M Arita, Y Ueno, S Fujiwara, M Hamada, T Hano, I Nishio, Y Masuyama
{"title":"[The pattern of left ventricular hypertrophy in hypertension and its relation to the hemodynamic and sympathetic responses to exercise].","authors":"M Arita, Y Ueno, S Fujiwara, M Hamada, T Hano, I Nishio, Y Masuyama","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>A wide spectrum of cardiac hypertrophy has been observed in hypertensive patients. In this study, the responses of hemodynamics and sympathetic drives to exercise among hypertensive patients with various types of left ventricular hypertrophy were investigated. Twenty-five patients with untreated essential hypertension (WHO I and II) were classified as those with and without asymmetric hypertrophy (with AH, n = 7; without AH, n = 18) by their echocardiographic patterns. Ten normotensives served as controls. Exercise was performed on a braked bicycle ergometer; the initial work load was 50 watt. The work load increased progressively by 25 watt at three minute-intervals to the target heart rate, exhaustion, or positive ST.T changes. Blood pressure, heart rate, plasma norepinephrine and hemodynamic parameters by echocardiography were estimated at rest and during exercise. Systolic blood pressure and increased heart rate by exercise in all groups. In patients with AH, a rapid increase was observed, and the increase in systolic blood pressure at submaximum exercise was significantly greater than those in normotensives or patients without AH (p less than 0.05). During exercise, endsystolic dimension decreased in normotensives and in patients without AH (p less than 0.01), but the change was not significant in patients with AH. Percent fractional shortening and percent systolic wall thickening of the interventricular septum and left ventricular posterior wall increased significantly in normotensives and in patients without AH (p less than 0.05), but they were unaltered in patients with AH. Although plasma norepinephrine significantly increased in all groups by exercise, the increase in patients with ASH was greater than those in the other groups (p less than 0.05). These results suggest that hyperresponsiveness of systolic blood pressure and heart rate to exercise may play a role in the pathogenesis of AH, and that this type of hypertrophy could be associated with abnormalities of the sympathetic nervous system.</p>","PeriodicalId":77734,"journal":{"name":"Journal of cardiography","volume":"16 1","pages":"95-104"},"PeriodicalIF":0.0000,"publicationDate":"1986-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of cardiography","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
A wide spectrum of cardiac hypertrophy has been observed in hypertensive patients. In this study, the responses of hemodynamics and sympathetic drives to exercise among hypertensive patients with various types of left ventricular hypertrophy were investigated. Twenty-five patients with untreated essential hypertension (WHO I and II) were classified as those with and without asymmetric hypertrophy (with AH, n = 7; without AH, n = 18) by their echocardiographic patterns. Ten normotensives served as controls. Exercise was performed on a braked bicycle ergometer; the initial work load was 50 watt. The work load increased progressively by 25 watt at three minute-intervals to the target heart rate, exhaustion, or positive ST.T changes. Blood pressure, heart rate, plasma norepinephrine and hemodynamic parameters by echocardiography were estimated at rest and during exercise. Systolic blood pressure and increased heart rate by exercise in all groups. In patients with AH, a rapid increase was observed, and the increase in systolic blood pressure at submaximum exercise was significantly greater than those in normotensives or patients without AH (p less than 0.05). During exercise, endsystolic dimension decreased in normotensives and in patients without AH (p less than 0.01), but the change was not significant in patients with AH. Percent fractional shortening and percent systolic wall thickening of the interventricular septum and left ventricular posterior wall increased significantly in normotensives and in patients without AH (p less than 0.05), but they were unaltered in patients with AH. Although plasma norepinephrine significantly increased in all groups by exercise, the increase in patients with ASH was greater than those in the other groups (p less than 0.05). These results suggest that hyperresponsiveness of systolic blood pressure and heart rate to exercise may play a role in the pathogenesis of AH, and that this type of hypertrophy could be associated with abnormalities of the sympathetic nervous system.