Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postinfarction angina carries a poor prognosis, with a 20-70% incidence of recurrent myocardial infarction (MI) or death within the subsequent 3-6 months. The pathophysiologic mechanisms causing postinfarction angina may include thrombus, complex coronary arterial lesions that form a nidus for thrombus formation, inadequate collateral supply following acute MI, or intimal endothelial dysfunction. The role of thrombus has been established in the pathophysiology of Q-wave MI, and thrombolytic treatment of patients presenting with acute transmural MI has been shown to salvage left ventricular function and to reduce mortality. However, thrombolytic therapy for the acute MI does not reduce the incidence of recurrent ischemia or infarction, as is evident from the 18-26% incidence of recurrent ischemia reported in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) and Thrombolysis in Myocardial Infarction (TIMI) trials. In the Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI) study the incidence of reinfarction was documented as 4% in the streptokinase group, which was actually significantly greater than in the placebo group (2%). In a randomized placebo-controlled study of thrombolysis for postinfarction angina, 29 patients were randomized to placebo (P group, n = 17) or to thrombolytic therapy (T group, n = 12). Patient groups were similar with respect to age, location of MI, ejection fraction, severity of coronary artery disease, and antianginal therapy. Patients underwent coronary angiography 6 +/- 1 days postinfarction. Filling defects consistent with intracoronary thrombus was seen in 11 of 12 T group patients and in 11 of 17 P group patients prior to treatment. Lysis occurred in 7 of 11 T patients and 1 of 11 P (p less than 0.02). Holter-detected silent ischemia was compared pre- and posttherapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thrombolysis in postinfarction angina. 189 59

The characteristics of ischemic episodes in exercise test and daily activities were observed in a silent myocardial ischemia (SMI) group and an anginal group (23 patients each). 15 patients in the SMI group were treated with nifedipine. In exercise test, the time of onset of ischemia was earlier and the ischemic threshold was lower in SMI group. During daily activities, the frequency of SMI was high. The heart rate just before onset of SMI was lower than the mean heart rate in 24-hour Holter monitoring. The highest frequency of SMI was found between 5 AM and 12 noon. Postinfarction patients had a higher frequency and a longer duration of SMI than noninfarction patients. The frequency and duration of SMI decreased in the 15 patients treated with nifedipine in SMI group. It is concluded that silent ischemic episodes were frequent and occurred easily. They might be associated with poor prognosis in CAD patients. Nifedipine was effective in reducing the frequency and duration of SMI in our patients.
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PMID:[Clinical characteristics of silent myocardial ischemia and the effect of nifedipine treatment]. 263 87

Acute myocardial infarction can be stratified into electrocardiographic subsets based on the presence or absence of new Q waves. This stratification has important clinical and prognostic utility. Coronary angiography during acute non-Q-wave compared with Q-wave infarction shows much higher infarct-related artery patency rates (about 75 vs. 10%) and increased coronary collateralization. Culprit legion morphology in non-Q-wave infarction commonly is complex. The frequent demonstration of recurrent clinical ischemia, or residual thallium-201 uptake abnormalities, and metabolic activity on persistent emission tomography suggest the presence of viable myocardium in the distribution of the non-Q-wave infarction usually represents 20-25% of acute myocardial infarctions. The University of California San Diego Collaborative Postinfarction Database and other large studies have found non-Q-wave infarctions to be more common in patients with a history of previous infarction and congestive heart failure, although their mortality during acute hospitalization is lower. However, in long-term followup to one year and beyond, non-Q-wave infarct mortality rates equal those of Q-wave infarction. Patients at low early and late risk of mortality include those with a first infarction who are under age 70, whereas patients with evidence of residual ischemia postinfarction are at increased risk of events. It is interesting to speculate that the settings of unstable angina pectoris, non-Q-wave infarction, and perhaps the picture after thrombolysis for acute myocardial infarction, have pathophysiologic similarities which may carry implications for future research and therapy.
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PMID:Non-Q-wave myocardial infarction: incidence, pathophysiology, and clinical course compared with Q-wave infarction. 269 Nov 40

Recurrent ischemia after acute myocardial infarction (AMI) has been largely associated with a poor prognosis. This study was carried out to analyze the relationship among different clinical variables and both postinfarction angina and reinfarction after AMI. A total of 452 consecutive patients (mean age 58.2 +/- 12 years) were admitted to the coronary care unit and were studied prospectively. More than half of the patients received some type of thrombolytic therapy. Death occurred in 45 patients (9.9%) during hospital stay. Postinfarction angina was diagnosed in 81 patients (17.9%) and reinfarction in 22 (4.9%). Patients who developed reinfarction had a high mortality rate (45.5%) compared with those who did not develop such an event (8.1%) (p < 0.0001; odds ratio: 9.4; 95% confidence interval 3.5-25.4). On the other hand, postinfarction angina had no significant association with mortality. Multivariate analysis revealed that a history of angina (> 1 week) was predictive of the occurrence of postinfarction angina and that the use of fibrinolytic treatment, prodromal symptoms, and postinfarction angina were significantly related to reinfarction. We conclude that several simple clinical variables are clear independent predictors of postinfarction angina and reinfarction following AMI and should be taken into account in routine clinical practice or when planning intervention trials.
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PMID:Prognostic value of clinical variables for recurrent ischemic events after acute myocardial infarction. 774 87

Objective. Postinfarction transneuronal degeneration refers to secondary neuronal death that occurs within a few days to weeks following the disruption of input or output to synapsed neurons sustaining ischemic insults. The thalamus receives its blood supply from the posterior circulation; however, infarctions of the middle cerebral arterial may cause secondary transneuronal degeneration in the thalamus. In this study, we presented the areas of ischemia and associated transneuronal degeneration following MCAo in a rat model. Materials and Methods. Eighteen 12-week-old male Sprague-Dawley rats were randomly assigned to receive middle cerebral artery occlusion surgery for 1, 7, and 14 days. Cerebral atrophy was assessed by 2,3,5-triphenyltetrazolium hydrochloride staining. Postural reflex and open field tests were performed prior to animal sacrifice to assess the effects of occlusion on behavior. Results. Myelin loss was observed at the lesion site following ischemia. Gliosis was also observed in thalamic regions 14 days following occlusion. Differential degrees of increased vascular endothelial growth factor expression were observed at each stage of infarction. Increases in myelin basic protein levels were also observed in the 14-day group. Conclusion. The present rat model of ischemia provides evidence of transneuronal degeneration within the first 14 days of occlusion. The observed changes in protein expression may be associated with self-repair mechanisms in the damaged brain.
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PMID:Transneuronal Degeneration of Thalamic Nuclei following Middle Cerebral Artery Occlusion in Rats. 2759 62