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Heart failure (HF) is a clinical syndrome caused by abnormalities of cardiac structure or function that result in impaired cardiac filling, ejection of blood, or both and, consequently, an inability to meet the circulatory needs of the body. There is substantial variation in its etiology, associated comorbidities, prognosis, and response to therapy. HF carries a significant burden on society, accounting for approximately 1 million hospitalizations and 65,000 deaths at a cost of $31 billion annually in the United States alone. In this chapter, we review the epidemiology of HF, with a specific focus on chronic HF.


Commonly encountered symptoms and signs of HF, such as dyspnea and edema, have been recognized for more than 2,500 years, dating back to ancient Greece and Rome.1 However, pathophysiologic understanding of HF was not well understood. Two millennia lapsed before William Harvey, in 1628, identified the heart as the pulsatile driver of blood through the vascular circulatory system.2 This discovery set the stage for understanding hemodynamic abnormalities in HF. In 1918, Starling described the relationship between cardiac volumes and output in the normal and failing heart.3 The advent of cardiac catheterization in the 1940s brought hemodynamic assessments into clinical medicine, but even then therapies for HF were limited to palliation of symptoms with digitalis and the toxic mercurial diuretics.4

Around World War II, cardiovascular disease was recognized as the leading cause of death in the United States and, in 1944, Franklin D. Roosevelt was diagnosed with hypertensive heart disease and cardiac failure.5 In the context of increasing awareness of the public health burden of cardiovascular disease, the National Heart Act was signed in 1948, establishing what is now known as the National Heart, Lung, and Blood Institute and initiating a new epidemiologic study (the Framingham Heart Study).5 In 1953, the cardiologist Inge Edler and physicist Hellmuth Hertz (Lund University, Sweden) developed echocardiography, which enabled a noninvasive estimation of cardiac structure and function.6 In the late 1950s, thiazide diuretics were introduced to alleviate congestive symptoms in HF. The 1950s and 1960s also marked a time when knowledge about the cellular and molecular basis of HF was increasing, with seminal observations implicating inflammation, adrenergic and neurohormonal activation, abnormal energetics, myocyte hypertrophy, and altered excitation-contraction coupling.7,8,9,10 A new era in HF therapy was also ushered in by the first heart transplant in 1967.11

A major barrier to understanding the risk factors and natural history of HF was a lack of uniform diagnostic criteria. Therefore, investigators at the Framingham Heart Study developed a set of clinical criteria for the diagnosis of HF that was first reported in 1971 (Fig. 69–1).12 Other algorithms for the diagnosis of HF, such as the Boston and Gothenburg criteria, were developed in the mid-to-late 1980s (see Fig. 69–1).13,14...

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