The heart is a truly remarkable organ, beating more than 40 million times per year and pumping over 7500 liters of blood a day; in a typical lifespan, its cumulative output would fill three supertankers. The cardiovascular system is the first organ system to become functional in utero (at approximately 8 weeks of gestation); without a beating heart and vascular supply, development cannot proceed, and the embryo dies. When the heart fails during postnatal life, the results are equally catastrophic. Indeed, cardiovascular disease is the leading cause of mortality worldwide and accounts for one in four of all deaths in the United States—approximately 1 death every minute, or 610,000 deaths each year (a greater mortality rate than for all forms of cancer combined). The annual economic impact of cardiac disease exceeds $200 billion, with ischemic heart disease contributing well over half. Moreover, roughly one third of these deaths are “premature,” occurring in individuals younger than 75 years of age; thus, an additional economic burden is imposed through lost years of productivity.
Although a wide range of diseases can affect the cardiovascular system, the pathophysiologic pathways that result in a “broken” heart distill down to six principal mechanisms:
Failure of the pump. In the most common situation, the cardiac muscle contracts weakly and the chambers cannot empty properly—so-called “systolic dysfunction.” In some cases, the muscle cannot relax sufficiently to permit ventricular filling, resulting in diastolic dysfunction.
Obstruction to flow. Lesions that prevent valve opening (e.g., calcific aortic valve stenosis) or cause increased ventricular chamber pressures (e.g., systemic hypertension or aortic coarctation) can overwork the myocardium, which has to pump against the obstruction.
Regurgitant flow. Valve pathology that allows backward flow of blood results in increased volume workload and may overwhelm the pumping capacity of the affected chambers.
Shunted flow. Defects (congenital or acquired) that divert blood inappropriately from one chamber to another, or from one vessel to another, lead to pressure and volume overloads.
Disorders of cardiac conduction. Uncoordinated cardiac impulses or blocked conduction pathways can cause arrhythmias that slow contractions or prevent effective pumping altogether.
Rupture of the heart or major vessel. Loss of circulatory continuity (e.g., a gunshot wound through the thoracic aorta) may lead to massive blood loss, hypotensive shock, and death.
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Heart failure, often referred to as congestive heart failure (CHF), is the common end point for many forms of cardiac disease and typically is a progressive condition with a poor prognosis. In the United States alone, over 5 million individuals are affected, resulting in well over 1 million hospitalizations annually, and a financial burden in excess of $32 billion. Roughly one half of patients die within 5 years of receiving a diagnosis of CHF, and 1 in 9 deaths in the United States include heart failure as a contributory cause.
CHF occurs when the heart cannot generate sufficient output to meet the metabolic demands of the tissues, or can only do so at higher-than-normal filling pressures; in a minority of cases, heart failure is a consequence of greatly increased tissue demands, as in hyperthyroidism, or decreased oxygen carrying capacity, as in anemia (highoutput failure). The onset of CHF is sometimes abrupt, as in the setting of a large myocardial infarct or acute valve dysfunction. In most cases, however, CHF develops gradually and insidiously owing to the cumulative effects of chronic work overload or progressive loss of myocardium.