This document provides guidelines for the treatment of dyslipidemia to reduce cardiovascular risk. It defines dyslipidemia as abnormal lipid levels measured in a blood sample. The guidelines classify risk based on LDL cholesterol, total cholesterol, and HDL cholesterol levels. They recommend screening adults over certain ages for lipid levels and cardiovascular risk. Risk is assessed using tools like the Framingham Risk Score. Treatment involves starting statin therapy, with the intensity based on a patient's risk category. Lifestyle changes and other medications may also be used. The guidelines aim to identify those who will benefit most from treatment to lower lipid levels and cardiovascular risk.
This document provides an overview of dyslipidemia including the physiology of lipid metabolism, the role of lipoproteins in atherosclerosis, screening and treatment approaches. It covers topics such as the exogenous and endogenous pathways of lipid metabolism, key enzymes involved, how lipids contribute to atherosclerosis, diagnostic evaluation, and management with an emphasis on statin therapy and other lipid-lowering drug classes and their mechanisms of action and side effects.
This document provides an overview of the management of dyslipidemia. It discusses lipoprotein classification and composition. It also outlines the non-pharmacological and pharmacological treatment approaches for different dyslipidemia scenarios, including various drug classes like statins, PCSK9 inhibitors, fibrates and their effects. It discusses treatment approaches for different patient groups such as those with cardiovascular disease, diabetes, chronic kidney disease, inflammatory conditions and others. The guidelines for screening and management of dyslipidemia in various clinical situations are summarized.
- The patient is a 50-year-old male smoker with hypertension for 6 years. His lipid profile shows a total cholesterol of 210 mg/dL, triglycerides of 180 mg/dL, LDL of 119 mg/dL, and HDL of 30 mg/dL.
- According to guidelines, he is at high cardiovascular risk due to smoking, hypertension, and lipid levels. Egypt is also considered a very high risk country.
- The appropriate measures for this high risk patient include lifestyle modifications plus high-intensity statin therapy, with an LDL cholesterol goal of less than 70 mg/dL. Monitoring is also needed.
Statin combinations aim to address residual cardiovascular risk from atherogenic dyslipidemia. While lowering LDL cholesterol is important, the number of lipoprotein particles is a stronger determinant of risk. Fibrates may help when triglycerides are high and HDL is low despite statins. Ezetimibe can lower LDL further when at maximum statin dose. Niacin reduces non-HDL cholesterol and Lp(a), but failed outcome trials question its benefit. Lifestyle changes and drugs like aspirin and clopidogrel may provide additional benefits when added to statins. Ongoing research evaluates new agents for refractory hypercholesterolemia and statin intolerance.
What’s new in Lipidology, Lessons from “recent guidelines“Arindam Pande
1. The 2018 ACC/AHA cholesterol guidelines provide 10 key take-home messages focusing on lifestyle management, statin therapy for various risk groups, and risk assessment approaches.
2. The guidelines emphasize lifestyle therapy and statins for secondary prevention, with an LDL-C goal of 70 mg/dL for very high risk patients to consider adding nonstatins.
3. They provide guidance on statin use for various primary prevention groups based on risk levels and discussion, including an expanded definition of intermediate risk factors.
This document outlines guidelines for screening and treating dyslipidemia. It discusses lipid handling in the body and pathophysiology of atherosclerosis. Current drug treatments include statins as first-line therapy, with bile acid sequestrants, nicotinic acid, fibrates, ezetimibe, and omega-3 fatty acids as alternatives. Newer drugs that inhibit PCSK9 are also mentioned. Treatment goals depend on risk level, with lifestyle changes recommended initially before adding drug therapy for higher risk patients.
1) Several early trials evaluated lipid lowering drugs such as mevastatin and lovastatin, which were isolated from fungi and shown to inhibit HMG CoA reductase. However, mevastatin was not marketed due to toxicity in dogs. Lovastatin was first marketed as Mevacor in 1987.
2) Large primary prevention trials such as WOSCOPS, AFCAPS/TexCAPS, CARDS and JUPITER demonstrated significant reductions in cardiovascular events with statin therapy compared to placebo in various populations with and without known heart disease.
3) Secondary prevention trials in patients with stable CAD such as 4S, CARE, LIPID and TNT showed that statin therapy reduces
This document discusses guidelines for treating diabetes and hypertension. It recommends that all diabetic patients have their blood pressure checked and receive non-pharmacological treatment. For those with BP above 140/90, single drug treatment should begin, while BP above 160/100 warrants two drugs. The preferred initial drugs are ACE inhibitors or ARB. Target blood pressure depends on cardiovascular risk factors. While cost is a consideration, affordable options exist like ACE/ARB plus thiazide diuretics or calcium channel blockers.
This document provides an overview of dyslipidemia including the physiology of lipid metabolism, the role of lipoproteins in atherosclerosis, screening and treatment approaches. It covers topics such as the exogenous and endogenous pathways of lipid metabolism, key enzymes involved, how lipids contribute to atherosclerosis, diagnostic evaluation, and management with an emphasis on statin therapy and other lipid-lowering drug classes and their mechanisms of action and side effects.
This document provides an overview of the management of dyslipidemia. It discusses lipoprotein classification and composition. It also outlines the non-pharmacological and pharmacological treatment approaches for different dyslipidemia scenarios, including various drug classes like statins, PCSK9 inhibitors, fibrates and their effects. It discusses treatment approaches for different patient groups such as those with cardiovascular disease, diabetes, chronic kidney disease, inflammatory conditions and others. The guidelines for screening and management of dyslipidemia in various clinical situations are summarized.
- The patient is a 50-year-old male smoker with hypertension for 6 years. His lipid profile shows a total cholesterol of 210 mg/dL, triglycerides of 180 mg/dL, LDL of 119 mg/dL, and HDL of 30 mg/dL.
- According to guidelines, he is at high cardiovascular risk due to smoking, hypertension, and lipid levels. Egypt is also considered a very high risk country.
- The appropriate measures for this high risk patient include lifestyle modifications plus high-intensity statin therapy, with an LDL cholesterol goal of less than 70 mg/dL. Monitoring is also needed.
Statin combinations aim to address residual cardiovascular risk from atherogenic dyslipidemia. While lowering LDL cholesterol is important, the number of lipoprotein particles is a stronger determinant of risk. Fibrates may help when triglycerides are high and HDL is low despite statins. Ezetimibe can lower LDL further when at maximum statin dose. Niacin reduces non-HDL cholesterol and Lp(a), but failed outcome trials question its benefit. Lifestyle changes and drugs like aspirin and clopidogrel may provide additional benefits when added to statins. Ongoing research evaluates new agents for refractory hypercholesterolemia and statin intolerance.
What’s new in Lipidology, Lessons from “recent guidelines“Arindam Pande
1. The 2018 ACC/AHA cholesterol guidelines provide 10 key take-home messages focusing on lifestyle management, statin therapy for various risk groups, and risk assessment approaches.
2. The guidelines emphasize lifestyle therapy and statins for secondary prevention, with an LDL-C goal of 70 mg/dL for very high risk patients to consider adding nonstatins.
3. They provide guidance on statin use for various primary prevention groups based on risk levels and discussion, including an expanded definition of intermediate risk factors.
This document outlines guidelines for screening and treating dyslipidemia. It discusses lipid handling in the body and pathophysiology of atherosclerosis. Current drug treatments include statins as first-line therapy, with bile acid sequestrants, nicotinic acid, fibrates, ezetimibe, and omega-3 fatty acids as alternatives. Newer drugs that inhibit PCSK9 are also mentioned. Treatment goals depend on risk level, with lifestyle changes recommended initially before adding drug therapy for higher risk patients.
1) Several early trials evaluated lipid lowering drugs such as mevastatin and lovastatin, which were isolated from fungi and shown to inhibit HMG CoA reductase. However, mevastatin was not marketed due to toxicity in dogs. Lovastatin was first marketed as Mevacor in 1987.
2) Large primary prevention trials such as WOSCOPS, AFCAPS/TexCAPS, CARDS and JUPITER demonstrated significant reductions in cardiovascular events with statin therapy compared to placebo in various populations with and without known heart disease.
3) Secondary prevention trials in patients with stable CAD such as 4S, CARE, LIPID and TNT showed that statin therapy reduces
This document discusses guidelines for treating diabetes and hypertension. It recommends that all diabetic patients have their blood pressure checked and receive non-pharmacological treatment. For those with BP above 140/90, single drug treatment should begin, while BP above 160/100 warrants two drugs. The preferred initial drugs are ACE inhibitors or ARB. Target blood pressure depends on cardiovascular risk factors. While cost is a consideration, affordable options exist like ACE/ARB plus thiazide diuretics or calcium channel blockers.
This document provides guidelines for the assessment and management of dyslipidemia from several major organizations. It discusses risk assessment tools for cardiovascular disease from ATP III, ADA, ACC/AHA, and QRISK2. It also compares statin intensity categories between NICE and ACC/AHA guidelines. The document recommends lifestyle modification as first-line treatment and the use of high-intensity statins for primary and secondary prevention of CVD according to the guidelines of NICE, ADA, and ACC/AHA.
El Prof. Alberico L. Catapano, profesor de Farmacología en la Facultad de Farmacia de la Universidad de Milán (Italia) y presidente de la European Atherosclerosis Society (EAS), participa en la sesión 'Nuevos enfoques y evidencias cone statinas en ECV y control lipídico', perteneciente a la 'Jornada Galáctica sobre Guías de Lípidos y objetivos a alcanzar en los pacientes de más alto riesgo cardiovascular' (Málaga, 4-5 abril, 2014).
Accede a la jornada completa en http://guiaslipidos.secardiologia.es
1) The patient has a 10.8% 10-year ASCVD risk, placing him in the intermediate risk category.
2) For patients in this category, guidelines recommend evaluating additional risk enhancers such as family history of premature CVD, metabolic syndrome, inflammation, and coronary artery calcium score.
3) Based on the assessment of risk enhancers, the guidelines recommend either moderate or high-intensity statin therapy.
This document provides guidelines for the management of dyslipidemia from the European Society of Cardiology in 2016. It discusses lipid profiling, total cardiovascular risk assessment, treatment strategies, lifestyle modifications, treatment targets, and choice of treatment. Lipid profiling is recommended for those with cardiovascular disease, at increased risk, or for risk stratification. LDL-C is the primary treatment target, while non-HDL-C and apoB are secondary targets. Lifestyle changes and statin therapy are first-line treatment, with fibrates, nicotinic acid or PCSK9 inhibitors as options for additional lowering of lipids. Guidelines for treatment targets and special populations are also covered.
Statins are highly effective LDL-c lowering agents that actually reduce clinical cardiovascular events. The 2013 ACC/AHA guidelines on the management of blood cholesterol recommend high-intensity statin therapy in individuals with high cardiovascular risk as assessed by the 10-year atherosclerotic cardiovascular disease risk calculator. However, a significant number of individuals do not tolerate or respond adequately to statins, and continue to have residual risk in spite of high intensity statin therapy.
There are some exciting developments in the field of lipidology. This decade has been labeled “The PCSK9 decade”. A new class of monoclonal antibodies directed against the PCSK9 glycoproteins appears very promising in further lowering LDL cholesterol and thereby cardiovascular risk. Evolocumab and alirucomab are novel PCSK9 inhibitors that can be given subcutaneously once or twice in a month, and have the potential to reduce LDL-cholesterol to very low levels without any major adverse effects.
Other classes of drugs like Apo-B antisense oligonucleotides (mipomersen), CETP inhibitors (especially anacetrapib), microsomal transfer protein inhibitors (lomitapide) also hold some promise. The future of lipid lowering therapy looks reassuring with these new developments.
Shashikiran Umakanth presented this at the Egyptian Association of Endocrinology, Diabetes & Atherosclerosis (EAEDA) 2014 conference at Alexandria, Egypt. This conference was help in association with Endocrine Society, USA and the European Association for the Study of Diabetes (EASD).
The document provides guidelines for cholesterol management and cardiovascular disease (CVD) risk assessment. It discusses guidelines for measuring cholesterol and lipid levels, calculating LDL and VLDL values, and assessing CVD risk. It recommends starting moderate- or high-intensity statin therapy for most adults aged 40-75 years with diabetes or LDL ≥70 mg/dL. For those without diabetes but with a CVD risk of 7.5% or higher, it recommends discussing statin therapy. The guidelines also provide recommendations for managing statin side effects, evaluating risk factors, and refining risk assessment using coronary artery calcium scoring. The main messages are to emphasize lifestyle changes, use high-intensity statins for high-risk patients, and consider patient risk
This document discusses guidelines for managing dyslipidemia with statins. It identifies 4 main groups that benefit from statin treatment based on their ASCVD risk: 1) those with clinical ASCVD, 2) those with LDL-C >190 mg/dL, 3) those with diabetes aged 40-75 with LDL-C 70-189 mg/dL, and 4) those aged 40-75 without clinical ASCVD or diabetes but with LDL-C 70-189 mg/dL and 10-year ASCVD risk >7.5%. The document reviews evidence that moderate- and high-intensity statin therapy lowers ASCVD risk across all baseline LDL-C levels above 70 mg/dL. It provides guidance on
This document provides guidelines and recommendations for lipid management:
1. It summarizes the 2013 ACC/AHA guidelines and 2016 ACC expert consensus, focusing on proven therapy rather than arbitrary lipid targets. Lifestyle changes like diet and exercise are encouraged for all.
2. Statins are recommended for four major groups to reduce ASCVD risk. High, moderate, and low intensity statin therapies are defined based on average LDL-C reduction.
3. For patients who are truly statin intolerant or require additional lowering, the document provides guidance on use of non-statin therapies like ezetimibe, basing selection on risk level and comorbidities.
The document provides guidelines for the practical management of dyslipidemia and drug resistant dyslipidemia. It discusses identifying risk factors to guide personalized therapy, assessing cardiovascular risk, screening recommendations for different populations, lipid tests to perform, and the approach to management for different patient groups including those with ASCVD, undergoing PCI, with diabetes, chronic kidney disease, or statin intolerance. It recommends statins, especially atorvastatin, for secondary prevention in ASCVD patients based on landmark trials showing reductions in cardiovascular events.
- Early initiation of high-intensity statin therapy in acute coronary syndrome patients significantly reduces mortality and morbidity rates compared to later initiation or lower-intensity statins. Clinical trials found a 16-36% reduction in major coronary events with early high-dose statin use.
- Guidelines recommend high-intensity statins like atorvastatin 80mg or simvastatin 80mg for acute coronary syndrome patients, though risks like side effects must be considered. Long-term statin therapy is also generally advised after acute coronary syndrome.
LDL Cholesterol Target :“ Lower the Better ”Arindam Pande
Lowering LDL cholesterol provides significant cardiovascular benefits and reduces risk, even in those with low baseline LDL levels or who achieve very low LDL levels with treatment. While residual risk remains even with intensive statin therapy to lower LDL well below current target levels, risk continues to decrease as LDL is further lowered. The lower the achieved LDL level, the lower the long-term risk of major cardiovascular events and atherosclerotic progression.
1) Statins are highly effective in reducing LDL-C and cardiovascular risk, playing a cornerstone role in lipid management. They work by inhibiting HMG-CoA reductase.
2) Atorvastatin has been extensively studied in large trials and shown to significantly reduce major cardiovascular events when doses are increased from 10 mg to 80 mg.
3) Studies in India found that high dose atorvastatin (80 mg) was well tolerated and more effective at reducing LDL-C and hs-CRP than lower doses in ACS patients. However, many ACS patients in India were not receiving statins as recommended.
This document summarizes clinical guidelines for cholesterol management and cardiovascular risk reduction. It compares the 2013 ACC/AHA guidelines to previous NCEP ATP III guidelines. The new guidelines have a focus on reducing atherosclerotic cardiovascular disease risk rather than just coronary heart disease risk. They recommend high-intensity statin therapy for more patient groups based on revised risk assessment categories and calculators. Key changes include expanding statin benefit to those with diabetes or a 7.5% or higher 10-year risk without cardiovascular disease. Management of high triglycerides is also discussed.
#flozins
🫀DAPA 🆚placebo in HFpEF
Now we have a positive trial!
⬇️18% in CV☠️ death or
worsening HF among LVEF>40%
⬇️ 21%heart failure
💥Results same for LVEF> 60% 🆚LVEF<60%
SGLT-2 inhibitors have shown promising cardiovascular and renal benefits:
1) Trials have found SGLT-2 inhibitors reduce the risk of cardiovascular death in patients with type 2 diabetes and established cardiovascular disease, as well as reducing heart failure hospitalizations in those with diabetes and cardiovascular risk factors.
2) Studies also show SGLT-2 inhibitors improve outcomes for patients with heart failure with reduced ejection fraction, reducing rates of heart failure hospitalization and mortality regardless of diabetes status or background heart failure therapies.
3) SGLT-2 inhibitors were also found to reduce the risk of renal death or progression to end-stage kidney disease in patients with type 2 diabetes and macroalbuminuria.
Dyslipidemia management an evidence based approachDr Vivek Baliga
In this presentation by Dr Vivek Baliga, he discusses the different available statins and how you can choose the right one in different clinical situations. See articles from Dr Baliga on http://drvivekbaliga.net
Ponencia realizada por el Prof. Alberto Zambon en la segunda sesión de CardioVascular Virtual Topic 2022, titulada Residual cardiovascular risk. What is the role of icosapent ethyl?
Dyslipidemia and Management of Dyslipidemia | Muhammad-Nizam-UddinMuhammad Nizam Uddin
Dyslipidemia and it's management is such a topic that one single PPT is not enough to express all sorts of problems or scopes. This PPT will give you an overview on "Dyslipidemia and it's management"
This document provides guidelines for the practice of treating dyslipidemia. It defines dyslipidemia as abnormal lipid levels measured in a blood sample, which can include hypercholesterolemia, low HDL levels, or hypertriglyceridemia. The document discusses various classification systems for different lipid levels and cardiovascular risk factors. It recommends screening and treatment approaches based on a patient's risk level as assessed by tools like the Pooled Cohort Equation or UKPDS risk engine. Key treatment involves starting statin therapy matched to a patient's risk level and potential side effects. The document also provides guidance on screening for familial hypercholesterolemia.
This document discusses cardiovascular disease (CVD) prevention and treatment goals for dyslipidemia. It notes that CVD is a leading cause of death in Europe and prevention is important. The importance of lifestyle modifications and controlling risk factors like lipids and blood pressure is emphasized. Treatment goals for low-density lipoprotein cholesterol (LDL-C) are personalized based on a patient's risk level, ranging from less than 130 mg/dL for low risk to less than 55 mg/dL for extreme risk. Additional goals for high-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, apolipoproteins, and triglycerides are provided. Compliance with statin therapy is important for achieving benefits.
This document provides guidelines for the assessment and management of dyslipidemia from several major organizations. It discusses risk assessment tools for cardiovascular disease from ATP III, ADA, ACC/AHA, and QRISK2. It also compares statin intensity categories between NICE and ACC/AHA guidelines. The document recommends lifestyle modification as first-line treatment and the use of high-intensity statins for primary and secondary prevention of CVD according to the guidelines of NICE, ADA, and ACC/AHA.
El Prof. Alberico L. Catapano, profesor de Farmacología en la Facultad de Farmacia de la Universidad de Milán (Italia) y presidente de la European Atherosclerosis Society (EAS), participa en la sesión 'Nuevos enfoques y evidencias cone statinas en ECV y control lipídico', perteneciente a la 'Jornada Galáctica sobre Guías de Lípidos y objetivos a alcanzar en los pacientes de más alto riesgo cardiovascular' (Málaga, 4-5 abril, 2014).
Accede a la jornada completa en http://guiaslipidos.secardiologia.es
1) The patient has a 10.8% 10-year ASCVD risk, placing him in the intermediate risk category.
2) For patients in this category, guidelines recommend evaluating additional risk enhancers such as family history of premature CVD, metabolic syndrome, inflammation, and coronary artery calcium score.
3) Based on the assessment of risk enhancers, the guidelines recommend either moderate or high-intensity statin therapy.
This document provides guidelines for the management of dyslipidemia from the European Society of Cardiology in 2016. It discusses lipid profiling, total cardiovascular risk assessment, treatment strategies, lifestyle modifications, treatment targets, and choice of treatment. Lipid profiling is recommended for those with cardiovascular disease, at increased risk, or for risk stratification. LDL-C is the primary treatment target, while non-HDL-C and apoB are secondary targets. Lifestyle changes and statin therapy are first-line treatment, with fibrates, nicotinic acid or PCSK9 inhibitors as options for additional lowering of lipids. Guidelines for treatment targets and special populations are also covered.
Statins are highly effective LDL-c lowering agents that actually reduce clinical cardiovascular events. The 2013 ACC/AHA guidelines on the management of blood cholesterol recommend high-intensity statin therapy in individuals with high cardiovascular risk as assessed by the 10-year atherosclerotic cardiovascular disease risk calculator. However, a significant number of individuals do not tolerate or respond adequately to statins, and continue to have residual risk in spite of high intensity statin therapy.
There are some exciting developments in the field of lipidology. This decade has been labeled “The PCSK9 decade”. A new class of monoclonal antibodies directed against the PCSK9 glycoproteins appears very promising in further lowering LDL cholesterol and thereby cardiovascular risk. Evolocumab and alirucomab are novel PCSK9 inhibitors that can be given subcutaneously once or twice in a month, and have the potential to reduce LDL-cholesterol to very low levels without any major adverse effects.
Other classes of drugs like Apo-B antisense oligonucleotides (mipomersen), CETP inhibitors (especially anacetrapib), microsomal transfer protein inhibitors (lomitapide) also hold some promise. The future of lipid lowering therapy looks reassuring with these new developments.
Shashikiran Umakanth presented this at the Egyptian Association of Endocrinology, Diabetes & Atherosclerosis (EAEDA) 2014 conference at Alexandria, Egypt. This conference was help in association with Endocrine Society, USA and the European Association for the Study of Diabetes (EASD).
The document provides guidelines for cholesterol management and cardiovascular disease (CVD) risk assessment. It discusses guidelines for measuring cholesterol and lipid levels, calculating LDL and VLDL values, and assessing CVD risk. It recommends starting moderate- or high-intensity statin therapy for most adults aged 40-75 years with diabetes or LDL ≥70 mg/dL. For those without diabetes but with a CVD risk of 7.5% or higher, it recommends discussing statin therapy. The guidelines also provide recommendations for managing statin side effects, evaluating risk factors, and refining risk assessment using coronary artery calcium scoring. The main messages are to emphasize lifestyle changes, use high-intensity statins for high-risk patients, and consider patient risk
This document discusses guidelines for managing dyslipidemia with statins. It identifies 4 main groups that benefit from statin treatment based on their ASCVD risk: 1) those with clinical ASCVD, 2) those with LDL-C >190 mg/dL, 3) those with diabetes aged 40-75 with LDL-C 70-189 mg/dL, and 4) those aged 40-75 without clinical ASCVD or diabetes but with LDL-C 70-189 mg/dL and 10-year ASCVD risk >7.5%. The document reviews evidence that moderate- and high-intensity statin therapy lowers ASCVD risk across all baseline LDL-C levels above 70 mg/dL. It provides guidance on
This document provides guidelines and recommendations for lipid management:
1. It summarizes the 2013 ACC/AHA guidelines and 2016 ACC expert consensus, focusing on proven therapy rather than arbitrary lipid targets. Lifestyle changes like diet and exercise are encouraged for all.
2. Statins are recommended for four major groups to reduce ASCVD risk. High, moderate, and low intensity statin therapies are defined based on average LDL-C reduction.
3. For patients who are truly statin intolerant or require additional lowering, the document provides guidance on use of non-statin therapies like ezetimibe, basing selection on risk level and comorbidities.
The document provides guidelines for the practical management of dyslipidemia and drug resistant dyslipidemia. It discusses identifying risk factors to guide personalized therapy, assessing cardiovascular risk, screening recommendations for different populations, lipid tests to perform, and the approach to management for different patient groups including those with ASCVD, undergoing PCI, with diabetes, chronic kidney disease, or statin intolerance. It recommends statins, especially atorvastatin, for secondary prevention in ASCVD patients based on landmark trials showing reductions in cardiovascular events.
- Early initiation of high-intensity statin therapy in acute coronary syndrome patients significantly reduces mortality and morbidity rates compared to later initiation or lower-intensity statins. Clinical trials found a 16-36% reduction in major coronary events with early high-dose statin use.
- Guidelines recommend high-intensity statins like atorvastatin 80mg or simvastatin 80mg for acute coronary syndrome patients, though risks like side effects must be considered. Long-term statin therapy is also generally advised after acute coronary syndrome.
LDL Cholesterol Target :“ Lower the Better ”Arindam Pande
Lowering LDL cholesterol provides significant cardiovascular benefits and reduces risk, even in those with low baseline LDL levels or who achieve very low LDL levels with treatment. While residual risk remains even with intensive statin therapy to lower LDL well below current target levels, risk continues to decrease as LDL is further lowered. The lower the achieved LDL level, the lower the long-term risk of major cardiovascular events and atherosclerotic progression.
1) Statins are highly effective in reducing LDL-C and cardiovascular risk, playing a cornerstone role in lipid management. They work by inhibiting HMG-CoA reductase.
2) Atorvastatin has been extensively studied in large trials and shown to significantly reduce major cardiovascular events when doses are increased from 10 mg to 80 mg.
3) Studies in India found that high dose atorvastatin (80 mg) was well tolerated and more effective at reducing LDL-C and hs-CRP than lower doses in ACS patients. However, many ACS patients in India were not receiving statins as recommended.
This document summarizes clinical guidelines for cholesterol management and cardiovascular risk reduction. It compares the 2013 ACC/AHA guidelines to previous NCEP ATP III guidelines. The new guidelines have a focus on reducing atherosclerotic cardiovascular disease risk rather than just coronary heart disease risk. They recommend high-intensity statin therapy for more patient groups based on revised risk assessment categories and calculators. Key changes include expanding statin benefit to those with diabetes or a 7.5% or higher 10-year risk without cardiovascular disease. Management of high triglycerides is also discussed.
#flozins
🫀DAPA 🆚placebo in HFpEF
Now we have a positive trial!
⬇️18% in CV☠️ death or
worsening HF among LVEF>40%
⬇️ 21%heart failure
💥Results same for LVEF> 60% 🆚LVEF<60%
SGLT-2 inhibitors have shown promising cardiovascular and renal benefits:
1) Trials have found SGLT-2 inhibitors reduce the risk of cardiovascular death in patients with type 2 diabetes and established cardiovascular disease, as well as reducing heart failure hospitalizations in those with diabetes and cardiovascular risk factors.
2) Studies also show SGLT-2 inhibitors improve outcomes for patients with heart failure with reduced ejection fraction, reducing rates of heart failure hospitalization and mortality regardless of diabetes status or background heart failure therapies.
3) SGLT-2 inhibitors were also found to reduce the risk of renal death or progression to end-stage kidney disease in patients with type 2 diabetes and macroalbuminuria.
Dyslipidemia management an evidence based approachDr Vivek Baliga
In this presentation by Dr Vivek Baliga, he discusses the different available statins and how you can choose the right one in different clinical situations. See articles from Dr Baliga on http://drvivekbaliga.net
Ponencia realizada por el Prof. Alberto Zambon en la segunda sesión de CardioVascular Virtual Topic 2022, titulada Residual cardiovascular risk. What is the role of icosapent ethyl?
Dyslipidemia and Management of Dyslipidemia | Muhammad-Nizam-UddinMuhammad Nizam Uddin
Dyslipidemia and it's management is such a topic that one single PPT is not enough to express all sorts of problems or scopes. This PPT will give you an overview on "Dyslipidemia and it's management"
This document provides guidelines for the practice of treating dyslipidemia. It defines dyslipidemia as abnormal lipid levels measured in a blood sample, which can include hypercholesterolemia, low HDL levels, or hypertriglyceridemia. The document discusses various classification systems for different lipid levels and cardiovascular risk factors. It recommends screening and treatment approaches based on a patient's risk level as assessed by tools like the Pooled Cohort Equation or UKPDS risk engine. Key treatment involves starting statin therapy matched to a patient's risk level and potential side effects. The document also provides guidance on screening for familial hypercholesterolemia.
This document discusses cardiovascular disease (CVD) prevention and treatment goals for dyslipidemia. It notes that CVD is a leading cause of death in Europe and prevention is important. The importance of lifestyle modifications and controlling risk factors like lipids and blood pressure is emphasized. Treatment goals for low-density lipoprotein cholesterol (LDL-C) are personalized based on a patient's risk level, ranging from less than 130 mg/dL for low risk to less than 55 mg/dL for extreme risk. Additional goals for high-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, apolipoproteins, and triglycerides are provided. Compliance with statin therapy is important for achieving benefits.
The American Heart Association and American College of Cardiology, in partnership with the National Heart, Lung and Blood Institute, have released new joint guidelines on cardiovascular disease prevention focusing on hyperlipidemia, hypertension, cardiovascular risk assessment, lifestyle interventions, and obesity. The guidelines provide recommendations on screening and treating dyslipidemia and cardiovascular risk through lifestyle modifications like diet, exercise, weight loss and smoking cessation as well as pharmacological interventions including statin therapy. The guidelines stratify treatment approaches based on levels of cardiovascular risk and recommend high or moderate intensity statins for primary and secondary prevention.
2. prof. bambang irawan cv assessment in met s and t2dm [compatibility mode]yoga buana
This document summarizes guidelines from several organizations on cardiovascular assessment and management of risk factors for patients with metabolic syndrome and diabetes. The guidelines address:
1) Definitions of metabolic syndrome from organizations like WHO, NCEP ATP III, IDF which include criteria like waist circumference, blood pressure, lipids, and glucose.
2) Cardiovascular risk assessment recommendations including considering patients with diabetes as high risk and using risk scores.
3) Management strategies focusing on lifestyle changes and treating multiple risk factors like dyslipidemia, hypertension, and hyperglycemia to reduce cardiovascular risk.
The guidelines provide recommendations for screening, risk assessment, treatment goals, and management of dyslipidemia to prevent cardiovascular disease. Key points include screening adults based on age and risk factors, using LDL-C and other lipid levels to determine risk stratification and treatment goals, and employing lifestyle changes and pharmacologic therapies like statins and fibrates to manage lipid levels and reduce risk. The guidelines aim to optimize dyslipidemia treatment to lower cardiovascular disease risk.
This document provides an overview of diabetic dyslipidemia and lipid management recommendations for patients with diabetes. It discusses that excess fat contributes to atherosclerosis and mortality in diabetes. It outlines traditional and non-traditional risk factors for cardiovascular disease. The spectrum of diabetic dyslipidemia includes quantitative changes like high triglycerides and qualitative changes in lipoprotein composition. Lifestyle modifications and statin therapy are recommended to improve lipid profiles and reduce cardiovascular risk according to guidelines. The appropriate screening, interpretation of results, and intensity of statin therapy depends on individual patient risk factors and characteristics.
This patient presents with multiple metabolic risk factors including obesity, elevated triglycerides and fasting blood glucose, and a family history of diabetes. While she does not meet the criteria for metabolic syndrome, her 10-year risk of heart disease is elevated. Her LDL cholesterol goal according to NCEP guidelines is less than 160 mg/dL. Fasting glucose would be most influential in determining her treatment plan given her risk factors.
Dyslipidemia, specially high LDL cholesterol is the key risk factor for cardiovascular diseases. The presentation discusses metabolism and structure of lipoproteins, their screening and interpretation, risk assessment methods, targets for various lipoproteins and its step by step treatment.
This document discusses cardiovascular risk reduction strategies for a patient with type 2 diabetes and a strong family history of cardiovascular disease. It reviews the cardiovascular safety data of various anti-diabetic medications and recommends intensifying treatment to achieve an A1C less than 7%, blood pressure lower than 130/80 mmHg, high-intensity statin therapy, and aspirin. For this patient's secondary prevention, drugs like liraglutide, empagliflozin, canagliflozin, and pioglitazone that have demonstrated cardiovascular benefits in clinical trials are preferable additions to metformin over sulfonylureas. While these newer anti-diabetic drugs have robust evidence for secondary prevention, data for their use in
Diabetic patients are at high risk for cardiovascular disease due to dyslipidemia and should be treated aggressively to target lipid levels. Lifestyle modifications such as diet, exercise, and weight management are first-line treatment along with statin therapy. Statins should be prescribed to diabetic patients over age 40 with one or more other cardiovascular risk factors, or to those of any age with existing cardiovascular disease, to reduce LDL cholesterol. The main treatment goals are lowering LDL cholesterol to less than 100 mg/dL for patients without cardiovascular disease and less than 70 mg/dL for those with cardiovascular disease.
Lipid-lowering therapy should be considered for primary prevention in asymptomatic healthy individuals based on their estimated 10-year risk of cardiovascular disease. Several risk assessment models can stratify individuals into low, moderate, or high risk categories. For those at high risk, lipid-lowering drugs may be recommended to reduce cholesterol and prevent future heart attacks and strokes. Monitoring of lipids, liver and muscle enzymes is important before and during treatment to check for side effects.
Targeting lipids: a primary and secondary care perspectiveInnovation Agency
Presentations by Dr Sue Kemsley and Dr Gavin Galasko from the first webinar of the Mastering Cholesterol webinar series on Thursday 26 January 2023, focusing on lipid management from a primary and secondary care perspective.
The document discusses the National Programme for Prevention and Control of Cancer, Diabetes, Cardiovascular Disease and Stroke (NPCDCS) in India. It notes that non-communicable diseases are emerging as a leading cause of death in India. The NPCDCS was initiated in 2010 to prevent and control common NCDs through lifestyle changes, early diagnosis, treatment, and capacity building. The program aims to reduce mortality from heart disease, stroke, cancer and other NCDs. It operates in 100 districts across 21 states using strategies like health promotion, screening, affordable diagnosis and treatment, and monitoring/evaluation.
This document provides an introduction and overview of dyslipidemia. It begins by defining dyslipidemia as lipid abnormalities involving elevated total cholesterol, LDL-C, triglycerides or low HDL-C. It then discusses why dyslipidemia is an important risk factor for cardiovascular disease. The document outlines how to measure lipids and classify different types of dyslipidemia. It emphasizes assessing global cardiovascular risk and provides details on risk stratification using tools like the Framingham Risk Score. The summary concludes by stating management of dyslipidemia should be based on a patient's global cardiovascular risk level.
This document discusses dyslipidemia, including its epidemiology, classification, diagnosis, screening, and management. Some key points:
- Dyslipidemia is characterized by abnormal lipid levels and contributes to atherosclerosis. It can be primary or secondary.
- The prevalence of dyslipidemia in Saudi Arabia ranges from 20-44% according to studies.
- Diagnosis involves measuring lipid levels through a serum profile. Treatment involves lifestyle changes and lipid-lowering drugs like statins.
- Statins are beneficial for both primary and secondary prevention of cardiovascular disease according to clinical trials. Guidelines recommend statin use for those with specific risk factors.
This document summarizes guidelines for cholesterol treatment and clinical trials evaluating lipid targets. It discusses the ATP III guidelines, major trials after ATP III including TNT, JUPITER, ACCORD-LIPID, and AIM-HIGH. It then reviews the 2013 ACC/AHA cholesterol treatment guidelines, including the 4 groups that benefit from statins, ASCVD risk assessment, and future directions. Clinical cases are used to illustrate guideline recommendations for statin treatment based on a patient's risk factors.
Dyslipidemia GL & Total Vascular Benefit .pptxWidiHadian3
1) New guidelines from the European Society of Cardiology/European Atherosclerosis Society classify patients into very high, high, moderate, and low risk categories for cardiovascular disease based on factors like documented atherosclerotic disease, diabetes, kidney disease, and risk scores.
2) Treatment targets for LDL-C levels are more aggressive, with goals of less than 1.4 mmol/L for very high risk patients, less than 1.8 mmol/L for high risk, and less than 2.6 mmol/L for moderate risk.
3) The guidelines recommend high-intensity statins as first-line therapy, then adding ezetimibe or PCSK9 inhibitors if goals are not
This document discusses a case of multiple endocrine neoplasia type 1 (MEN1) in a 46-year-old female patient and her brother. The patient presented with symptoms of hypoglycemia and was found to have hyperparathyroidism, a pituitary adenoma, and insulinomas. Genetic testing confirmed a MEN1 gene mutation. Her brother also had features of MEN1 including acromegaly, hyperparathyroidism, and insulinomas. MEN1 is a rare genetic disorder characterized by tumors of the parathyroid glands, anterior pituitary, and pancreatic islet cells. Early detection of MEN1-associated tumors through genetic screening and biochemical monitoring of at-risk family members
This document discusses drug-induced liver injury (DILI). It begins by stating that multiple drugs can cause hepatotoxicity through various mechanisms. It then discusses the epidemiology of DILI, noting that its worldwide annual incidence is estimated between 1.3 to 19.1 per 100,000 exposed individuals. The document outlines the pathogenesis, clinical presentation, diagnosis, classification, histology, and management of DILI. Regarding histology, it describes various patterns of injury that can be seen such as hepatocellular necrosis, cholestasis, steatosis, and sinusoidal obstruction syndrome. The primary treatment for DILI is withdrawal of the causative drug, with specific therapies for certain cases like
1) Aortic stenosis is a narrowing of the aortic valve that obstructs blood flow from the left ventricle to the aorta.
2) The most common presenting symptoms are dyspnea on exertion, exertional dizziness, and exertional angina, reflecting the stiff left ventricle's inability to increase cardiac output during exercise.
3) On examination, the carotid pulse is weak and slow rising, and a crescendo-decrescendo murmur is best heard at the right upper sternal border when leaning forward.
This document discusses drug overdoses, including definitions, common drugs involved, risk factors, evaluation and treatment. It notes that overdoses can be intentional or accidental and are a major cause of morbidity and mortality worldwide. The most common drugs involved in overdoses are opioid analgesics and benzodiazepines. Men ages 45-49 have the highest death rates. Evaluation involves assessing vital signs and mental status while treatment focuses on stabilization, supportive care, prevention of further exposure, and administration of antidotes if available.
Scorpion stings, especially from the Indian red scorpion, are a major public health problem in tropical countries. The venom causes an autonomic storm that can lead to hypertension, pulmonary edema, hypotension and shock. Early symptoms include local pain, vomiting, sweating and priapism. Delayed treatment can result in high morbidity and mortality. Management involves fluid resuscitation, prazosin to block alpha receptors, vasodilators, antivenom and intensive care as needed for pulmonary edema or hypotension. Prevention focuses on reducing places scorpions may hide and using pesticides in endemic areas.
This document discusses acute HIV infection and CDC criteria for diagnosis. It defines acute HIV infection as occurring within approximately six months of infection. Symptoms may include fever, lymphadenopathy, sore throat, rash, and others nonspecific symptoms. Diagnosis is made by detecting HIV RNA during the window period before antibodies develop or with a positive combination antigen/antibody test and negative antibody-only test. Early diagnosis is important for individual treatment and reducing transmission.
head ache dizziness and sphincter disturbance s.pptxSruthi Meenaxshi
This document discusses several topics related to sensory disturbances:
1) It describes the anatomy of the sensory system and how sensations are transmitted from receptors to the central nervous system.
2) It defines different types of sensory loss or disturbances like hypoesthesia, anesthesia, hypalgesia, and hyperpathia.
3) It outlines how to perform a sensory examination to localize lesions, including testing touch, proprioception, vibration, temperature, and pain. Higher cortical sensations can also be examined.
Inflammatory Bowel Disease (IBD) represents a spectrum of chronic inflammatory conditions of the digestive tract including Ulcerative Colitis and Crohn's Disease. IBD is caused by an inappropriate immune response to intestinal bacteria in genetically predisposed individuals. Symptoms include diarrhea, abdominal pain, and weight loss. Treatment involves medications to reduce inflammation like aminosalicylates, corticosteroids, immunosuppressants, and biologics that target tumor necrosis factor-alpha. The goals of treatment are to induce and maintain remission of symptoms and prevent disease complications.
1. Premature ventricular contractions are early occurring, widened QRS complexes originating from the left or right ventricle that have a distinct morphology different from the normal sinus rhythm.
2. Ventricular tachycardia is defined as three or more successive ventricular complexes at a rate greater than 100 beats per minute and shows atrioventricular dissociation.
3. Ventricular fibrillation is identified by the complete absence of properly formed QRS complexes and P waves, with irregular ventricular activation above 300 beats per minute leading to cardiac arrest.
Digoxin toxicity can cause various arrhythmias due to its effects on intracellular calcium levels and vagal tone. Life-threatening arrhythmias may occur at plasma digoxin levels above 2.0 ng/mL. Hypokalemia and age over 65 increase toxicity risk. Symptoms include ectopic atrial tachycardia with block, various forms of AV block, and junctional rhythms. Distinguishing features between arrhythmias is important for appropriate treatment.
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/ARVC) is a genetic heart condition characterized by structural abnormalities and fatty infiltration of the right ventricle, leading to ventricular arrhythmias and sudden cardiac death. It is a common cause of sudden cardiac death in young athletes. Clinical features include palpitations, syncope, chest pain, and dyspnea. Diagnosis relies on a combination of ECG findings, echocardiogram abnormalities of the right ventricle, and genetic testing.
Left ventricular noncompaction (LVNC) is a heart muscle disorder characterized by excessive trabeculations and deep recesses in the left ventricle. It is diagnosed using echocardiography or cardiac MRI based on specific criteria. Symptoms vary and include heart failure, arrhythmias, and thromboembolic events like stroke. The cause involves abnormal heart muscle development during fetal life. Genetic factors are involved in some cases. Treatment focuses on managing symptoms and complications. Prognosis depends on the severity of symptoms and complications.
Vector borne diseases recent concepts in management and elimination targets...Sruthi Meenaxshi
This document discusses vector-borne diseases and strategies for their management and elimination. It begins by stating that vector-borne diseases account for 17% of infectious diseases globally, with malaria being the main contributor. Vectors transmit diseases between humans or animals. Vector management aims to optimize control and reduce incidence. Mosquitoes transmit diseases like malaria, dengue, chikungunya, Japanese encephalitis, and lymphatic filariasis. The National Vector Borne Disease Control Program integrates control of these diseases. Malaria elimination targets aim for transmission interruption in certain states by 2020 and nationwide by 2030. Integrated vector control includes insecticide spraying, bed nets, and source reduction.
This document discusses atrial septal defect (ASD) closure procedures. It describes that ASDs are often asymptomatic until adulthood but can lead to complications if left untreated. Preprocedural assessment includes echocardiography and additional imaging if needed. Surgical closure is preferred for primum, sinus venosus, and coronary sinus defects. Percutaneous closure is an alternative to surgery for secundum ASDs of appropriate size and anatomy. Percutaneous closure has comparable efficacy to surgery but shorter hospital stays and fewer complications. Complications of percutaneous closure include device embolization, arrhythmias, and erosion.
Echocardiography is the main tool for evaluating prosthetic heart valves. Transthoracic echocardiography (TTE) is generally used to assess normal valve function and identify dysfunction like stenosis or regurgitation. Transesophageal echocardiography (TEE) provides better imaging of valve structure and is helpful for evaluating regurgitation and complications like endocarditis. Echocardiograms establish a baseline after valve implantation and monitor for issues like pannus, thrombus, infection or degeneration over time. TTE and TEE are complementary, with TEE used when TTE is inadequate or clinical suspicion remains after a TTE.
Ventricular septal defects (VSDs) are openings in the wall separating the ventricles of the heart. There are four main types classified by location: membranous, muscular, supracristal, and inlet VSDs. Echocardiography is useful for diagnosing VSDs and assessing their characteristics like location, size, and impact on cardiac function. VSDs range from small and asymptomatic to large defects causing heart failure or pulmonary hypertension. Surgical or catheter-based closure may be required for large VSDs.
A 45 year old woman presented with shortness of breath on exertion. Echocardiography showed an atrial septal defect (ASD). ASDs are congenital heart defects where the wall separating the left and right atria is incomplete. The most common type is secundum ASD, which accounts for 70-75% of cases. ASDs allow blood to shunt from the left to the right atrium, overloading the right heart and lungs over time if not repaired. Echocardiography is the primary test to diagnose ASDs.
Echocardiography plays a key role in the diagnosis and management of infective endocarditis. It can identify valvular vegetations, abscesses, fistulas and other complications. The presence of an oscillating intracardiac mass or abscess on valves or endocardial surfaces are major echocardiographic criteria for the diagnosis. Transesophageal echocardiography is recommended if transthoracic is nondiagnostic or for complications. Follow up echos are important to monitor vegetation size with treatment and check for complications. Differentiating infective vegetations from other intracardiac masses or artifacts is important.
This document discusses different types of atrioventricular (AV) block and their classification. It describes:
- First, second, and third degree AV blocks, as well as high-grade block. Second degree block is further divided into Mobitz type I (Wenckebach) and type II.
- Etiologies of AV block.
- Class I indications for pacemaker placement, which include complete AV block and various types of symptomatic second degree block.
- Examples of ECGs demonstrating Wenckebach phenomenon, Mobitz type II block, complete heart block with and without myocardial infarction. Causes like muscular dystrophy are also discussed.
Pictorial and detailed description of patellar instability with sign and symptoms and how to diagnose , what investigations you should go with and how to approach with treatment options . I have presented this slide in my 2nd year junior residency in orthopedics at LLRM medical college Meerut and got good reviews for it
After getting it read you will definitely understand the topic.
PGx Analysis in VarSeq: A User’s PerspectiveGolden Helix
Since our release of the PGx capabilities in VarSeq, we’ve had a few months to gather some insights from various use cases. Some users approach PGx workflows by means of array genotyping or what seems to be a growing trend of adding the star allele calling to the existing NGS pipeline for whole genome data. Luckily, both approaches are supported with the VarSeq software platform. The genotyping method being used will also dictate what the scope of the tertiary analysis will be. For example, are your PGx reports a standalone pipeline or would your lab’s goal be to handle a dual-purpose workflow and report on PGx + Diagnostic findings.
The purpose of this webcast is to:
Discuss and demonstrate the approaches with array and NGS genotyping methods for star allele calling to prep for downstream analysis.
Following genotyping, explore alternative tertiary workflow concepts in VarSeq to handle PGx reporting.
Moreover, we will include insights users will need to consider when validating their PGx workflow for all possible star alleles and options you have for automating your PGx analysis for large number of samples. Please join us for a session dedicated to the application of star allele genotyping and subsequent PGx workflows in our VarSeq software.
NAVIGATING THE HORIZONS OF TIME LAPSE EMBRYO MONITORING.pdfRahul Sen
Time-lapse embryo monitoring is an advanced imaging technique used in IVF to continuously observe embryo development. It captures high-resolution images at regular intervals, allowing embryologists to select the most viable embryos for transfer based on detailed growth patterns. This technology enhances embryo selection, potentially increasing pregnancy success rates.
Giloy in Ayurveda - Classical Categorization and SynonymsPlanet Ayurveda
Giloy, also known as Guduchi or Amrita in classical Ayurvedic texts, is a revered herb renowned for its myriad health benefits. It is categorized as a Rasayana, meaning it has rejuvenating properties that enhance vitality and longevity. Giloy is celebrated for its ability to boost the immune system, detoxify the body, and promote overall wellness. Its anti-inflammatory, antipyretic, and antioxidant properties make it a staple in managing conditions like fever, diabetes, and stress. The versatility and efficacy of Giloy in supporting health naturally highlight its importance in Ayurveda. At Planet Ayurveda, we provide a comprehensive range of health services and 100% herbal supplements that harness the power of natural ingredients like Giloy. Our products are globally available and affordable, ensuring that everyone can benefit from the ancient wisdom of Ayurveda. If you or your loved ones are dealing with health issues, contact Planet Ayurveda at 01725214040 to book an online video consultation with our professional doctors. Let us help you achieve optimal health and wellness naturally.
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdfOsvaldo Bernardo Muchanga
GASTROINTESTINAL INFECTIONS AND GASTRITIS
Osvaldo Bernardo Muchanga
Gastrointestinal Infections
GASTROINTESTINAL INFECTIONS result from the ingestion of pathogens that cause infections at the level of this tract, generally being transmitted by food, water and hands contaminated by microorganisms such as E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter, Staphylococcus, Rotavirus among others that are generally contained in feces, thus configuring a FECAL-ORAL type of transmission.
Among the factors that lead to the occurrence of gastrointestinal infections are the hygienic and sanitary deficiencies that characterize our markets and other places where raw or cooked food is sold, poor environmental sanitation in communities, deficiencies in water treatment (or in the process of its plumbing), risky hygienic-sanitary habits (not washing hands after major and/or minor needs), among others.
These are generally consequences (signs and symptoms) resulting from gastrointestinal infections: diarrhea, vomiting, fever and malaise, among others.
The treatment consists of replacing lost liquids and electrolytes (drinking drinking water and other recommended liquids, including consumption of juicy fruits such as papayas, apples, pears, among others that contain water in their composition).
To prevent this, it is necessary to promote health education, improve the hygienic-sanitary conditions of markets and communities in general as a way of promoting, preserving and prolonging PUBLIC HEALTH.
Gastritis and Gastric Health
Gastric Health is one of the most relevant concerns in human health, with gastrointestinal infections being among the main illnesses that affect humans.
Among gastric problems, we have GASTRITIS AND GASTRIC ULCERS as the main public health problems. Gastritis and gastric ulcers normally result from inflammation and corrosion of the walls of the stomach (gastric mucosa) and are generally associated (caused) by the bacterium Helicobacter pylor, which, according to the literature, this bacterium settles on these walls (of the stomach) and starts to release urease that ends up altering the normal pH of the stomach (acid), which leads to inflammation and corrosion of the mucous membranes and consequent gastritis or ulcers, respectively.
In addition to bacterial infections, gastritis and gastric ulcers are associated with several factors, with emphasis on prolonged fasting, chemical substances including drugs, alcohol, foods with strong seasonings including chilli, which ends up causing inflammation of the stomach walls and/or corrosion. of the same, resulting in the appearance of wounds and consequent gastritis or ulcers, respectively.
Among patients with gastritis and/or ulcers, one of the dilemmas is associated with the foods to consume in order to minimize the sensation of pain and discomfort.
“Psychiatry and the Humanities”: An Innovative Course at the University of Mo...Université de Montréal
“Psychiatry and the Humanities”: An Innovative Course at the University of Montreal Expanding the medical model to embrace the humanities. Link: https://www.psychiatrictimes.com/view/-psychiatry-and-the-humanities-an-innovative-course-at-the-university-of-montreal
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Are you looking for a long-lasting solution to your missing tooth?
Dental implants are the most common type of method for replacing the missing tooth. Unlike dentures or bridges, implants are surgically placed in the jawbone. In layman’s terms, a dental implant is similar to the natural root of the tooth. It offers a stable foundation for the artificial tooth giving it the look, feel, and function similar to the natural tooth.
How to Control Your Asthma Tips by gokuldas hospital.Gokuldas Hospital
Respiratory issues like asthma are the most sensitive issue that is affecting millions worldwide. It hampers the daily activities leaving the body tired and breathless.
The key to a good grip on asthma is proper knowledge and management strategies. Understanding the patient-specific symptoms and carving out an effective treatment likewise is the best way to keep asthma under control.
2. Dyslipidemia – Definition
• is, quite simply “abnormal lipid levels”, as
measured on a blood sample and which
reflects one of several disorders in the
metabolism of lipoproteins. It may be
classified as:
• hypercholesterolemia
• low levels of High Density Lipoproteins (HDL)
• hypertriglyceridemia
3. ATP III Classification
LDL cholesterol
<100 Optimal
100-129 Near optimal/above
optimal
130-159 Borderline high
160-189 high
>190 Very high
Total cholestrol
<200
200-239
>240
HDL cholestrol
>40
>60
Desirable
Borderline high
High
Low
high
12. Question 1
41 yo M evaluated in PCP appointment. He is
healthy with no symptoms, is sedentary and
obese. PMH and FHx non-contributory. He does
not smoke, drink, or use illicit drugs. He takes no
meds. On exam, BP 132/82, HR 80, and BMI 32.
Labs show total cholesterol 251, LDL 172, HDL
35, TG 220, HbA1c 5%.
Estimated 10 year risk for ASCVD is 3.4%
13. Which of the following is the most appropriate
management of this patient’s hyperlipidemia?
A: Ezetimibe
B: High-intensity rosuvastatin
C: Moderate intensity rosuvastatin
D. Niacin
E: Therapeutic Lifestyle modification
14. Question 2
80 yo M was hospitalized for a 5 day history of
acute leg ischemia treated with angioplasty and
stenting. Now asymptomatic. PMH significant
for CKD stage III and HTN on diltiazem, lisinopril,
ASA and plavix. Exam is normal.
Labs: AST 20, Total cholesterol 170, LDL 97, HDL
44, Cr. 1.8, TG 147 and GFR 35
15. Question 2
Which of the following is the most appropriate
therapy for secondary prevention of
cardiovascular disease in this patient?
A: High intensity rosuvastatin
B: Moderate intensity rousvastatin
C: Niacin
D: No additional Treatment
16. Question 3
48 yo M evaluated during follow up appointment. 3
months ago, he had a STEMI and underwent PCI
with bare metal stent of Left circumflex artery. He
was started on high intensity rosuvastatin at the
time. LFT’s normal and Cr level was normal. He is
now asymptomatic, no chest pain or muscle
pain.His meds are aspirin, metoprolol, lisinopril,
rosuvastatin, and plavix.
Exam and vitals normal. No muscle or abdominal
tenderness.
17. Question 3
Which of the following is the most appropriate
laboratory study to obtain at this visit?
A: Alanine aminotransferase level
B: Creatine Kinase Level
C: Fasting Lipid Panel
D. High sensitivity C-reactive protein level
18. Introduction
• Treatment of dyslipidemia is a cornerstone of
preventive cardiology, and reduction in low-
density lipoprotein (LDL-C) in select
populations reduces risk of atherosclerotic
cardiovascular disease (ASCVD) events in both
primary and secondary prevention.
19. Current Major Lipid Treatment
guidelines
1. 2014 American College of Cardiology/American Health Association
(ACC/AHA),4
2. 2014 U.S. Veterans Affairs/Department of Defense (VA-DoD).9
3. 2016 Canadian Cardiovascular Society (CCS),5
4. 2016 European Society of Cardiology/European Atherosclerosis
Society (ESC/EAS),6
5. 2016 US Preventive Services Task Force (USPSTF),7,8
6. 2017, American Association of Clinical Endocrinologist (AACE)
Examining differences between dyslipidemia guidelines can help
identify areas requiring further research and also potential
opportunities for harmonization of guidelines.
20. Lipid guidelines
• Previous ATP III (Adult Treatment Panel III)
looked at LDL goals in combination with
patient’s risk.
• Current ACC/AHA does not focus on pure lab
values, but on overall atherosclerotic
cardiovascular risk disease
21. Who should be tested ??
• USPSTF recommends screening:
– Men: >35yo
– Women: >45yo at increased increased risk
– Increased risk is defined as having: diabetes, CHD, family history of CHD in males <50yo and in
females <60yo, smokers, HTN, obesity
• All patients aged 40-79 years old should have their
10year risk for ASCVD using Pooled Cohort Equation
• Of note, European Federation of Clinical Chemistry and
Laboratory Medicine recommended in April 2016 non-
fasting measurements in most patients.
26. Who needs treatment?
• Group1: Clinical ASCVD
– ACS, history of MI, angina, stroke, TIA, PAD
• Group2: LDL >190
– Rule out secondary causes
• Group 3: All Diabetics without clinical ASCVD
– 40-75yo with LDL 70-189mg/dL
• Group 4: 10 year ASCVD risk >7.5%
– with LDL 70-189mg/dL
27. Management
• Start statin
– Select appropriate dose
for patient
– Keep potential side effects
and drug interactions in
mind
– If high/moderate intensity
not tolerate, use max
dose tolerated
28. • Intensity of Statin:
– Established ASCVD
• Age > 75 moderate intensity statin
• Age <75 high intensity statin
– LDL cholesterol >190mg/dL
• High intensity statin
– Diabetes 40-75yo w/LDL 70-189mg/dL and no ASCVD
• ASCVD 10 year risk >7.5% high intensity statin
• ASCVD 10 year risk < 7.5% moderate intensity statin
– No ASCVD or DM, but 10 year ASCVD > 7.5%
– Moderate to high intensity statin
– Adults >76 yo w/o history of ASCVD
• Insufficient evidence to recommend for/against statins
29.
30.
31.
32. The risk of ASCVD and ASCVD-related mortality is substantially greater in
the presence of multiple risk factors. Since epidemiologic evidence indicates
that ASCVD risk factors frequently cluster, it should be expected that many
individuals have multiple risk factors.
Recommendations associated with this question:
What are the risk factors for ASCVD ?
R1. Identify risk factors that enable personalized and optimal therapy for
dyslipidemia. (Grade A; BEL 1).
Abbreviation: ASCVD, atherosclerotic cardiovascular disease.
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497
33. Major Atherosclerotic Cardiovascular
Disease Risk Factors
Abbreviations: apo, apolipoprotein; ASCVD, atherosclerotic cardiovascular disease; HDL-C, high-density lipoprotein cholesterol;
hsCRP, highly sensitive C-reactive protein; LDL, low-density lipoprotein; LDL-C, low-density lipoprotein cholesterol; Lp-PLA2,
lipoprotein-associated phospholipase; PCOS, polycystic ovary syndrome.
AACE POSWC. Endocr Pract. 2005;11:126-134; ADA. Diabetes Care. 2017;40(Suppl 1):S1-S135; Brunzell JD, et al. Diabetes
Care.2008;31:811-822; Cromwell WC, et al. J Clin Lipidol. 2007;1:583-592;
MAJOR RISK FACTORS ADDITIONAL RISK FACTORS NON TRADITIONAL RISK
FACTORS
Advancing age
Increased Total Serum
cholesterol level
Increased Non HDL – C
Increased LDL – C
Low HDL –C
Diabetes Mellitus
Hypertension
Stage 3 or 4 chronic kidney
disease
Cigarette smoking
Family history of ASCVD
Obesity , abdominal
obesity
Family history of
hyperlipidemia
Increased small , dense
LDL-C
Increased APO – B
Increased LDL particle
concentration
Fasting / Postprandial
Hypertriglyceridemia
PCOS
Increased Lipoprotein (a)
Increased Clotting factors
Increased inflammation
markers (hs- CRP , LP-
PLA2)
Increased homocysteine
Apo E4 isoform
Increased uric acid
Increased Tgrich remnants
34. How can be the risk assessed?
R4. The 10-year risk of a coronary event (high, intermediate, or low)
should be determined by detailed assessment using one or more of the
following tools (Grade C; BEL 4, upgraded due to cost-effectiveness):
• Framingham Risk Assessment Tool
• MESA 10-year ASCVD Risk with Coronary Artery Calcification Calculator
• Reynolds Risk Score, which includes hsCRP and family history of premature ASCVD
• UKPDS risk engine to calculate ASCVD risk in individuals with T2DM
R7. When the HDL-C concentration is greater than 60 mg/dL, one risk
factor should be subtracted from an individual’s overall risk profile (Grade
B; BEL 2).
• R8. A classification of elevated TG should be incorporated into risk assessments to aid in
treatment decisions (Grade B; BEL 2).
Abbreviations: ASCVD, atherosclerotic cardiovascular disease; HDL-C, high-density lipoprotein cholesterol; hsCRP, high-sensitivity CRP;
MESA, Multi-Ethnic Study of Atherosclerosis; T2DM, type 2 diabetes mellitus; TG, triglycerides
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
39. ASCVD Risk Categories
• Low risk:
– No risk factors
• Moderate risk:
– 2 or fewer risk factors and a calculated 10-
year risk of less than 10%
• High risk:
– An ASCVD equivalent including diabetes
or stage 3 or 4 CKD with no other risk
factors, or individuals with 2 or more risk
factors and a 10-year risk of 10%-20%
• Very high risk:
– Established or recent hospitalization for
ACS; coronary, carotid or peripheral
vascular disease; diabetes or stage 3 or 4
CKD with 1 or more risk factors; a
calculated 10-year risk greater than 20%;
or HeFH
• Extreme risk:
– Progressive ASCVD, including unstable
angina that persists after achieving an
LDL-C less than 70 mg/dL, or established
clinical ASCVD with diabetes, stage 3 or 4
CKD, and/or HeFH, or in those with a
history of premature ASCVD (<55 years
of age for males or <65 years of age for
females)
– This category was added in this CPG based
on clinical trial evidence and supported by
meta-analyses that further lowering of
LDL-C produces better outcomes in
individuals with ACS. IMPROVE-IT
demonstrated lower rates of
cardiovascular events in those with ACS
when LDL-C levels were lowered to 53
mg/dL combining ezetimibe with statins.
Abbreviations: ACS, acute coronary syndrome; ASCVD, atherosclerotic cardiovascular disease; CKD, chronic kidney disease; CPG, clinical practice guideline; HeFH,
heterozygous familial hypercholesterolemia; LDL-C, low-density lipoprotein cholesterol; IMPROVE-IT, Improved Reduction of Outcomes: Vytorin Efficacy
International Trial.
AACE/ACE CPG. 2017;epub ahead of print; Cannon, CP, et al. N Engl J Med. 2015;372(25):2387-239; Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice.
2017;23(4):479-497.
40. Who should be screened and when ?
Familial Hypercholesterolemia
• R9. Individuals should be screened for FH when there is a family
history of:
• Premature ASCVD (definite MI or sudden death before age 55 years
in father or other male first-degree relative or before age 65 years
in mother or other female first-degree relative) or
• Elevated cholesterol levels (total, non-HDL, and/or LDL) consistent
with FH (Grade C; BEL 4, upgraded due to cost-effectiveness).
Adults With Diabetes
• R10. Annually screen all adult individuals with T1DM or T2DM for
dyslipidemia (Grade B; BEL 2).
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-
497
41. Who should be screened and when ?
Young Adults (Men Aged 20-45 Years, Women Aged 20-55 Years)
• R11. Evaluate all adults 20 years of age or older for dyslipidemia every 5
years as part of a global risk assessment (Grade C; BEL 4, upgraded due
to cost-effectiveness).
Middle-Aged Adults (Men Aged 45-65 Years, Women Aged 55-65
Years)
• R12. In the absence of ASCVD risk factors, screen middle-aged individuals for
dyslipidemia at least once every 1 to 2 years. More frequent lipid testing is
recommended when multiple global ASCVD risk factors are present (Grade A; BEL 1).
• R13. The frequency of lipid testing should be based on individual clinical circumstances
and the clinician’s best judgment (Grade C; BEL 4, upgraded due to cost-effectiveness).
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice.
2017;23(4):479-497
42. • R14. Annually screen older adults with 0 to 1
ASCVD risk factor for dyslipidemia (Grade A; BEL
1).
• R15. Older adults should undergo lipid
assessment if they have multiple ASCVD global
risk factors (i.e., other than age) (Grade C; BEL 4,
upgraded due to cost-effectiveness).
• R16. Screening for this group is based on age and
risk, but not gender; therefore, older women
should be screened in the same way as older men
(Grade A; BEL 1).
Older Adults (Older Than 65 Years)
43. Whom to screen ?
*Men younger than 55 years and women younger than 65 years of age in first-degree relative. BMI, body
mass index.
44. How to screen ?
ApoB, apolipoprotein B; eGFR, estimated glomerular filtration rate; HDL-C,high-density lipoprotein cholesterol; LDL-C, low-
density lipoprotein cholesterol; TC, total cholesterol; TG, triglycerides
45. Familial Hypercholesterolemia:
Diagnosis
• FH diagnostic criteria include lipid levels and family history, physical
symptoms (if any), and genetic analysis (if available)1
• Three clinical diagnostic tools:2-3
• Simon Broome Register Diagnostic Criteria
• Dutch Lipid Clinic Network Diagnostic Criteria
• U.S. MEDPED
• Factors that lead to an FH diagnosis include:
• Premature ASCVD, fasting LDL-C >190 mg/dL, the presence of tendon
xanthomas, full corneal arcus in individuals <40 years of age, or a family
history of high cholesterol and/or premature ASCVD1
• While genetic testing may identify FH, it is not commonly used in the
United States due to cost and lack of payer coverage1
Abbreviations: ASCVD, atherosclerotic cardiovascular disease; FH, familial hypercholesterolemia; LDL-C, low-density lipoprotein
cholesterol; MEDPED, Make Early Diagnoses Prevent Early Deaths Program Diagnostic Criteria.
1. Bouhairie VE, et al. Cardiol Clin. 2015;33:169-179; 2. Haralambos K, et al. Curr Opin Lipidol. 2016;27:367-374; 3. Turgeon RD, et al.
Can Fam Physician. 2016;62:32-37.
46. Familial Hypercholesterolemia:
Prevalence and Risk
• FH is caused by genetic mutations passed on by:
• One parent (heterozygous, HeFH)1
• Both parents (homozygous, HoFH)1
• HoFH prevalence ranges from 1 in 160,000 to 1 in 250,0002,3
• Individuals with HoFH have extremely high LDL-C levels (>500 mg/dL) and premature CV risk4
• Many with HoFH experience their first coronary event in childhood or adolescence4
• HeFH prevalence ranges from 1 in 200 to 1 in 2503
• Individuals with HeFH can present with LDL-C levels 90 to 500
mg/dL and have premature CV risk4
• On average, individuals with HeFH experience their first
coronary event at age 42 (about 20 years younger than the
general population)4
• Early treatment is recommended for all individuals with FH, with a
goal of reducing LDL-C levels by 50% from baseline3
Abbreviations: CV, cerebrovascular; FH, familial hypercholesterolemia; HeFH, heterozygous familial hypercholesterolemia; HoFH, homozygous familial
hypercholesterolemia; LDL-C, low-density lipoprotein cholesterol.
1. Zimmerman MP. Am Health Drug Benefits. 2015;8:436-442; 2. Goldstein J, et al. The Metabolic and Molecular Bases of Inherited Disease. 7th ed. New
York, NY: McGraw-Hill; 1995: 1981-2030; 3. Bouhairie VE, et al. Cardiol Clin. 2015;33:169-179; 4. Turgeon RD, et al. Can Fam Physician. 2016;62:32-37.
47. Which screening tests should be
used?
Fasting Lipid Profile
• R19. Use a fasting lipid profile to ensure the most precise lipid assessment; this should
include total cholesterol, LDL-C, TG, and non-HDL-C (Grade C; BEL 4, upgraded due to cost-
effectiveness).
• R20. Lipids, including TG, can be measured in the non-fasting state if fasting determinations
are impractical (Grade D).
LDL-C
• R21. LDL-C may be estimated using the Friedewald equation: LDL-C = (total cholesterol –
HDL-C) – TG/5; however, this method is valid only for values obtained during the fasting state
and becomes increasingly inaccurate when TG levels are greater than 200 mg/dL, and
becomes invalid when TG levels are greater than 400 mg/dL (Grade C; BEL 3).
• R22. LDL-C should be directly measured in certain high-risk individuals, such as those with
fasting TG levels greater than 250 mg/dL or those with diabetes or known vascular disease
(Grade C; BEL 3).
HDL-C
• R23. Measurement of HDL-C should be included in screening tests for
dyslipidemia (Grade B; BEL 2).
Abbreviations: HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TG, triglycerides.
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
48. Which screening tests should be
used?
Non-HDL-C
• R24. Non-HDL-C (total cholesterol minus HDL-C) should be calculated to assist risk
stratification in individuals with moderately elevated TG (200 to 500 mg/dL), diabetes,
and/or established ASCVD (Grade B; BEL 2).
• R25. If insulin resistance is suspected, non-HDL-C should be evaluated to gain useful
information regarding the individual’s total atherogenic lipoprotein burden (Grade D).
Triglycerides
• R26. TG levels should be part of routine lipid screening: moderate elevations (≥150 mg/dL)
may identify individuals at risk for insulin resistance syndrome and levels ≥200 mg/dL may
identify individuals at substantially increased ASCVD risk (Grade B; BEL 2).
Apolipoproteins
• R27. Apo B and/or an apo B/apo A1 ratio calculation and evaluation may be useful in at-risk
individuals (TG ≥150, HDL-C <40, prior ASCVD event, T2DM, and/or insulin resistance
syndrome [even at target LDL-C levels]) to assess residual risk and guide decision-making
(Grade A; BEL 1).
• R28. Apo B measurements (reflecting the particle concentration of LDL and all
other atherogenic lipoproteins) may be useful to assess the success of
LDL-C–lowering therapy (Grade A; BEL 1).
Abbreviations: apo, apolipoprotein; ASCVD, atherosclerotic cardiovascular disease; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-
density lipoprotein cholesterol; T2DM, type 2 diabetes mellitus; TG, triglycerides.
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497
49. Additional screening test
Coronary artery
calcification
• R33. Coronary
artery
calcification
measurement
has been shown
to be of high
predictive value
and is useful in
refining risk
stratification to
determine the
need for more
aggressive
treatment
strategies (Grade
B; BEL 2).
hsCRP
• R30. Use hsCRP
to stratify ASCVD
risk in individuals
with a standard
risk assessment
that is borderline,
or in those with
an intermediate
or higher risk
with an LDL-C
concentration
less than 130
mg/dL (Grade B;
BEL 2).
Lp-PLA2
• R31. Measure
lipoprotein-
associated
phospholipase A2
(Lp-PLA2), which
in some studies
has
demonstrated
more specificity
than hsCRP, when
it is necessary to
further stratify an
individual’s
ASCVD risk,
especially in the
presence of
hsCRP elevations
(Grade A; BEL 1).
Homocysteine
• R32. The routine
measurement of
homocysteine,
uric acid,
plasminogen
activator
inhibitor-1, or
other
inflammatory
markers is not
recommended
because the
benefit of doing
so is not
sufficiently
proven (Grade
D).
Carotid intima
media thickness
• R34. Carotid
intima media
thickness may be
considered to
refine risk
stratification to
determine
the need for
more aggressive
ASCVD
preventive
strategies (Grade
B; BEL 2).
Abbreviations: apo, apolipoprotein; ASCVD, atherosclerotic cardiovascular disease; HDL-C, high-density lipoprotein cholesterol; LDL-C,
low-density lipoprotein cholesterol; T2DM, type 2 diabetes mellitus; TG, triglycerides.
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497
50. •R5. Special attention should be given to assessing women for ASCVD risk by determining the
10-year risk (high, intermediate, or low) of a coronary event using the Reynolds Risk Score or
the Framingham (Grade C; BEL 4, upgraded due to cost-effectiveness).
Risk Assessment
•R72. Women should be evaluated for their ASCVD risk and be treated with pharmacotherapy if
lifestyle intervention is insufficient (Grade C; BEL 4; upgraded due to potential benefit).
•R73. Hormone replacement therapy for the treatment of dyslipidemia in postmenopausal
women is not recommended (Grade A; BEL 1).
•An HDL-C concentration <40 mg/dL is an established independent risk factor for ASCVD in both
men and women. However, because HDL-C levels tend to be higher in women than in men, an
HDL-C concentration <50 mg/dL in women is also considered a marginal risk factor.
•In stark contrast to findings in men, very low HDL-C (<40 mg/dL) is an independent risk factor
for ASCVD development and mortality in women, even in the presence of total cholesterol
concentrations less than 200 mg/dL or normal LDL-C and/or TG levels. Compared with women
with high HDL-C, women with low HDL-C have a nearly 3-fold elevated risk of ASCVD.
Treatment options
What special consideration should be given for women ?
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497
52. What are lipid treatment goals?
R35. Treatment goals for dyslipidemia should be personalized according to
levels of risk (Grade A; BEL 1).
R36. For individuals at low risk (i.e., with no risk factors), an LDL-C goal of
less than 130 mg/dL is recommended (Grade A; BEL 1).
R37. For individuals at moderate risk (i.e., with 2 or fewer risk factors and a
calculated 10-year risk of less than 10%), an LDL-C goal of less than 100
mg/dL is recommended (Grade A; BEL 1).
R38. For individuals at high risk (i.e., with an ASCVD equivalent including diabetes or
stage 3 or 4 CKD with no other risk factors, or individuals with 2 or more risk factors
and a 10-year risk of 10%-20%), an LDL-C goal of less than 100 mg/dL is
recommended (Grade A; BEL 1).
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
53. R39. For individuals at very high risk (i.e., with established or recent
hospitalization for ACS; coronary, carotid or peripheral vascular disease; diabetes
or stage 3 or 4 CKD with 1 or more risk factors; a calculated 10-year risk greater
than 20%; or HeFH), an LDL-C goal of less than 70 mg/dL is recommended (Grade
A; BEL 1).
R40. For individuals at extreme risk (i.e., with progressive ASCVD, including unstable
angina that persists after achieving an LDL-C less than 70 mg/dL, or established clinical
ASCVD in individuals with diabetes, stage 3 or 4 CKD, and/or HeFH, or in individuals
with a history of premature ASCVD (<55 years of age for males or <65 years of age for
females), an LDL-C goal of less than 55 mg/dL is recommended (Grade A; BEL 1).
R41. An LDL-C goal of <100 mg/dL is considered “acceptable” for children and
adolescents, with 100 to 129 mg/dL considered “borderline” and 130 mg/dL or
greater considered “high” (based on recommendations from the American
Academy of Pediatrics) (Grade D).
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
54. High-Density Lipoprotein Cholesterol
•R42. HDL-C should be greater than 40 mg/dL, but also as high as possible, primarily through the use of
lifestyle interventions (e.g., weight loss, physical activity, and tobacco cessation), and if risk factors are
present (e.g., borderline elevated LDL-C levels, a family history of premature ASCVD, or a personal
history of ASCVD), also through the use of pharmacotherapy primarily focused on reducing LDL-C
(Grade A; BEL 1).
Non–High-Density Lipoprotein Cholesterol
•R43. For most individuals, a non–HDL-C goal (total cholesterol minus HDL-C) 30 mg/dL higher than the
individual’s specific LDL-C goal is recommended (Grade D).
•R44. For individuals at extreme risk, a non-HDL-C goal 25 mg/dL higher than the individual-specific
LDL-C goal is recommended (Grade A; BEL 1).
Apolipoproteins
•R45. For individuals at increased risk of ASCVD, including those with diabetes, an optimal apo B goal is
less than 90 mg/dL, while for individuals with established ASCVD or diabetes plus 1 or more additional
risk factor(s), an optimal apo B goal is less than 80 mg/dL, and for individuals at extreme risk, an
optimal apo B goal is less than 70 mg/dL (Grade A; BEL 1).
Triglycerides
•R46. TG goals of less than 150mg/dL are recommended (Grade A; BEL 1).
55. Treatment goals
AACE/ACE 2017;epub ahead of print; Baigent C, et al. Lancet. 2010;376:1670-1681; Boekholdt SM, et al. J Am Coll Cardiol. 2014;64(5):485-494;
Brunzell JD, et al. Diabetes Care. 2008;31:811-822; Cannon CP, et al. N Engl J Med. 2015;372(25):2387-2397; Heart Protection Study
Collaborative
Group. Lancet. 2002;360:7-22; Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497; Ridker PM, J Am Coll Cardiol.
2005;45:1644-1648; Sever PS, et al. Lancet. 2003;361:1149-1158; Shepherd J, et al. Lancet. 2002;360:1623-1630; Weiner DE, et al. J Am Soc
Nephrol. 2004;15(5):1307-1315.
56. TREATMENT GOALS
Barter PJ, et al. J Intern Med. 2006;259:247-258; Boekholdt SM, et al. J Am Coll Cardiol. 2014;64(5):485-494; Brunzell JD, et al. Diabetes Care. 2008;31:811-822;
Cannon CP, et al. N Engl J Med. 2015;372(25):2387-2397; Grundy SM, et al. Circulation. 2004;110:227-239; Heart Protection Study Collaborative Group. Lancet.
2002;360:7-22; Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497; Lloyd-Jones DM, et al. Am J Cardiol. 2004;94:20-24; McClelland RL,
et al. J Am Coll Cardiol. 2015;66(15):1643-1653; NHLBI. NIH Publication No. 02-5215. 2002; Ridker PM, J Am Coll Cardiol. 2005;45:1644-1648; Ridker PM, et al. JAMA.
2007;297(6):611-619; Sever PS, et al. Lancet. 2003;361:1149-1158; Shepherd J, et al. Lancet. 2002;360:1623-1630; Smith SC Jr, et al. Circulation. 2006;113:2363-2372;
Stevens RJ, et al. Clin Sci. 2001;101(6):671-679; Stone NJ. Am J Med. 1996;101:4A40S-48S; Weiner DE, et al. J Am Soc Nephrol. 2004;15(5):1307-1315.
57. CLASSIFICATION OF ELEVATED
TRIGLYCERIDE LEVELS
Einhorn D, et al. Endocr Pract. 2003;9:237-252; Frick MH, et al. NEJM. 1987;317:1237-1245; Jellinger P,
Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497; Keech A, et al. Lancet. 2005;366:1849-
1861; NHLBI. NIH Publication No. 02-5215. 2002; Tenaknen L, et al. Arch Intern Med. 2006;166:743-748.
TG levels that are even moderately elevated (≥150 mg/dL) may identify
individuals at risk for the insulin resistance syndrome. TG levels ≥200 mg/dL
may indicate a substantial increase in ASCVD risk. Hypertriglyceridemia is
also commonly associated with a procoagulant state and hypertension.
58. What treatments are available for
dyslipidemia?
Treatment categories for dyslipidemia:
– Lifestyle changes
• Physical activity
• Medical nutrition therapy
• Smoking cessation
– Pharmacologic therapy
• Statins
• Fibrates
• Omega-3 fish oil
• Niacin
• Bile acid sequestrants
• Cholesterol absorption inhibitors
• PCSK9 inhibitors
• MTP inhibitor
• Antisense apo B oligonucleotide
• Combination therapies
Abbreviations: apo, apolipoprotein; MTP, microsomal transfer protein;
PCSK9, proprotein convertase subtilisin/kexin type 9.
59. Non pharmacological lipid treatment
Physical Activity
• R48. A reasonable and feasible approach to fitness therapy (i.e., exercise programs that include at least 30 minutes of
moderate-intensity physical activity [consuming 4-7 kcal/min] 4 to 6 times weekly, with an expenditure of at least 200
kcal/day) is recommended; suggested activities include brisk walking, riding a stationary bike, water aerobics,
cleaning/scrubbing, mowing the lawn, and sporting activities (Grade A; BEL 1).
• R49. Daily physical activity goals can be met in a single session or in multiple sessions throughout the course of a day (10
minutes minimum per session); for some individuals, breaking activity up throughout the day may help improve adherence
with physical activity programs (Grade A; BEL 1).
• R50. In addition to aerobic activity, muscle-strengthening activity is recommended at least 2 days a week (Grade A; BEL 1).
Medical Nutrition Therapy
• R51. For adults, a reduced-calorie diet consisting of fruits and vegetables (combined ≥5 servings/day), grains (primarily whole
grains), fish, and lean meats is recommended (Grade A; BEL 1).
• R52. For adults, the intake of saturated fats, trans-fats, and cholesterol should be limited, while LDL-C-lowering
macronutrient intake should include plant stanols/sterols (~2 g/ day) and soluble fiber (10-25 g/day) (Grade A; BEL 1).
• R53. Primary preventive nutrition consisting of healthy lifestyle habits is recommended in all healthy children (Grade A; BEL
1).
Smoking Cessation
• R54. Tobacco cessation should be strongly encouraged and facilitated (Grade A; BEL 2; upgraded due to potential benefit).
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497
60. Statins, Fibrates
Statins
• R56. Statin therapy is recommended as the primary pharmacologic agent to achieve target LDL-C goals on the basis
of morbidity and mortality outcome trials (Grade A; BEL 1).
• R57. For clinical decision making, mild elevations in blood glucose levels and/or an increased risk of new-onset
T2DM associated with intensive statin therapy do not outweigh the benefits of statin therapy for ASCVD risk
reduction (Grade A, BEL 1).
• R58. In individuals within high-risk and very high-risk categories, further lowering of LDL-C beyond established
targets with statins results in additional ASCVD event reduction and may be considered (Grade A, BEL 1).
• R59. Very high-risk individuals with established coronary, carotid, and peripheral vascular disease, or diabetes, who
also have at least 1 additional risk factor, should be treated with statins to target a reduced LDL-C treatment goal of
<70 mg/dL (Grade A, BEL 1).
• R60. Extreme risk individuals should be treated with statins or with combination therapy to target an even lower
LDL-C treatment goal of <55 mg/dL (Grade A, BEL 1).
Fibrates
• R61. Fibrates should be used to treat severe hypertriglyceridemia (TG >500 mg/dL) (Grade A; BEL 1).
• R62. Fibrates may improve ASCVD outcomes in primary and secondary prevention when
TG concentrations are 200 mg/dL and HDL-C concentrations <40 mg/dL (Grade A; BEL 1).
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497
61. Statin
Main Considerations
• Liver function test prior to therapy and as clinically indicated thereafter
• Myalgias and muscle weakness in some individuals
• Potential for drug-drug interaction between some statins and CYP450 3A4 inhibitors,
cyclosporine, warfarin, and protease inhibitors
• Myopathy/rhabdomyolysis in rare cases; increased risk with coadministration of some drugs
(see product labeling)
• Simvastatin dosages should not exceed 40 mg in most individuals; dosages of 80 mg are no
longer recommended except in those who have tolerated 80 mg for 12 months or more
without muscle toxicity
• Do not exceed 20 mg simvastatin daily with amlodipine or ranolazine
• Plasma elevations of rosuvastatin may be higher among Asian persons than other ethnic
groups
• New-onset diabetes is increased in individuals treated with statins; however, it is dose-
related, occurs primarily in individuals with MetS, appears to be less common with
pravastatin and possibly pitavastatin, and occurs overall to a lesser extent than the associated
decrease in ASCVD
Metabolic Effects
• Primarily ↓ LDL-C 21%-55% by competitively inhibiting rate-limiting step of cholesterol
synthesis in the liver, leading to upregulation of hepatic LDL receptors
• Effects on TG and HDL-C are less pronounced (↓ TG 6%-30% and ↑ HDL-C 2%-10%)
Bissonnette S, et al. Can J Cardiol. 2006;22:1035-1044; Denke M, et al. Diab Vasc Dis Res. 2006;3:93-102; Jellinger P,
Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497; Preiss D, et al. JAMA. 2011;305: 2556-2564
62. Statin and dosages
Agent
Usual recommended
starting daily dosage
Dosage range
Method of
administration
Statins
Lovastatin 20 mg 10-80 mg Oral
Pravastatin 40 mg 10-80 mg Oral
Simvastatin 20-40 mg 5-80 mga Oral
Fluvastatin 40 mg 20-80 mg Oral
Atorvastatin 10-20 mg 10-80 mg Oral
Rosuvastatin 10 mg 5-40 mg Oral
Pitavastatin 2 mg 2-4 mg Oral
Simvastatin, 80 mg, not approved for therapy unless individual has been on
treatment for more than 1 year without myopathy.
Crestor (rosuvastatin calcium); [PI]; 2016; Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497; Lescol
(fluvastatin sodium) [PI]; 2012 Lipitor (atorvastatin calcium) [PI]; 2015; Livalo (pitavastatin) [PI]; 2013; ; Mevacor (lovastatin) [PI];
2014; Pravachol (pravastatin sodium) [PI]; 2016; Zocor (simvastatin) [PI]; 2015.
63. Fibrates
Metabolic Effects:
• Primarily ↓ TG 20%-35%, ↑ HDL-C 6%-18% by stimulating lipoprotein lipase activity
• Fenofibrate may ↓ TC and LDL-C 20%-25%
• Lower VLDL-C and LDL-C; reciprocal rise in LDL-C transforms the profile into a less
atherogenic form by shifting fewer LDL particles to larger size
• Fenofibrate ↓ fibrinogen level
Abbreviations: HDL-C, high-density lipoprotein cholesterol; LDL, low-density lipoprotein, LDL-C, low-density lipoprotein cholesterol; TC, total
cholesterol; TG, triglycerides; VLDL-C, very low-density lipoprotein cholesterol.
Aguilar-Salinas CA, et al. Metabolism. 2001;50:729-733; Athyros VG, et al. Coron Artery Dis. 1995;6:25-1256; Avellone G, et al. Blood Coagul
Fibrinolysis. 1995;6:543-548; Bröijersen A, et al. Arterioscler Thromb Vasc Biol. 1996;16:511-516; Bröijersén A, et al. Thromb Haemost.
1996;76:171-176; Davidson MH, et al. Am J Cardiol. 2007;99:3C-18C; Farnier M, et al. Eur Heart J. 2005;26:897-905; Guyton JR, et al. Arch
Intern Med. 2000;160:1177-1184; Hottelart C, et al. Nephron. 2002;92:536-541; Insua A, et al. Endocr Pract. 2002;8:96-101; Jellinger P,
Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497; Kockx M, et al. Thromb Haemost. 1997;78:1167-1172; Lopid
(gemfibrozil) [PI] 2010; McKenney JM, et al. J Am Coll Cardiol. 2006;47:1584-1587; Syvänne M, et al. Atherosclerosis. 2004;172:267-272;
Tricor (fenofibrate) [PI]; 2010; Trilipix (fenofibric acid) [PI]; 2016; Westphal S, et al. Lancet. 2001; 358:39-40.
64. Fibrates metabolic effects and main
consideration
Main Considerations:
Gemfibrozil may ↑ LDL-C 10%-15%
GI symptoms, possible cholelithiasis
May potentiate effects of orally administered anticoagulants
Gemfibrozil may ↑ fibrinogen level
Gemfibrozil and fenofibrate can ↑ homocysteine independent of vitamin
concentrations
May cause muscle disorders; myopathy/rhabdomyolysis when used with
statin
Fibrates are associated with increased serum creatinine levels, which may
not reflect renal dysfunction
Fenofibrate dose should be cut by two-thirds and gemofibrozil by one-half
when eGFR is 15-60, and fibrates should be avoided when eGFR is <15
Can improve diabetic retinopathy
65. Omega 3 fish oil
Metabolic Effects:
• ↓ TG 27%-45%, TC 7%-10%, VLDL-C 20%-42%, apo B 4%, and non-HDL-C 8%-14%
in individuals with severe hypertriglyceridemia most likely by reducing hepatic
VLDL-TG synthesis and/or secretion and enhancing TG clearance from circulating
VLDL particles. Other potential mechanisms of action include: increased ß-
oxidation; inhibition of acyl-CoA; 1,2-diacylglyceral acyltransferase; decreased
hepatic lipogenesis; and increased plasma lipoprotein activity.
• Icosapent ethyl ↓ LDL-C 5%, whereas, omega-3-acid ethyl esters ↑ LDL-C 45%
66. Omega 3 fatty aids
Assess TG levels prior to initiating and periodically during therapy.
Omega-3-acid ethyl esters can increase LDL-C levels. Monitor LDL-C levels during
treatment.
May prolong bleeding time. Monitor coagulation status periodically in patients receiving
treatment with omega-3 fatty acids and other drugs affecting coagulation.
Monitor ALT and AST levels periodically during treatment in patients with hepatic
impairment. Some patients may experience increases in ALT levels only.
Exercise caution when treating patients with a known hypersensitivity to fish and/or
shellfish.
67. Omega 3 fattyacids
Assess TG levels prior to initiating and periodically during therapy.
Omega-3-acid ethyl esters can increase LDL-C levels. Monitor LDL-C levels during
treatment.
May prolong bleeding time. Monitor coagulation status periodically in patients
receiving treatment with omega-3 fatty acids and other drugs affecting coagulation.
Monitor ALT and AST levels periodically during treatment in patients with hepatic
impairment. Some patients may experience increases in ALT levels only.
Exercise caution when treating patients with a known hypersensitivity to fish and/or
shellfish.
68. Agent
Usual recommended
starting daily dosage
Dosage range
Method of
administration
Bile acid sequestrants
Cholestyramine 8-16 g 4-24 g Oral
Colestipol 2 g 2-16 g Oral
Colesevelam 3.8 g 3.8-4.5 g Oral
Metabolic Effects:
• Primarily ↓ LDL-C 15%-25% by binding bile acids and preventing their
reabsorption in the ileum (causing hepatic cholesterol depletion and LDL-
receptor upregulation)
• Colesevelam ↓ glucose and hemoglobin A1C (~0.5%); FDA-approved to
treat T2DM
Abbreviations: A1C, glycated hemoglobin; FDA, Food and Drug Administration; LDL, low-density lipoprotein; LDL-C, low-
density lipoprotein cholesterol; T2DM, type 2 diabetes mellitus; TG, triglyceride.
Colestid (colestipol hydrochloride) [PI]; 2014; Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-
497; Prevalite (cholestyramine for oral suspension, USP) [PI]; 2015; WelChol (colesevelam hydrochloride) [PI]; 2014; Zieve FJ,
et al. Ther. 2007;29:74-839:74-83.
69. Bile acid sequestrants
• Main Considerations:
•May ↑ serum TG
•Frequent constipation and/or bloating, which
can reduce adherence
•Many potential drug interactions (decreased
drug absorption), less so with colesevelam (see
product labeling)
•May reduce absorption of folic acid and fat-
soluble vitamins such as vitamins A, D, and K
70. Metabolic Effects
• Primarily ↓ LDL-C 10%-18% by inhibiting intestinal absorption of cholesterol and
decreasing delivery to the liver, leading to upregulation of hepatic LDL receptors
• ↓ Apo B 11%-16%
• In combination with statins, additional ↓ LDL-C 25%, total ↓ LDL-C 34%-61%
• In combination with fenofibrate, ↓ LDL-C 20%-22% and ↓ apo B 25%-26% without
reducing ↑ HDL-C
Main Considerations
• Myopathy/rhabdomyolysis (rare)
• When coadministered with statins or fenofibrate, risks associated with those
drugs remain (e.g., myopathy/ rhabdomyolysis, cholelithiasis)
71. Niacin
• Metabolic Effects:
• ↓ LDL-C 10%-25%, ↓ TG 20%-30%, ↑ HDL-C 10%-35%
by decreasing hepatic synthesis of LDL-C and VLDL-C
• ↓ Lipoprotein (a)
• Transforms LDL-C to less atherogenic form by increasing
average particle size and also decreases LDL particle
concentration
Usual recommended
starting daily dosage
Dosage range
Method of
administration
Niacin (nicotinic acid)
Immediate release 250 mg 250-3,000 mg Oral
Extended release 500 mg 500-2,000 mg Oral
72. Niacin
• Main Considerations:
• Potential for frequent skin flushing, pruritus,
abdominal discomfort, hepatoxicity (rare but
may be severe), nausea, peptic ulcer, atrial
fibrillation
• Deleterious effect on serum glucose at higher
dosages
• Increases uric acid levels; may lead to gout
73. Metabolic Effects:
• ↓LDL-C 48%-71%, ↓ non-HDL-C 49%-58%, ↓TC 36%-42%,
↓Apo B 42%-55% by inhibiting PCSK9 binding with LDLRs,
increasing the number of LDLRs available to clear LDL, and
lowering LDL-C levels
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-
497; Praluent (alirocumab) [PI] 2015; Repatha (evolocumab) [PI]; 2016.
74. • Main Considerations:
• Require subcutaneous self-injection; refrigeration generally needed
• Overall levels of adverse reactions and discontinuation very low
• Adverse reactions with significantly different rates between drug and
placebo were: local injection site reactions and influenza
• The most common adverse reactions with similar rates for drug vs. placebo
were:
• Alirocumab: nasopharyngitis, influenza, urinary tract infections,
diarrhea, bronchitis, and myalgia
• Evolocumab: nasopharyngitis, back pain,
and upper respiratory tract infection
75. MTP Inhibitor
Metabolic Effects:
• ↓ Up to LDL-C 40%, TC 36%, apo B 39%, TG 45%, and non-HDL-C 40% (depending
on dose) in individuals with HoFH by binding and inhibiting MTP, which inhibits
synthesis of chylomicrons and VLDL
Abbreviations: ALT, aspartate amino transferase; AST, amino alanine transferase; FDA, Food dministration; HDL-C, high-density lipoprotein
cholesterol; HoFH, homozygous familial hypercholesterolemia; LDL-C, low-density lipoprotein cholesterol; MTP, microsomal transfer protein; REMS,
Risk Evaluation and Mitigation Strategy; TG, triglycerides; VLDL, very low-density lipoprotein.
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497; Juxtapid (lomitapide) [PI]; 2012.
76. MTP Inhibitor
• Main Considerations:
• Can cause increases in transminases (ALT, AST); monitoring of ALT,
AST, alkaline phosphatase, and total bilirubin prior to initiation, and
of ALT and AST during treatment, is required per FDA REMS
• Causes increases in hepatic fat (steatosis) with or without
concomitant elevated transminases, which may be a risk for
progressive liver diseases
• Also causes steatosis of the small intestine with resulting abdominal
pain and steatorrhea unless a very-low-fat diet is followed; may also
cause fat-soluble vitamin deficiency unless vitamin supplements are
taken
• Caution should be exercised when used with other drugs with
potential hepatoxicity; because of hepatoxicity risk, only available
through REMS program
77. • Metabolic Effects
• ↓ LDL-C 21%, TC 19%, apo B 24%, and non-HDL-C
22% in individuals with HoFH by degrading mRNA
for apo B-100, the principal apolipoprotein
needed for hepatic synthesis of VLDL (and
subsequent intra-plasma production of IDL and
LDL)
Agent
Usual recommended
starting daily dosage
Dosage range
Method of
administration
Anti-sense apolipoprotein B oligonucleotide
Mipomersen
(SQ injection)
200 mg once weekly 200 mg once weekly SQ
78. mipomersen
• Main Considerations:
• Can cause increases in transminases (ALT,
AST); monitoring of ALT, AST, alkaline phosphatase, and
total bilirubin before initiation, and of ALT and AST
during treatment is recommended
• Causes increases in hepatic fat (steatosis) with or
without concomitant elevated transminases, which may
be a risk for progressive liver diseases
• Caution should be exercised when used with other drugs
with potential hepatoxicity; because of hepatoxicity risk,
only available through REMS program
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497; Kynamro
(mipomersen sodium) Injection [PI]; 2016
79. How should treatment be monitored?
• R75. Reassess individuals’ lipid status 6 weeks after therapy initiation and
again at 6-week intervals until the treatment goal is achieved (Grade D;
BEL 4).
R76. While on stable lipid therapy, individuals should be tested at 6- to 12-month
intervals (Grade D; BEL 4).
R77. While on stable lipid therapy, the specific interval of testing should depend on
individual adherence to therapy and lipid profile consistency; if adherence is a
concern or the lipid profile is unstable, the individual will probably benefit from more
frequent assessment (Grade C; BEL 4; upgraded due to potential benefit).
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497
80. R79. Liver transaminase levels should be measured before and 3 months after niacin
or fibric acid treatment initiation because most liver abnormalities occur within 3
months of treatment initiation. Liver transaminase levels should be measured
periodically thereafter (e.g., semiannually or annually) (Grade C; BEL 4; upgraded
due to potential benefit).
R80. Creatine kinase levels should be assessed and the statin discontinued, at least
temporarily, when an individual reports clinically significant myalgias or muscle
weakness on statin therapy (Grade C; BEL 4; upgraded due to potential benefit).
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-
497
R78. More frequent lipid status evaluation is recommended in situations such as
deterioration of diabetes control, use of a new drug known to affect lipid levels,
progression of atherothrombotic disease, considerable weight gain, unexpected
adverse change in any lipid parameter, development of a new ASCVD risk factor, or
convincing new clinical trial evidence or guidelines that suggest stricter lipid goals
(Grade C; BEL 4; upgraded due to potential benefit).
81. •Lipid Association of India (LAI)
expert consensus statement on
management of dyslipidemia in
Indians 2017: Part 2
SS Iyengar et al. Lipid Association of India (LAI) expert consensus
statement on management of
dyslipidemia in Indians 2017: part 2, Clinical Lipidology, 12:1, 56-109
Focus on Dyslipidaemia and
Comorbidities
82. Objective of the guideline
Lipid Association of India (LAI) part 2 recommendations refer to
specific patient populations. These part 2 LAI recommendations
focus on comorbidities associated with Dyslipidemia and also
focuses on specific patient groups.
These include patients with heart failure, chronic kidney disease,
non-alcoholic fatty liver disease, cerebrovascular disease, thyroid
disorders, inflammatory joint diseases, familial
hypercholesterolemia and human immunodeficiency virus
infection.
Guideline also consider women, the elderly and post-
transplantation patients.
83. Dyslipidemia in Heart Failure
Besides lifestyle measures, statins may be
administered to patients with ischemic HF
with NYHA Class II-III symptoms.
Patients with advanced symptomatic HF
require individualized care, in these groups,
intensive statin therapy with a goal to achieve
50% reduction in LDL-C levels is justified.
Statins are also recommended for ischemic HF
patients awaiting heart transplantation.
HF: Heart Failure, LDL-C; Low-density Lipoprotein, NYHA: New York Heart
Association class
84. Dyslipidemia in Heart Failure
Statins are not recommended in NYHA Class IV HF.
However, three points can be considered in patients
with advanced HF. Firstly, no excess of side effects.
Secondly, the degree of LDL-C lowering did not
correlate with event rate. Thirdly, there were fewer
hospitalizations
Statin therapy is not recommended in advanced HF
patients who have a short life expectancy (e.g. because
of comorbidities like malignancy).
Statins are not recommended in non-ischemic HF or
dilated cardiomyopathy
85. Dyslipidemia in CKD
Follow-up measurement of lipid levels should be performed routinely (at treating
physicians’ discretion) in subjects with CKD until the LDL-C and non- HDL-C target
is achieved.
Therapeutic lifestyle modification should be recommended to all patients.
A combination of statins/statin plus ezetimibe is recommended for all adults over
the age of 40 years with eGFR < 60 mL/min/1.73 m2.
Adults between the ages of 18 and 39, with CKD should be treated with statins if
they have one of the following:
– - Known CAD, stroke or peripheral arterial disease
– - Diabetes mellitus
– - Life time risk of ASCVD >30%
Kodachrome Kidney Disease, LDL-C: Low-density Lipoprotein, HDL-C: High-density
Lipoprotein, eGFR: Estimated Glomerular Filtration Rate,, CAD: coronary artery disease,
ASCVD: Atherosclerotic cardiovascular risk factors
86. Dyslipidemia in CKD
Patients who are already receiving lipid-lowering therapy at the
time of starting dialysis should continue to receive these agents.
In adults with dialysis-dependent CKD who are not on statins,
statins could be considered at the lowest dose possible and should
be titrated up carefully to achieve the LDL-C level for very high risk
patients
All adult kidney transplant recipients should receive statin
therapy.
Statins should be started at a lower dose in all subjects with eGFR
<30 ml/min with gradual escalation to the recommended dose
along with monitoring for any adverse events
Kodachrome Kidney Disease, LDL-C: Low-density Lipoprotein, HDL-C:
High-density Lipoprotein, eGFR: Estimated Glomerular Filtration Rate,,
CAD: coronary artery disease, ASCVD: Atherosclerotic cardiovascular
88. Dyslipidemia in NAFD
The available evidence suggests that the risk for
serious liver injury from statins is quite rare and
patients with NAFLD and dyslipidemia are not at an
increased risk for statin-induced hepatotoxicity. Hence,
statins could be used by physicians to treat
dyslipidemia in patients with NAFLD.
There are few data to suggest usage of statins as a
treatment option for NAFLD. However, it continues to
be a matter of debate and treatment of NAFLD with
statins cannot be recommended at present.
NAFD: Non-alcoholic fatty liver disease
89. Dyslipidemia in NAFD
The available evidence suggests that the risk for
serious liver injury from statins is quite rare and
patients with NAFLD and dyslipidemia are not at
an increased risk for statin-induced
hepatotoxicity. Hence, statins could be used by
physicians to treat dyslipidemia in patients with
NAFLD.
There are few data to suggest usage of statins as
a treatment option for NAFLD. However, it
continues to be a matter of debate and
treatment of NAFLD with statins cannot be
recommended at present.
NAFD: Non-alcoholic fatty liver disease
90. Dyslipidemia in Cerebrovascular
Disease
Acute ischemic stroke: Starting a statin is probably
beneficial. Continue statin if patient is already receiving it.
Statins are not contraindicated if patient is thrombolysis. It
may be given by nasogastric tube in patients with dysphagia.
Acute ICH: Do not initiate statin if patient is not already on
it. Do not discontinue statin if patient is already on a statin.
Optimal blood pressure control is essential in those already
on a statin.
Primary prevention of stroke: Statin treatment is
recommended in adults with diabetes, or CAD, to lower the
risk of a first stroke.
Secondary prevention of stroke: Statins are beneficial in
preventing a second ischemic stroke, but do not prevent
fatal stroke.
Patients with previous haemorrhagic stroke: Statins are
best avoided in patients with previous lobar haemorrhage,
but may be beneficial in preventing stroke in patients with
previous basal-ganglionic haemorrhage who have a high risk
for ischemic events.
ICH: Intracerebral Hemorrahge
91. All patients with dyslipidemia should be screened for thyroid dysfunction.
Patients with dyslipidemia and overt hypothyroidism should be treated
initially with thyroxine.
In patients with underlying risk for CAD, start low dose thyroxine and
titrate upwards slowly. Assess CVD risk and start lipid-lowering drugs as
per LAI recommendation for primary prevention of CVD.
Patients without underlying risk for CAD: wait for the patient to become
euthyroid.
Statins or fibrates alone or in combination in patients with dyslipidemia
and uncontrolled hypothyroidism carry a higher risk of myopathy.
Thyroid replacement in patients with sub-clinical hypothyroidism if serum
TSH is >10 mIU/L, patients have high initial cholesterol levels or are
elderly, are smokers or are positive for anti-thyroid peroxidase antibodies.
In patients with established vascular disease requiring thyroxine and lipid-
lowering therapy, caution should be exercised with thyroxine dose to
prevent onset of ischemic symptoms.
Dyslipidemia in Thyroid Disorder
CAD: coronary artery disease, CVD: Cardiovascular disease, TSH: Thyroid stimulating
hormone
92. CVD risk assessment for IJD patients should be
carried out [including total cholesterol and
HDL-C (fasting or non-fasting)] during the
stable disease state once every 5 years.
The use of statins and CVD risk management
should follow the same principles as discussed
in the Part1 of this consensus document.
Management of ASCVD risk in
inflammatory joint diseases (IJD)
CVD: Cardiovascular disease, HDL-C: High density lipoprotein
93. Familial Hypercholeterolemia (FH)
Lipid profile estimation of children to be done at 2 years of age
in those with family history of FH and premature ASCVD.
LAI recommends the Simon Broome criteria for the diagnosis of
FH.
In an established case of FH, LAI recommends estimation of
Lp(a) levels.
Genetic testing and cascade screening should be performed
wherever feasible.
Look for other ASCVD risk factors and manage them
appropriately.
Strict dietary recommendations and lifestyle modifications as
advised.
Drug therapy to be started at age 8 years or earlier in
individualised cases.
LDL-C targets to be achieved:<70 mg/dL for HoFH and <100
mg/dL for HeFH in children and in adults <50 mg/dL in HoFH
and 70 mg/dL in HeFH or at least 50% reduction in LDL-C from
the baseline.
HeFH: Heterozygous FH; HoFH: Homozygous FH; HF: Heart Failure, Lp(a): Lipoprotein,
LDL-C: Low-denisty lipoprotein
94. Inherited Hypertriglyceridaemia
All subjects should be screened for
hypertriglyceridaemia with a fasting lipid profile. A
non-fasting lipid profile may be performed as an
initial step, but fasting TG estimation will be needed
if TG is found to be high in the non-fasting sample
Exclude and treat secondary causes
Aggressive therapeutic lifestyle changes should be
implemented
Subjects with TG > 200 mg/dL and <500 mg/dL –
treat with a statin
Subjects with TG ≥ 500 mg/dL-treat with fibrates to
prevent acute pancreatitis and later add statin to
achieve non-HDL-C goal
Preferred drugs: Fibrates and high dose omega fatty
acids; the role of niacin is controversial.
TG; Triglycerides, HDL-C: High-density lipoprotein
95. Lipids targets in HIV patients as recommended by
LAI
Dyslipidemia in HIV
Effect of different statins in HIV patients with
dyslipidemia
LDL-C: Low-denisty lipoprotein, HDL-C: High density
96. Lifestyle modifications with special emphasis on
smoking cessation, weight reduction and calorie
restriction are important.
The recommendations for the evaluation and
treatment of dyslipidemia as suggested by LAI
regarding target goals for lipids should be strictly
followed to help guide therapy.
At least, evidence available in the Indian
population suggests the same.
Dyslipidemia in HIV
HIV: Human Immunodeficiency Virus, LDL-C: Low-density lipoprotein
97. Different types of statins are available to lower
plasma lipids to guideline levels in patients with HIV,
but they differ in their pharmacokinetic properties
and drug interaction profiles. Simvastatin and
lovastatin are contraindicated in patients taking PIs.
The other statins atorvastatin and rosuvastatin
(apart from simvastatin and lovastatin) have better
therapeutic effect in lowering LDL-C in HIV
dyslipidemia. The addition of ezetimibe is another
option. Fenofibrate and fish oil can be used in statin-
unresponsive HIV dyslipidemia.
Dyslipidemia in HIV
HIV: Human Immunodeficiency Virus, LDL-C: Low-density lipoprotein
98. Dyslipidemia in Women
Women with collagen vascular disorders, PCOS,
preeclampsia, pregnancy-induced hypertension and
gestational diabetes are at higher ASCVD risk.
The dyslipidemia management is similar in both men and
women. However, in elderly frail women, treatment should
be started with low dose statin in view of higher incidence of
muscle-related adverse effects except in the very high risk
group.
Statins remain the first-line cholesterol-lowering drug
therapy for primary and secondary prevention in women.
Statin dosage should be increased to the maximally tolerated
dose before adding a non-statin drug if goal levels of LDL-C
and non-HDL-C are not achieved.
Non-statin drugs may be considered as a primary drug for
women with contraindications for, or intolerance to, statin
therapy.
PCOS: Polycystic ovarian syndrome, LDL-C: Low-denisty lipoprotein, HDL-C:
High density lipoprotein
99. Dyslipidemia in Elderly
CVD is the most common cause of death in the elderly. As in
the young, elderly patients with dyslipidemia have an
increased risk for CVD. • Secondary causes of dyslipidemia
such as hypothyroidism, diabetes, CKD and drug effects
should be considered in elderly patients.
The RRR of lipid-lowering therapy in elderly patients is similar
to that in younger patients; however, the absolute benefit is
higher than in younger patients.
Reductions in events with statin therapy are apparent within
a few weeks to months even in older patients.
RRR: Relative Risk Reduction, CKD: Chronic kidney disease, CVD: Cardiovascular
100. Dyslipidemia in Elderly
Side effects of lipid-lowering therapy are similar in the old
and young. However, in very elderly frail patients, lower
doses may be appropriate.
Secondary prevention: Statin therapy should be instituted in
all appropriate elderly patients as above with treatment goals
similar to younger patients. Dose of statins may need to be
individualized in the elderly based on frailty and other
comorbidities.
Primary prevention: Elderly subjects with a reasonable life
expectancy should be treated similar to younger patients as
per risk stratification algorithm proposed in the previously
published LAI expert consensus statement
RRR: Relative Risk Reduction, CKD: Chronic kidney disease, CVD: Cardiovascular
101. Post-Heart Transplantation
Baseline lipid levels should be obtained for all
patients after heart transplantation.
The strict control of modifiable risk factors
including hypertension, diabetes, dyslipidemia,
smoking and obesity should be reinforced.
In adults, the use of statins beginning 1 to 2
weeks after heart transplantation is
recommended regardless of cholesterol levels.
CAV: Cardiac Allograft Vasculopathy, LDL-C: Low-denisty
102. Post-Heart Transplantation
Pravastatin shows the least interaction with
cyclosporine to produce myopathy, making it the
drug of choice.
Rosuvastatin up to 10 mg/day may be given as a
second choice.
Addition of a statin to a cyclosporine–sirolimus
regimen produces multiple beneficial effects like
reduced cholesterol levels, decreased acute
rejection episodes, decreased incidence of CAV
and improved survival.
In heart transplant recipients, a strategy of
lowest achievable LDL-C levels with maximally
tolerated dose of statin by slowly up-titrating the
statin dose is justified.
CAV: Cardiac Allograft Vasculopathy, LDL-C: Low-denisty
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