Background: Appropriate systolic coaptation of the anterior and posterior mitral leaflets depends on normal anatomy and function of the different components of the mitral valve apparatus: annulus, leaflets, chordae, papillary muscles, and the left ventricular (LV) wall. Mitral regurgitation (MR) consists in systolic retrograde flow from the LV to the left atrium (LA) because of the lack of adequate coaptation of the leaflets and a pressure gradient between the two cavities. It is important to distinguish between primary MR due to organic disease of one or more components of the mitral valve apparatus and secondary MR which is not a valve disease, but represents the valvular consequences of a LV disease. Secondary MR is defined as functional MR, due to LV remodelling by idiopathic cardiomyopathy or coronary artery disease. In the latter clinical setting, secondary functional MR is called ischaemic MR. Mitral valve leaflets undergo multiple changes in response to myocardial ischemia and the mechanical stretch imposed by LV remodelling The mitral valve has the possibility of increasing its surface to match LV dilation and prevent MR. Ischemic MR has the specificity of self-aggravating in a vicious circle as it promotes the dilation of the LV which, in turn, leads to additional LV remodelling and exacerbated MR. This phenomenon is facilitated by the fact that ischemic LV seems more vulnerable to MR. Early intravenous anti-coagulation along with anti-platelets is the cornerstone for the management of acute coronary syndrome patients. The primary aim of early anti-coagulation is to reduce the ischaemic burden in the myocardium without increasing the haemorrhagic events. Acute coronary syndrome (ACS) occurs due to complete or incomplete coronary thrombosis following atherosclerotic plaque rupture. ACS includes the patients having unstable angina (UA), non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI).