Medical treatment:
There are only a few studies that focus on the impact of medical treatment on CIMR. Medical treatment of CIMR may lead to a reduction in MR severity, and/or it may lead to
attenuation or reversion of post-MI LV remodeling. Several studies suggest that angiotensin-converting enzyme inhibitors, nitrates and diuretics can lead to a partial shorter long-term reduction in MR by increasing the transmitral valve pressure gradient through either afterload or preload reduction [27 - 29]. In addition, inotropic vasopressors, such as dobutamine, can decrease CIMR [30]. As shown by the SAVE (Survival And Ventricular Enlargement) and SOLVD (Studies of Left Ventricular Dysfunction) studies, ACE inhibition can attenuate [31], arrest [32] or reverse [33] post-MI LV remodeling. In addition, the CAPRICOR (Carvedilol PostInfarct Survival Controlled Evaluation) and CARMEN (Carvedilol and ACE Inhibitor Remodeling Mild Heart Failure Evaluation Trial) studies showed that the combination of ACE inhibition and b-blockade inhibits [34] or synergistically reverses LV negative remodeling. There are, however, no data from large trials that show a decrease in the incidence of CIMR after attenuation or reversal of LV remodeling with ACE inhibition and b-blockade [36]. Despite the use of these drugs CIMR remains common. Cardiac resynchronization therapy (CRT) significantly and immediately reduces functional MR and CIMR due to
improved coordinated timing of the PM insertion sites [36] and increased closing force. Long-term CRT (up to 12 months) results in progressive structural and functional LV reverse remodeling, improved LV systolic and diastolic function and decreased MR severity in patients with moderate-to-severe heart failure and dyssynchronous ventricular contraction [37]. This effect is also evident during exercise, preventing the increase of MR during exercise [38]. However, approximately 30% of CHF patients treated with CRT do not respond to treatment [39]. Independent predictors of lack of response to CRT are ischemic heart disease, severe MR and LV end-diastolic dimension 75 mm [40]. This indicates that patients with CIMR are less likely to benefit from CRT, especially in advanced stages of LV dilatation and tenting [37].