Acute Coronary Syndromes: Diagnosis and Management, Part II

Department of Hospital Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA.
Mayo Clinic Proceedings (Impact Factor: 6.26). 11/2009; 84(11):1021-36. DOI: 10.1016/S0025-6196(11)60674-5
Source: PubMed


At the most severe end of the spectrum of acute coronary syndromes is ST-segment elevation myocardial infarction (STEMI), which usually occurs when a fibrin-rich thrombus completely occludes an epicardial coronary artery. The diagnosis of STEMI is based on clinical characteristics and persistent ST-segment elevation as demonstrated by 12-lead electrocardiography. Patients with STEMI should undergo rapid assessment for reperfusion therapy, and a reperfusion strategy should be implemented promptly after the patient's contact with the health care system. Two methods are currently available for establishing timely coronary reperfusion: primary percutaneous coronary intervention and fibrinolytic therapy. Percutaneous coronary intervention is the preferred method but is not always available. Antiplatelet agents and anticoagulants are critical adjuncts to reperfusion. This article summarizes the current evidence-based guidelines for the diagnosis and management of STEMI. This summary is followed by a brief discussion of the role of noninvasive stress testing in the assessment of patients with acute coronary syndrome and their selection for coronary revascularization.

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    • "Primary percutaneous coronary intervention (PCI) in the infarct-related artery (IRA) is now considered the gold standard for patients with acute ST-elevation myocardial infarction (STEMI) [1,2]. Multivessel disease (MVD) is relatively common in patients with STEMI, with a reported prevalence ranging from 50% in highly selected subjects enrolled in randomized clinical trials, such as the CADILLAC study [3], to 80% in those included in more comprehensive registries or those with cardiogenic shock, such as in the SHOCK trial [4,5]. "
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    ABSTRACT: The importance of achieving complete revascularization by percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (MI) remains unclear. To compare short-term exercise capacity following acute ST-elevation myocardial infarction (STEMI), in patients receiving PCI with stenting, between those completely revascularized (CR) and those incompletely revascularized (IR). We retrospectively reviewed 326 patients [single-vessel disease (SVD) group, 118 patients; CR group, 112 patients; IR group, 96 patients] who underwent cardiopulmonary exercise testing 7-30 days after STEMI to measure peak oxygen uptake (VO2peak), oxygen uptake at anaerobic threshold (VO2AT), and peak oxygen pulse. Demographic data, presence of concomitant diseases, STEMI characteristics, and echocardiography and angiography findings were evaluated. Most patients were male (89.0%) and mean age was 55.6 +/- 11.2 years. Ischemic ST deviation occurred in 7.1%, with no significant difference between groups. VO2peak and VO2AT did not differ significantly between groups, despite a trend to be lower in the CR and IR groups compared with the SVD group. Peak oxygen pulse was significantly higher in the SVD group than in the IR group (p = 0.005). After adjustment for age, gender, body mass index, cardiovascular risk factors, MI characteristics and echocardiography parameters, CR was not an independent predictor of VO2peak (OR = -0.123, 95% confidence interval [CI] -2.986 to 0.232, p = 0.093), VO2AT (OR = 0.002, 95%CI 1.735 to 1.773, p = 0.983), or peak oxygen pulse (OR = -0.102, 95%CI -1.435 to 0.105, p = 0.090). CR in patients treated with PCI for multivessel disease might show no benefit on short-term exercise tolerance over IR.
    Journal of Cardiothoracic Surgery 03/2014; 9(1):50. DOI:10.1186/1749-8090-9-50 · 1.03 Impact Factor
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    • "The association of platelet activation with acute CVDs justifies anti-platelet therapy as a standard of care for those at high risk of atherothrombosis [111]. Current anti-platelet drugs have been developed to target specific signaling pathways mainly implicated in the thrombus formation, and their ever increasing clinical use has resulted in clear benefits in "
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    ABSTRACT: Cardiovascular diseases are one of the leading causes of morbidity and mortality in industrialized countries, and although many processes play a role in the development of vascular disease, thrombosis is the primary event that precipitates stroke and acute coronary syndromes. The blood platelets are of significant importance in medicine. These cells are involved in many physiological processes, particularly haemostasis through their ability to aggregate and form clots in response to activation. In addition, these dynamic cells display activities that extend beyond thrombosis, including an important role in initiating and sustaining vascular inflammation. The expansion of knowledge from basic and clinical research has highlighted the critical position of platelets in several inflammatory diseases such as arthritis and atherosclerosis. Platelets are emerging as important mediators of inflammation and provide important signals to mediate phenotype of other blood and vascular cells. The important role of platelets in arterial thrombosis and the onset of acute myocardial infarction after atherosclerotic plaque rupture make inhibition of platelet aggregation a critical step in preventing thrombotic events associated with stroke, heart attack, and peripheral arterial thrombosis. However, the use of platelet inhibitors for thrombosis prevention must seek a delicate balance between inhibiting platelet activation and an associated increased bleeding risk. The aim of this review is to up-date the knowledge on platelets physiology and dysfunction in pathologies, such as diabetes mellitus, hypercholesterolemia, and hypertension, emphasizing the link between platelets and the inflammation-related atherosclerosis. The review evaluates the opportunities offered by the novel platelet inhibitors to efficiently alleviate the thrombotic events.
    Thrombosis Research 02/2012; 129(2):116-26. DOI:10.1016/j.thromres.2011.09.026 · 2.45 Impact Factor
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