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      Presence and Extent of Cardiac Magnetic Resonance Microvascular Obstruction in Reperfused Non-ST-Elevated Myocardial Infarction and Correlation with Infarct Size and Myocardial Enzyme Release

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          Objective: Microvascular obstruction (MO) is a factor of adverse outcome in patients with ST-elevated myocardial infarction (STEMI). We assessed the presence and extent of MO and its relationship with infarct size and left ventricular (LV) functional parameters after acute non-ST-elevated myocardial infarction (NSTEMI). Methods: Twenty-five patients with first acute NSTEMI underwent a cine and first-pass perfusion cardiac magnetic resonance (CMR) study, with late gadolinium enhancement imaging 72 h after myocardial infarction. Results: MO was detected in 32% of patients, and its extent comprised 0.5–3.1% of the total LV mass (mean 1.9 ± 1.2%). Patients with MO had a significantly larger infarct size than patients without (14.1 ± 5.9 vs. 5.3 ± 4.1% LV mass; p < 0.001). There was no significant difference between both groups for the LV functional parameters and LV ejection fraction (58.5 ± 6.8 vs. 62.6 ± 9.6%; p = 0.29). Patients with MO showed a higher troponin I release (570 ± 364 vs. 148 ± 103 IU; p = 0.003) and a higher creatine kinase release (29,887 ± 18,263 vs. 10,287 ± 5,283 IU; p = 0.007). Conclusions: In patients with acute NSTEMI, MO has a frequency similar to that observed in patients with STEMI and also correlates with the infarct extent. The prognostic significance on clinical outcome remains to be shown in this specific population.

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          Most cited references 16

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          Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: A comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge.

          Intravenous administration of 80 mg of recombinant tissue plasminogen activator (rt-PA, 40, 20, and 20 mg in successive hours) and streptokinase (SK, 1.5 million units over 1 hr) was compared in a double-blind, randomized trial in 290 patients with evolving acute myocardial infarction. These patients entered the trial within 7 hr of the onset of symptoms and underwent baseline coronary arteriography before thrombolytic therapy was instituted. Ninety minutes after the start of thrombolytic therapy, occluded infarct-related arteries had opened in 62% of 113 patients in the rt-PA and 31% of 119 patients in the SK group (p less than .001). Twice as many occluded infarct-related arteries opened after rt-PA compared with SK at the time of each of seven angiograms obtained during the first 90 min after commencing thrombolytic therapy. Regardless of the time from onset of symptoms to treatment, more arteries were opened after rt-PA than SK. The reduction in circulating fibrinogen and plasminogen and the increase in circulating fibrin split products at 3 and 24 hr were significantly less in patients treated with rt-PA than in those treated with SK (p less than .001). The occurrence of bleeding events, administration of blood transfusions, and reocclusion of the infarct-related artery was comparable in the two groups. Thus, in patients with acute myocardial infarction, rt-PA elicited reperfusion in twice as many occluded infarct-related arteries as compared with SK at each of seven serial observations during the first 90 min after onset of treatment.
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            The "no-reflow" phenomenon after temporary coronary occlusion in the dog.

            The role of microvascular damage in the genesis of the "no-reflow" phenomenon was investigated in the left ventricular myocardium of dogs subjected to temporary occlusions of a major coronary artery for 40 and 90 min. Intravenous carbon black or thioflavin S (a fluorescent vital stain for endothelium) were used to demonstrate the distribution of coronary arterial flow in control and damaged myocardium. These tracers were injected simultaneously with release of the coronary occlusion or after 5 or 20 min of reflow of coronary arterial blood. After 40 min of ischemia plus arterial reperfusion, usually the tracers were evenly distributed throughout the damaged tissue at each time of reperfusion. On the other hand, when reflow was allowed after 90 min of ischemia, portions of the inner half of damaged myocardium were not penetrated by the tracers. Electron microscopic study of this poorly perfused tissue revealed severe capillary damage; endothelial cells with large intraluminal protrusions and decreased pinocytic vesicles were common. Also, occasional intraluminal fibrin thrombi were noted, as well as extravascular fibrin deposits and erythrocytes. Myocardial cells were swollen in both poorly perfused and well-perfused irreversibly injured tissue. Contraction bands and mitochondrial Ca(2+) accumulation were prominent features of irreversible injury with reflow at 40 min but were not noted after 90 min of ischemia in areas with poor perfusion. These results suggest that 40 min of ischemia were tolerated by the capillary bed of the dog heart without serious capillary damage or perfusion defects, but that 90 min of ischemic injury was associated with the "no-reflow" phenomenon, i.e., failure to achieve uniform reperfusion. This failure of reflow was associated with extensive capillary damage and myocardial cell swelling. Death of severely ischemic myocardial cells in this model occurs before the onset of capillary damage and the no-reflow phenomenon.
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              Impact of age on management and outcome of acute coronary syndrome: observations from the Global Registry of Acute Coronary Events (GRACE).

              Evidence-based cardiac therapies are underutilized in elderly patients. We assessed differences in practice patterns, comorbidities, and in-hospital event rates, by age and type of acute coronary syndrome (ACS). We studied 24165 ACS patients in 102 hospitals in 14 countries stratified by age. Approximately two-thirds of patients were men, but this proportion decreased with age. In elderly patients (> or = 65 years), history of angina, transient ischemic attack/stroke, myocardial infarction(MI), congestive heart failure, coronary artery bypass graft (CABG) surgery, hypertension or atrial fibrillation were more common, and delay in seeking medical attention and non-ST-segment elevation MI were significantly higher. Aspirin, beta-blockers, thrombolytic therapy, statins and glycoprotein IIb/IIIa inhibitors were prescribed less, while calcium antagonists and angiotensin-converting enzyme inhibitors were prescribed more often to elderly patients. Unfractionated heparin was prescribed more often in young patients, while low-molecular-weight heparins were similarly prescribed across all age groups. Coronary angiography and percutaneous intervention rates significantly decreased with age. The rate of CABG surgery was highest among patients aged 65-74 years (8.1%) and 55-64 years (7.7%), but reduced in the youngest (4.7%) and oldest (2.7%) groups. Major bleeding rates were 2-3% among patients aged 6% in those > or = 85 years. Hospital-mortality rates, adjusted for baseline risk differences, increased with age (odds ratio: 15.7 in patients > or = 85 years compared with those < 45 years). Many elderly ACS patients do not receive evidence-based therapies, highlighting the need for clinical trials targeted specifically at elderly cohorts, and quality-of-care programs that reinforce the use of such therapies among these individuals.

                Author and article information

                S. Karger AG
                March 2009
                04 November 2008
                : 113
                : 1
                : 50-58
                Hôpital Cardiovasculaire Louis Pradel, Université de Lyon, Hospices Civils de Lyon, Lyon, France
                167042 Cardiology 2009;113:50–58
                © 2008 S. Karger AG, Basel

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                Figures: 3, Tables: 3, References: 32, Pages: 9
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