Harsh Agrawal

Obesity and heart failure: epidemiology, pathophysiology, clinical manifestations, and management

Obesity is a risk factor for heart failure (HF) in both men and women. The mortality risk of overweight and class I and II obese adults with HF is lower than that of normal weight or underweight adults with HF of comparable severity, a phenomenon referred to as the obesity paradox. Severe obesity produces hemodynamic alterations that predispose to changes in cardiac morphology and ventricular function, which may lead to the development of HF. The presence of systemic hypertension, sleep apnea, and hypoventilation, comorbidities that occur commonly with severe obesity, may contribute to HF in such patients. The resultant syndrome is known as obesity cardiomyopathy. Substantial weight loss in severely obese persons is capable of reversing most obesity-related abnormalities of cardiac performance and morphology and improving the clinical manifestations of obesity cardiomyopathy.

Cardiac effects of obesity: pathophysiologic, clinical, and prognostic consequences-A review

Obesity produces various hemodynamic alterations and changes in cardiac morphology that predispose to ventricular dysfunction and heart failure (HF). Obesity may serve as a risk factor for or the primary cause of HF. Obesity is also associated with impairment of cardiorespiratory fitness. An obesity paradox exists with respect to mortality in those with HF wherein overweight and mildly to moderately obese individuals have a better prognosis than underweight or normal weight persons. Cardiorespiratory fitness is an important determinant of the prognosis in obesity. Many of the alterations in cardiac structure and function as well as the clinical manifestations of HF are reversible with substantial weight loss in moderately to severely obese individuals.

Improved Transplant-Free Survival in Patients With Systemic Sclerosis–Associated Pulmonary Hypertension and Interstitial Lung Disease

Survival in patients with systemic sclerosis (SSc)–associated pulmonary hypertension (PH) and interstitial lung disease (ILD) is poor. Evidence supporting the efficacy of aggressive pulmonary arterial hypertension (PAH)–targeted therapy in this population is limited. The aim of this study was to investigate transplant‐free survival in patients with isolated SSc‐related PAH or SSc‐related PH‐ILD who were treated with aggressive PAH‐targeted therapy.

Pharmacological and Non Pharmacological Strategies in the Management of Coronary Artery Disease and Chronic Kidney Disease

Patients with advanced chronic kidney disease (CKD), including those treated with dialysis, are at high risk for the development of cardiovascular disease (CVD). CVD accounts for 45-50% of deaths among dialysis patients. Therapy of acute and chronic coronary heart disease (CHD) that is effective in the general population is frequently less effective in patients with advanced CKD. Drug therapy in such patients may require dose modification in some cases. Oral anti-platelet drugs are less effective in those with advanced CKD than in persons with normal or near normal renal function. The intravenous antiplatelet drugs eptifibatide and tirofiban both require dose reductions in patients with advanced CKD. Enoxaparin requires dose reduction in early stage CKD and is contraindicated in hemodialysis patients. Unfractionated heparin and warfarin maybe used without dose adjustment in CKD patients. Atenolol, acetbutolol and nadolol may require dose adjustments in CKD. Metoprolol and carvedilol do not. Calcium channel blockers and nitrates do not require dose adjustment, whereas ranolazine does. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers may safely be used in CKD patients with close observation for hyperkalemia. The safety of spironolactone in such patients is questionable. Statins are less effective in reducing cardiovascular complication in CKD patients and their initiation is not recommended in dialysis patients. Coronary artery bypass grafting is associated with higher short-term mortality, but better long-term morbidity and mortality than percutaneous coronary interventions in patients with advanced CKD with non-ST segment ACS and chronic CHD.

Infection and Lupus: Which Causes Which?

Infection is a leading cause of morbidity and mortality among patients with systemic lupus erythematous (SLE). Dysfunction of the innate and adaptive immune systems increases the risk of infection in patients with SLE. Infectious agents have also been theorized to play a role in the pathogenesis of SLE. This article summarizes our current knowledge of the infectious risk SLE patients face as a result of their underlying disease including abnormal phagocytes and T cells as well as the increased risk of infection associated with immunosuppressive agents used to treat disease. Pathogens thought to play a role in the pathogenesis of disease including EBV, CMV, human endogenous retroviruses (HERVs), and tuberculosis will also be reviewed, as well as the pathologic potential of microbial amyloids and the microbiome.

Heart Failure and Obesity in Adults: Pathophysiology, Clinical Manifestations and Management

Obesity is both a risk factor and a direct cause of heart failure (HF) in adults. Severe obesity produces hemodynamic alterations that predispose to changes in left ventricular morphology and function, which, over time, may lend to the development of HF (obesity cardiomyopathy). Certain neurohormonal and metabolic abnormalities as well as cardiovascular co-morbidities may facilitate this process. Substantial purposeful weight loss is capable of reversing most of the alterations in cardiac performance and morphology and may improve functional capacity and quality of life in patents with obesity cardiomyopathy.

Antithrombotics in atrial fibrillation and coronary disease.

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia and approximately 18–45% of AF patients have concomitant coronary artery disease (CAD). Several studies have demonstrated that oral anticoagulation is the mainstay of therapy for stroke prevention in AF. Similarly, antiplatelet therapy including aspirin and P2Y12 inhibitor is recommended in the management of acute coronary syndrome and stable CAD. Despite the high prevalence of CAD with AF, practice guidelines are scarce on the appropriate antithrombotic regimen due to lack of large-scale randomized clinical trials. The use of direct thrombin and factor Xa inhibitors for stroke prevention in AF has also complicated the possible combinations of antithrombotic therapies. This review aims to discuss the available evidence regarding aspirin as an antithrombotic strategy, the role of novel anticoagulants and the specific clinical situations where aspirin may be beneficial in patients with AF and CAD.

Does pharmacotherapy improve cardiovascular outcomes in hemodialysis patients

Cardiovascular disease (CVD) occurs commonly in patients with chronic kidney disease (CKD) including those treated with hemodialysis (HD), and is associated with poor outcomes in this population. Pharmacologic management of hypertension, dyslipidemia, acute and chronic coronary artery disease, and atrial fibrillation in the general population is supported by the results of high‐quality, randomized, controlled clinical trials. Pharmacotherapy of these disorders in the general population is effective in improving clinical outcomes. In contrast, information concerning the effect of pharmacotherapy on mortality and cardiovascular outcomes in patients with CKD, and particularly in HD patients, is limited. Available data suggest that, in general, pharmacotherapy of hypertension and dyslipidemia, anti‐platelet therapy of CVD, and anticoagulant therapy in patients with atrial fibrillation are less effective in HD patients than in the general population or even in patients with early stage of CKD.