The impact of cigarette smoking on infarct location and in-hospital outcome following acute ST-elevation myocardial infarction.

Introduction: Smoking, which is a major modifiable risk factor for coronary artery diseases, affects cardiovascular system with different mechanisms. We designed this study to investigate the association of smoking with location of ST-segment elevation myocardial infarction (STEMI), and short-term outcomes during hospitalization. Methods: In 1017 consecutive patients with anterior/inferior STEMI, comprehensive demographic, biochemical data, as well as clinical complications and mortality rate, were recorded. Patients were allocated into two groups based on smoking status and compared regarding the location of myocardial infarction, the emergence of clinical complications and in-hospital mortality in univariate and multivariate logistic regression analysis. Results: Among 1017 patients, 300 patients (29.5%) were smoker and 717 patients (70.5 %) were non-smoker. Smokers were significantly younger and had lower prevalence of diabetes, hyperlipidemia and hypertension. Inferior myocardial infarction was considerably more common in smokers than in non-smokers (45.7% vs. 36%, P = 0.001). Heart failure was developed more commonly in non-smokers (33.9% vs. 20%, P = 0.001). In-hospital mortality was significantly lower in smokers (6.7% vs. 17.3%, P = 0.001). After adjustment for confounding variables, smoking was independently associated with inferior myocardial infarction and lower heart failure [odds ratio: 1.44 (1.06-1.96), P = 0.01 and odds ratio: 0.61 (0.40-0.92), P = 0.02, respectively]. However, in-hospital mortality was not associated with smoking after adjustment for other factors [odds ratio: 0.69 (0.36-1.31), P = 0.2]. Conclusion: Smoking is independently associated with inferior myocardial infarction. Although smokers had lower incidence of heart failure, in-hospital mortality was not different after adjustment for other factors.

Effect of Vitamin D in the Prevention of Myocardial Injury Following Elective Percutaneous Coronary Intervention: A Pilot Randomized Clinical Trial.

Myocardial injury following elective percutaneous coronary intervention (PCI) occurs in about one-third of patients and is associated with mortality. Platelet aggregation, thrombosis formation, and inflammation are the main causes of cardiac injury during PCI. Vitamin D plays a key role in the cardiovascular system by exerting antiplatelet, anticoagulant, and anti-inflammatory properties. There is no published study that investigated the effect of vitamin D in the prevention of cardiac injury following elective PCI. In a randomized clinical trial, 99 patients admitted for elective PCI were randomized into vitamin D (n = 52) and control (n = 47) groups. The intervention group received 300 000 IU vitamin D orally 12 hours before PCI. The cardiac biomarkers were checked at baseline, 8 and 24 hours after PCI. hs-CRP was also measured at baseline and after 24 hours. The increase in CK-MB was documented in 20 patients (42%) in the control group and 18 patients (34.6%) in the intervention group (P = .417). Furthermore, the increase in cTnI occurred in 4 patients (8%) and 2 patients (3.3%) in the control and intervention groups, respectively (P = .419). No significant changes were noted in the level of cardiac biomarkers. In the vitamin D group, the mean difference in CK-MB between 8 and 24 hours was significantly lower (P = .048). The mean difference in hs-CRP was significantly lower in the vitamin D group (P = .045). This study could not show a clear effect of vitamin D in the prevention of cardiac injury during elective PCI. Further outcome-based studies are needed to describe the role of vitamin D in the prevention of periprocedural myocardial injury.

The effect of prethrombolytic cyclosporine-A injection on clinical outcome of acute anterior ST-elevation myocardial infarction.

INTRODUCTION: Reperfusion injury reduces the benefits of early reperfusion therapies after acute ST-elevation myocardial infarction (STEMI). Cyclosporine-A (CsA) is a potent inhibitor of opening of the mitochondrial permeability transition pore, which has been shown to play a key role in myocardial reperfusion injury. The impact of this treatment on clinical outcomes of acute STEMI remains unknown. Our aim was to investigate the clinical outcomes of using this drug in patients with acute anterior STEMI receiving thrombolytic treatment (TLT). METHODS: In this double-blinded randomized clinical trial, 101 patients with acute anterior STEMI who were candidate for TLT, were enrolled and randomly assigned into treatment or control groups. Patients in the treatment group received an intravenous bolus injection of 2.5 mg/kg of CsA immediately before TLT. The patients in the control group received an equivalent volume of normal saline. Infarct size, occurrence of major arrhythmias, heart failure, left ventricular ejection fraction (LVEF), TLT-related complications, in-hospital and 6-month mortality rates were investigated. RESULTS: There were no significant differences among the demographics, myocardial enzyme release, occurrence of major arrhythmias [9 (18%) vs. 12 (23.5%), P = 0.80], heart failure [18 (36%) vs. 19 (38.3%), P = 0.83], LVEF at first day [34.7 ± 9.9% vs. 33.5 ± 8.1%, P = 0.50] or at discharge [37.7 ± 10% vs. 36.1 ± 8.2%, P = 0.43], and in-hospital [4 (8%) vs. 6 (11.8%), P = 0.74] or 6-month mortality rates [9 (18%) vs. 10 (19.6%), P = 0.99] between the CsA vs. the control group. CONCLUSION: In this study, the prethrombolytic administration of CsA was not associated with a reduction in the infarct size or any improvement in clinical outcomes.