Other possible causes of HF include congenital heart disease, myocarditis, infiltrative disease, peripartum cardiomyopathy, human immunodeficiency virus (HIV), connective tissue disease, amyloidosis, substance abuse, long-standing alcohol use, obesity, diabetes mellitus (DM), hyperthyroidism (can cause high-output HF), pulmonary hypertension (can cause right HF), constrictive pericarditis (can cause HFpEF), pulmonary embolism (can cause right HF), and chemotherapies (like doxorubicin). CMP categorizes into five types, which can be genetic or acquired: dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), restrictive cardiomyopathy (RCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), and other unclassified cardiomyopathies (isolated noncompaction of the left ventricle and Takotsubo syndrome are also in this category). Ĭardiomyopathies (CMP): CMP is a disease in which there are functional and structurally heart muscle abnormalities in the absence of CAD, HBP, valvular, or congenital heart disease.
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The Systolic Blood Pressure Intervention Trial (SPRINT) has shown that lowering the systolic BP to a target goal of less than 120 mmHg in HBP patients without diabetes had lower rates of HF with 38% lower relative risk comparing to systolic BP goal of less than140 mmHg. Control of BP is of paramount importance in improving the prognosis of HF. LVH increases the myocardial stiffness and can cause ischemia, which leads to HFpEF or HFrEF. If blood pressure (BP) remains uncontrolled, apoptosis and fibrosis may result. The heart must pump up blood against a higher afterload caused by HBP, which increases the myocardial mass as a compensatory mechanism to maintain a normal CO and that causes left ventricular hypertrophy (LVH). HBP increases vascular resistance and activates the renin-angiotensin-aldosterone system (RAAS). The high prevalence of HBP makes it a possible cause of HF in around one-fourth to one-third of cases. High blood pressure (HBP): HBP is an independent risk factor for CAD. However, the role of coronary revascularization in reducing HF-related morbidity and mortality is still controversial, and viability testing may be useful to select the population that may benefit from revascularization. CAD is a strong predictor of mortality in patients with acute HF. Several tachyarrhythmias such as atrial fibrillation/atrial flutter or non sustained ventricular tachycardia is common in patients with CAD and can deteriorate the cardiac function more. Myocardial infarction (MI) also causes dyssynchronous contraction of the infarcted segment, subsequent remodeling of the ventricle, ventricular dilatation with annular dilation, and mitral regurgitation that predispose to HF and decrease the CO. This scar formation may also correlate with aneurysm formation, and that further impairs contractile performance and relaxation.
Coronary artery disease (CAD): chronic and acute ischemia causes direct damage to the myocardium and leads to remodeling and scar formation, resulting in inadequate relaxation in diastole and impaired contraction in systole, which decreases contractility and cardiac output (CO).
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