HEART FAILURE
Heart failure is a condition that develops slowly as the heart muscle weakens and results in the inability of the heart to keep an adequate supply of blood flowing through the body. Heart failure occurs when the heart has been damaged by a heart attack, long-term high blood pressure, an abnormality of the heart valves, coronary artery disease, and/or an infection such as endocarditis or myocarditis. Because the weakened heart must work harder to meet the demands of the body, in its advanced stages the disease causes people to feel tired and short-of-breath.
The lack of proper circulation causes fluid to build up in the organs, which results in severe congestion in tissues and swelling, or edema, especially in the feet and legs. In its most advanced stage, heart failure causes fluid to build up in the lungs, interfering with breathing.
Physicians often assess the patient's stage of heart failure according to the New York Heart Association (NYHA) functional classification criteria. The NYHA classification is based on symptoms measured against everyday functional activities and range from mild to severe classifications. The four function classes of the NYHA are Class I and II, which are mild stages of the disease, Class III is moderate and Class IV is severe heart failure in which the person is unable to carry out any physical activity without extreme discomfort.
Treatment is usually with drugs that induce diuresis and provoke vasodialtion, decreasing vascular resistance and blood input into the heart, ultimately reducing heart size. These therapies allow blood to flow more easily making the heart work easier and more efficiently. Current guidelines for treating heart failure indicate a combination drug regimen, which includes ACE inhibitors, angiotensin receptor blockers (ARBs), beta-blockers, spironolactone, diuretics and digitalis.
There is clinical data that suggests that hypertension in African Americans is less well controlled with ACE inhibitor therapy. Other studies have shown similar differences between white heart failure patients and African Americans with heart failure. Black heart failure patients also have different morbidity and mortality than do whites; dying at a rate 40-50% faster than the corresponding white population.
It is postulated that heart failure in African Americans is associated with a deficit in the vascular production of nitric oxide. The effect of BiDil® could be explained by a replenishment of nitric oxide to the vascular tissue. ACE inhibitors, ARBs, beta-blockers and spironolactone act through different mechanisms that ultimately contract blood vessels.
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