A rare case of thromboembolism in a 21-year old female with elevated factor VIII.
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In this article we present the history of a previously healthy female adolescent, who was seen at our hospital with abdominal pain. This was the result of a large floating thrombus in the aorta. Widespread embolism occurred, which lead to the loss of a limb and a left hemicolectomy. Although our patient is a smoker, used oral contraceptives and was found to have a heterozygote mutation at the factor V Leiden gene, the most important factor contributing to her thrombophilia is thought to be her significantly elevated factor VIII. We stress an aggressive diagnostic and therapeutic approach in young patients with unknown embolism in order to avoid the grave consequences of delay. (+info)
Postconditioning fails to improve no reflow or alter infarct size in an open-chest rabbit model of myocardial ischemia-reperfusion.
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Postconditioning (PoC) with brief intermittent ischemia after myocardial reperfusion has been shown to lessen some elements of postischemic injury including arrhythmias and, in some studies, the size of myocardial infarction. We hypothesized that PoC could improve reflow to the risk zone after reperfusion. Anesthetized, open-chest rabbits were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion. In protocol 1, rabbits were randomly assigned to the control group (n = 10, no further intervention after reperfusion) or to the PoC group, which consisted of four cycles of 30-s reocclusions with 30 s of reperfusion in between starting at 30 s after the initial reperfusion (4 x 30/30, n = 10). In protocol 2, rabbits were assigned to the control group (n = 7) or the PoC group, which received PoC consisting of four cycles of 60-s intervals of ischemia and reperfusion starting at 30 s after the initial reperfusion (4 x 60/60, n = 7). No reflow was determined by injecting thioflavine S (a fluorescent marker of capillary perfusion), risk zone by blue dye, and infarct size by triphenyltetrazolium chloride. In protocol 1, there were no statistical differences in hemodynamics, ischemic risk zone, or infarct size (35 +/- 6% of the risk zone in the PoC group vs. 29 +/- 4% in the control group, P = 0.38) between the groups. Similarly, in protocol 2, PoC failed to reduce infarct size compared with the control group (45 +/- 4% of the risk zone in the PoC group vs. 42 +/- 6% in the control group, P = 0.75). There was a strong correlation in both protocols between the size of the necrotic zone and the portion of the necrotic zone that contained an area of no reflow. However, PoC did not affect this relationship. PoC did not reduce infarct size in this model, nor did it reduce the extent of the anatomic zone of no reflow, suggesting that this intervention may not impact postreperfusion microvascular damage due to ischemia. (+info)
Myocardial contrast echocardiography in ST elevation myocardial infarction: ready for prime time?
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Impact of culprit plaque composition on the no-reflow phenomenon in patients with acute coronary syndrome: an intravascular ultrasound radiofrequency analysis.
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BACKGROUND: The difference in the culprit plaque composition of acute coronary syndrome (ACS) patients with and without the no-reflow phenomenon has not been fully evaluated. METHODS AND RESULTS: Intravascular ultrasound radiofrequency data of culprit plaques were obtained and analyzed in 49 ACS patients. The no-reflow phenomenon was defined as a decrease of at least 1 grade in 'Thrombolysis In Myocardial Infarction' flow immediately after mechanical dilatation compared with before mechanical dilatation, with no evidence of thrombus, spasm, or dissection. The no-reflow phenomenon was observed in 9 individuals. Culprit plaques with the no-reflow phenomenon contained a higher percentage of necrotic core component and a smaller percentage of fibrous component than plaques in the patients without the no-reflow phenomenon (necrotic core component, 22.1+/-9.3% vs 11.7+/-7.9%, p=0.0011; fibrous component, 59.6+/-11.2% vs 68.3+/-10.2%, p=0.027). Multivariate analysis identified the percentage of necrotic core component as an independent predictor of the no-reflow phenomenon after adjustment for plaque geometry and procedural factors (odds ratio, 1.7; 95% confidence interval, 1.1 to 2.5; p=0.015). CONCLUSION: Culprit plaques of patients with the no-reflow phenomenon differ from those in patients without the no-reflow phenomenon. (+info)
Distribution and determinants of myocardial perfusion grade following late mechanical recanalization of occluded infarct-related arteries postmyocardial infarction: a report from the occluded artery trial.
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