Retrospective and prospective research on hypertension-related end-organ damage.
Persistent inappropriate blood pressure elevation leads to the development of left ventricular hypertrophy, progressive atherosclerosis, and structural changes in the arterial tree. These changes result in clinical manifestations such as ischemic cardiac and cerebral events, congestive heart failure, renal failure, and peripheral vascular insufficiency. This article reviews the 5-year course of 439 patients with primary hypertension who were seen at a time (1946-1953) when potent antihypertensive therapy was not widely used. At the end of 5 years, 55% of the men (78 of 143) and 28% of the women (83 of 296) were dead. The principal causes of death were coronary insufficiency, congestive heart failure, cerebral infarction and hemorrhage, accelerated hypertension, renal failure, and dissecting aneurysm of the aorta. Coronary insufficiency and accelerated hypertension predominated in men, whereas women died principally of cerebral events and congestive heart failure. The 439 patients were stratified according to the level of their office blood pressure on the first visit, the severity of the changes in the optic fundi, the degree of left ventricular hypertrophy determined by electrocardiogram, cardiac enlargement determined by roentgenogram and their renal function, as measures of end-organ damage. Patients who had higher initial blood pressures showed more evidence of end-organ damage than patients with lower initial pressures. The higher the initial blood pressure or the more advanced the evidence of end-organ damage, the greater was the 5-year mortality. The mortality was particularly high in patients who had already sustained a clinical cardiovascular event before entry into the study and in those with malignant hypertension or gross cardiomegaly.(ABSTRACT TRUNCATED AT 250 WORDS)
Perloff
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Moffitt Hospital, University of California, San Francisco 94143, USA.
D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001161:Arteriosclerosis / Q000209:etiology / Q000401:mortality; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D018660:Blood Pressure Monitoring, Ambulatory; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000401:mortality / Q000517:prevention & control; D002544:Cerebral Infarction / Q000209:etiology / Q000401:mortality; D015331:Cohort Studies; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000209:etiology / Q000401:mortality; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy / Q000401:mortality; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000401:mortality; D015993:Life Tables; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology / Q000401:mortality; D011379:Prognosis; D016016:Proportional Hazards Models; D011446:Prospective Studies; D051437:Renal Insufficiency / Q000209:etiology / Q000401:mortality; D012189:Retrospective Studies
D000959:Antihypertensive Agents