Relationship between peripheral monocytosis and nonrecovery of left ventricular function in patients with left ventricular dysfunction complicated with acute myocardial infarction.

BACKGROUND: Although ischemic heart failure is a major cause of mortality after acute myocardial infarction (AMI), the factors that may influence the nonrecovery of left ventricular function (LVF) after an AMI are still unclear. The aim of this study was to identify predictors of nonrecovery of LVF in patients with left ventricular (LV) dysfunction (defined as an echocardiographic ejection fraction (EF)<40%) complicated with AMI who undergo successful primary percutaneous coronary intervention (PCI).

METHODS AND RESULTS: LVF recovery was defined as improvement of LVEF more than 10% compared with baseline LVEF at follow-up. One hundred and eight patients with LV dysfunction after AMI were divided into 2 groups according to the LVF recovery at follow-up: patients with LVF recovery (n=64) vs patients without LVF recovery (n=44). The follow-up LVEF was measured at 8+/-4 months after PCI. Patients without LVF recovery were older (76+/-13 years vs 59+/-14 years, p=0.023) and the baseline peak monocyte count, creatine kinase, and troponin I levels were significantly higher in patients without LVF recovery than in patients with LVF recovery. Delta LVEF (follow-up LVEF-baseline LVEF) correlated with baseline peak monocyte count (r=-0.417, p<0.001), baseline peak creatine kinase (r=-0.269, p=0.005), and baseline peak troponin I levels (r=-0.256, p=0.007). Multivariate analyses showed that baseline peak monocyte count and old age were the independent predictors of nonrecovery of LVF (hazard ratio; 3.38, 95% confidence interval (CI): 1.16-5.43, p=0.012, and hazard ratio; 2.38, 95% CI: 1.09-4.87, p=0.025, respectively).

CONCLUSION: Peripheral monocytosis is associated with nonrecovery of LVF in patients with LV dysfunction complicating an AMI who underwent successful primary PCI. These results suggest an important role of monocytes in the expansion of the infarct and the development of chronic ischemic heart failure after reperfusion therapy.