Background Bacterial infections can trigger acute coronary syndromes. This study aimed to examine bacterial footprints in the aspirate of infarct-related artery.
Patients and methods We studied 140 patients with ST-elevation myocardial infarction who underwent a primary coronary intervention using thrombus aspiration catheters. The aspirate was sent for bacteriological
and pathological examinations and immunoassay for pneumolysin toxin.
Results Bacterial culture showed different bacteria
in 14 samples. Leukocyte in ltrate 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], 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 signi cantly different between the 2 groups with and without bacteria [4 (28.6%) vs. 20 (18.6%) events, respectively, odds ratio (OR) 1.8 (95% CL: 06–6.3), P = 0.5]. Patients with bacteria, heavy in ltration, and pneumolysin had insigni cant higher events compared with those without [10/35 (28.6%)
Introduction
One emerging paradigm suggests that bacterial infection can contribute toward the pathogenesis of acute coronary syndromes (ACSs) [1]. The formation of platelet thrombi on the surface of complicated coronary plaques is consid- ered an essential step in the evolution of ACS [2]. Acute infections can promote the development of thrombi in var- ious ways [3]. Platelets can be activated directly by patho- gens and the in ammatory response that they elicit [4]. In addition, acute infections can cause coronary vasoconstric- tion and further narrow the lumen in atherosclerotic coro- nary segments, stimulating shear-induced platelet activity [5]. The host response to acute infections can trigger, has- ten, or facilitate ACS on the basis of generalized and local in ammatory and thrombogenic changes [6].
The clinical trials to date have not provided an adequate support for the clinical use of antibiotics in the primary or secondary prevention of coronary artery disease [7].
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vs. 16/105 (15.2%) events, OR 2.2 (95% CL: 0.92–5.43), P = 0.13]. However, the difference was not signi cant. By multivariate analysis, bacteria, leukocyte in ltration, and pneumolysin were not predictors for in-hospital clinical events. Higher WBCs and younger age were signi cant predictors of bacterial footprints (P < 0.0001 and P = 0.04, respectively).
Conclusion 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.