P5585Diagnosis of acute myocardial infarction in patients presenting with left bundle branch block

Abstract

in patients presenting with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) is not well-described in contemporary era. Purpose: The purpose of the study is to investigate the association between proximal and non-proximal location of culprit coronary lesion and short-term outcomes of patients with STEMI treated with PCI. Methods: We retrospectively analysed 3,283 patients with STEMI enrolled in the Victorian Cardiac Outcomes Registry (VCOR). Multivariable logistic regression was used to assess the effect of proximal lesion location (located prior to the first major branch of the three coronary arteries) versus non-proximal location (lesion located elsewhere) on in-hospital and 30-day MACE (defined as a composite of mortality, myocardial infarction, stent thrombosis or unplanned coronary revascularisation). Results: Compared to the non-proximal group (n=1,907, 58%), the proximal group (n=1,376, 42%) presented with more cardiogenic shock (12.4% vs. 5.7%), out-of-hospital arrest (11.8% vs. 7.9%) 65, p=0.159). A subgroup analysis was conducted on stable patients; excluding those with cardiogenic shock, out-of-hospital cardiac arrest and those requiring mechanical circulatory support. Proximal lesion location was also shown to be not an independent predictor of 30-day MACE (HR 1.27, 95% CI 0.84-1.91, p=0.26). Predictors of 30-day MACE Conclusion:Despite the presence of higher risk characteristics among patients with proximal lesion location presenting with STEMI, the proximity of the lesion was not associated with worse outcomes at 30 days in the contemporary era of PCI and adjunctive medical therapy. Background: Statins are a mainstay of primary and secondary prevention of cardiovascular disease. They have been reported to induce plaque regression but the underlying mechanisms remain speculative. Purpose: We hypothesize that statins inhibit local macrophage proliferation in atherosclerotic lesions by lowering systemic cholesterol levels. Methods and results: ApoE−/− mice and APOE*3-Leiden.huCETP mice were fed a high cholesterol diet (HCD) containing 1.25% cholesterol for 12 weeks to induce atherosclerosis followed by a low cholesterol diet (LCD) containing 0.05% cholesterol for an additional 4 weeks to prepare for therapeutic intervention. Here we compared the effects of continued LCD, with LCD plus 0.01% atorvastatin, and cholesterol free diet. Atorvastatin resulted in a significant decrease of total plasma cholesterol by 50% in APOE*3-Leiden.huCETP but not in unresponsive ApoE−/− mice. Consequently, macrophage numbers declined in statin treated APOE*3-Leiden.huCETP mice with reduced proliferation as assessed by Ki67 staining. Similarly, diet induced cholesterol lowering dampened local macrophage proliferation. In ApoE−/− mice, however, statin treatment did not lower plasma cholesterol levels and did not alter macrophage proliferation, thus arguing against relevant pleiotropic statin effects. Background: Patients with suspected acute myocardial infarction (A...