Mechanistically, the valve and subvalvular apparatus work in a tightly coupled and coordinated fashion. The loop from the papillary muscles to the mitral annulus is completed by the chordae tendineae continuing into the mitral leaflets, which then are attached to the annular ring.

A normal kinetics and sequence of contraction of the papillary muscles (PMs) is basic for an optimal valve competence. The increased interpapillary distance, PM malalignment and the consequent increase of the traction force exerted by the chordae may lead to apical tethering or tenting of the leaflets and mitral incompetence associated with restricted systolic leaflet motion (type IIIb).

PMs dysfunction in patients with coronary artery disease has been thought to contribute to mitral regurgitation [3, 12, 19–21]. The PMs are particularly susceptible to ischemia, more so the posteromedial PM (generally supplied by the posterior descending coronary artery) than the anterolateral PM (customarily supplied by branches of the left anterior descending and the circumflex coronary arteries) [20, 22]. The posteromedial PM is perfused by one major coronary artery in 63 % of cases and by two vessels in the remainder; the anterior PM has two-vessel perfusion in 71 % of normal individuals [19].

Myocardial infarction leading to PMs dysfunction occurs more frequently when the blood supply to the PM is provided by one vessel, as is more often the case with the posteromedial PM after an inferior myocardial infarction.

Posteromedial PM tip displacement probably results from failure of the ischemic posterior PM to shorten during systole, lengthening of the ischemic PM over time, and also dyskinesia of the ischemic LV wall subtenting the PM [23].

The nonischemic anterior PM also may play a role in apical leaflet restriction because this normally shortening anterior PM is displaced apically at end-systole relative to baseline.

The primary mechanism of SMR is the regional or global LV dysfunction, even though the mitral valve is structurally normal, and is a common complication in both ICM and DCM patients [24, 25].

Geometric changes associated with ventricular remodeling, such as posteromedial PMs dislocation in the lateral axis, may lead to leaflet tenting or tethering, as reflected by a larger distance from the plane of the anterior annulus to the posteromedial PM tip and increased annular diameter [12, 26].

The term “secondary or functional” describe collectively MR related to severe LV systolic dysfunction with pronounced LV dilation (ejection fraction <30 %) regardless of etiology [27]. IMR, by contrast, refers to mitral insufficiency caused by the adverse consequences of coronary disease with more asymmetric ventricular remodeling, most often affecting the inferior and lateral LV wall.

The geometry of the MV related to unilateral PM displacement (regional LV dysfunction) is different from that related to bilateral PM displacement (global LV dysfunction) on the basis of anatomic knowledge that each PM distributes the chordae only to the ipsilateral half of both leaflets. This is the patophisiological bases of the echocardiographyc difference between asymmetric and symmetric thetering (Figs. 2.2 and 2.3 ).

Echocardiographic studies in patients with dilated nonischemic cardiomyopathy confirm enlarged LV diameter and sphericity to be major predictors of MR in addition to the tenting or apical tethering of the chordae tendineae and valve leaflets, whereas sphericity also can accompany progression of MR in end-stage coronary disease [28, 29].

IMR is, by contrast, not so much dependent on global LV dilation but rather on a more localized LV insult [12, 21].

Anteroapical infarcts lead to apical thinning and akinesia and inferior infarcts cause inferior akinesia or dyskinesia and progressive IMR, for the major substantial perturbation of the mitral subvalvular apparatus [1].

Over time, as the left ventricle dilates and changes shape after the ischemic event (postinfarction remodeling), the degree of IMR progresses [26, 30].

In literature, IMR associated with anterior infarction is usually accompanied by greater LV and mitral annular dilation in the septal-lateral (also known as “anteroposterior”) axis, more impressive annular flattening, and lower ejection fraction relative to inferior MI [31–33].