The influence of sympathetic nervous activity on regression of cardiac hypertrophy.
Pharmacotherapeutical means of reversing cardiac hypertrophy (prazosin, clonidine and nifedipine) were analysed in concentrically, as well as eccentrically, hypertrophied left ventricles. Regression of cardiac hypertrophy, i.e. a therapeutic intervention on a critical precursor of hypertensive congestive heart failure, can be obtained by various antihypertensive agents. Prazosin, calcium channel blockers, clonidine and angiotensin converting enzyme inhibitors as well as a combined treatment regimen using alpha-receptor blockers together with diuretics and vasodilators can all induce regression of hypertrophy associated with an improvement in left ventricular function. Moreover, an improved coronary reserve may reduce the ischaemic risk of the hypertrophied myocardium. However, not all antihypertensive drugs seem equally effective in bringing about coronary regression of left ventricular hypertrophy (LVH). No regression or little regression has been found with diuretic monotherapy despite a satisfactory reduction in blood pressure. On the other hand, a trend towards a regression has been observed in patients in whom treatment with clonidine significantly reduced catecholamines.
D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D006332:Cardiomegaly / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D002395:Catecholamines / Q000097:blood; D003326:Coronary Circulation; D003327:Coronary Disease / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D000959:Antihypertensive Agents; D002395:Catecholamines