Hypertension, or a history of hypertension, accounts for nearly half of all cases of congestive heart failure. There is clear-cut evidence of a close relationship between blood pressure and atherosclerosis. The Systolic Hypertension Europe (Syst-Eur) and Hypertension Optimal Treatment (HOT) studies showed that aggressive blood pressure lowering produces substantial gains in stroke and coronary event prevention. Lowering blood pressure to below 140/90 mm Hg is achievable, tolerable and highly effective. ACE inhibitors, P-blockers, and calcium channel blockers are the first-line drugs in established coronary heart disease, ACE inhibitors the first-line therapy in diabetics, and calcium channel blockers or thiazides the first line in systolic hypertension. Three or four drugs may be required to lower the blood pressure adequately.
In the Veterans Affairs Cooperative Study on Antihyper-trtnsive Agents in diastolic hypertension (90 to 114 mm hg), antihypertensive therapy not only decreased allcause mortality, but also decreased the risk of heart failure. In the Systolic Hypertension in the Elderly Program (SHEP) in over 60-year-olds with isolated systolic hypertension (160 to 219 mm Hg systolic and <90 mm Hg '.':astolic), hypertensive therapy decreased the risk not only of stroke by 36%, but also of heart failure by 49%; in the subgroup with a previous myocardial infarction, it decreased the risk of heart failure by 81%. Richards et al recently showed that antecedent hypertension interacts with age, neurohumoral activation and early ventricular remodeling to increase the risk of heart failure after myocardial infarction. In their population with acute myocardial infarction, plasma neurohormones were significantly higher in hypertensives than in normotensives 1 to 4 days and 3 to 5 months after infarction. From similar baseline values, left ventricular volumes increased significantly in hypertensives compared to normotensives. The left ventricular ejection fraction rose significantly in normotensives, but not hypertensives. Together with higher inpatient and postdischarge mortality, hypertensive patients incurred more inpatient heart failure and more late heart failure requiring readmission. The association of antecedent hypertension with adverse outcome was amplified by age >64 years, more marked neurohumoral activation (N-ter-minal brain-type natriuretic peptide [N-BNP] >120 pmol/L) and more pronounced left ventricular dilation (left ventricular end-systolic volume [LVESV] >78 mL). Mortality and morbidity were also greater in the patients with antecedent hypertension, despite significantly more ACE-inhibitor and diuretic therapy than in normotensives. Multivariate analysis identified antecedent hypertension as a persistent independent risk for heart failure. The effects of chronic hypertension that predispose to adverse outcome after myocardial infarction include increased coronary vascular resistance, decreased coronary reserve, preexisting muscle fiber hyperplasia, and augmented interstitial collagen, together with pos= sible impaired responsiveness of the coronary vasculature to vasoactive transmitters. Thus, the hypertensive heart is more vulnerable to adverse left ventricular remodeling and progression to frank congestive heart failure for a given infarct size.
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