Bacterial Footprints in Aspirate of Infarct-Related Artery in ST-Elevation Myocardial Infarction patients underwent primary percutaneous coronary intervention


Bacterial infections can trigger acute coronary syndromes. This study aimed to examine bacterial footprints in the aspirate of infarct-related artery.


We studied 140 patients with ST-elevation myocardial infarctionwho underwent a primary coronary intervention using thrombus aspiration catheters. The aspirate was sent for bacteriological and pathological examinations and immunoassay for pneumolysin toxin.


Bacterial culture showed different bacteria in 14 samples. Leukocyte infiltrate was detected in all pathologically examined samples. Pneumolysin toxin was detected in only two samples. Patients with bacteria had similar baseline data as those without, except for the median age [46 (44-50) vs. 55 (47-62) years, P=0.001, respectively], white blood cells, and white blood cells (WBCs) (16670 vs. 7550 cells/µl, P<0.0001, respectively). In hospital-major clinical events (death, stroke, reinfarction, lethal arrhythmia, and heart failure) were not significantly different between the 2 groups with and without bacteria [4 (28.6%) vs. 20 (18.6%) events, respectively, odds ratio (OR) 1.8 (95% CI: 06-6.3), P=0.5].

Patients with bacteria, heavy infiltration, and pneumolysin had insignificant higher events compared with those without [10/35 (28.6%) vs. 16/105 (15.2%) events, OR 2.2 (95% CI: 0.92-5.43), P=0.13]. However, the difference was not significant. By multivariate analysis, bacteria, leukocyte infiltration, and pneumolysin were not predictors for in-hospital clinical events. Higher WBCs and younger age were significant predictors of bacterial footprints (P<0.0001 and P=0.04, respectively).


Bacterial footprints existed in the aspirate of infarct-related artery of ST-elevation myocardial infarction patients. Predictors were higher WBCs and younger age. Bacterial markers were not predictors for in-hospital clinical events. The presence of bacterial footprints supports the infectious hypothesis of atherosclerosis.