Indices of Remodeling
IMR is a common complication of the LV global or local pathological remodeling caused by acute and chronic coronary artery diseases[2]. It often represents the pathological result of increased tethering forces and decreased MV coaptation, which finally leads to IMR[33]. IMR is common and seriously affects the prognosis. Even mild IMR can have adverse effects on survival. There is a strong grade relationship between IMR severity and survival rate[34]. The full closure of the MV leaflets is a balance between two opposing forces: the closing force of the LV contraction and the tethering force of the chordae tendineae (Figure 1 )[35]. IMR is in a self-perpetuating cycle due to the imbalance caused by either a decrease in the closing force or an increase in the tethering force[36].
IMR occurs when the MV leaflets do not adequately cover the MV orifice in systolic period. Two main mechanisms of IMR are generally accepted: ischemic LV dysfunction and non-ischemic dilated cardiomyopathy. IMR results from LV remodeling, which directly affects the spatial relationship between LV and MV. This deformation finally affects the leaflet coaptation and valve competency. The following mechanisms play roles in the pathophysiology of IMR: 1. PM dysfunction: During systole, PM contraction is important to keep the MV leaflets close in the LV. PM ischemia can lead to hypokinesia and detectable MR[37]. The anterolateral PM has a dual blood supply, however, the posteromedial papillary muscle has a solitary blood supply[38]. Because of the vascular anatomy of the PM, the posterior PM is more susceptible to ischemia[39]. 2. MA function: The MA enlargement and flattening also contributes to the development of IMR. The abnormal MA shape, and/or the loss of the saddle-shape, would result in increase of the leaflet stress and abnormal leaflet remodeling[40]. 3. Mechanical coordination of systole: a loss of ventricular mechanical coordination after myocardial infarction would decrease the closing forces during systole, which is thought to be a factor in deteriorating IMR[41]. The disordered contraction of the LV near the PM would increase the tethering forces[42]. Dyssynchrony between atrial and ventricular systole would generate diastolic MR[43]. Due to the MR, the time required to reach the maximal coaptation during acute ischemia is prolonged, which would result in severe MR even during “early systole” and maximal coaptation[44].
IMR is believed to initiate from LV remodeling caused by increased diastolic wall stress and persistent increased end-systolic volume[45]. The lateral and apical PM displacement secondarily affects the MV coaptation, resulting in the valve incompetence. In IMR, the tethering forces exerted by the chordae are increased while the closing forces are reduced due to LV systolic dysfunction. The PM displacement result from from a regional LV remodeling or the global LV dilation after MI, so one or both PM can be affected. When abnormal wall motion and local remodeling in a specific region lead to adequate MV tethering to generate IMR[46]. MV tethering is symmetric in the global remodeling, while asymmetric tethering mainly occurs following localized LV remodeling and mostly affects the posterior PM[47].