Definition
Dr. Carpentier has defined the triad of MR by focusing on the etiology, lesion and dysfunction, as such IMR can have a specific definition. The etiology of IMR is due to coronary artery disease (CAD) and virtually is always associated with AMI. The primary lesion in IMR is leaflet tethering resulting from left ventricle (LV) remodeling secondary to an acute ischemic insult. Multiple studies have shown that the inferior/inferoposterior MI is more commonly associated with IMR[5]. The dysfunction of IMR rises from posteriormedial and apical displacement of the papillary muscle (PM), which leads to a measurable “tethering distance” and ultimately results in apical tenting and restriction of the free margin of the leaflets and poor leaflet coaptation [6]. Tethering of secondary chordae can lead to a “seagull” deformation of the anterior leaflet, which has been targeted in certain repair series. Ischemic heart disease (IHD) results in LV and mitral annular remodeling[8]. As a consequence, LV remodeling can lead to changes in the geometry of the mitral valve apparatus leading to MR[9].
It is noteworthy that IMR and FMR fundamentally have different pathophysiology, albeit IMR and FMR have been frequently used interchangeably in the literature. IMR is associated with LV remodeling, yet the degree of LV chamber remodeling differs due to the location of the AMI. Echocardiographic studies in patients with dilated non-ischemic cardiomyopathy confirm enlarged LV diameter and sphericity to be the major predictors of MR in addition to the tenting or apical tethering of the chordae tendineae and valve leaflets. However, IMR, especially in the inferior or infero-posterior AMI, is not as much dependent on global LV dilatation but rather on a more localized LV insult. Generally, IMR is more likely after inferior/inferoposterior AMI rather that anterior AMI. IMR associated with anterior infarction is usually accompanied by greater LV and mitral annular dilatation in the septal-lateral (S-L) (also known as “antero-posterior”) axis, more impressive annular flattening, and lower ejection fraction (EF) relative to inferior MI. It appears that anterior infarction does not sufficiently affect critical annular-subvalvular spatial relationships that are perturbed by a smaller posterolateral infarct. As such, IMR in the presence of anterior AMI develops due to chronic remodeling and progressive LV dysfunction, which results in development of IMR. Thus, IMR associated with anterior MI may be more similar to the clinical spectrum to FMR characterized by severely depressed LV function, global LV dilatation, and annular enlargement. On the other hand, an inferior MI is associated with less global LV dilatation and systolic dysfunction but more substantial perturbation of the mitral subvalvular apparatus[10].