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End-organ damage: does it really matter how we prevent it?

B. Dahlöf*

Sahlgrenska University Hospital/Östra, Göteborg, Sweden

* Björn Dahlöf, MD, Department of Medicine, Ostral Hospital, SE-41685 Göteborg, Sweden

Abstract

Studying left ventricular hypertrophy (LVH) allows the most comprehensive evaluation of end-organ damage prevention. Clinical trials show that renin-angiotensin-aldosterone system blockade confers protective effects that are not simply due to antihypertensive activity. Angiotensin II receptor blockers (ARBs), which offer specific and complete inhibition of the action of angiotensin II at the level of the angiotensin II type 1 (AT1) receptor, have proves more effective than other antihypertensive classes in reversing LVH and interstitial collagen accumulation. The Losartan Intervension For Endpoint reduction in hypertension (LIFE) study, for example, showed that a losartan-based therapy resulted in better LVH regression than an atenolol-based one, despite similar blood pressure control with both treatment regimens. Other clinical studies demonstrated that ARB-induced reduction in fibrosis is linked to functional improvement. It is still not known whether more effective angiotensin II blockade will provide more complete LVH reversal, improve cardiac function, prevent damage to other target organs and enhance prognosis. To find the answer, The ONgoing Telmisartan Alone and in combination with Ramipril GLobal Endpoint Trial (ONTSRGET) Trial Programme will compare 24-h active AT1 blockade with telmisartan versus established angiotensin-converting enzyme (ACE) inhibition using ramipril versus AT1 blockade plus ACE inhibition.

Key Words: Endotheliall dysfunction • Left ventricular hypertrophy • Renin-angiotensin-aldosterone system • Target organ damage • Treatment


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