ABSTRACT
Left ventricular hypertrophy [LVH] is a sequelae of sustained prolonged systemic hypertension Initially it is a compensatory mechanism but later on the left ventricular hypertrophy carriers the risk of arrhythmias, congestive cardiac failure, angina, systolic as well as diastolic dysfunction, greater intensity and risk of myocardial infarction and cardiac rupture. The Framingham Heart Study and other studies have shown LVH as an independent risk factor for cardiovascular morbidity and mortality. Some classes of drug cause regression of LVH e.g. ACE inihibitor, AT[1] receptor blockers, calcium channel blockers, B blockers and methyldopa. The effect of diuretics on regression are equivocal. we gave indapamide 2.5mg to 7 pts with echocardiographic evidence of LVH and found that LVID [mm] [mean + SEM] decreased from 50.7 +/- 1.2 to 50.20 +/- 1.70, IVST [mean + SEM] decreased from 14.10 +/- 0.4 to 11.9 +/- 0.30, PWT [mean +SEM] decreased from 13.0 +/- 0.3 to 11.2 +/- 0.2 and LVMI [mean +SEM] decreased from 176.42 +/- 6.13 to 145.25 + 6.04g/m[2]