Congestive heart failure
Congestive heart failure
Congestive heart failure (CHF) is a state of abnormal cardiac function. CHF is not a single entity but a symptom complex that may represent the consequence of mechanical abnormalities, myocardial abnormalities, and/or disturbances of cardiac rhythm. In turn, it affects virtually every organ system in the body. Congestive heart failure is a common clinical syndrome. In the US, there are approximately 4.8 million patients with congestive heart failure. The incidence and prevalence increases with increasing age and it has been estimated that 1.5% of all adults and 6 to 10% of adults aged more than age 65 years have congestive heart failure.
The most frequent causes for heart failure are myocardial infarction, pressure overload, volume overload, viral myocarditis, toxic cardiomyopathy and mutations in genes encoding for sarcomeric or cytoskeletal proteins. Myocardial damage with subsequent neurohumoral and cytokine activation induce chamber remodeling and phenotype alteration which then result in myocardial failure.
Although there is no single unifying pathogenetic theory, a number of biochemical abnormalities have been described in heart failure. There is agreement that the efficiency of the heart as a pump is reduced in the low-output, systolic heart failure that occurs in ischemic heart disease and dilated cardiomyopathy. The “external work” performed by the left ventricle is depressed, whereas its energy consumption is normal or almost so.15 Thus, the dilated, failing heart is energy-inefficient. Second, alterations in cardiac energy metabolism are frequently observed in systolic heart failure. Relative ischemia of the subendocardium occurs in ventricular hypertrophy and dilatation.
Congestive heart failure (CHF) promotes an array of biologic changes that are largely designed to compensate for reduced flow. These include activation of the sympathetic nervous system and the renin-angiotensin system, as well as the release of arginine vasopressin. The ultimate expression of these compensatory mechanisms is heightened vascular tone, increased sodium and water retention and antidiuresis. The peripheral circulation is normally under the fine control of circulating and neuronally released moieties, which can directly or indirectly alter vascular tone. Angiotensin II appears to be a key element in this regard because of its multiple biologic activities. Direct arteriolar vasoconstriction, facilitation of norepinephrine release and stimulation of aldosterone are some of the activities that are likely to be of major importance in the syndrome of CHF.