Effect of atrial natriuretic peptide on left ventricular remodelling in patients with acute myocardial infarction.

Atrial natriuretic peptide (ANP) is a member of the natriuretic peptide family that exerts various biological effects via acting on the receptor-guanylyl cyclase system, increasing the content of intracellular cyclic guanosine monophosphate (cGMP). ANP was first identified as a diuretic/natriuretic and vasodilating hormone, but subsequent studies revealed that ANP has a very important function in the inhibition of the renin-angiotensin-aldosterone system (RAAS), endothelin synthesis, and sympathetic nerve activity. Evidence is also accumulating from recent work that ANP exerts its cardioprotective functions not only as a circulating hormone but also as a local autocrine and/or paracrine factor. ANP inhibits apoptosis and hypertrophy of cardiac myocytes, and inhibits proliferation and fibrosis of cardiac fibroblasts. Reperfusion of the ischaemic myocardium by percutaneous coronary intervention (PCI) reduces the infarct size and improves left ventricular (LV) function in patients with acute myocardial infarction (AMI). However, the benefits of PCI in AMI are limited by reperfusion injury. Animal studies have shown that ANP inhibits ischaemia/reperfusion injury, and reduces infarct size. We and others have recently shown that the intravenous administration of ANP inhibits RAAS, sympathetic nerve activity and reperfusion injury, prevents LV remodelling, and improves LV function in patients with AMI. ANP has a variety of cardioprotective effects and is considered to be a very promising adjunct drug for the reperfusion therapy in patients with AMI.