Obesity cardiomyopathy (OCM) is a recently described form of heart muscle disorder. However, with the prevalence of obesity rapidly rising, research interest on its deleterious effect on cardiac morphology and function has been on the increase. However, with morphological and functional features mimicking those of dilated cardiomyopathy, research on OCM has been reduced to a sub-type or a secondary cause of dilated cardiomyopathy (DCM). Considerable debate also persists as to whether isolated obesity can directly cause cardiomyopathy in humans since its effect on cardiac function and structure cannot be isolated from those of comorbidities such as hypertension, dyslipidemia, glucose intolerance and coronary artery disease. With such extraneous factors, research on IOC has been fragmented and at most inconsistent. The purpose of the present review and meta-analysis is to synthesize current scholarly and practitioner understanding of IOC with a focus on broadening the knowledge on diagnosis and clinical management.

Drug-induced cardiomyopathy (CM) is a potentially reversible form of acquired CM and a common consequence of exposure to numerous medically prescribed drugs. It is particularly a common serious adverse side effect of anticancer and antiretroviral therapies. The two drugs may have significantly improved longevity in cancer and HIV-infected patients respectively but their cardiotoxic effects threaten to undermine their therapeutic efficacy and reduce survival in affected patients. Hospitalization due to drug-induced CM also places a considerable burden on the healthcare system in terms of reduced drug efficacy and patient management. Early detection is clinically important for improve efficacy in the management of drug-induced CM as well as the prevention of the progression into heart failure. Thus, prescribers should be fully aware of drugs with the potential to cause CM and the clinical value of monitoring the cardiotoxic effects of these drugs. Thus, the present paper provides a systematic review of literature and meta-analysis of diagnosis and management methods. The aim is to broaden the understanding of the major causative drugs, pathophysiology, diagnosis and management of drug-induced CM.

Virtually, any kind of tachycardia may lead to the development of tachycardiainduced cardiomyopathy. This term refers to left ventricular dysfunction and dilated cardiomyopathy pattern that occur as a consequence of persistent tachycardia. Impaired left ventricular function in the presence of tachycardia can be found accidentally, but it is often associated with progressive symptoms and signs of heart failure that force the individual to seek medical help. A hallmark of tachycardiainduced cardiomyopathy is the reversibility of both hemodynamic and structural changes after cessation of the index tachycardia. However, contractile dysfunction and structural changes may persist even weeks after the rhythm/rate correction. Therefore, tachycardia-induced cardiomyopathy should be considered as a probable reason of ventricular dysfunction and dilatation in any patient presenting with dilated cardiomyopathy pattern, despite that the initial rhythm is not pathological or the heart rate is well controlled. This review summarizes our current knowledge about this specific form of cardiomyopathy.

Arrhythmogenic right ventricular dysplasia (ARVD) is a serious heart muscle disease, often inherited. It is implicated as a leading cause of exercise-related sudden death primarily in young adults and athletes. Developing a precise understanding of its prevalence, clinical course and manifestation would improve early detection and help institute prompt and appropriate therapeutic management. Thus, this review article aggregates current research-based evidence on ARVD. The intention is to advance the current understanding and status of ARVD to improve diagnosis and survival rates. Particularly, this article reviews clinical description, classification, epidemiology, clinical manifestation, prognosis, risk factors, pathophysiology, etiology, differential diagnosis and clinical management of ARVD.

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The clinical syndrome of heart failure (HF) has traditionally been associated with low or normal cardiac output accompanied by increased systemic vascular resistance. This association has led to the present under-appreciation of a minority group of HF patients presenting with high cardiac output but with normal cardiac function, clinically termed high-output HF. In these patients, the pathophysiological hallmark is decreased systemic vascular resistance. Because these patients lack proven therapies, treatment relies on evidence-based therapies developed for low-cardiac output HF. With a paucity of clinical trial data, evidence based from case reports suggest some of the established HF medications such as vasodilators and inotropes can be potentially detrimental for patients with high-output HF. These findings demonstrates an unmet clinical need for in-depth understanding of the pathophysiology, aetiology and clinical course of high-output HF, which forms the basis for the present review.

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Research on heart failure (HF) has traditionally focused on the left-ventricular heart failure (LHF) with little consideration for the right-ventricular heart failure (RHF). Thus, precise knowledge of the role of the right ventricle (RV) in health and disease has lagged far behind that of the left ventricle (LV). Recently, increased recognition of the importance of RV failure in the development of HF has motivated increased research interest to improve clinical management of HF. However, research on RHF has remained fragmented and precise diagnostic and therapeutic methods are not well established. The present paper seeks to conduct a review of published research evidence including two meta-analyses of diagnosis and clinical management methods to advance knowledge on clinical status, diagnosis and management of RHF.