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)

Indium-111-Fab antimyosin antibody accumulation was studied in an 81-yr-old patient who was treated twice for unstable angina on ECG, signs of apicoseptal infarction, anterolateral and inferior ischemia without clinical evidence of an acute coronary event. During the last hospitalization, 9 and 3 mo after the previous ones, additional ischemia in the inferoposterior wall was demonstrated. Antimyosin was administered to detect acute infarction but pump failure developed and the patient died. Autopsy confirmed all stages of infarction on the anterior and lateral walls, predominant fibrosis in the apicoseptal region and predominant acute necrosis in the inferior wall. Macroscopic and scintigraphic examinations of transverse slices gave concordant results. A mixture of infarctions and normal tissue was confirmed by histologic findings. Antimyosin antibody accumulation was seen in areas of acute necrosis or bordering areas of reduced uptake in myocardium with remote damage, probably caused by prolonged episodes of unstable angina without evident acute coronary event.
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PMID:Indium-111-antimyosin uptake in acute and remote myocardial infarction: comparison with pathohistologic findings. 155 46

To assess the long-term prognostic significance of total ischemic time (silent plus painful ischemia) and silent ischemia in patients with unstable angina whose condition stabilized with medical treatment, 76 patients were studied. All patients underwent Holter ambulatory electrocardiographic (ECG) monitoring for greater than or equal to 48 h beginning within the 1st 12 h of the hospital stay. Forty-three patients (Group A) had a total ischemic time greater than or equal to 60 min, whereas 33 patients (Group B) had a total ischemic time less than 60 min. More than 78% of the ischemic episodes in patients in Group A and 62% of those in Group B were silent (p less than 0.05); nine patients in Group A and six in Group B had only silent episodes. Patients in Group A frequently showed three-vessel disease (65% vs. 18%, p less than 0.01), angiographic findings of subtotal occlusion of the coronary arteries (TIMI grade I) (76.7% vs. 42.4%, p less than 0.01) and ischemic alterations in the rest ECG (51.2% vs. 30.3%, p less than 0.05). During a 6-year follow-up period, 15 patients in Group A and 8 in Group B experienced myocardial infarction (p less than 0.05); 9 patients in Group A and 4 in Group B required coronary artery surgery (p less than 0.05) and 10 patients in Group A and 4 in Group B died of cardiac causes (p less than 0.01). Multivariate analysis showed three-vessel disease to be the most important predictor of cardiac mortality and morbidity (p = 0.025); it was followed in predictive power by a total ischemic time greater than or equal to 60 min and by left ventricular dysfunction. The presence of silent ischemia was not shown to be an independent predictor of long-term morbidity and mortality. In conclusion, patients with unstable angina and a total ischemic time greater than or equal to 60 min frequently have silent ischemic episodes on Holter ECG monitoring, a greater extent of coronary atherosclerosis and ischemic alterations of the rest ECG. The long-term prognosis of patients with unstable angina whose condition stabilizes with medical treatment depends on the extent of coronary atherosclerosis and on the longer duration of total ischemic time but not on the presence of silent ischemia.
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PMID:Unstable angina: role of silent ischemia and total ischemic time (silent plus painful ischemia), a 6-year follow-up. 156 18

We report a case of unstable angina in an active phase of polymyositis. A 51 year-old man was admitted with a diagnosis of polymyositis and unstable angina with ST elevation on prolonged rest chest pain. Rest anginal attack which had been refractory to conventional antianginal medications was controlled by high dose of glucocorticosteroid. Electrocardiography revealed multifocal premature ventricular contraction. Since silent ischemia on exercise persisted, percutaneous transluminal coronary angioplasty (PTCA) was performed on a stenotic lesion in the left anterior descending artery. Since there was recurrent anginal attack, re-PTCA was carried out at the same site. He was discharged in a good condition. This case is considered to be associated with cardiac involvement of polymyositis because of ventricular arrhythmia, persistent increased serum levels of CPK-MB, and the marked benefits of corticosteroid against unstable angina. In addition, clinical manifestations, coronary arteriographic findings, and increased plasma levels of thrombin-antithrombin III complex suggest that cardiac involvement in polymyositis accelerates intracoronary thrombus formation and/or coronary spasm.
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PMID:[A case of unstable angina pectoris associated with an active phase of polymyositis]. 158 49

Unstable angina is a broad clinical diagnosis that includes patients at different levels of risk for an unfavorable outcome. Although, as in other categories of coronary artery disease, the state of left ventricular function and the extent of coronary artery disease will determine long-term prognosis, recognition of clinical markers of an early unfavorable course may be of value in defining management strategies. This review focuses on the relevance of baseline clinical characteristics and noninvasive data in assessing the prognostic significance of unstable angina in light of its presenting features. Recurrence of chest pain within 48 h after admission carries a reduction in likelihood of survival of about 20% in patients with progressive or prolonged angina. Similarly, ECG changes on admission have a negative prognostic implication, particularly in rest angina, as they predict recurrence of ischemia, myocardial infarction or need for revascularization in 80% of the patients. In variant angina, determinants of prognosis are level of disease activity, as judged by recurrence of pain, ECG changes and use of calcium channel antagonists. Patients with angina after a myocardial infarction who have more than one episode of either angina or silent ischemia in 24 h have a 10% reduction in probability of survival during the 1st year compared with that of asymptomatic patients. An abrupt course, or the rapidity with which symptoms develop, is the main determinant of prognosis in new onset angina. Thus, recurrent angina and ECG changes appear to be relevant prognostic markers in the patient subsets considered; if these are present, early coronary angiography must be performed and revascularization procedures should be considered without delay.
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PMID:Unstable angina: outcome according to clinical presentation. 159 63

The relation between coronary artery lesion morphology and associated segmental left ventricular (LV) dysfunction in patients with unstable angina is unclear. Fifty-two patients with angina occurring at rest who underwent cardiac catheterization within 3 days of the last episode of pain and had no enzymatic evidence for myocardial necrosis were evaluated. Coronary artery narrowings deemed responsible for the ischemic episodes were analyzed with regard to the artery involved, maximal diameter of the narrowing, presence of thrombus, and complex appearance. Time to catheterization, age, sex and electrocardiographic evidence of ischemia were also noted. Segmental LV dysfunction in the territory supplied by the "culprit lesion" was present in 58% of patients. It occurred significantly more often with lesion location in the left anterior descending coronary artery, and was less frequent with lesions in the left circumflex and ramus coronary arteries. Ischemic electrocardiographic changes were more sensitive in predicting LV dysfunction with culprit lesion location in the left anterior descending or right coronary artery. LV dysfunction could not be predicted by any other parameter analyzed. It is concluded that postischemic LV dysfunction occurs frequently in rest angina, especially when the severest narrowing is in the left anterior descending coronary artery.
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PMID:Frequency and predictors of left ventricular segmental dysfunction in patients with recent rest angina. 159 64

In 121 patients (93 males, mean age 53.9 years), percutaneous transluminal coronary angioplasty (PTCA) of 140 lesions was performed as treatment of symptomatic, single or multiple vessel disease, with the following clinical syndromes: stable angina pectoris (Group I) in 59 cases (48.8%), unstable angina (Group II) in 40 (33%), and angina or residual ischemia after thrombolysis for myocardial infarction (MI) (Group III) in 22 patients (18.2%). PTCA was successfully accomplished in 123 of 140 segments (87.8%), with a reduction in mean luminal stenosis from 87.3 +/- 13% (range 70-100) to 15 +/- 10% (range 0-30, p less than 0.00001). Successful results were obtained in 85.9% of patients (104/121) and they were 84.7%, 82.5% and 95.5% in Groups I, II and III, respectively. The procedure failed in 17 cases (14.0%), and within this group, 14 complications occurred (11.6%): 2 deaths (1.6%), 3 cases of MI, acute closure in 4, and emergency coronary bypass surgery in 5 patients. Late evaluation (6-8 months) revealed clinical and functional improvement in 71/98 patients (72.4%), and recurrent ischemic symptoms (no improvement) in 27 cases. Coronary angiography performed in 20, showed restenosis in 10, and progressive disease in 7 patients. In conclusion, PTCA is an effective therapeutic option in selected cases of symptomatic ischemic heart disease with suboptimal results to medical management alone.
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PMID:[Coronary angioplasty as the treatment in different myocardial ischemic syndromes: a report of 121 consecutive cases]. 159 28

It has been suggested that unstable angina at rest, like acute myocardial infarction, might be associated with a thrombotic process. In order to study the hypothesis that myocardial ischemia during exercise could also be associated with an activation of blood coagulation and/or fibrinolysis, we investigated the presence of plasma markers of a prethrombotic or thrombotic state (thrombin-antithrombin III complexes TAT, prothrombin fragment F1 + 2, and D-dimers DD) in 100 consecutive patients with confirmed or suspected coronary artery disease during ergometric test with myocardial thallium-201 scintigraphy. Symptoms and scintigrams allowed to define three groups of patients: those showing no ischemia (n = 79) and those with symptomatic (n = 8) or silent myocardial ischemia (n = 13). Before exercise, DD and TAT levels were not significantly different among the three groups. On the other hand, the F1 + 2 levels were slightly albeit significantly higher in the patients without ischemia than in the patients with symptomatic or silent ischemia. After exercise, no significant difference was found between the three groups. Exercise induced a significant and parallel increase in both the TAT and the F1 + 2 levels (but not of the DD levels) in the three groups. Thus, our study does not support the hypothesis that myocardial ischemia, silent or symptomatic, is associated with an activation of plasma coagulation and fibrinolysis that can be distinguished from the exercise-induced thrombin generation.
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PMID:Effects of exercise test on plasma markers of an activation of coagulation and/or fibrinolysis in patients with symptomatic or silent myocardial ischemia. 160 40

Objective signs of myocardial ischemia without angina pectoris or its equivalents define the syndrome of silent myocardial ischemia. Its significance lies in the prevalence and prognostic implications. As a prevalence, asymptomatic coronary heart disease can be found in 2.5% of men 40 to 60 years old. Silent myocardial ischemia is frequently found in patients with unstable coronary syndromes. The Framingham Study showed 25% of all myocardial infarctions as unrecognized by patients and physicians. The prognostic implications of silent myocardial ischemia are shown in large studies on prognosis of pathologic exercise-ECG's. Asymptomatic patients with pathologic exercise-ECG have always been recognized as having a significantly increased risk of myocardial infarction and death. Recently, many studies showed a worse prognosis for patients with asymptomatic transient ischemia on Holter-ECG. This can be found in patients with stable angina pectoris, unstable angina pectoris, patients with peripheral arterial disease, and patients after myocardial infarction. It becomes clear that prognosis is not defined by the pain, but by the severity of ischemia. Silent ischemia has to be viewed together with the severity of the underlying coronary heart disease. This synopsis will define the necessary steps for further diagnosis and treatment.
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PMID:[Clinical importance of silent ischemia]. 160 22

Clinical data on 10,451 high-dose (up to 0.84 mg/kg over 10 minutes) dipyridamole-echocardiography tests (DET) performed in 9,122 patients were prospectively collected from 33 echocardiographic laboratories, each contributing greater than 100 tests. All patients were studied for documented or suspected coronary artery disease (1,117 early [less than 18 days] after acute myocardial infarction and 293 had unstable angina). Significant side effects including major adverse reactions and minor but limiting side effects occurred in 113 patients (1.2%). Major adverse reactions occurred in 7 cases (0.07%). In 6 of these cases, adverse reactions were associated with echocardiographically assessed ischemia and included 1 prolonged cardiac asystole (complicated by acute myocardial infarction and coma, with death after 23 days), 1 short-lasting cardiac asystole, 2 myocardial infarctions, 1 pulmonary edema and 1 sustained ventricular tachycardia. In all 6 cases, the cardiologist-echocardiographer performing the study had a limited experience (less than 100 tests) with DET, and at off-line reading in 5 cases, the obvious echo-positivity preceded the onset of complications by 1 to 5 minutes. The only ischemia-independent major side effect was a short-lasting cardiac asystole that was reversed by aminophylline and atropine. Significant side effects associated with echocardiographically assessed ischemia occurred in 89 additional cases (21 with and 68 without concomitant echocardiographically assessed myocardial ischemia). The most frequent of these side effects was hypotension or bradycardia, or both, which occurred in 40 patients with negative and 6 with positive DET. In all cases, side effects promptly subsided after aminophylline. In 1,857 cases, the high dose was not given for echo-positivity before the eighth minute.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety of intravenous high-dose dipyridamole echocardiography. The Echo-Persantine International Cooperative Study Group. 162 16

The pathophysiologic mechanisms responsible for the clinical syndrome known as unstable angina pectoris are complex but provide a framework for a rational medical approach to this ischemic condition. The combined use of nitrates, beta-blockers, calcium antagonists, antiplatelet agents, and anticoagulants has been shown to reduce recurrent ischemia, and the latter therapies have reduced the incidence of progression to myocardial infarction and death. A rational risk stratification scheme, which utilizes the presenting symptoms, electrocardiographic, and anatomic information to identify patients for whom additional revascularization procedures are warranted, is presented.
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PMID:Medical therapy of unstable angina pectoris. 167 28


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