Regression of Cardiac Hypertrophy with Antihypertensive Therapy Long term gallopamil causes regression of left ventricular hypertrophy . ..

The effects of long term gallopamil treatment on left ventricular hypertrophy and function in hypertensive patients were assessed in an open study. 26 previously untreated pat ients, with BP > 140/90mm Hg and left ventricular hypertrophy, received gallopamil 50mg bid for 14.9 months then 50mg tid (n = 13) for up to 22.3 months (n = 13).

After 8.2 months of gallopamil therapy , the interventricular septal thickness decreased by 7% (p < 0.01), posterior wall thickness decreased by 9.9% (p < 0.001) and the left ventricular mass index decreased by 11.9% (p < 0.01) . Over the next 6.7 months, these parameters were unaltered. However, after 22.3 months of treatment , there were further reductions in the left ventricular mass index (319%, p < 0.001) , posterior wall thickness (183%, p < 0.001) and interventricular septal thickness (16.9%, p < 0.001) . After 22.3 months, the relative wall thickness left ventricular end-diastoiic and end-systolic dimensions were also significantly reduced but fractional shortening remained unaltered . Mean BP decreased from 157/103 to 136/84mm Hg (p < 0.001) after 4 weeks and to 134/85 (p < 0001) after 14.9 months of therapy. Exercise BP at a work load of 100W also decreased from 205/ 115 to 194/ 103mm and to 190/94mm Hg , respectively.

Thus, " , , long term treatment with the calcium antagonist gal/opamil induces a significant antihypertensive effect accompanied by a regression of LVH [left ventricular hypertrophy] , , .. , Franz IW . 6ehr V Ke telhut R. Agrawal B J ournal of Card iovascular Pharmacology to (Suppl t o) SI 78·S181. 1987

... and nifedipine and captopril reduce left ventricular thickness and mass The effects of long term captopril and nifedipine treatment on left ventricular mass and volume were

assessed in 16 pat ients with mild to moderate hypertension . Following a 15-day washout period , patients received captopril 50-100 mg/ day (n = 8) or nifedipine 20-40 mg/day (8) for 6 months.

After 6 months' treatment , supine BP had decreased from a mean of 148/101 to 130/90mm Hg (p < 0.01) in captopril recipients and from 145/98 to 127/85mm Hg (p < 0.01) in nifedipine patients . Following isotonic e xercise , nifedipine recipients only showed a decrease in the diastolic BP increment from 13 to 5mm Hg (p < 0.01). The left ventricular end-d iastol ic volume increased significantly in both captopril and nifedipine recipients . There were no significant changes in the left ventricular systolic function . The end-diastolic posterior wall thickness and septum thickness were significantly reduced by both captopril and nifedipine. However , there were no changes in the end-systolic posterior wall thickness and septum thickness with therapy. The left ventricular mass and the mass/volume index were reduced significantly in both treatment groups There was no significant correlation between the reduction in BP and the changes i n left ventricular mass and volume.

Antihypertensive therapy with captopril and nifedipine reduced left ventricular thickness and mass, which " , , might be attributed to an improvement in diastolic function and to a reduction in wall tension rather than to an effective regression of left ventricular hypertrophy', She,ban I Arca ro G . COVI G. Accardi R. Zenoron, C. et al Journal of Cardiovascular Pharmacology 10 (Suppl 10) S187·S191 1 987 7U~

0156-2703/ 88/ 0827-0015 / 0S01.00/0 © ADIS Press INPHARMA ' 27 Aug 1988 15