Pathophysiological aspects of the renin-angiotensin-aldosterone system in acute myocardial infarction.

Abstract

Our understanding of the renin-angiotensin-aldosterone system (RAAS) has advanced considerably in recent years. The RAAS plays a central role in the control of salt and water balance, and in the regulation of blood pressure and cardiovascular homeostasis. The haemodynamic changes in the period after myocardial infarction stimulate intense activation of both the circulating and the local RAAS. This acts through its end-products, angiotensin II and aldosterone, to promote sodium and fluid retention, and to increase cardiac contractility and systemic vascular tone. There is increasing evidence that, in the long term, this apparently adaptive response may be harmful, and might contribute to the development of some of the complications seen after infarction. Angiotensin II is capable of inducing coronary as well as systemic vasoconstriction, and may therefore prolong the duration of ischaemia. The response of the RAAS after infarction can be modified pharmacologically. Angiotensin converting enzyme (ACE) inhibitor drugs are already the mainstay of treatment in heart failure, and have now been shown to have a crucial role in the prevention of ventricular remodelling after myocardial infarction. Although the precise mechanism of this benefit is unclear, it provides further incentives to develop more effective strategies capable of suppressing neurohumoral activity following infarction.