ABSTRACTS

DETEFWINANTS OF LEFT VENTRICULAIl HYPERTROPHY AND FUNCTION IN HYPEXTENSION. Freddy Abi-Samra, MD; Fetnat M. Fouad, ND, FACC; Yoshi- yuki Nakashima, MD; Robert C. Tarazi, MD, FACC; Emmanuel L. Bravo, MD, Research Division, Cleveland Clinic Founda- tion, Cleveland, Ohio.

revels of blood pressure have given at best only partial explanation for LV changes in hypertension. Determinants of LV behavior in hypertension were therefore studied in 74 patients (53-M. 21-F; Age: median-50; range: 16-79), using cuff systolic pressure and M-mode echocardiograk to measure LV mass index , percent LV systolic shortening, velocity of circumferential fiber shorteninp (Vcf), as well as meridional peak systolic stress (PSS) and end- systolic stress (ESS). At the time of study, 29 patients were untreated while 45 were taking different drug regi- mens. In the group as a whole, LV mass correlated only with systolic pressure (r = 0.38, p< 0.01) and ESS (r = 0.33, p< 0.01). Vcf and percent shortening did not corre- late with blood pressure or PSS but were both inversely related to ESS (r = -0.74 and -0.80 respectively; p<O.Ol). In addition, LV mass was inversely related to PSS (r = -0.32, p< 0.01). The results were similar when treated and untreated subgroups were looked at separately. These data suggest that in patients with hypertension (1) LV hypertrophy correlates poorly with systolic pressure or mechanical stress (r2 = 14%); (2) increasing LV mass tended to normalize PSS but not ESS and, (3) LV perfor- mance decreased as ESS rose. Thus, ESS appeared as one of the more significant determinants of LV function in hypertension.

ECHOCARDIOGRAPHIC DOCUMENTATION OF REGRESSION OF LEFT VENTRICULAR HYPERTROPHY PRODUCED BY THE TREATMENT OF ESSENTIAL HYPERTENSION Robert C. Schlant, MD, FACC; Joel M. Felner, MD, FACC; 8rent A. Blumenstcin, PhD; Neil B. Shulman, MD; Steven 8. Heymsfield, MD; W. Dollas Hall, MD; and Gary L. Wollam, MD, Emory University School of Medicine, Atlanta, GA

Ninety-five patients (meun age 48 * 11 .Bl yrs.) with previously unctnnplicrrted and untreated diastolic hypertension over 90 mmHg were followed by echocardiogrophy over 5 years of treatment. Significant changes occurred in heart rate (HR), ventricular septal thickness (VST), left ventricular posterior wall thickness (LVPWT), left ventricular end-diastolic volume index (LVEDVI), and end- systolic volume index (LVESVI), ejection fmction (EF), and left ientriculor mass index (LVMI).

Initial Blood pressure, mmHg 155.s22.4/101.@9.5 HR, beats/min 66.9 f 10.6 VST, mm 12.0 f 2.7 LVPWT, mm 11.2 f 2.2 LVEDVI, ml/m2 89.3 f 41.9 LVESVI, ml/m2 28.8 f 17.6 EF LVMI, grn/m2

.6a2 * .09 204.5 ??69.3

5-Yeor

134.9+21.0/88.2*11.7 59.4 f 10.6 9.0 ??1.0 10.1 * 1.6 102.Oh33.1 22.2 f 11.0 .79 f .06 161.6i40.8

The dota document that the treatment of hypertension produces significant and sustained decreases in left ventricular hypertrophy in association with improved left ventricular function.

THE TIME COURSE OF REGRESSION OF LEFT VENTRICULAR HYPERTROPHY IN TREATED HYPERTENSIVE PATIENTS Gary L. Wollam, MD; W. Dallas Hall, MD; Margaret B. Douglas, M.C.H.; Brent A. Blumenstein, Ph.D.; Merril L. Knudtson, MD; Joel M. Felner, MD, FACC; Robert C. Schlant, MD, FACC; &uory University, Atlanta, Ga.

Regression of left ventricular hypertrophy (LVH), as evidenced by the ECG and echocardiogram (ECHO), has been observed with antihypertensive treatment. However, the initial time course has not been well established. In a prospective study, 29 black hypertensive patients with posterior wall thickness at end-diastole (PW'I'd) L 11 mm were treated with hydrochlorothiazide (7 patients), methyldopa (6) 01‘ both (16). ECHO and ECG were performed in each of the 29 patients at baseline and after one month, three months, six months and 12 months of therapy. PWTd, left ventricular mass index (LVMI) and maximal summed precordial voltage on ECG (Sv'l or SVz + RVs or RVs) decreased significantly after one month in all three treatment groups. Changes in ventricular septal thickness (IVSTd) were not significant.

Baseline 1 Month 12 Months P* Systolic BP (mm HE) ----iz- 175 134 c.01 Diastolic BP (mm fig) 112 89 86 c.01 ECG Voltage (mm) 38 36 34 c.01 PWTd (mm) 12.9 12.0 11.7 c.01 IVSTd (mm) 12.3 11.9 12.3 >.05 LVMI (g/m*) 143 126 120 c.01 *Significance of the changes between the baseline and follow-up periods.

These data suggest that evidence of regression of LVH may be detected as early as one month after arterial pressure is controlled and continues during the initial year of treatment.

SEPTAL THICKNESS AS A MARKER OF CHANGES IN LEFT VENTRICULAR MUSCLE MASS DURING SHORT-TERM THERAPY WITH HYDROCHLOROTHIAZIDE. Jan I.M. Drayer, MD; Julius M. Gardin, MD, FACC; Michael A. Weber, MD, FACC; and Wilbert S. Aronow, MD, FACC; Hyper- tension Center and Section of Cardiology, VA Medical Center, Long Beach, University of California, Irvine, California

Recent studies suggest that the response of the LV muscle wall to increased blood pressure mainly involves increases in thickness of the interventricular septum. Moreover, regression of hypertrophy has been reported to be more pronounced at the level of the septum than at the posterior wall, and to occur during treatment with sympatholytic agents rather than during diuretic therapy. In this study we report changes in echocardiographic parameters of LV muscle mass observed in 20 hypertensive patients during short- term therapy with hydrochlorothiazide. Although blood pressure fell significantly from 155 f 3/104 f 2 to 144 f 3/98 f 2mm Hg (FQOOS), septal thickness (VSD) or posterior wall (LVWTD) thickness (VSD 10.7 f 0.3 to 10.5 f 0.2mm and LVWTD 9.4 f 0.3 to 9.4 i 0.3mm, ns) did not change. VSD was significantly greater than LVWTD before and during therapy (PUJ.001). VSD decreased in 9 patients, and all of these patients also showed a decrease in LV cross sectional area. VSD did not change or increased in I1 patients, and only one of these patients showed an increase in cross sectional area. However, LV transversal dimension decreas- ed in 8 of these patients. This study .confirms that hypertrophy induced by hypertension occurs to a greater extent in the septum than in the posterior wall. In contrast to earlier studies, the parameters of LV muscle mass decreased in 45% of the patients studied, even during short-term diuretic therapy. Decreases in septal thickness reflect decreases in other parameters of muscle mass. However, apparent increases in septal thickness may occur, usually associated with decreases in LV transversal dimension. Therefore, the diuretic-induced increases in LV wall thickness and septal thickness probably reflect adaptive changes of cardiac muscle tissue secondary to the decreased size of LV cavity.

March 1992 The American Journal of CARDIOLOGY Volume 49 951