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Segment Elevation Myocardial Infarction (segment + elevation_myocardial_infarction)
Selected AbstractsSelection of glycoprotein IIb/IIIa inhibitors for upstream use in patients with diabetes experiencing unstable angina or non-ST segment elevation myocardial infarction.JOURNAL OF CLINICAL PHARMACY & THERAPEUTICS, Issue 6 2004What have we learned in the last 10 years? Summary Coronary disease accounts for the majority of deaths among patients with diabetes and the thrombotic milieu accelerated by diabetes results in unstable angina (UA), non-ST segment elevation myocardial infarction (NSTEMI) or ST-segment elevation myocardial infarction (STEMI) or death. Upstream use of a glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitor with percutaneous coronary intervention (PCI) as part of an early invasive approach is preferred. However substantial numbers of patients present to rural or non-teaching hospitals without immediate access to a catheterization laboratory. Enhanced GP IIb/IIIa receptor mobilization, TXA2 production and platelet activation together present an extensive thrombotic challenge that may not be overcome with current doses of GP IIb/IIIa inhibitors when used without PCI. Heterogeneity of platelet aggregometric analysis may have identified GP IIb/IIIa doses used in clinical trials that may not fully overcome the thrombotic challenge in patients with diabetes. GUSTO-IV ACS failed to demonstrate a difference in mortality when used without PCI. The PURSUIT trial provided evidence that eptifibatide decreases death or non-fatal myocardial infarction (MI) in the main group and in the diabetic subgroup. Reductions in this primary endpoint were driven by the reduction in non-fatal MI. The PRISM and PRISM-PLUS trials demonstrated a reduction in death, MI or refractory ischaemia at 48 h or 7 days in the main cohort but not specifically in patients with diabetes. Data supporting use of GP IIb/IIIa inhibitors are inconsistent, raising the question of whether these agents should be used at all without PCI. Variability in experimental methodology of platelet aggregometry and selection of anticoagulant used during dose finding studies may have generated doses that are insufficient to overcome the thrombotic burden. A new marker of active inflammation, sCD40L is found to be upregulated at subtherapeutic doses of GP IIb/IIIa inhibitors, suggesting that rebound inflammatory processes may partially account for absence of clear evidence of benefit with some GP IIb/IIIa inhibitors in patients with diabetes experiencing UA/NSTEMI. [source] Does Proximal Location of Culprit Lesion Confer Worse Prognosis in Patients Undergoing Primary Percutaneous Coronary Intervention for ST Elevation Myocardial Infarction?JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2006KISHORE J. HARJAI M.D. ST segment elevation myocardial infarction (STEMI) from proximally located culprit lesion is associated with greater myocardium at jeopardy. In STEMI patients treated with thrombolytics, proximal culprit lesions are known to have worse prognosis. This relation has not been studied in patients undergoing primary percutaneous coronary intervention (PCI). In 3,535 STEMI patients with native coronary artery occlusion pooled from the primary angioplasty in myocardial infarction database, we compared in-hospital and 1-year outcomes between those with proximal (n = 1,606) versus nonproximal (n = 1,929) culprit lesions. Patients with proximal culprits were more likely to die and suffer major adverse cardiovascular events (MACE) during the index hospital stay (3.8% vs 2.2%, P = 0.006; 8.2% vs 5.8%, P = 0.0066, respectively) as well as during 1-year follow-up (6.9% vs 4.5%, P = 0.0013; 22% vs 17%, P = 0.003, respectively) compared to those with nonproximal culprits. After adjustment for baseline differences, proximal culprit was independently predictive of in-hospital death (adjusted odds ratio% 1.58, 95% confidence intervals, CI 1.05,2.40) and MACE (OR 1.41, CI 1.06,1.86), but not 1-year death or MACE. In addition, proximal culprit was independently associated with higher incidence of ventricular arrhythmias and sustained hypotension during the index hospitalization. The univariate impact of proximal culprit lesion on in-hospital death and MACE was comparable to other adverse angiographic characteristics, such as multivessel disease and poor initial thrombolysis in myocardial infarction flow, and greater than that of anterior wall STEMI. In conclusion, proximal location of the culprit lesion is a strong independent predictor of worse in-hospital outcomes in patients with STEMI undergoing primary PCI. [source] Electrocardiographic Body Surface Mapping: Potential Tool for the Detection of Transient Myocardial Ischemia in the 21st Century?ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2009Monique R. Robinson D.Phil Coronary artery disease (CAD) is one of the leading causes of cardiovascular mortality and morbidity worldwide. CAD presents as a wide spectrum of clinical disease from stable angina to ST segment elevation myocardial infarction. The 12-lead electrocardiogram (ECG) has been the main tool for the diagnosis of these events for almost a century but is limited in its diagnostic ability. For patients with suspected angina, the exercise tolerance test is often used to provoke and detect stress-induced ischemia but does not provide a definitive answer in a substantial proportion of patients. Body surface mapping (BSM) is a technique that samples multiple points around the thorax to provide a more comprehensive electrocardiographic data set than the conventional 12-lead ECG. Moreover, recent preliminary data demonstrate that BSM can detect and display transient regional myocardial ischemia in an intuitive fashion, employing subtraction color mapping, making it potentially valuable for diagnosing CAD causing transient regional ischemia. Research is ongoing to determine the full extent of its utility. [source] Reproducible microvascular dysfunction with dobutamine infusion in Takotsubo cardiomyopathy presenting with ST segment elevationCATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 5 2006Stacy D. Brewington MD Abstract Takotsubo (ampulla) cardiomyopathy, or broken heart syndrome, is an underrecognized cardiac illness that usually presents as an acute coronary syndrome in postmenopausal females. The disorder is frequently associated with episodes of mental or physical stress, implicating an abnormal cardiac response to increased catecholamines. Although death has been reported during the index event, the long-term prognosis is good with full recovery of left ventricular function. We present a case of Takotsubo cardiomyopathy mimicking anterior ST segment elevation myocardial infarction precipitated by dobutamine stress testing. Reinfusion of dobutamine in the catheterization laboratory reproduced symptoms with angiography and intravascular ultrasound supporting the theory of abnormal microvascular circulation as the etiology of Takotsubo cardiomyopathy. Acute and delayed magnetic resonance imaging demonstrated no infarction with complete recovery of ventricular function. © 2005 Wiley-Liss, Inc. [source] | ||||||||||