Abstract
Introduction: The objective was to examine the role of statins in modulating post-STEMI inflammation and related mortality. Methods: A total of 404 patients with STEMI were reviewed. Demographics, comorbidities, laboratory values, and outcomes were collected. The patients were grouped as STATIN and NOSTAT based on the use of statin drugs at the time of admission. Ninety-seven patients were receiving statin drugs. Results: The patients in the STATIN group were more likely to be hypertensive (53.6%), diabetic (37.1%) and to have previous coronary revascularization (9.3%). Following propensity matching of 89 patients in STATIN group to an equal number of patients in NOSTAT controls had lower neutrophil count 7.8 (6.8-8.4) compared to those in the NOSTAT group 9.1 (7.9-10.1). Although there was no difference in-hospital mortality between the two groups, the incidence of pump failure was lower in the STATIN group (5.6% vs. 15.7%; P < 0.01). Conclusion: Statin treatment prior to STEMI mitigates the cellular inflammatory response after the myocardial infarction, as evidenced by lower leukocyte and neutrophil cell counts in the STATIN group.
Highlights
The objective was to examine the role of statins in modulating post-ST elevation myocardial infarction (STEMI) inflammation and related mortality
STEMI was determined using the definition and criteria provided by American College of Cardiology and European Society of Cardiology; in short: STEMI was defined as an increase in cardiac troponin-I along with new ST-segment elevation measured from J point at least 0.2 mV in two adjacent V1-V3 leads or at least 0.1 mV in other leads within 24 hours after the onset of chest pain.[18]
There were no statistical differences in demographics, comorbidities, or laboratory values between the two groups, except for hyperlipidemia, which remained statistically higher in the STATIN group as this variable was not included in the propensity matching calculation (Table 1)
Summary
The objective was to examine the role of statins in modulating post-STEMI inflammation and related mortality. Acute ST elevation myocardial infarction (STEMI) is associated with a significant local inflammatory response is initiated in the myocardium and propagates systemically into the blood stream Proximal inflammatory cytokines such as tumor necrosis factor alpha (TNFa) and variety of chemokines are scant in healthy hearts, their levels spike up during myocardial infarct.[1,2,3] Elevation of acute phase reactants such as C-reactive protein and increased peripheral white blood cell count, especially neutrophils, are common manifests of systemic inflammation during an acute coronary syndrome.[4,5] Various investigators have reported associations between increased neutrophil count in peripheral blood and short-term post-STEMI adverse outcomes, including mortality.[6,7,8] It has been imperative for both clinicians and reseachers in the field of cardiovascular medicine to successfully mitigate the exuberent inflammatory responses during an acute coronary event with the aim of limiting the extent of the myocardial injury and thereby improving the outcome following STEMI.
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