This study used a Mendelian randomization approach to test whether elevated nonfasting glucose levels are causally associated with increased risk of ischemic heart disease (IHD) and myocardial infarction (MI). The study found that:
1) Risk of IHD and MI increased with higher nonfasting glucose levels.
2) Genetic variants associated with higher fasting glucose were also associated with higher nonfasting glucose levels.
3) These glucose-increasing genetic variants were associated with increased risk of IHD and MI.
4) Instrumental variable analysis estimated that a 1 mmol/L increase in nonfasting glucose due to genetic variants was associated with a 25% increased risk of IHD and 69% increased
Prevalence of Chronic Kidney disease in Patients with Metabolic Syndrome in S...asclepiuspdfs
Background and Objective: Chronic kidney disease (CKD) which is an increasingly important clinical and public health issue is associated with cardiovascular disease. Epidemiologic studies have also linked metabolic syndrome (MetS) with an increased risk of incident CKD. Therefore, the present study was designed retrospectively to find the prevalence and potential risk factors of CKD in patients with MetS in Saudi Arabia.
HIGH SENSITIVE C-REACTIVE PROTEIN (hs-CRP) AND ITS CORRELATION WITH ANGIOGRAP...M A Hasnat
Association between the plasma hs-CRP levels and the severity of coronary
stenosis in subjects remains controversial. This cross sectional study was performed in the
Department of Cardiology, Dhaka Medical College during July 2008 to December 2009, to determine whether the concentrations of hs-CRP correlate with the coronary atherosclerotic disease assessed by coronary angiography.
Prevalence of Chronic Kidney disease in Patients with Metabolic Syndrome in S...asclepiuspdfs
Background and Objective: Chronic kidney disease (CKD) which is an increasingly important clinical and public health issue is associated with cardiovascular disease. Epidemiologic studies have also linked metabolic syndrome (MetS) with an increased risk of incident CKD. Therefore, the present study was designed retrospectively to find the prevalence and potential risk factors of CKD in patients with MetS in Saudi Arabia.
HIGH SENSITIVE C-REACTIVE PROTEIN (hs-CRP) AND ITS CORRELATION WITH ANGIOGRAP...M A Hasnat
Association between the plasma hs-CRP levels and the severity of coronary
stenosis in subjects remains controversial. This cross sectional study was performed in the
Department of Cardiology, Dhaka Medical College during July 2008 to December 2009, to determine whether the concentrations of hs-CRP correlate with the coronary atherosclerotic disease assessed by coronary angiography.
Copeptin as a Novel Biomarker in the Diagnosis of Acute Myocardial Infarction...Premier Publishers
To evaluate the diagnostic value of Copeptin as a novel biomarker in early diagnosis of Acute Myocardial Infarction. 56 patients with acute Myocardial Infarction (STEMI) and 25 healthy controls who were admitted to the Cardiology and Clinical Pathology Departments, national heart institute (NHI) from October 2015 to April 2016. The kit used a double-antibody sandwich enzyme-linked immune-sorbent assay (ELISA) to assay the level of Human Copeptin in samples. As regard copeptin, the median range of copeptin level was 242.5pg/ml in patient group and 75pg/ml in control group. The comparative study between the two groups shows a significant difference (p < 0.05) Conclusion: Copeptin is a reliable diagnostic tool in patients with AMI (STEMI) with sensitivity 85.7%, specificity 86.7%, PPV 96% and NPV 61.9%.
Crimson Publishers: Insulin Therapy and Cardiovascular Outcome Trials (CVOTs)...CrimsonGastroenterology
The therapeutic management of diabetes may on its own increase the risk of cardiovascular (CV) risk markers – directly or indirectly – through their pharmacological actions (e.g. side effects as hypoglycaemia), or some metabolic changes (e.g. Weight-Gain, increased BP, etc.). As these risks may not have been anticipated or immediately noticed during clinical trials, 1 post hoc analyses and epidemiological follow up of clinical trials have raised concerns about the CV safety of some drugs used in the management of diabetes.
Implication of preoperative glycosylated hemoglobin level on short term outco...Dr.Debmalya Saha
ABSTRACT
Background: Diabetes mellitus is one of the significant risk factors for adverse outcomes after coronary artery bypass surgery. The glycosylated haemoglobin i.e. HbA1c is a reliable diagnostic test to know the long-term glycemic status. The objective of the study is to investigate the implication of preoperative HbA1c level on short term outcomes after coronary artery bypass grafting (CABG).
Method: Total 218 patients were studied, and the data were collected retrospectively. Patients are distributed into group 1 with HbA1c≤7 (good glycemic control) and group 2 with HbA1c>7 (poor glycemic control). The parameters studied for short term outcomes were revision due to bleeding, duration of mechanical ventilation, cerebrovascular accident (CVA), atrial fibrillation (AF), renal failure requiring dialysis, infective complications like sternal and leg wound infection, mediastinitis, pneumonia, urinary tract infection (UTI), sepsis; length of ICU stay and in-hospital mortality.
Result: In comparison to group 1, patients of group 2 showed statistically significant more morbidity in view of short-term outcomes in this study.
Conclusion: HbA1c>7 is associated with statistically significant adverse short-term outcomes after CABG.
The prevalence and severity of obesity is increasing dramatically
among children and adolescents in many parts of the
world, whereas prevalence rates are estimated to increase in
the next decades [1]. In children, excess body fat appears to
be strongly associated with the clustering of risk factors, such
as hyperglycemia, dyslipidemia, and hypertension, which
play a key role in the pathogenesis of the metabolic syndrome
(MetS) [2].
Obesity and the MetS risk in children have been
recently associated with systemic inflammatory markers,
in particular C-reactive protein (CRP) [3, 4], implying
that low-grade inflammation can already exist in childhood
and may be a potential link between the obesity and the
MetS. Among behavioral variables, cardiorespiratory fitness
has a protective role in MetS and inflammatory factors;
however, it is not entirely clear if the interrelations among
cardiorespiratory fitness, MetS risk, and inflammation in
children are independent or partly due to the mediating
effect of obesity, since the existing data are limited and
equivocal [5, 6].
Recent evidence indicates that the prevalence rates
of childhood obesity in Greece remain high [1, 7] and
often coexist with low cardiorespiratory fitness [8] and
an unfavorable cardiometabolic risk profile [9]. For the
Greek pediatric population these data suggest an increased
cardiovascular morbidity in adulthood, given that highrisk
children and adolescents are likely to become highrisk
adults [10]. Although the relationship among obesity
and dyslipidemia in Greek children has been thoroughly
investigated [9, 11], there is a paucity of data regarding the
clustering of metabolic risk factors, inflammation, and their
relationship with cardiorespiratory fitness. The present study
was undertaken in an attempt to investigate the prevalence of
theMetS and examine the associations among cardiorespiratory
fitness, MetS risk, and CRP in 11-year-old children.
Efficiency of Use of Dietary Supplement Arteroprotect® In Prevention of Cardi...inventionjournals
Cardiovascular diseases are the leading cause of death in most developed countries and in many developing countries. The main cause of cardiovascular disease in 95% cases is supposed to be atherosclerosis, and the symptoms occur when the process is already at an advanced stage of disease. Present study was conducted to examine an efficiency of ARTEROprotect® (by Abela Pharm, Serbia) in prevention of cardiovascular diseases. The study was conducted by 76 doctors in primary health centers throughout the Republic of Serbia as a prospective clinical study of two groups of subjects. The study group included 4031 subjects (1785 males and 2246 females) who were taking ARTEROprotect® , while the control group consisted of 2564 subjects (1135 males and 1428 females) who were not taking it. Based on the results, dietary supplement ARTEROprotect® , used alone, could contribute to lowering levels of cholesterol, triglycerides, LDL-cholesterol; in combination with a statin it can achieve the target value of LDL- and HDL-cholesterol.
Microalbuminuria in Saudi Adults with Type 1 Diabetes Mellitus_Crimson Publis...CrimsonPublishersIOD
Background: Diabetes mellitus is among the most common chronic non-communicable diseases. The development of microalbuminuria in type 1 diabetes increases the risk for renal and cardiovascular disease.
Methods: A cross sectional study was conducted at the Primary Health Care Clinics at King Fahad Armed Forces Hospital, Jeddah, Saudi Arabia. A total of 334 Saudi with type 1 diabetes were randomly selected.
Results: Total of 334 patients with T2DM included in this study; 102 (30.5%) male and 232 (69.5%) female with mean age 25.8±3.4. MA was present in 99 (29.6%). MA was not significantly more prevalent in female (69.4%) with female predominance (sex ratio male: female) 1:2.3. HTN with MA was significantly more prevalent in 51(51.5%) of MA group with odd ratio 1.7 (1.2-2.4), p=0.001 with no siginificant difference between both gender. Patients with MA have significant higher HbA1c than patients with normal buminuria and there was a significant difference between gender (p< 0.0001) and when compared to HbA1c groups (p=0.002).
Conclusion: The frequency of microalbuminuria in patients with type 1 diabetes in this study is high. It is mandatory to have adequate diagnostic, therapeutic and educational resources in addition to competent physicians who can manage microalbuminuria in diabetic patients by using a continuing, comprehensive and coordinated approach.
Sample Work of an Meta-Analysis | Hire a Meta-Analysis Expert: Pubrica.comPubrica
Pubrica has a broad experience in all aspects of Scientific Medical Writing, Editing, and Publishing. A global leader in comprehensive manuscript publication support service for academic and scientific journals, We provide a wide range of services that include Scientific medical research writing, Clinical data analysis, Literature review, Meta-analysis, medical Communication and medico-marketing solutions to healthcare/pharmaceutical/food and beverage companies.
Find freelance Meta-Analysis professionals, consultants, freelancers and get your project done - https://bit.ly/30V8QUK
Why Pubrica:
When you order our services, we promise you the following – Plagiarism free, always on Time, outstanding customer support, written to Standard, Unlimited Revisions support and High-quality Subject Matter Experts.
Contact us:
Web: https://pubrica.com/
Blog: https://pubrica.com/academy/
Email: sales@pubrica.com
WhatsApp : +91 9884350006
United Kingdom : +44-1143520021
Association of the HLA-B alleles with carbamazepine-induced Stevens–Johnson s...UniversitasGadjahMada
Carbamazepine (CBZ) is a common cause of life-threatening cutaneous adverse drug reactions such as Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). Previous studies have reported a strong association between the HLA genotype and CBZ-induced SJS/TEN.We investigated the association between the HLA genotype and CBZ-induced SJS/TEN in Javanese and Sundanese patients in Indonesia. Nine unrelated patients with CBZ-induced SJS/TEN and 236 healthy Javanese and Sundanese controls were genotyped for HLA-B and their allele frequencies were compared. The HLA-B*15:02 allele was found in 66.7% of the patients with CBZ-induced SJS/TEN, but only in 29.4% of tolerant control (p = 0.029; odds ratio [OR]: 6.5; 95% CI: 1.2–33.57) and 22.9% of healthy controls (p = 0.0021; OR: 6.78; 95% CI: 1.96– 23.38). These findings support the involvement of HLA-B*15:02 in CBZ-induced SJS/TEN reported in other Asian populations. Interestingly, we also observed the presence of the HLA-B*15:21 allele. HLA-B*15:02 and HLA-B*15:21 are members of the HLA-B75 serotype, for which a greater frequency was observed in CBZ-induced SJS/TEN (vs tolerant control [p = 0.0078; OR: 12; 95% CI: 1.90–75.72] and vs normal control [p = 0.0018; OR: 8.56; 95% CI: 1.83–40]). Our findings suggest that screening for the HLA-B75 serotype can predict the risk of CBZ-induced SJS/TEN more accurately than screening for a specific allele.
Association of cardio metabolic risk factors, serum nitric oxide metabolite a...iosrjce
IOSR Journal of Dental and Medical Sciences is one of the speciality Journal in Dental Science and Medical Science published by International Organization of Scientific Research (IOSR). The Journal publishes papers of the highest scientific merit and widest possible scope work in all areas related to medical and dental science. The Journal welcome review articles, leading medical and clinical research articles, technical notes, case reports and others.
Copeptin as a Novel Biomarker in the Diagnosis of Acute Myocardial Infarction...Premier Publishers
To evaluate the diagnostic value of Copeptin as a novel biomarker in early diagnosis of Acute Myocardial Infarction. 56 patients with acute Myocardial Infarction (STEMI) and 25 healthy controls who were admitted to the Cardiology and Clinical Pathology Departments, national heart institute (NHI) from October 2015 to April 2016. The kit used a double-antibody sandwich enzyme-linked immune-sorbent assay (ELISA) to assay the level of Human Copeptin in samples. As regard copeptin, the median range of copeptin level was 242.5pg/ml in patient group and 75pg/ml in control group. The comparative study between the two groups shows a significant difference (p < 0.05) Conclusion: Copeptin is a reliable diagnostic tool in patients with AMI (STEMI) with sensitivity 85.7%, specificity 86.7%, PPV 96% and NPV 61.9%.
Crimson Publishers: Insulin Therapy and Cardiovascular Outcome Trials (CVOTs)...CrimsonGastroenterology
The therapeutic management of diabetes may on its own increase the risk of cardiovascular (CV) risk markers – directly or indirectly – through their pharmacological actions (e.g. side effects as hypoglycaemia), or some metabolic changes (e.g. Weight-Gain, increased BP, etc.). As these risks may not have been anticipated or immediately noticed during clinical trials, 1 post hoc analyses and epidemiological follow up of clinical trials have raised concerns about the CV safety of some drugs used in the management of diabetes.
Implication of preoperative glycosylated hemoglobin level on short term outco...Dr.Debmalya Saha
ABSTRACT
Background: Diabetes mellitus is one of the significant risk factors for adverse outcomes after coronary artery bypass surgery. The glycosylated haemoglobin i.e. HbA1c is a reliable diagnostic test to know the long-term glycemic status. The objective of the study is to investigate the implication of preoperative HbA1c level on short term outcomes after coronary artery bypass grafting (CABG).
Method: Total 218 patients were studied, and the data were collected retrospectively. Patients are distributed into group 1 with HbA1c≤7 (good glycemic control) and group 2 with HbA1c>7 (poor glycemic control). The parameters studied for short term outcomes were revision due to bleeding, duration of mechanical ventilation, cerebrovascular accident (CVA), atrial fibrillation (AF), renal failure requiring dialysis, infective complications like sternal and leg wound infection, mediastinitis, pneumonia, urinary tract infection (UTI), sepsis; length of ICU stay and in-hospital mortality.
Result: In comparison to group 1, patients of group 2 showed statistically significant more morbidity in view of short-term outcomes in this study.
Conclusion: HbA1c>7 is associated with statistically significant adverse short-term outcomes after CABG.
The prevalence and severity of obesity is increasing dramatically
among children and adolescents in many parts of the
world, whereas prevalence rates are estimated to increase in
the next decades [1]. In children, excess body fat appears to
be strongly associated with the clustering of risk factors, such
as hyperglycemia, dyslipidemia, and hypertension, which
play a key role in the pathogenesis of the metabolic syndrome
(MetS) [2].
Obesity and the MetS risk in children have been
recently associated with systemic inflammatory markers,
in particular C-reactive protein (CRP) [3, 4], implying
that low-grade inflammation can already exist in childhood
and may be a potential link between the obesity and the
MetS. Among behavioral variables, cardiorespiratory fitness
has a protective role in MetS and inflammatory factors;
however, it is not entirely clear if the interrelations among
cardiorespiratory fitness, MetS risk, and inflammation in
children are independent or partly due to the mediating
effect of obesity, since the existing data are limited and
equivocal [5, 6].
Recent evidence indicates that the prevalence rates
of childhood obesity in Greece remain high [1, 7] and
often coexist with low cardiorespiratory fitness [8] and
an unfavorable cardiometabolic risk profile [9]. For the
Greek pediatric population these data suggest an increased
cardiovascular morbidity in adulthood, given that highrisk
children and adolescents are likely to become highrisk
adults [10]. Although the relationship among obesity
and dyslipidemia in Greek children has been thoroughly
investigated [9, 11], there is a paucity of data regarding the
clustering of metabolic risk factors, inflammation, and their
relationship with cardiorespiratory fitness. The present study
was undertaken in an attempt to investigate the prevalence of
theMetS and examine the associations among cardiorespiratory
fitness, MetS risk, and CRP in 11-year-old children.
Efficiency of Use of Dietary Supplement Arteroprotect® In Prevention of Cardi...inventionjournals
Cardiovascular diseases are the leading cause of death in most developed countries and in many developing countries. The main cause of cardiovascular disease in 95% cases is supposed to be atherosclerosis, and the symptoms occur when the process is already at an advanced stage of disease. Present study was conducted to examine an efficiency of ARTEROprotect® (by Abela Pharm, Serbia) in prevention of cardiovascular diseases. The study was conducted by 76 doctors in primary health centers throughout the Republic of Serbia as a prospective clinical study of two groups of subjects. The study group included 4031 subjects (1785 males and 2246 females) who were taking ARTEROprotect® , while the control group consisted of 2564 subjects (1135 males and 1428 females) who were not taking it. Based on the results, dietary supplement ARTEROprotect® , used alone, could contribute to lowering levels of cholesterol, triglycerides, LDL-cholesterol; in combination with a statin it can achieve the target value of LDL- and HDL-cholesterol.
Microalbuminuria in Saudi Adults with Type 1 Diabetes Mellitus_Crimson Publis...CrimsonPublishersIOD
Background: Diabetes mellitus is among the most common chronic non-communicable diseases. The development of microalbuminuria in type 1 diabetes increases the risk for renal and cardiovascular disease.
Methods: A cross sectional study was conducted at the Primary Health Care Clinics at King Fahad Armed Forces Hospital, Jeddah, Saudi Arabia. A total of 334 Saudi with type 1 diabetes were randomly selected.
Results: Total of 334 patients with T2DM included in this study; 102 (30.5%) male and 232 (69.5%) female with mean age 25.8±3.4. MA was present in 99 (29.6%). MA was not significantly more prevalent in female (69.4%) with female predominance (sex ratio male: female) 1:2.3. HTN with MA was significantly more prevalent in 51(51.5%) of MA group with odd ratio 1.7 (1.2-2.4), p=0.001 with no siginificant difference between both gender. Patients with MA have significant higher HbA1c than patients with normal buminuria and there was a significant difference between gender (p< 0.0001) and when compared to HbA1c groups (p=0.002).
Conclusion: The frequency of microalbuminuria in patients with type 1 diabetes in this study is high. It is mandatory to have adequate diagnostic, therapeutic and educational resources in addition to competent physicians who can manage microalbuminuria in diabetic patients by using a continuing, comprehensive and coordinated approach.
Sample Work of an Meta-Analysis | Hire a Meta-Analysis Expert: Pubrica.comPubrica
Pubrica has a broad experience in all aspects of Scientific Medical Writing, Editing, and Publishing. A global leader in comprehensive manuscript publication support service for academic and scientific journals, We provide a wide range of services that include Scientific medical research writing, Clinical data analysis, Literature review, Meta-analysis, medical Communication and medico-marketing solutions to healthcare/pharmaceutical/food and beverage companies.
Find freelance Meta-Analysis professionals, consultants, freelancers and get your project done - https://bit.ly/30V8QUK
Why Pubrica:
When you order our services, we promise you the following – Plagiarism free, always on Time, outstanding customer support, written to Standard, Unlimited Revisions support and High-quality Subject Matter Experts.
Contact us:
Web: https://pubrica.com/
Blog: https://pubrica.com/academy/
Email: sales@pubrica.com
WhatsApp : +91 9884350006
United Kingdom : +44-1143520021
Association of the HLA-B alleles with carbamazepine-induced Stevens–Johnson s...UniversitasGadjahMada
Carbamazepine (CBZ) is a common cause of life-threatening cutaneous adverse drug reactions such as Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). Previous studies have reported a strong association between the HLA genotype and CBZ-induced SJS/TEN.We investigated the association between the HLA genotype and CBZ-induced SJS/TEN in Javanese and Sundanese patients in Indonesia. Nine unrelated patients with CBZ-induced SJS/TEN and 236 healthy Javanese and Sundanese controls were genotyped for HLA-B and their allele frequencies were compared. The HLA-B*15:02 allele was found in 66.7% of the patients with CBZ-induced SJS/TEN, but only in 29.4% of tolerant control (p = 0.029; odds ratio [OR]: 6.5; 95% CI: 1.2–33.57) and 22.9% of healthy controls (p = 0.0021; OR: 6.78; 95% CI: 1.96– 23.38). These findings support the involvement of HLA-B*15:02 in CBZ-induced SJS/TEN reported in other Asian populations. Interestingly, we also observed the presence of the HLA-B*15:21 allele. HLA-B*15:02 and HLA-B*15:21 are members of the HLA-B75 serotype, for which a greater frequency was observed in CBZ-induced SJS/TEN (vs tolerant control [p = 0.0078; OR: 12; 95% CI: 1.90–75.72] and vs normal control [p = 0.0018; OR: 8.56; 95% CI: 1.83–40]). Our findings suggest that screening for the HLA-B75 serotype can predict the risk of CBZ-induced SJS/TEN more accurately than screening for a specific allele.
Association of cardio metabolic risk factors, serum nitric oxide metabolite a...iosrjce
IOSR Journal of Dental and Medical Sciences is one of the speciality Journal in Dental Science and Medical Science published by International Organization of Scientific Research (IOSR). The Journal publishes papers of the highest scientific merit and widest possible scope work in all areas related to medical and dental science. The Journal welcome review articles, leading medical and clinical research articles, technical notes, case reports and others.
Health Outcomes, Quality, and Cost: Opportunities for Pediatric EndocrinologyJoyce Lee
My talk for the Paul Kaplowitz Endowed Lectureship for contributions to quality and cost-effective care in Pediatric Endocrinology at the Pediatric Endocrine Society Meeting 2016. Thank you so much Dr. Kaplowitz! And a hat tip to Lawson Wilkins, who developed learning health systems ages ago.
Atherotech’s VAP+ is a simple non-fasting blood test that directly measures your cardiovascular risk and disease progression that breaks down lipid abnormalities into three categories: triglycerides, cholesterol and hereditary components. The basic lipid does NOT fully assess cardiovascular risk/disease. Often, misclassifying the high risk patients approximately 60% of the time; and inaccurately reports a falsely low LDL, the main target of therapy. Why would anyone with family history of cardiovascular disease NOT want this complete assessment at NO additional cost????
Call 202-527-1953 to find out where to get your VAP+ test done, today!
*Additional markers included in the VAP+ report are LDL-P, Lp(a), remnants (IDL, VLDL3), ApoB and Apo A1.
Lipids are a heterogenous group of
water –insoluble ( hydrophobic ) organic
molecules. Presentation on how they affect the body and what to do to prevent their effects.
Lipid profile is an important group of tests used to diagnose hyperlipidemias. it is also used in Investigating Myocardial infarction , Diabetes mellitus & nephrotic syndrome
Hemorheological indexes, living habits, medical history and genetics factor are primary risk factors in Coronary Heart Disease (CHD). In the present study the relation of all factors to the severity of CHD was examined. The data of 282 patients (mean age: 60±9 years) diagnosed with CHD and 229 healthy controls (mean age: 59±7 years) from Wenzhou Medical University were analyzed.
Functional genomics has led to an improvement of our understanding of CVD and can be translated to clinical utility. Gene-based pre-symptomatic prediction of illness, finer diagnostic sub-classifications and improved risk assessment tools will permit earlier and more targeted intervention. Pharmacogenetics will guide our therapeutic decisions and monitor response to therapy. Personalised medicine requires the integration of clinical information, stable and dynamic genomics and molecular phenotyping.
It is now possible to systematically search the entire human genome for common variants that are associated with a particular phenotype. (HGP, HAP MAP)
Does Type of Dialysis Affect BNP in Fluid Overload Patients?Premier Publishers
Brain Natriuretic Peptide (BNP) levels are important as predictors of heart failure in end-stage renal disease (ESRD) patients undergoing hemodialysis (HD) and continuous ambulatory peritoneal dialysis (PD). Twenty-four HD patients and 35 PD patients were included in the study. Each patient underwent an echocardiographic examination besides the determination of BNP, high-sensitivity C-reactive protein (hs-CRP) and homocysteine (Hcy). BNP, left ventricular mass (LVM), left ventricular mass index (LVMI) and Hcy levels were significantly higher in HD group (p<0.05); hs-CRP levels were significantly higher in PD group (p=0.029). Predialysis BNP was significantly higher than the postdialysis BNP (p=0.003). There was a significant correlation between LVMI and BNP in PD (r=0.527, p=0.009) and predialysis BNP in HD (r=0.417, p=0.043) groups. In conclusion, BNP levels were found to be significantly correlated with LVMI in HD and PD patients. Hemodialysis patients had higher BNP and LVMI levels. This may be due to the hemodynamic changes which occur with the hemodialysis.
Recent Trends in Genomic Biomarkers - Pepgra HealthcarePEPGRA Healthcare
Cardiovascular disease is a significant health concern worldwide despite having many genomics developments providing valuable new candidates for better biomarkers and novel therapeutic targets. The main integration of new technologies promises the discovery and validation of better biomarkers of the presence of cardio disease, its progression, and the response to treatment in this blog. Some of the features are:
1. Analyzing the Gene expression
2. Genome-wide association studies
3. Linkage analysis
4. Wrapping up...
Continue Reading: http://bit.ly/3bqq3Np
Contact us:
UK: +44-1143520021
US/Canada: +1-972-502-9262
India: +91-9884350006
Email id: sales.cro@pepgra.com
Website: www.pepgra.com
Recent trends in genomic biomarkers pepgra healthcarePEPGRA Healthcare
Cardiovascular disease is a significant health concern worldwide despite having many genomics developments providing valuable new candidates for better biomarkers and novel therapeutic targets. The main integration of new technologies promises the discovery and validation of better biomarkers of the presence of cardio disease, its progression, and the response to treatment in this blog. Some of the features are:
1. Analyzing the Gene expression
2. Genome-wide association studies
3. Linkage analysis
4. Wrapping up...
Continue Reading: http://bit.ly/3bqq3Np
Contact us:
UK: +44-1143520021
US/Canada: +1-972-502-9262
India: +91-9884350006
Email id: sales.cro@pepgra.com
Website: www.pepgra.com
A comparative analysis of biochemical and hematological parameters in diabeti...amsjournal
This study evaluated the biochemical and the hematological parameters in diabetic and non- diabetic patients. The measured biochemical parameters were fasting blood sugar, serum alanine aminotransferase (SGPT/ALT), total cholesterol, urea, creatinine and hematological parameters were hemoglobin, total white blood cell, neutrophil, lymphocyte,monocyte, eosinophil and ESR. There were 403 diabetic and 320 non-diabetic subjects included in this study and the study was carried out in BIRDEM (Bangladesh Institute of Research & Rehabilitation in Diabetes, Endocrine and Metabolic Disorders) General Hospital). It was observed that the mean values of SGPT/ALT (p<0.001),><0.001)><0.001)><0.001),><0.004),><0.001) of hematological parameters were significantly higher in diabetic patients than in the non-diabetic patients. In univariate analysis, all biochemical parameters and only four hematological parameters were found significantly associated with fasting blood sugar after adjusted with age and sex. The fasting blood sugar correlates highly with the other biochemical parameters but less or none with the hematological parameters. Our findings demonstrated that control of increased biochemical parameters and abnormal hematological levels in the early stage of diabetes mellitus may help the patients to raise quality of life.
Análisis de desempeño de laboratorios clínicos en la derterminación de glucos...Bladimir Viloria
Análisis de evaluación el desempeño de los Laboratorios Clínicos del estado Carabobo en la determinación
de las concentraciones séricas de glucosa y creatinina.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
2. (rs2191349) (6), and ADRA2A (rs10885122) (8), which
were selected as the variants associated with the largest
effects on fasting glucose levels in genome-wide association
studies specifically aiming to identify variants associated
with plasma glucose levels, and not previously associated
with IHD and MI (9). Furthermore, the genetic variants
have no major effects on other risk factors and, therefore,
can be used to study the impact of longstanding differences
in plasma glucose levels without known pleiotropic effects.
We tested the hypothesis that there is a potential causal
association between elevated nonfasting glucose levels and
increased risk of IHD and MI. As most subjects are in the
nonfasting state the majority of a 24-h cycle, and thus
exposed to higher glucose levels than observed through
fasting measurements, it may be more important to study
nonfasting than fasting glucose levels. First, we tested
whether elevated nonfasting glucose levels are associated
with increased risk of IHD; second, whether the selected
genotypes (5,8,10,11) are associated with elevated nonfast-
ing glucose levels; and finally, whether genotypes are asso-
ciated with increased risk of IHD and MI both as single site
genotypes and combined in instrumental variable analyses.
Methods
Subjects. Studies were approved by institutional review
boards and Danish ethical committees, and conducted
according to the Declaration of Helsinki. Participants were
all white persons and of Danish descent, and gave informed
consent. None appeared in Ͼ1 study.
The CCHS. The CCHS (Copenhagen City Heart Study)
is a prospective study of the general population initiated in
1976 to 1978 with follow-up examinations in 1981 to 1983,
1991 to 1994, and 2001 to 2003, and endpoints ascertained
from 1976 through May 2011 (12). Participants were
selected to reflect the adult Danish population ages 20 to
80ϩ years. Data were obtained from a questionnaire, a
physical examination, and from blood samples at each
examination. Baseline nonfasting plasma glucose levels were
available on 16,568 participants attending the 1976 to 1978,
1981 to 1983, 1991 to 1994, and/or 2001 to 2003 examina-
tions. Baseline was defined as the first examination a subject
participated in. Blood samples for deoxyribonucleic acid
(DNA) extraction were available on 10,603 participants
attending the 1991 to 1994 and 2001 to 2003 examinations.
The CGPS. The CGPS (Copenhagen General Population
Study) is a cross-sectional/prospective study of the general
population initiated in 2003 with ongoing enrollment (13–
15) and endpoints ascertained from 1976 through May
2011. Participants were selected and examined exactly as in
the CCHS. At the time of genotyping, 48,614 subjects had
been included.
The CIHDS. The CIHDS (Copenhagen Ischemic Heart
Disease Study) comprises 5,109 patients from the greater
Copenhagen area referred for coronary angiography in 1991 to
2010 and 10,231 controls without IHD ascertained as for the
CGPS (13–15). In addition to a
diagnosis of IHD, these patients
also had stenosis/atherosclerosis
on coronary angiography and/or a
positive exercise electrocardiogra-
phy test, and/or MI.
Ischemic heart disease and
myocardial infarction. In all
studies, information on diagnosis
of IHD and MI according to
WHO International Classifica-
tion of Diseases (ICD) (ICD8: 410–414 and 410; and
ICD10: I20–I25 and I21) was collected and verified from
1976 through May 2011 by reviewing all hospital admis-
sions and diagnoses entered in the national Danish Patient
Registry and all causes of death in the national Danish
Causes of Death Registry. Ischemic heart disease was
angina pectoris and MI, the latter determined on the basis
of characteristic chest pain, electrocardiographic changes,
and/or elevated cardiac enzymes following the changes in
diagnostic criteria over time (16). Follow-up was 100%
complete, that is, no subject was lost to follow-up in any
study.
Genotypes. Genotyping for GCK (rs4607517), G6PC2
(rs560887), ADCY5 (rs11708067), DGKB (rs2191349), and
ADRA2A (rs10885122) was by TaqMan, ABI Prism
7900HT Sequence Detection System (Applied Biosystems,
Foster City, California). Each run included a known non-
carrier, a heterozygous, and a homozygous control verified
by sequencing. After 2 reruns, call rates for genotypes where
Ͼ99.9% for all assays. We also genotyped the MTNR1B
(rs10830963) variant, but it did not associate with nonfast-
ing glucose levels (observed per allele effect, nonfasting:
Ϫ0.025 [SEM 0.01]) as reported for fasting glucose levels in
genome-wide association studies (per allele effect in litera-
ture: 0.072 [SEM 0.005]) (5,8), and were therefore ex-
cluded from further analysis.
Biochemical analyses. Colorimetric assays were used to mea-
sure nonfasting plasma glucose, total cholesterol, and high-density
lipoprotein (HDL) cholesterol (Konelab, Boehringer Mannheim,
Germany). Blood samples were taken at random irrespective of
content of or of time since the last meal.
Other covariates. Body mass index (BMI) was weight (kg)
divided by height squared (m2
); metabolic syndrome was
defined as fulfilling 3 of the following 5 criteria: waist
circumference Ն102 cm for men and Ն88 cm for women,
triglycerides Ն1.7 mmol/l (150 mg/dl) or drug treatment for
elevated triglycerides, HDL Ͻ1.0 mmol/l (40 mg/dl) in
men and Ͻ1.3 mmol/l (50 mg/dl) in women or drug
treatment for low HDL, systolic blood pressure Ն130 mm
Hg and/or diastolic blood pressure Ն85 mm Hg or antihy-
pertensive drug treatment, fasting glucose Ն5.56 mmol/l
(100 mg/dl), or antidiabetic medication (17); diabetes mel-
litus was self-reported diabetes, use of antidiabetic medica-
tion, a nonfasting plasma glucose Ͼ11.0 mmol/l, and/or
hospitalization or death due to diabetes (ICD8: 249–250;
Abbreviations
and Acronyms
BMI ؍ body mass index
CI ؍ confidence interval
HDL ؍ high-density
lipoprotein
IHD ؍ ischemic heart
disease
MI ؍ myocardial infarction
2357JACC Vol. 59, No. 25, 2012 Benn et al.
June 19/26, 2012:2356–65 Nonfasting Glucose and Ischemic Heart Disease
3. ICD10: E10–E11, E13–E14); hypertension was defined as
systolic blood pressure Ն140 mm Hg (Ն135 mm Hg for
diabetic subjects), diastolic blood pressure Ն90 mm Hg
(Ն85 mm Hg for diabetics), and/or use of antihyperten-
sive medication prescribed specifically for hypertension;
current smoking, menopause status, and statin use were
also self-reported.
Statistical analyses. Data were analyzed by 2 authors
(M.B. and B.G.N.) using Stata/IC version 11.1 (StataCorp,
College Station, Texas). Two-sided p Ͻ 0.05 was signifi-
cant. For trend tests using Cuzick nonparametric test and
extension of a Wilcoxon rank sum test, groups of subjects
classified by nonfasting glucose levels, genotypes, or number
of alleles were ranked according to increasing nonfasting
glucose levels and coded as 0, 1, 2, 3, and so forth.
First, to test whether nonfasting glucose associate with
increased risk of IHD and MI, Kaplan-Meier curves were
used to estimate cumulative incidence, and Cox regression
models with age as time scale and left truncation (delayed
entry) were used to estimate hazard ratios for IHD and MI
in the prospective CCHS. Analyses were conducted using
results from each participant’s first glucose measurement in
the 1976 to 1978, 1981 to 1983, 1991 to 1994, or 2001 to
2003 examinations (i.e., baseline), and data from the serial
examinations of other risk factors were used as time-
dependent covariates for multifactorial adjustment. Risk of
IHD and MI was estimated as a function of nonfasting
glucose levels in groups of 1-mmol/l (18-mg/dl) increases
versus Ͻ5.0 mmol/l (Ͻ90 mg/dl) and as a continuous variable,
and was corrected for regression dilution bias using a factor of
0.45 (Online Figs. 1 and 2) (18). Analyses were adjusted for:
1) age and sex; 2) multifactorially for age, sex, current smoking,
menopause, and statin use; 3) multifactorially including BMI;
4) multifactorially including total cholesterol and HDL cho-
lesterol; 5) multifactorially including hypertension; and 6)
multifactorially including all of the above.
Second, to test whether genotype associate with elevated
nonfasting glucose levels, per allele effects of genotypes were
calculated in the CCHS and CGPS combined to obtain
maximal power; we used a method by Falconer, taking allele
frequency and mean nonfasting glucose levels for each
genotype into account (19).
Third, to test whether genetically elevated nonfasting
glucose levels associate with increased risk of IHD, we
tested for association between genotype and IHD and MI
risk using logistic regression in the CCHS, CGPS, and
CIHDS combined to obtain maximal power. Analyses were
adjusted for age and sex only, as genotypes were randomly
distributed across the covariates.
Finally, instrumental variable analysis by 2-stage least-
squares regression was used to assess a potential causal
relationship between elevated nonfasting glucose levels and
increased IHD and MI risk using genetic variants as
instruments for elevated nonfasting glucose levels in an
additive model; we used the CCHS, CGPS, and CIHDS
combined to obtain maximal power. Strength of the geno-
types as instruments (association of genotype with plasma
glucose) was evaluated by F-statistics from the first-stage
regression, where F Ͼ10 indicates sufficient strength to
ensure the validity of the instrumental variable analysis,
while R2
in percent is a measure of percent contribution of
genotype to the variation in plasma glucose (4). Causal odds
ratios were estimated using the multiplicative generalized
method of moments estimator implemented in the user-
written Stata command “ivpois.” Altman’s method (20) was
used to compare the causal odds ratio from the instru-
mental variable analysis with the observational multifac-
torially adjusted hazard ratio from Cox regression. Use of
Ͼ1 genotype as instrumental variable reduces risk of bias
Characteristics of ParticipantsTable 1 Characteristics of Participants
Characteristics CCHS CGPS CIHDS
n 16,568 48,614 15,340
Ischemic heart disease* 4,184 4,862 5,109
Myocardial infarction* 2,327 2,038 1,892
Age, yrs 51 (40–59) 58 (47–67) 57 (48–66)
Women 53% 56% 46%
Body mass index, kg/m2
24.3 (22.2–26.8) 25.6 (23.2–28.5) 25.6 (23.2–28.5)
Total cholesterol, mmol/l 6.0 (5.2–6.8) 5.6 (4.9–6.3) 5.5 (4.7–6.3)
HDL cholesterol, mmol/l 1.4 (1.1–1.7) 1.6 (1.3–2.0) 1.5 (1.2–1.9)
Diabetes mellitus 2.1% 3.7% 13.2%
Hypertension 47% 71% 55%
Current smoking 53% 20% 26%
Menopause, women only 49% 66% —
Statin use 1.5% 11% —
Values are n, mean (range), or %. *Number of disease events at end of follow-up. Other data are from enrollment into the studies: In the CCHS
(Copenhagen City Heart Study), values are from the first participation in the study in either 1976 to 1978, 1981 to 1983, 1991 to 1994, or 2001
to 2003; in the CGPS (Copenhagen General Population Study), from enrollment 2003 to 2010; and in the CIHDS (Copenhagen Ischemic Heart
Disease Study), from enrollment 1994 to 2010. To convert glucose in mmol/l to mg/dl, multiply by 18; to convert cholesterol in mmol/l to mg/dl,
multiply by 39.
HDL ϭ high-density lipoprotein.
2358 Benn et al. JACC Vol. 59, No. 25, 2012
Nonfasting Glucose and Ischemic Heart Disease June 19/26, 2012:2356–65
4. due to pleiotropy, but may result in an overestimation of
the causal risk estimate (21). This can be evaluated using
effect estimates (strength of the association between
genotype and glucose level) from previous independent
studies. To do this, we repeated the instrumental variable
analyses using effect estimates from published genome-
wide association studies (effect sizes shown in Fig. 2)
(5,6,8).
Results
Characteristics of the 80,522 participants in the 3 study
populations are shown in Table 1; IHD developed in 14,155
subjects and MI in 6,247. Age, BMI, total cholesterol levels,
frequency of male sex, metabolic syndrome, diabetes melli-
tus, use of insulin or oral antidiabetic medication, hyperten-
sion, smoking, menopause (women only), and statin use
were higher at higher nonfasting plasma glucose levels,
whereas HDL cholesterol levels were lower (Online
Table 1). Variation in nonfasting plasma glucose levels as a
function of time since the last meal in hours is shown in
Online Figure 1. Median values ranged from 5.66 mmol/l at
0 to 1 h after a meal to 5.08 mmol/l Ͼ8 h after a meal (range
0.58 mmol/). Regression dilution on plasma glucose levels
from the 1976 to 1978 to the 1981 to 1983 examination is
shown in Online Figure 2, and was used to correct associ-
ation between nonfasting glucose and risk of IHD and MI
for regression dilution bias.
Nonfasting glucose and IHD and MI observational
estimates. Risk of IHD and MI increased stepwise with
increasing nonfasting glucose levels (Figs. 1 and 2). Subjects
with a level Ͼ11 mmol/l had their event on average 20 years
before subjects with levels Ͻ5 mmol/l (Fig. 1). Age- and
sex-adjusted hazard ratio for IHD was 6.9 (95% confidence
interval [CI]: 4.2 to 11.2) in subjects with nonfasting plasma
glucose levels Ն11 mmol/l (Ն198 mg/dl) versus Ͻ5 mmol/l
(Ͻ90 mg/dl). Corresponding estimates were 6.2 (95% CI:
3.8 to 10.2) when adjusting multifactorially; 4.7 (95% CI:
2.8 to 7.7) multifactorially including BMI; 3.8 (95% CI: 2.2
to 6.5) multifactorially including total and HDL choles-
terol; 5.8 (95% CI: 3.6 to 9.5) multifactorially including
hypertension; and 2.3 (95% CI: 1.3 to 4.2) multifactorially
including all the above. Corresponding values for MI were
9.2 (95% CI: 4.6 to 18.2), 8.3 (95% CI: 4.2 to 16.6), 6.8
(95% CI: 3.4 to 13.7), 6.0 (95% CI: 2.8 to 13.0), 7.5 (95%
CI: 3.8 to 15.0), and 4.8 (95% CI: 2.1 to 11.2).
Genotype and nonfasting glucose. Homozygotes versus
noncarriers associated with the following increases in
nonfasting plasma glucose levels: GCK (rs4607517) 2.7%
(95% CI: 1.5% to 3.8%), G6PC2 (rs560887) 2.5% (1.9%
to 3.2%), ADCY5 (rs11708067) 1.5% (0.7% to 2.2%),
DGKB (rs2191349) 0.8% (0.3% to 1.3%), and ADRA2A
(rs10885122) 0.5% (Ϫ1.1% to 2.0%) (Fig. 3). Combining
genotypes by number of glucose-increasing alleles, an
increasing number of glucose-increasing alleles associated
with an up to 4.8% (3.6% to 6.0%) increase in nonfasting
glucose levels.
Genotype and IHD and MI. Assuming that increased
nonfasting glucose levels have a causal effect on risk of IHD
and MI, lifelong increased glucose levels due to genetic
variants should confer a similar increase in risk of IHD and
MI as that observed for increased glucose levels encountered
in the general population. For example, the 4.8% increase in
nonfasting glucose levels seen for 8 glucose-increasing alleles
(Fig. 3) would theoretically predict an increased risk of IHD
and MI with hazard ratios of 1.04 (95% CI: 1.03 to 1.05) and
1.04 (95% CI: 1.03 to 1.05) (Online Fig. 3). In accordance
with this, the observed odds ratio for IHD increased as a
function of the glucose-increasing alleles with the largest
glucose-increasing effects (p trend ϭ 0.01) (Online Fig. 3); the
Figure 1
Cumulative Incidence Using Kaplan-Meier
Estimates of IHD and MI
Cumulative incidence using Kaplan-Meier estimates of (A) ischemic heart dis-
ease (IHD) and (B) myocardial infarction (MI) in percent as a function of age at
event. Subjects with IHD or MI before study enrollment were excluded, result-
ing in 16,318 subjects followed up for as long as 35 years with respect to inci-
dent events. Solid line indicates Ͻ5 mmol/l; long-dashed line indicates 5 to
6.9 mmol/l; shorter-dashed line indicates 7 to 8.9 mmol/l; shortest-dashed
line indicates 9 to 10.9 mmol/l; and dotted line indicates Ն11 mmol/l.
2359JACC Vol. 59, No. 25, 2012 Benn et al.
June 19/26, 2012:2356–65 Nonfasting Glucose and Ischemic Heart Disease
5. Figure 2 Risk of IHD and MI as a Function of Baseline Nonfasting Plasma Glucose Levels in General Population
Nonfasting plasma glucose levels were measured in 16,568 subjects who participated in the 1976 to 1978, 1981 to 1983, 1991 to 1994, and/or 2001 to 2003
examinations of the Copenhagen City Heart Study. Results are shown for (A) ischemic heart disease (IHD) and (B) myocardial infarction (MI). Participants with IHD or MI
before study enrollment were excluded, resulting in 16,318 subjects followed up for as long as 35 years with respect to incident events. Basic multifactorial adjustment
was for age, sex, current smoking, menopause, and statin use. The fully multifactorially adjusted model additionally included body mass index, total cholesterol, high-
density lipoprotein (HDL) cholesterol, and hypertension. CI ϭ confidence interval; HR ϭ hazard ratio.
2360 Benn et al. JACC Vol. 59, No. 25, 2012
Nonfasting Glucose and Ischemic Heart Disease June 19/26, 2012:2356–65
6. various risk factors except glucose levels were equally distrib-
uted among the genotypes, confirming that these genotypes are
largely unconfounded by such factors (Online Table 2). Results
for MI were similar (Online Fig. 3).
Nonfasting glucose and IHD and MI causal estimates.
A potential causal effect of increased nonfasting glucose
levels on increased risk of IHD and MI was also examined
using instrumental variable analysis. A 1-mmol/l (18-mg/
Figure 2 Continued
2361JACC Vol. 59, No. 25, 2012 Benn et al.
June 19/26, 2012:2356–65 Nonfasting Glucose and Ischemic Heart Disease
7. dl) increase in nonfasting glucose levels due to genotypes
associated with a causal odds ratio for IHD of 1.25 (95% CI:
1.03 to 1.52) and MI of 1.69 (95% CI: 1.28 to 2.23), and
the observed multifactorially adjusted hazard ratio for a
similar increase was 1.18 (95% CI: 1.15 to 1.22) for IHD
and 1.09 (95% CI: 1.07 to 1.11) for MI (Fig. 4). The
corresponding causal odds ratios for IHD and MI were 1.36
(95% CI: 1.05 to 1.77) and 1.54 (95% CI: 1.05 to 2.27),
respectively, using effect estimates for per allele increases in
fasting glucose levels from the literature.
Discussion
The main finding of this study is that both observational
and genetically elevated nonfasting glucose levels are asso-
ciated with increased risk of IHD and MI. This finding is
compatible with elevated glucose levels per se being causally
related to the development of IHD and MI.
Overall, evidence for or against a causal contribution of
glucose to the pathogenesis of macrovascular disease, in-
cluding IHD and MI, can come from 5 types of evidence;
that is, conventional epidemiology, mechanistic studies,
animal models, randomized intervention trials, and Men-
delian randomization studies like the present (22,23).
1) Previous prospective epidemiologic studies showed that
elevated fasting glucose levels associate with increased IHD
and MI risk even at nondiabetic glucose levels (1,2). Our
results using nonfasting glucose levels are in agreement with
this, and confirm that even after adjustment for obesity,
dyslipidemia, and hypertension, elevated IHD and MI risk
remain. 2) Results from in vitro and animal studies have
suggested several mechanisms by which glucose may con-
tribute to macrovascular disease: increased glucose levels,
free fatty acids, and insulin resistance together leads to
oxidative stress, activation of protein kinase C isoforms,
formation of advanced glycation end product, and nonen-
zymatic glycation of low-density lipoprotein, apolipopro-
teins, and clotting factors, collectively resulting in vasocon-
striction, inflammation, and thrombosis (2,24,25). 3) In
animal models with experimental hypercholesterolemia or
genetic predisposition for atherosclerosis, elevated glucose
Gene Genotype
No. of
participants
Mean (standard error) P-trend
Change in glucose levels, %
(95% confidence interval)
Per allele effect,
mmol/L (SEM)
Per allele effect,
mmol/L (SEM);
GWAS (5,6,8)
Risk allele
frequency;
GWAS
GCK rs4607517,G>A
)700.0(260.0)610.0(370.00100.0<511,84GG
)4.1-6.0(0.1560,81AG
81.0)8.3-5.1(7.2517,1AA
G6PC2 rs560887,C>T
)400.0(460.0)900.0(860.00100.0<193,6TT
)5.1-2.0(9.0586,82TC
82.0)2.3-9.1(5.2147,23CC
ADCY5 rs11708067,A>G
)300.0(720.0)110.0(930.00100.0<880,4GG
)9.0-6.0-(1.0715,52GA
87.0)2.2-7.0(5.1292,83AA
DGKB rs2191349,T>G
)7800.0(640.0)700.0(220.00100.0<730,61GG
)0.1-1.0(5.0539,33GT
25.0)3.1-3.0(8.0029,71TT
ADRA2A rs10885122,G>T
)400.0(220.0)220.0(710.0020.0988TT
)7.1-5.1-(1.0325,31TG
78.0)0.2-1.1-(5.0394,35GG
Glucose increasing alleles
0100.0<310,23-0
)1.2-3.0-(9.0364,64
)7.2-5.0(6.1726,415
)1.4-8.1(9.2099,916
)6.4-3.2(4.3980,617
)0.6-6.3(8.4640,78
Nonfasting glucose, mmol/L
Figure 3 Nonfasting Plasma Glucose Levels as a Function of Genotype in General Population
Glucose-increasing alleles were combinations of genotypes with glucose-increasing effects; the most common genotype combinations are shown, whereas the rarer com-
binations were excluded because of reduced statistical power. This was examined in 67,914 participants from the Copenhagen City Heart Study and the Copenhagen
General Population Study combined, irrespective of other cardiovascular risk factors or treatment for diabetes mellitus. Estimates of effect on fasting plasma glucose
levels reported from genome-wide association studies (GWAS) using plasma glucose level as the phenotype are reported in the right column. To convert mmol/l glucose
to mg/dl, multiply by 18.
2362 Benn et al. JACC Vol. 59, No. 25, 2012
Nonfasting Glucose and Ischemic Heart Disease June 19/26, 2012:2356–65
8. levels may directly cause macrovascular disease (24,26). 4) A
meta-analysis of randomized intervention trials (27–32)
showed that intensive glycemic control in patients with
diabetes mellitus was associated with a 15% reduction in risk
of IHD (3). However, in all included studies, intensive
glycemic control also had beneficial effects on obesity,
dyslipidemia, and/or hypertension, obscuring the isolated
effect of reduced glucose levels, and this issue remains
unresolved. 5) Using a Mendelian randomization approach
free from reverse causation and unconfounded by obesity,
dyslipidemia, and hypertension, we here found that both
observational and genetic lifelong elevated nonfasting or
fasting glucose levels associate with increased risk of IHD
and MI. In the present study, we use genotypes associated
with glucose levels in the nondiabetic range and not asso-
ciated with diabetes mellitus in our general population
samples, suggesting that the increased risk of IHD is more
likely due to glucose per se, rather than mediated through
diabetes mellitus. A recent Mendelian randomization study
support that elevated fasting plasma glucose levels may also
be causally related to increased intima-media thickness (33).
Therefore, these 5 different types of evidence collectively
suggest that elevated plasma glucose per se might be causally
related to the development of IHD and MI.
From a clinical standpoint, our confirmation of increased
nonfasting glucose as a marker of increased IHD risk
suggests that nonfasting values may be used in risk stratifi-
cation, whereas for diagnostic purposes, fasting values are
required. Although nonfasting/post-prandial glucose levels
are more variable than fasting levels, risk of cardiovascular
disease is more strongly associated with nonfasting/post-
prandial hyperglycemia than fasting hyperglycemia (34).
The exact reason for this is not known, but it has been
observed that persons with impaired glucose tolerance, a
Figure 4 Summary of Causal Effects of Increased Nonfasting Glucose on Increased Risk of IHD and MI
Studies’ summary of the causal effect of increased nonfasting glucose on increased risk of ischemic heart disease (IHD) and myocardial infarction (MI). This was tested
in the Copenhagen City Heart Study, the Copenhagen General Population Study, and the Copenhagen Ischemic Heart Disease Study combined; 6,448 participants were
not genotyped for lack of deoxyribonucleic acid; and for participants genotyped, numbers vary slightly from genotype to genotype. The causal effect of increased nonfast-
ing glucose levels on risk of IHD and MI was estimated by the association between a 1-mmol/l (18-mg/dl) genetic increase in nonfasting glucose levels and risk of IHD
and MI, using instrumental variable analysis by 2-stage least-squares regression and given as an odds ratio (OR) with a 95% confidence interval (CI). This risk is com-
pared to the observational prospective increased risk of IHD and MI, respectively, associated with a 1-mmol/l (18-mg/dl) increase in nonfasting glucose in the general
population, the Copenhagen City Heart Study, given as a multifactorially adjusted Cox regression hazard ratio (HR) with a 95% CI. Odds ratios for a 1-mmol/l (18-mg/dl)
genetic increase in nonfasting glucose levels are also given for individual and combined genotypes. F-statistics (evaluation of strength of instrument) and R2
(contribution
of genotype to variation in plasma glucose levels in percent) are from the first-stage regression analysis. In the second-stage regression analysis studying the associa-
tion between genotype and risk, imputed glucose values were included in part of the cases in the Copenhagen Ischemic Heart Disease Study. The causal effect of a
1-mmol/l (18-mg/dl) genetic increase in nonfasting glucose levels on risk of IHD and MI was also estimated using effect sizes for genotypes previously reported from
genome-wide association studies specifically aimed at identifying genes associated with plasma glucose levels. The p value is for significance of hazard ratio/odds ratio.
The p value comparison is between the estimate from observational epidemiology and the causal estimate from instrumental variable analysis. To convert mmol/l glu-
cose to mg/dl, multiply by 18.
2363JACC Vol. 59, No. 25, 2012 Benn et al.
June 19/26, 2012:2356–65 Nonfasting Glucose and Ischemic Heart Disease
9. diagnostic group known to have a high risk of cardiovascular
disease, have elevated nonfasting/post-prandial glucose lev-
els, but usually fasting blood glucose levels within the
normal range (35). The use of nonfasting glucose measure-
ments may explain the relatively high observational risk
estimates in the present study compared to others (1), but
this difference may also in part be because we were able to
adjust for regression dilution bias (18).
Strengths of the present study are that we had sufficient
statistical power to document increased risk of IHD and MI
as a function of glucose-increasing genotypes. Another
strength of the present study was that all participants were
white persons of Danish descent, thus effectively excluding
admixture as a potential problem in our study.
A potential limitation of the present Mendelian random-
ization approach is that, apart from their involvement in
glucose regulation and metabolism, the presently studied
genetic variants may have pleiotropic effects on other
cardiovascular risk factors or directly on IHD and MI risk
unrelated to nonfasting glucose levels. However, we did not
find any consistent associations with age, BMI, levels of
total cholesterol or HDL cholesterol, or frequency of
metabolic syndrome, diabetes mellitus, use of insulin or oral
antidiabetic medication, hypertension, current smoking,
menopause, or statin use across genotypes. Nevertheless, the
ADCY5 and DGKB genes are reported to be involved in
symphacetic and parasymphacetic regulation of heart rate
(10) and may have an effect on IHD and MI risk through 1
of these pathways. Furthermore, ADRA2A is directly in-
volved in lipolysis and is associated with risk of attention
deficit/hyperactive disorder (11). Except for increased birth
weight reported to be associated with GCK genotype, no
pleiotropic effects have been reported for the GCK and
G6PC2 genes with the largest effects on nonfasting glucose
levels in the present study. Using Ͼ1 genotype reduces the
effect of unknown pleiotropy of the genotypes and reduces the
influence of a genotype directly associated with risk of IHD
and MI unrelated to nonfasting glucose levels, but may result
in an overestimation of the causal risk (4). Another potential
limitation of the present study is the modest contribution of
genotypes to the variation in nonfasting glucose levels (weak
instrument bias and unreliable instruments bias) and the use of
5 genotypes as instruments. To evaluate this, we first used F
statistics to test the strength of the instruments and found that
3 of 5 instruments were excellent, and combined, all 5
genotypes were good instruments (F Ͼ10). We then repeated
the instrumental variable analyses using effect estimates from
published genome-wide association studies. The causal esti-
mate using external independent effect sizes corresponded with
the causal estimate from the present study populations, sug-
gesting that such a bias is unlikely. Also, we studied white
subjects only, and therefore our results may not necessarily
translate to other races. A known limitation of prospective
studies using a baseline nonfasting measurement for classifica-
tion is misclassification due to regression dilution bias, which is
the fact that extreme values at baseline tend to attenuate over
time and regress toward the mean value of measurements (4).
In the present study, we corrected for this using results from
subjects with Ͼ1 measurement over time to estimate the
degree of regression dilution.
Conclusions
Both elevated observational and genetic nonfasting glucose
levels are associated with increased risk of IHD and MI.
These data are compatible with a causal association.
Acknowledgments
The authors thank Hanne Damm and Dorthe Uldall
Andersen for assisting with the large-scale genotyping. The
authors are indebted to the staff and participants of the
CCHS, the CGPS, and the CIHDS for their important
contributions.
Reprint requests and correspondence: Dr. Børge G. Nordest-
gaard, Department of Clinical Biochemistry, Herlev Hospital,
Copenhagen University Hospital, Herlev Ringvej 75, Herlev
DK-2730, Denmark. E-mail: Boerge.Nordestgaard@regionh.dk.
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Key Words: cardiovascular disease y diabetes mellitus y
epidemiology y nonfasting y plasma glucose y post-prandial.
APPENDIX
For supplemental figures and tables,
please see the online version of this article.
2365JACC Vol. 59, No. 25, 2012 Benn et al.
June 19/26, 2012:2356–65 Nonfasting Glucose and Ischemic Heart Disease