Heart failure with preserved ejection fraction (HFpEF) is now recognized as a major and growing public health problem worldwide. This heart failure subtype disproportionately affects women and the elderly and is commonly associated with other cardiovascular comorbidities, such as hypertension, diabetes and chronic kidney disease. There are uncertainties and debates regarding the definition, diagnosis and pathophysiology with the consequence that all outcome trials performed so far cannot yield an effective treatment as in heart failure with reduced ejection fraction (HFrEF). Here we present an overview of epidemiology, pathophysiology, diagnosis and therapeutic approaches emerging from large outcome clinical trials.
Part of the book: Cardiomyopathies
Heart failure (HF) represents fatal endpoint of all cardiovascular diseases. Acute and chronic HF is a complex, heterogeneous syndrome consisting of many overlapping syndromes making its diagnosis and treatment more challenging. There is no single test for diagnosis of HF, and diagnosis is based on clinical judgment driven by a combination of history, physical examination, and appropriate tests. Despite improvements in clinical management within the last 50 years, it has still been a disease of poor prognosis. Attempts to further improve its prognosis can only be achieved by understanding pathophysiology of HF clearly and finding, developing, and using appropriate and new clinical biochemical markers for diagnosis of each different clinical subtype and hence unique intervention of that specific subtype of HF. This review is an overview of biomarkers, which are either currently used in the clinical practice or hold promise for future use in patients with both chronic and acute HF.
Part of the book: Biomarker
Ventricular tachycardia (VT) is a common arrhythmia seen in patients with heart failure (HF) and is now seen more frequently as these patients survive longer with modern therapies. In patients with HF, half of the deaths are sudden due to life-threatening ventricular arrhythmias, including VT. Although disease modifying drugs, such as beta blockers, mineralocorticoid drugs, and angiotensin receptor neprilysin inhibitors, prevent the occurrence of VT to some extent, the mainstay of therapy is the antiarrhythmic drug therapy, implantable cardioverter-defibrillator (ICD) implantation, and traditional radiofrequency catheter ablation. Autonomic nerve system modulation and stereotactic body radiation therapy have emerged as novel techniques for the management of refractory VT cases. Patients with refractory VT and repetitive ICD shocks should be further evaluated regarding the candidacy for left ventricular assist device and transplantation.
Part of the book: Practical Applications of Electrocardiogram
Graves’ disease is an autoimmune thyroid disease and a common cause of hyperthyroidism. Thyroid hormones have multiple adverse effect on cardiovascular system through many direct and indirect mechanisms. They increases heart rate, cardiac contractility, systolic and mean pulmonary artery pressure, cardiac output, diastolic relaxation, and myocardial oxygen consumption, whereas decrease systemic vascular resistance and diastolic pressure. All these hemodynamic changes in cardiovascular system can eventually lead to heart failure, tachyarrhythmias, systemic and pulmonary hypertension, if left untreated. Cardiovascular complications of Graves’ disease are frequent and important cause of increased morbidity and mortality. This chapter reviews the cardiovascular complications of Graves’ hyperthyroidism with underlying mechanisms and treatment.
Part of the book: Graves' Disease