The importance of the renin-angiotensin system in reversal of left ventricular hypertrophy.
BACKGROUND
The renin-angiotensin system has an important effect on the development of cardiac hypertrophy and the regulation of left ventricular function, in particular by promoting cardiac interstitial fibrosis.
In both experimental and human studies, ACE inhibitors have shown a clear tendency to perform better than other types of antihypertensive therapy in reversing cardiac structural changes. A recent meta-analysis of 109 studies showed that ACE inhibitors were more effective than beta-blockers, calcium antagonists and diuretics in reducing left ventricular mass. Furthermore, cardiac hypertrophy was reversed to a significantly greater extent with enalapril than hydrochlorothiazide in a long-term study of previously untreated men. Multivariate analyses of the results from that study showed that the reversal of cardiac hypertrophy was independently related to the blockade of the circulating renin-angiotensin system. Furthermore, experimental studies have shown that ACE inhibition can induce reversal of left ventricular hypertrophy even without a fall in blood pressure.
The novel angiotensin II blocker losartan has, like ACE inhibitors, shown significant effects on cardiovascular structure in animal models.


CONCLUSIONS
Blockade of the renin-angiotensin system with ACE inhibitors seems to have independent significance for the reversal of cardiac hypertrophy. However, we still do not know whether it is the attenuation of angiotensin II (locally or systemically), apart from a fall in blood pressure, that is the most important effect of ACE inhibition. Therefore, results from future studies on the ability of angiotensin II antagonists to affect left ventricular hypertrophy, in comparison with ACE inhibitors, are awaited with great interest, especially regarding the differential effects on myocyte hypertrophy and interstitial fibrosis.
Dahlöf
B
B
Department of Medicine, University of Göteborg, Ostra Hospital, Sweden.
D000804:Angiotensin II / Q000037:antagonists & inhibitors*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000503:physiopathology; D012084:Renin-Angiotensin System / Q000187:drug effects*
D000806:Angiotensin-Converting Enzyme Inhibitors; D000804:Angiotensin II