Abstract and Introduction
Abstract
Almost 6 million people in the United States have heart failure. When heart failure develops, cardiac output decreases and compensatory mechanisms activate. One of these mechanisms is cardiac fibrosis, a scarring process that over time impacts cardiac structure and function. Historically, cardiac fibrosis has not been a focus for treatment; however, it is now believed that therapy directed at cardiac fibrosis could reduce the progression of heart failure and other cardiovascular diseases. Medications that target the renin-angiotensin system, transforming growth factor-beta, and endothelin are in various stages of development.
Introduction
Heart failure is a complex clinical syndrome in which structural or functional abnormalities impair the heart's ability to fill with or pump blood. Affecting nearly 6 million people in the United States, heart failure is the leading reason for hospitalization in patients aged 65 years and older, as well as a major cause of impaired quality of life and chronic disability.
Heart failure can result from systolic dysfunction, diastolic dysfunction, or both. The most common risk factors for developing heart failure include coronary heart disease (often with myocardial infarction [MI]), hypertension, diabetes, and cardiomyopathy.
Heart failure is initiated by any event that impairs the heart's ability to contract and/or relax, resulting in reduced cardiac output. As cardiac output decreases, compensatory mechanisms activate to restore cardiac output through increased preload, tachycardia, vasoconstriction, ventricular hypertrophy, and remodeling. At the cellular level, ventricular hypertrophy and remodeling are accompanied by cardiomyocyte hypertrophy, necrosis, apoptosis, fibroblast proliferation, and increased deposition of fibrous collagen, the last two of which are collectively termed cardiac fibrosis. This article will focus on cardiac fibrosis, including its mediators, assessment, and potential treatments.