Alterations in left ventricular torsion and diastolic recoil after myocardial infarction with and without chronic ischemic mitral regurgitation.

BACKGROUND Chronic ischemic mitral regurgitation (CIMR) is associated with heart failure that continues unabated whether the valve is repaired, replaced, or ignored. Altered left ventricular (LV) torsion dynamics, with deleterious effects on transmural gradients of oxygen consumption and diastolic filling, may play a role in the cycle of the failing myocardium. We hypothesized that LV dilatation and perturbations in torsion would be greater in animals in which CIMR developed after inferior myocardial infarction (MI) than in those that it did not. METHODS 8+/-2 days after marker placement in sheep, 3-dimensional fluoroscopic marker data (baseline) were obtained before creating inferior MI by snare occlusion. After 7+/-1 weeks, the animals were restudied (chronic). Inferior MI resulted in CIMR in 11 animals but not in 9 (non-CIMR). End-diastolic septal-lateral and anterior-posterior LV diameters, maximal torsional deformation (phi(max), rotation of the LV apex with respect to the base), and torsional recoil in early diastole (phi(5%), first 5% of filling) for each LV free wall region (anterior, lateral, posterior) were measured. RESULTS Both CIMR and non-CIMR animals demonstrated derangement of LV torsion after inferior MI. In contrast to non-CIMR, CIMR animals exhibited greater LV dilation and significant reductions in posterior maximal torsion (6.1+/-4.3 degrees to 3.9+/-1.9 degrees * versus 4.4+/-2.5 degrees to 2.8+/-2.0 degrees; mean+/-SD, baseline to chronic, *P<0.05) and anterior torsional recoil (-1.4+/-1.1 degrees to -0.2+/-1.0 degrees versus -1.2+/-1.0 degrees to -1.3+/-1.6 degrees ). CONCLUSIONS MI associated with CIMR resulted in greater perturbations in torsion and recoil than inferior MI without CIMR. These perturbations may be linked to more LV dilation in CIMR, which possibly reduced the effectiveness of fiber shortening on torsion generation. Altered torsion and recoil may contribute to the "ventricular disease" component of CIMR, with increased gradients of myocardial oxygen consumption and impaired diastolic filling. These abnormalities in regional torsion and recoil may, in part, underlie the "ventricular disease" of CIMR, which may persist despite restoration of mitral competence.