Asynchrony and left ventricular remodeling after acute myocardial infarction in the BONAMI trial

Objectives We evaluated the time-course of both LV asynchrony and remodeling in patients with reperfused myocardial infarction (MI) enrolled in the BONAMI trial.

Methods BONAMI was a randomized, multicentre controlled trial assessing cell therapy in patients with acute MI. Briefly, 101 patients with reperfused acute MI, LVEF < 45% and decreased viability were randomized to cell therapy (n=52) or to control (n=49). Patients underwent Tl-201 SPECT, equilibrium RNA and echocardiography at baseline, 3 month and 1 year follow-up. LV asynchrony was assessed by the standard deviation (SD) and mode of the LV phase histogram.

Results Eighty-three patients with comprehensive follow-up at 1 year were included. LV remodeling was defined by a 20% increase in LV end-systolic volume index (ESVI) from baseline to 1 year (n=43). Baseline LVEF, WMSI and perfusion defect size were significantly impaired in patients with LV remodeling (all P<0.001). Peak troponin was increased (P=0.04) in patients with LV remodeling. By contrast, LV mechanical asynchrony parameters (LV SD and LV mode) did not differ at baseline between the 2 groups. Along with the worsening of LV remodeling there was a significant increase in LV SD (75.1±24.0 to 85.5±37.9 ms, P=0.01) and LV mode (290±48 to 357±56 ms, P<0.0001) from baseline to 1 year follow-up. Treatment allocated (control or bone marrow cell) did not modify the time-course of LV remodeling and asynchrony. At 1 year LV SD was highly correlated with LV ESVI (r=0.54), EDVI (r=0.55), EF (r=-0.41) and WMSI (r=0.39, all P<0.0001) and with Tl-201 defect size (r=0.33, P=0.003).

Conclusions LV remodeling 1 year after acute MI is associated with (i) progressive LV asynchrony as demonstrated by RNA and (ii) viability, without impact of cell therapy on this process. (ClinicalTrials.gov number NCT00200707).