Connections Between Hepatic and Cardiovascular Disease,Diagnostic criteria for cirrhotic cardiomyopathy 2005 and 2019.New CCM criteria based
on contemporary CV imaging parameters
LV Systolic Function.
LV Diastolic Dysfunction.cardiac evaluation algorithm for liver transplant candidates
SEMINAR PRESENTATION ON CONTRAST INDUCED NEPHROPATHY BY PHARM D STUDENT
IT INCLUDES COMPLETE OVERVIEW OF THE TOPIC CIN.
POST CONTRAST ACUTE KIDNEY INJURY( PC-AKI) WITH TREATMENT AND MANAGEMENT.
SEMINAR PRESENTATION ON CONTRAST INDUCED NEPHROPATHY BY PHARM D STUDENT
IT INCLUDES COMPLETE OVERVIEW OF THE TOPIC CIN.
POST CONTRAST ACUTE KIDNEY INJURY( PC-AKI) WITH TREATMENT AND MANAGEMENT.
download link : https://www.dropbox.com/s/a8ug16pfkvv1bzp/Cardiorenal%20syndrome.ppt?m
Join us on our facebook group: NephroTube...............Follow our blog: www.nephrotube.blogspot.com
Contrast induced nephropathy (CIN) is agenerally reversible form of acute kidney injury (AKI) that occurs soon after the administration of radiocontrast media.
HCM is a common genetic heart disease reported in populations globally
Inherited in an autosomal dominant pattern
The distribution of HCM is equal by sex, although women are diagnosed less commonly than men
The prevalence of unexplained asymptomatic hypertrophy in young adults has been reported to range from 1:200 to 1:500
Portal biliopathy is defined as abnormalities in the intrahepatic and extrahepatic biliary tract, gallbladder and cystic duct secondary to portal hypertension
download link : https://www.dropbox.com/s/a8ug16pfkvv1bzp/Cardiorenal%20syndrome.ppt?m
Join us on our facebook group: NephroTube...............Follow our blog: www.nephrotube.blogspot.com
Contrast induced nephropathy (CIN) is agenerally reversible form of acute kidney injury (AKI) that occurs soon after the administration of radiocontrast media.
HCM is a common genetic heart disease reported in populations globally
Inherited in an autosomal dominant pattern
The distribution of HCM is equal by sex, although women are diagnosed less commonly than men
The prevalence of unexplained asymptomatic hypertrophy in young adults has been reported to range from 1:200 to 1:500
Portal biliopathy is defined as abnormalities in the intrahepatic and extrahepatic biliary tract, gallbladder and cystic duct secondary to portal hypertension
Presentation given by Sonia Eiras from the Health Research Institute of Santiago de Compostela (IDIS) in the framework of the Emergence Forum Barcelona
Biocat organized the Barcelona Emergence Forum (April 10-11th, 2014, Congress Palace, Montjuïc) supported by the TRANSBIO SUDOE, a translational cooperation project dedicated to innovation in life sciences in South-West Europe. The Barcelona Emergence Forum contributed to bringing together Academics, Companies, Investment Entities, Technology Platforms and Technology Transfer Offices from Spain, France and Portugal to set up collaborative projects on Human Health & Agro-food Innovation.
More information at: http://www.b2match.eu/emergenceforum2014
Cardiology: Treatment of Heart FailureVedica Sethi
Abstract Heart Failure (HF) is the most widely recognized cardiovascular disorder behind medical clinic affirmation for individuals more established than 60 years old. Hardly any regions in medication have advanced as surprisingly as HF treatment in the course of recent decades. Be that as it may, progress has been reliable just for ceaseless HF with diminished discharge part. In intensely decompensated HF and HF with safeguarded discharge part, none of the medications tried to date have been conclusively demonstrated to improve endurance. Deferring or forestalling HF has gotten progressively significant in patients who are inclined to HF. The anticipation of declining interminable HF and hospitalisations for intense decompensation is likewise critical. The target of this paper is to give a compact and down to earth rundown of the accessible medication medicines for HF. The most ideal proof based medication treatment (counting inhibitors of the renin–angiotensin– aldosterone framework and β blockers) is helpful just when ideally actualized. Notwithstanding, usage may be testing. To accept that ailment the executives projects can be useful in giving a multidisciplinary, comprehensive way to deal with the conveyance of ideal clinical consideration. Keywords; heart failure, multidisciplinary approach, Beat-blocker, RAAS framework
The cardio-metabolic continuum.
Hypertension and global cardio-metabolic risk
Hypertension Continuum Stages
What is the total cardiovascular risk?
What is the residual cardiovascular risk?
Global “Cardio-metabolic” Residual Risk Reduction
Residual CV risk rising from obesity.Metabolic syndrome.From NAFLD (Non-Alcoholic Fatty Liver Disease)
to MAFLD (Metabolic dysfunction-Associated Fatty Liver Disease)
Congestive Heart FailureAbstractThe primary function of the he.docxmaxinesmith73660
Congestive Heart Failure
Abstract
The primary function of the heart is to pump blood to all organs of the body, delivering oxygen and nutrients to the tissues and at the same removing waste products. At rest, organs need a certain amount of blood for this function. During activity, there are greater demands on the heart and more blood perfusion is required. To meet this varying demands, the heart rate and force of contraction of the heart may change and the blood vessels vasodilate to deliver more blood to the organs. In an individual with congestive heart failure (CHF), the heart is not able to meet these demands or is not able to work efficiently as it should. There are many causes of CHF some of which are reversible. However, heart failure can be sudden and present with a variety of symptoms such as dyspnea. Over time the architecture of the heart changes as it enlarges-this also alters the geometry of the valves leading to mitral valve regurgitation which makes heart failure worse. Overall, the prognosis of patients with heart failure is guarded and they have a poor quality of life.
Introduction
Heart failure is a pathological medical disorder where there is an abnormality of heart function, which results in an inability to pump blood to the rest of the body resulting in poor perfusion of the organs (Dumitru & Ooi, 2015). Heart failure may be due to systolic dysfunction where the pumping action of the hart is reduced or it may be diastolic where the heart chambers do not fill adequately because of stiffness in the walls. The clinical signs of heart failure depend on whether there is right or left heart failure. Heart failure is classified by the New York Heart Association based on presence of symptoms and the degree of effort needed to trigger them as follows:
· Class I patients have no limitation of physical activity
· Class II patients have slight limitation of physical activity
· Class III patients have marked limitation of physical activity
· Class IV patients have symptoms even at rest and are unable to carry on any physical activity without discomfort
Pathophysiology
The pathophysiology of heart failure is complex because of presence of compensatory mechanisms at all levels of the organization of the heart and other systemic influences. It is only when these network of organizations become overwhelmed that heart failure occurs. In summary the inefficient heart pumping results in back-up of fluids to lungs (Left sided failure) or peripheral tissues (Right sided failure). Compensatory mechanisms that occur include changes in myocyte size (ie hypertrophy) and activation of various neurohumoral systems. There is release of catecholamines by the sympathetic nerves to enhance myocardial contractility, activation of the activation of the renin-angiotensin-aldosterone system and other vasoregulating adjustments to maintain mean arterial pressure and perfusion of vital organs (Urso et al, 2015).
Etiology
The majority of patients who present.
Pro / Con Debate on Central Blood Pressuremagdy elmasry
The Basis : Forward & Reflected Pulse Waves
Central BP - Pro Side of the Argument
Central BP - Con Side of the Argument
Central BP - Consensus on Clinical Application
FDA-cleared devices for central BP and arterial stiffness assessment
Value of measuring central BP in clinComparative effect of
anti-hypertensive drugs and nitrates
on central systolic BP
ical practice
isolated systolic hypertension in the young
Diagnosis and Management of Cardiovascular Involvement in Friedreich Ataxia
GAA 7-34 times→Normal
GAA 100-1700 times→FRDA
Current Research
into Drug Treatments
for Friedreich ataxia
Best Practice in Rare Diseases
Although CNS involvement dominates the clinical presentation of FRDA ,
CV involvement dictates its prognosis, accounting for ~ 59% of deaths among FRDA patients .
The prognosis is particularly poor for those with progressive LV systolic dysfunction.
Should we screen for and treat childhood dyslipidemia?
The Rationale for ASCVD Prevention by Primordial and Primary Strategies
Pediatric guidelines
Selective Screening
2Treatment algorithm of childhood dyslipidemia
-8 years & 12-16 years
Dyslipidemia and lipid lowering-therapy {LLT}
in women through the course of life. Lipid loering drug safety profile .Aging is associated with an increasing burden of morbidity, especially for CVDs.
Elderly population should be screened for
Main CV risk factors :
T2D , HTN , Smoking , Dyslipidemia & Obesity
Comorbidities : CKD
Geriatric conditions: Functional Impairment
Linking HFpEF and Chronic kidney disease magdy elmasry
Cardio-renal interactions
Introducing nephro-cardiology
{ or cardio-nephrology }
Where are we in 2022 with HFpEF ?CKD in HFpEF { or HFpEF in CKD } Cardiorenal
Syndrome .Four-step
HFA-PEFF diagnostic algorithm
heterogeneity in patients with HFpEF.Phenotyping HFpEF :
Beyond EF.Management of HFpEF .patients with HF on dialysis
Drug Treatment of Chronic Coronary Syndrome: Focus Issue on Ranolazinemagdy elmasry
Chronic Coronary Syndromes .Old and New Anti-anginal Drugs.Sodium channel blocker(Ranolazine)Angina / ischaemiac relief .
Voltage-gated sodium channels (NaVChs).Patient profile to guide drug treatment of
chronic coronary syndromes .Therapeutic algorithm for chronic stable angina according to heart rate and blood pressure.Treatment Options for Microvascular angina / Vasospastic angina.Ranolazine in arrhythmias
Ranolazine in ischemic reperfusion injury
Ranolazine in pulmonary hypertension
Ranolazine in heart failure
Ranolazine in the prevention of chemotherapy‑induced cardiotoxicity
Role in diabetes mellitus
Ranolazine in peripheral arterial disease
Ranolazine in myotonia‑congenita
Ranolazine in hypertrophic cardiomyopathy.Antiarrhythmic properties of ranolazine.Amiodarone +Ranolazine
Strategies to improve adherence to antihypertensive medicationmagdy elmasry
Challenges in hypertension treatment.What is the definition of medication non-adherence?Who is at risk? How should
patients at risk be screened and identified?What are the negative impacts of non-adherence?What is the
practical approach for improving adherence? The ABC taxonomy for medication adherence
Adherence :3 quantifiable components: initiation , implementation , and discontinuationThe five dimensions
of non-adherence
.
Do T2DM drugs have CV benefit for Type 1 Diabetes ?magdy elmasry
T1D Exchange , average A1C levels have not improved .How can adjunctive therapies ( added to insulin ) can help?
The Removal Trial.Three main clinical trials :
DEPICT with dapagliflozin ,
EASE with empagliflozin , and
inTANDEM with sotagliflozin.
Takotsubo syndrome diagnostic criteria.
position papers :Mayo clnic ,HFA and InterTAK Diagnostic Criteria.Takotsubo Syndrome and COVID-19.Noninvasive Multimodality Imaging
in the Diagnosis and Management
of Patients with Takotsubo Syndrome
CVD in cancer survivors.Screening of cancer survivors.Chest Radiotherapy .JACC Scientific Expert Panel
( J Am Coll Cardiol 2019;74:905–27 )manifestations of chest and mediastinal radiotherapy .
Anti-Diabetics For Cardiac Patients The Proper Selectionmagdy elmasry
Cardiovascular Disease and Type 2 Diabetes.Tight glycaemic control can reduce microvascular complications of T2DM, but does not lower CV risk sufficiently.
Multifactorial intervention, comprising of lowering lipid levels and BP, and use of aspirin, has been shown to reduce vascular complications and mortality.Shifting the Paradigm in Diabetes Care
Treating Diabetes Beyond A1C :Considerations for Cardiovascular Protection.
Peripartum Cardiomyopathy .BOARD scheme for the therapy of patients with acut...magdy elmasry
Definition of peripartum cardiomyopathy;Risk factors for the development of PPCM .Environmental Factors
Vasculohormonal (pregnancy).Genetic Factors Titin-truncating
Variants (TTNtv) .Secretion of prolactin by the anterior pituitary gland, upregulation of endothelial microRNA-146a (miRNA-146a), and placental secretion of soluble fms-like tyrosine kinase receptor 1 (sFlt-1) lead to endothelial dysfunction and cardiomyocyte death.Antisense therapy against microRNA-146a
Prolactin inhibition.bromocriptine .biomarkers in peripartum cardiomyopathy
Thyroid Hormones and Cardiovascular Function and Diseasesmagdy elmasry
Thyroid hormone system.
Thyroid hormone action on the CVS.
Thyroid hormones and cardioprotection.
How does thyroid disease affect the heart?
- Thyroid disease and CV risk factors.
- Thyroid dysfunction and CVD.
Thyroid hormones : a future therapeutic option?
New recommendations for a thyroid and CVD.
Thyroid and CV drugs.
Chronic Obstructive Pulmonary Disease and Heart Failure The challenges facin...magdy elmasry
Chronic Obstructive Pulmonary Disease and Heart Failure
The challenges facing cardiologists and pulmonologists,
prevalence of heart failure in COPD patients .Association of Cardiovascular Disease With Respiratory Disease,An atypical presentation of myocardial infarction (MI) should be considered in every patient presenting with COPD exacerbation ,Cardiovascular and pulmonary disease in the context of inflammation
(“CardioPulmonary Continuum”),The cornerstones of therapy are beta-blockers and beta-agonists ,which as their modes of action suggest oppose each other’s action
The main hemodynamic interactions that may impact on the diagnosis of multiple and mixed Multiple and Mixed Valvular Heart Diseases:HOW TO USE IMAGINGThe interplay of multiple valve pathology.The clinical challenge of concomitant aortic and mitral valve stenosis
.
.
Cancer-Associated Thrombosis.From LMWH to DOACsmagdy elmasry
Cancer-Associated Thrombosis.Risk factors for CAT. Certain types of cancer are associated with higher risk of CAT. Anticoagulant therapy for VTE in patients with cancer
Should You Use DOACs for Cancer-Associated VTE?.Criteria for DOAC use in cancer patients requiring anticoagulation .DOACs + AntiCancer agents
The Progression of Hypertensive Heart Disease.From hypertension to heart failuremagdy elmasry
Staging of Hypertensive Heart Disease.Precipitants and clinical sequelae related to LVH and myocardial fibrosis.Imaging in hypertensive heart disease .Differential diagnosis of LVH.Concentric LVH .Eccentric LVH . Concentric remodeling .linking hypertension and atrial fibrillation
Role of the Renin–Angiotensin–Aldosterone System Inhibition Beyond BP Reductionmagdy elmasry
Hypertension Mediated Organ Damage : How We Prevent It?The Role Of RAAS In Cardiovascular Continuum.Changes in Arterial Diameter in Patients with Arteriosclerosis or Atherosclerosis.Not All Angiotensin-Converting Enzyme Inhibitors Are Equal.Question : ACEIs vs. ARBsIs One Class Better For Cardiovascular Diseases?BP Variability .Central BP
.
Vascular Age &
Arterial Stiffness.Achieving BP Goals.
Cardio-Renal Protection Through Renin–Angiotensin–Aldosterone System Inhibitionmagdy elmasry
Physiological and detrimental roles of RAAS molecules in cardiac, vascular tissues and kidneys.‘cardiovascular continuum’ Barriers In Optimizing RAAS Inhibition.The effects of angiotensin II inhibition and improvement in bradykinin availability
HDL-cholesterol concentrations are inversely associated with CVD.When we consider cardiovascular mortality in women in terms of HDL.Causes of low HDL cholesterol.Lipoprotein subfractions suffer a shift after menopause towards a more atherogenic lipid profile.associations of HDL-C and HDL-P with cIMT and CHD.MESA (Multi-Ethnic Study of therosclerosis. Functional Versus Dysfunctional HDL. High concentrations of HDL - cholesterol are associated with high all-cause mortality in men and women.Improvement of HDL function without necessarily raising HDL-C
Fourth Universal Definition Of Myocardial Infarction (2018)magdy elmasry
Reasons for the elevation of cardiac troponin values
because of myocardial injury.
Spectrum of myocardial injury, ranging from no injury to myocardial infarction. Criteria For MI.Types of MI.Myocardial Infarction with Non-Obstructive Coronary Arteries(MINOCA)
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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!
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.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
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.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
4. In their clinical practice, physicians can face heart diseases (chronic or acute
heart failure) affecting the liver and liver diseases (liver cirrhosis, NAFLD/NASH )
affecting the heart. Systemic diseases (e.g., alcohol abuse, drugs, inflammation,
autoimmunity, infections) can also affect both heart and liver.
Cardiologist and Hepatologist Crosstalk
5. Interactions between the heart and the liver
The heart as a cause of liver disease*
The liver as a cause of heart disease**
Conditions affecting both the
liver and the heart***
*Chronic or acute heart failure→ congestive hepatopathy (cardiac cirrhosis)
and ischemic hepatopathy (acute cardiogenic liver injury)
**Liver cirrhosis→ cirrhotic cardiomyopathy
***Alcoholism→alcoholic cardiomyopathy & alcoholic liver cirrhosis
6. The scope of the presentation
How does the heart react when the liver is diseased?
The heart matters when the liver shatters !
Cirrhotic Cardiomyopathy
7. Arterial vasodilatation leads to redistribution of the blood volume with development of
central hypovolaemia, hyperdynamic circulation, and cardiac dysfunction.
AVP: vasopressin, CBV: central blood volume, ET: endothelin, RAAS: renin–angiotensin–aldosterone
system, SNS: sympathetic nervous system, SVR: systemic vascular resistance.
Role of hepatocellular dysfunction and portosystemic shunting in the
development of extrahepatic vasodilatation in cirrhosis.
9. Working definition of cirrhotic cardiomyopathy
as defined by the expert consensus committee at the World Congress of
Gastroenterology in Montreal, Canada in 2005.
Cirrhotic patient with
Abnormal
contractile
response to
stress
Diastolic
dysfunction
Absence of
another
clinically
significant
cardiac disease
11. CCM is a condition easily tolerated, remaining asymptomatic for months to years because of the near-
normal cardiac function at rest, manifesting only under conditions of physical or pharmacological
stress.
So , the diagnosis of CCM is difficult →Therefore, the exact prevalence cannot be defined
There is only
very limited data
about
epidemiology, as
well as actual
prevalence of this
condition at
present time. No Data
13. Liver cirrhosis and
portal hypertension
Splanchnic vasodilatation
Central hypovolemia
Hyperdynamic circulation
Cirrhotic cardiomyopathy
The sequence in development of cirrhotic
cardiomyopathy in liver cirrhosis.
14. The figure reviews the most important cellular and molecular pathogenic
mechanisms involved in cirrhotic cardiomyopathy
European Heart Journal(2013)34,2804
Down-regulation
Up-regulation
Increased
inhibitory effects
of cardio
depressant
substances
such as
haemoxygenase
(HO), carbon
monoxide (CO),
nitric oxide
synthase (NOS)-
induced nitric
oxide (NO)
release, and
tumour necrosis
factor-a (TNF-a).
Altered function
Inhibition
Increased fluidity
Alterations
Decreased content of G-protein
Alterations
16. Cirrhosis is a progressive liver disease characterized by diffuse fibrosis, which evolution is
divided in compensated and decompensated cirrhosis, where its development shows variceal
hemorrhage, jaundice, ascites and hepatic encephalopathy.
As the disease develops, reactive oxygen species increase as well as inflammation.
A second insult is a trigger for acute-on-chronic liver failure (ACLF) to occur, leading the
patient to multi-organ failure or even death if he does not receive a liver transplant.
Upwards arrows indicated ‘an increase’. ROS, reactive oxygen species.Clin Mol Hepatol Vol26 No1 Jan 2020
The clinical course of cirrhosis.
Cirrhotic cardiomyopathy is independent of the etiology
of the liver cirrhosis but related to severity and survival.
17. Compensated
cirrhosis
Decompensated
cirrhosis
Liver transplant
or death
Vasodilatation
Hyper- dynamic state
↑ Cardiac output
↓Cardiac output
The clinical course of cirrhosis.
Clinical Heart failure
Normal/Increased LVEF
LV diastolic dysfunction
Clinically Silent
(Oligo symptomatic
or even asymptomatic)
Decreased LVEF
LV diastolic dysfunction
Furthermore,
cirrhotic
cardiomyopathy is
an important cause
of perioperative
morbidity and
mortality for liver
transplant recipients
19. CCM : a diagnostic challenge
Lack of universally accepted diagnostic criteria.
CCM remains an ill-defined entity among cardiologists
20. Diagnostic criteria for cirrhotic cardiomyopathy ,
as defined by the expert consensus committee at the World Congress of
Gastroenterology in Montreal, Canada in 2005.
21. Diagnostic criteria for cirrhotic cardiomyopathy , as defined by the expert consensus
committee at the World Congress of Gastroenterology in Montreal, Canada in 2005.
2005
22. The Cirrhotic Cardiomyopathy Consortium
is a multidisciplinary
( hepatology , anesthesia , and cardiology )
international group whose focus is to improve the
understanding of cirrhotic cardiomyopathy, its
management and outcomes.
2019
23. The Cirrhotic Cardiomyopathy Consortium
CCM in the
spectrum of HF
New CCM
criteria based on
contemporary
CV imaging
parameters
Potential additional
markers of CCM
The group met in October 2018 at the Mayo Clinic (Minnesota) and
subsequently worked together to develop this document (2019)
25. Symptomatic HF
Cirrhotic Cardiomyopathy in the Spectrum of HF
Based on this classification,
patients with ESLD or
metabolic syndrome and its
components without
structural heart disease might
be classified as stage A,
whereas those considered
to have CCM on the basis
of LV remodeling and/or
systolic or diastolic
dysfunction in the absence
of clinical HF symptoms
might be classified as
stage B HF.
However, identification
of stage C HF due to
CCM in ESLD may be
complicated by the fact
that symptoms of HF
may be masked or
confounded by those of
advanced cirrhosis,
which can also limit
functional capacity.
Asymptomatic HF
The 4 Stages of Heart Failure (AHA/ACC)
26. Stage A
HF.
Stage B
HF.
Symptomatic
HF.
Majority of cirrhotic patients have LVDD
LVDD is an early manifestation f cardiac dysfunction in patients with liver cirrhosis.
LVDD predicts poor prognosis in patients with decompensated liver cirrhosis
ESLD LVDD
27. New CCM criteria based
on contemporary CV imaging parameters
• LV Systolic Function.
• LV Diastolic Dysfunction.
28. Redefining CCM Criteria :
Alignment with Contemporary Metrics for Assessing Cardiac Dysfunction
LV Systolic Function : LVEF / GLS
Global longitudinal strain (GLS) can identify myocardial
contractile dysfunction in those with preserved LVEF
Affected by LV
loading conditions
In adults, GLS < -16% is abnormal,
GLS > -18% is normal,
and GLS -16% to -18% is borderline.
Liver cirrhosis
“ESLD”
The vasodilatory
state
results in
decreased
afterload
and
consequently
normal or even
increased LVEF
Oligo symptomatic
or even asymptomatic
Diminished LVEF or diminished GLS in the absence of known cardiac disease (e.g., other
cardiomyopathies such as ischemic, rheumatic, etc.) should be considered diagnostic of CCM
29. LV Diastolic Dysfunction.
4 Criteria
3 Criteria
Application of these modern criteria should supersede the 2005 Montreal CCM criteria, which rely on parameters that
are impacted both by loading conditions and by heart rate, which can vary significantly in patients with ESLD
30. Evaluation of diastolic function in patients with end-stage liver disease
*In this algorithm, only medial annulus velocity is recommended. After applying the modified criteria, filling
pressure is first assessed, then diastolic function is graded based on E/A ratio.
**For values of PV, IVRT, and strain assessment in patients with indeterminate diastolic function, refer to next Fig.
Advanced diastolic dysfunction (grade 2 or 3) in patients with ESLD in the absence of known heart disease is
diagnostic of cirrhotic cardiomyopathy. It is critical to exclude coexisting comorbidities : DM,HTN,CAD
Abbreviations: LA, left atrium; PV, pulmonary vein; IVRT, isovolumetric relaxation time.
31. Additional assessment to reclassify patients with indeterminate diastolic function
based on previous Fig. into normal versus different grades of diastolic dysfunction.
Pictured are still frames of pulmonary vein pressures, values of isovolumetric relaxation
(IVRT), Left atrial systolic strain (LAS), and LV global longitudinal strain (LVS) for normal
and different stages of diastolic function.
34. Methods Markers
Echo There are suggestions to improve diagnostic criteria
considering dysfunction of right ventricle , biventricular
diastolic dysfunction at rest, large left and right atria,
higher systolic pulmonary arterial pressure and left
ventricular mass and evaluate systolic function
assessment using tissue strain imaging .
Dobutamine Stress
Echo
Abnormal or blunted contractile reserve
Cardiopulmonary
Exercise Testing
(CPET)
Exercise limitation and low pVO₂ (peak oxygen
consumption)
Cardiac Biomarkers Elevated levels of BNP/NT-proBNP (+imaging-based
markers)
ECG :of limited value Prolonged QT interval (>440 milliseconds)
CMRI More sensitive than DSE at detecting subclinical LV
dysfunction in CCM
Potential Additional Markers of CCM
38. AHA/ACC and ESC guidelines→no specific strategies to manage cirrhotic
cardiomyopathy→ follow the HF guidelines for the treatment of cirrhotics affected by
cardiomyopathy, with consideration for special conditions in patients with markedly
reduced SVR
At present there are no therapeutic guidelines with regards to
the management of cirrhotic cardiomyopathy
39. Treatment Optimization in Heart Failure
Cardiologists :
Taking responsibility in optimizing patient
care in heart failure
Placement of a transjugular intrahepatic
portosystemic shunt (TIPS) is a minimally invasive
procedure for the treatment of the major
complications of portal hypertension
Liver transplantation (LT) is thought to be
the only treatment for CCM.
40. Volume 13, 2019 - Issue 5
Liver transplantation
ameliorates most of the
abnormalities seen in
cirrhotic
cardiomyopathy, but no
specific treatment can
yet be recommended.
The outcome of invasive
procedures and liver
transplantation is influenced
by the presence of cardiac
dysfunction.
Therefore, a cautious cardiac
evaluation should be included in the
patient evaluation prior to liver
transplantation.
Expert commentary
41. Patients Cirrhotics without cardiomyopathy Cirrhotics with cardiomyopathy
After TIPS • Clinical findings:
1. Heart failure (rare, and mild)
2. Ascites (rare)
3. Liver and renal failure (rare)
4. Death (extremely rare)
• Clinical findings:
1. Heart failure (more frequent)
2. Ascites (more frequent)
3. Liver and renal failure (more frequent)
4. Death (more frequent)
5. Further prolongation QT interval
After liver
transplant
• Clinical findings:
1. Normalization of portal-hepatic
hemodynamics
2. Amelioration of cardiac
autonomic function after 12
postoperative months
• ECG:
Normalizaton of QT prolungation in
50 % of subjects within 12 months
• Clinical findings:
1. Normalization of portal-hepatic
hemodynamics
2. Early myocardial depression
3. Early drop in cardiac index and oxygen
delivery
4. Normalization of cardiac structure and
function by 9–12 postoperative months
• ECG:
Normalization of QT prolongation in 50 % of
subjects within 12 months
Clinical and diagnostic comparison between cirrhotics with and without
cardiomyopathy after TIPS & after liver transplant
Kathirvel Subramaniam Tetsuro Sakai ,Editors, 2017
42. Cardiologists may be asked to help
hepatologists and surgeons in the diagnosis and treatment
of this syndrome before and after liver transplantation.
Noteworthy, the subjects that suffer from cirrhotic cardiomyopathy may progress to heart failure
after TIPS and liver transplantation (these interventions generate a sudden increase in the preload
and, consequently, a rise in LVFP → acute pulmonary edema)
CVD is a common cause of morbidity and
mortality after liver transplantation.
43. Published in Current opinion in organ transplantation 2019
Risk factors and prevention of cardiovascular disease in liver transplant recipients
44. Liver transplant waiting list
E.M. Zardi et al. / Journal of Cardiology 67 (2016) 125–130
Consider therapy with :
Furosemide
Spironolactone
B-blockers
ACEI/ARB
Optimize and monitor volume status
and hemodynamics
Monitor ECG
45. Loop-diuretics →to treat hypervolemia
Aldosterone antagonists →to reduce the frequency of
hospitalization and mortality & to reduce the hepatic-venous
pressure(HVP) gradient, the LV wall thickness, and the LVEDV
Beta-blockers → to reduce the prolonged QT interval & to reduce
the hyperdynamic load
Carvedilol is a potent agent to reduce portal pressure
( Low dose : 12.5 mg.)
ACE-Is /ARBs (and vasodilators in general) →are not useful in
conditions of severe systemic vasodilation such as those observed
in cirrhotics with cardiomyopathy
( They should be used in the early phases of cirrhosis because of the
risk of hypotension and hepatic-renal syndrome in later phases )
However, there are still some issues that deserve to be addressed.
47. Redefining Criteria for CCM
(Manhal Izzy et al , Hepatology, VOL. 0, NO. 0, 2019 on behalf of The Cirrhotic Cardiomyopathy Consortium)
b. Proposed criteria by the Cirrhotic Cardiomyopathy Consortium (2019)
Systolic Dysfunction Advanced Diastolic Dysfunction† Areas for Future Research Which
Require Further Validation
Any of the following
•LV ejection fraction ≤50%
•Absolute* GLS <18% or
>22%
≥3 of the following
•Septal e′ velocity
<7 cm/second
•E/e′ ratio ≥15
•LAVI >34 mL/m2
•TR velocity >
2.8 m/second‡
•Abnormal chronotropic
or inotropic response§
•Electrocardiographic
changes
•Electromechanical
uncoupling
•Myocardial mass change
•Serum biomarkers
•Chamber enlargement
•CMRI||
* GLS is reported as a negative value in echocardiography reports. Changes in GLS should be described as changes in the
absolute value.† Refer to Fig. for echocardiographic changes in early diastolic dysfunction. They were not included in this
table given their decreased specificity as they can occur due to aging.‡ In the absence of evidence of primary pulmonary
hypertension or portopulmonary hypertension.§ Examples include absence of or blunted contractile or diastolic reserve
on exercise stress testing, dobutamine stress testing, or at rest on CMRI.|| Myocardial extracellular volume as a
surrogate for myocardial fibrosis can be assessed using this modality.
Abbreviation: e′, early diastolic mitral annular velocity.
48. Proposed cardiac evaluation algorithm for liver transplant candidates
Current Transplantation Reports (2019) 6:328–337
Editor's Notes
Mechanisms of cirrhotic cardiomyopathy. The figure reviews the most important mechanisms involved in cirrhotic cardiomyopathy: Desensitisation and downregulation of β-adrenergic receptors with decreased content of G-protein (Gαi: inhibitory G protein; Gαs: stimulatory G protein) and following impaired intracellular signalling; alterations in particular in M2 muscarinic receptors; upregulation of cannabinoid 1-receptor stimulation; altered plasma membrane cholesterol/phospholipid ratio; increased inhibitory effects of haemooxygenase (HO), carbon monoxide (CO), nitric oxide (NO), and tumour necrosis factor-α (TNF-α); reduced density of potassium channels; changed function and fluxes through L-type calcium channels; altered ratio and function of collagens and titins. Many post-receptor effects are mediated by adenylcyclase (AC) inhibition or stimulation. PKA: Protein kinase A. World J Gastroenterol. Nov 14, 2014; 20(42): 15499-15517
Cirrhosis is a progressive chronic liver disease characterized by diffuse fibrosis, severe interruption of intrahepatic venous flow, portal hypertension and hepatic insufficiency. Epidemiological studies indicate the existence of an increase in the prevalence of liver cirrhosis worldwide.1 The natural evolution of cirrhosis is divided into two stages; a compensated cirrhosis, which is defined as the period between the onset of cirrhosis and the appearance of the first major complication of the disease and the decompensated cirrhosis, which defines the period following the development of ascites, gastrointestinal hemorrhage due to rupture of esophageal varices and hepatic encephalopathy
Echocardiographic evaluation of cirrhotic cardiomyopathy. An example of a liver cirrhotic patient with Child-Pugh C, and severe diastolic dysfunction grade 3. Panel A. Pulsed wave Doppler at the level of mitral inflow: E = peak velocity blood flow in early diastole; A = peak velocity blood flow in late diastole; E/A ratio = the ratio between peak velocity blood flow in early diastole to peak velocity blood flow in late diastole; E/A = 2.2 suggesting a restrictive pattern (grade 3) of diastolic dysfunction. Panel B: TDI evaluation of myocardial velocities at the level of mitral annulus: S′ = systolic velocity; E′ = early diastolic velocity; A’ = late diastolic velocity; E′ medial = early diastolic velocity at septal site; E/E′ = 35 suggesting high left ventricular filling pressure. Panel C: LAvol = left atrial volume; LAVi = left atrial indexed volume (LAvol/BSA); LAVi = 60 ml/m2 suggesting an important LA dilatation. Panel D: GLS = global longitudinal strain of the left ventricle. GLS = -13% suggesting a significantly decreased longitudinal systolic dysfunction