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].