Etiology

There are numerous and varied causes of HF.​​​[7][9]

Common causes of chronic HF include:

  • Coronary artery disease/ischemic heart disease

  • Hypertension

  • Valvular disease

  • Myocarditis.

Other causes include:

  • Infiltrative diseases: amyloidosis, hemochromatosis, sarcoid

  • Congenital heart diseases

  • Pericardial disease

  • Toxin-induced: heroin, alcohol, cocaine, amphetamines, lead, arsenic, cobalt, phosphorus

  • Infection: bacterial, fungal, viral (HIV), Borrelia burgdorferi (Lyme disease), parasite (e.g., Trypanosoma cruzi [Chagas disease])

  • Endocrine disorders: diabetes mellitus, thyroid disease, hypoparathyroidism with hypocalcemia, pheochromocytoma, acromegaly, growth hormone deficiency

  • Systemic collagen vascular diseases: lupus, rheumatoid arthritis, systemic sclerosis, polyarteritis nodosa, hypersensitivity vasculitis, Takayasu syndrome, polymyositis, reactive arthritis

  • Chemotherapy-induced: e.g., adriamycin/anthracyclines, trastuzumab

  • Nutritional deficiencies: e.g., thiamine, protein, selenium, L-carnitine

  • Pregnancy: peripartum cardiomyopathy

  • Familial cardiomyopathy

  • Tachycardia-induced cardiomyopathy

  • Stress cardiomyopathy

  • Radiation therapy

  • Carcinoid heart disease.

Although Chagas disease is an uncommon cause of congestive HF in Europe and North America, it is an important cause of HF in Central and South America.​​[2][7]

Some of these conditions tend to increase metabolic demand, which may not be matched by a sufficient increase in cardiac output by the failing heart. Tachyarrhythmias also decrease the diastolic ventricular filling time and increase myocardial oxygen demand. Uncontrolled hypertension depresses systolic function by increasing the afterload against which the failing ventricle must pump blood, and may be the first clinical manifestation.

It should be emphasized that many of these causes may be completely reversible given appropriate and timely treatment/intervention (e.g., revascularization for stunned or hibernating myocardium; standard therapy for peripartum or hypertensive cardiomyopathy; valvuloplasty or valve replacement for valvular heart disease; standard treatment and adjunctive rate control therapy for tachycardia-induced cardiomyopathy and cardiomyopathy related to sepsis and stress).[7][10][11]​ Other causes, such as scarred myocardium or infiltrative cardiomyopathy, are currently considered irreversible.

Pathophysiology

The understanding of the pathophysiology of HF has evolved significantly over the last decades, from the hemodynamic model to the neurohormonal paradigm.[12] HF represents a complex syndrome in which an initial myocardial insult results in the overexpression of multiple peptides with different short- and long-term effects on the cardiovascular system. Neurohormonal activation is recognized to play a pivotal role in the development as well as the progression of HF. In the acute phase, neurohormonal activation seems to be beneficial in terms of maintaining adequate cardiac output and peripheral perfusion. Sustained neurohormonal activation, however, eventually results in increased wall stress, dilation, and ventricular remodeling, which contribute to disease progression in the failing myocardium, which eventually leads to further neurohormonal activation. Left ventricular remodeling is the process by which mechanical, neurohormonal, and possibly genetic factors alter ventricular size, shape, and function. Remodeling occurs in several clinical conditions, including myocardial infarction, cardiomyopathy, hypertension, and valvular heart disease; its hallmarks include hypertrophy, loss of myocytes, and increased interstitial fibrosis. One potential deleterious outcome of remodeling, as the left ventricle dilates and the heart assumes a more globular shape, is the development of mitral regurgitation. Mitral regurgitation results in an increasing volume overload on the overburdened left ventricle that further contributes to remodeling and progression of disease and symptoms.

Classification

Universal definition and classification of heart failure: classifications of HF according to ejection fraction[1]

  • HF with reduced EF (HFrEF): HF with left ventricular ejection fraction (LVEF) ≤40%.

  • HF with mildly reduced EF (HFmrEF): HF with LVEF 41% to 49%.

  • HF with preserved EF (HFpEF): HF with LVEF ≥50%.

  • HF with improved EF (HFimpEF): HF with a baseline LVEF of ≤40%, a ≥10-point increase from baseline LVEF, and a second measurement of LVEF of >40%.

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