The Role of Beta-Blockers in the Treatment of Chronic Heart Failure
In 1988 Sir James Whyte Black was honored with a Nobel Prize for medicine for his efforts in the discovery of the beta blocker propanolol and the histamine receptor agonist cimetidine. Beta blockers were originally developed to treat angina pectoris but were discovered to also treat hypertension, tachycardia, an myocardial infarctions. The discovery of propanolol was said to be the greatest discovery since digitalis. The mechanism of beta blockers treating CHF is not exact but may include a “reduction in circulating levels of vasoconstrictors, reductions in blood pressure, heart rate and myocardial oxygen consumption, up regulation of myocardial B-1- receptor density, thereby improving contractile function, a reduction in myocardial gene production of inflammatory cytokines, and increase in diastolic perfusion, and normalization of the expression of several myocardial genes involved in the development of pathologic hypertrophy”. The role of beta blockers has changed throughout the decades in part due to the changing theory of heart failure. Heart failure was thought to be a sole state of decline in systolic function and later updated to reflect it as a complex disorder which consisted of a decrease in cardiac output and compensatory neurohormonal mechanisms. Chronic neurohormonal activation allows for an increase in heart rate and cardiac output, which increases myocardial oxygen demand, ischemia and oxidative stress. In 1975, Waagstein conducted a clinical study testing the role of beta blockers on chf patients. The patients had clinical CHF and tachycardia at rest. Their normal treatment which included a diuretic and digitalis was not altered. The patients were given either alprenolol or practolol for two to twelve months. The results indicated favorable effects as hemodynamics improved, an increase in physical working capacity, and a reduction in heart size. Several more clinical trials...
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