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)

We investigated the mechanisms of exercise-induced precordial ST depression in prior inferior myocardial infarction in single vessel disease, and attempted to differentiate ST depression in single vessel from multivessel disease. Subjects were categorized as; Group I (n = 18), with inferior myocardial infarction and single vessel disease without (n = 11; Ia) and with (n = 7; Ib) exercise-induced precordial ST depression and group II (n = 10), inferior myocardial infarction with multivessel disease. The subjects were examined using 12-lead exercise ECG, stress T1-201 myocardial imaging and stress radionuclide ventriculography. Compared to group Ia, exercise-induced precordial ST depression in group Ib was associated with extensive infarction extending into the inferoseptal left ventricular wall by T1-201 myocardial imaging. Worsening of septal wall motion was also more frequently observed on stress radionuclide ventriculography. For detecting multivessel disease in prior inferior myocardial infarction, exercise ECG and radionuclide ventriculography had poor specificity and predictive value compared to stress T1-201 myocardial imaging. We conclude that exercise-induced precordial ST depression observed in patients with prior inferior myocardial infarction due to single vessel disease reflects a peri-infarction ischemia in the inferoseptal wall of the left ventricle. Great caution is necessary when predicting multivessel disease in prior inferior myocardial infarction using exercise ECG. Stress T1-201 myocardial imaging is the most accurate diagnostic means for this purpose.
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PMID:[Exercise-induced precordial ST depression in patients with prior inferior myocardial infarction with single vessel disease]. 281 51

Patients with acute inferior myocardial infarction commonly have ST segment depression in the anterior precordial leads. This may reflect either reciprocal changes from the inferior ST elevation or primary ST depression from additional anterior subendocardial ischemia. From a biophysical perspective reciprocal changes should be uniformly anticipated from basic dipole theory. Detection will vary with the size, location, orientation, and electrical intensity of the lesion and with the ECG lead system deployed to register the anterior changes. Alternatively, acute occlusion of the right coronary artery may produce ischemia in the anterior left ventricular wall supplied by a stenotic anterior descending coronary artery. Anterior ischemia may result from the abnormal hemodynamics or the reduced collateral flow produced by acute right coronary artery occlusion. Thus both mechanisms are based on sound physiologic principles. A review of the clinical literature suggests that such patients represent a heterogeneous group. In some instances coexistent anterior ischemia is present, whereas in others the anterior ST depression is the passive reflection of inferior ST elevation augmented in many cases by a large infarct size or more extensive posterobasal or septal involvement.
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PMID:Physiologic bases for anterior ST segment depression in patients with acute inferior wall myocardial infarction. 305 9

To investigate the mechanisms and clinical significance of precordial (V1-V4) ST segment depression during acute inferior myocardial infarction, stress thallium-201 scintigrams and coronary angiograms were obtained within four to eight weeks after the onset of myocardial infarction in 37 patients experiencing their first acute inferior myocardial infarction. Among 18 patients with precordial ST depression (group 1), 11 with concomitant disease of the left anterior descending artery (LAD) had positive results on exercise test, whereas in seven patients without LAD lesion, only two had positive exercise test (p less than 0.01). In 19 patients without precordial ST depression (group 2), 11 had severe stenosis in the LAD. However, among these 11 patients, only two had positive exercise tests. Patients with precordial ST depression demonstrated a higher frequency of positive exercise tests than those without it (p less than 0.01). On stress thallium-201 scintigraphy, a perfusion defect involving the inferior wall was present in all patients, but additional anterior wall ischemia was present in only five of the 18 patients in group 1. These five patients had chest pain on exercise tests and a severe stenosis greater than 90% in the LAD. There was no significant difference in the frequency of additional posterolateral wall infarction between groups 1 and 2. In 18 patients in group 1, sigma ST (total degrees of ST segment depression in leads V1, V2, V3, and V4 in the acute stage) was significantly greater in 11 patients with LAD lesion than in seven without (p less than 0.05), and sigma ST greater than five mm was observed in 12 of 13 patients who had additional anterior wall ischemia and posterolateral wall infarction on stress thallium-201 scintigraphy (p less than 0.05). Myocardial revascularization, such as aortocoronary bypass surgery or percutaneous transluminal coronary angioplasty (PTCA), was performed in six of the 18 patients in group 1 in the chronic stage, but in only one of the 19 patients in group 2. Thus, in patients with initial acute inferior myocardial infarction, those with precordial ST depression seemed to be a high-risk group. It was suggested that, during the early stage of myocardial infarction, this abnormality on electrocardiograms is related to the summation of effects of anterior wall ischemia and posterolateral wall infarction. Furthermore, the sigma ST evaluation is useful in differentiating a mirror image of inferior wall infarction from anterior wall ischemia and posterolateral wall infarction as the mechanism of precordial ST depression.
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PMID:[Clinical significance of precordial ST segment depression during acute inferior myocardial infarction]. 322 18

The authors report a fifty-year-old woman with acute inferior myocardial infarction in whom left atrial mobile thrombus was found by echocardiography. They believe this to be the first echocardiographic documentation of such a thrombus after acute myocardial infarction. The combination of the stagnant flow in the left atrium due to atrial ischemia, the low output state due to left ventricular dysfunction, and the hemoconcentric tendency from use of diuretics might have played a role in the present thrombus formation. The thrombus was safely lysed without complication after intravenous urokinase.
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PMID:Transient left atrial mobile thrombus in acute myocardial infarction--a case report. 334 6

We investigated the mechanisms of exercise-induced precordial ST-segment depression on the electrocardiogram in prior inferior myocardial infarction with single-vessel disease and attempted to differentiate the ST-segment depression between single- and multi-vessel disease. Subjects included three groups: group Ia (n = 11), inferior myocardial infarction with single-vessel disease that showed no precordial ST-segment depression; group Ib (n = 7), inferior myocardial infarction with single-vessel disease accompanied by precordial ST-segment depression; and group II (n = 10), inferior myocardial infarction with multi-vessel disease. The subjects underwent 12-lead exercise electrocardiography, stress Tl-201 myocardial imaging and stress radionuclide ventriculography. Exercise-induced precordial ST-segment depression observed in group Ib was associated with large infarction and infarction extending into the inferoseptal wall of the left ventricle on myocardial image. On stress ventriculography, worsening of the septal wall motion was more frequently observed in group Ib than in group Ia. Coronary arteriography revealed a higher rate of rich collateral vessels to the infarcted zone in group Ib than in group Ia. When we compared the diagnostic ability for detecting multi-vessel disease in prior inferior myocardial infarction, although sensitivity was not different among three tests, both exercise electrocardiography and radionuclide ventriculography had poor specificity and predictive value compared to stress Tl-201 myocardial imaging. Thus we concluded that exercise-induced precordial ST-segment depression observed in prior inferior myocardial infarction with single-vessel disease should reflect a peri-infarctional ischemia located in the inferoseptal wall of the left ventricle, and that stress Tl-201 myocardial imaging is the most accurate method for diagnosing multi-vessel disease in prior inferior myocardial infarction.
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PMID:Exercise-induced precordial ST-segment depression in prior inferior myocardial infarction with single-vessel disease; with special reference to its mechanisms and distinction from multi-vessel disease. 334 75

The clinical usefulness of radionuclide ventriculography (RNV) was evaluated in patients with right ventricular ischemia. The subjects consisted of 25 patients with acute inferior myocardial infarction, 19 patients with old myocardial infarction and six patients with angina pectoris who had severe stenosis of the right coronary artery. In patients with acute inferior myocardial infarction, follow-up radionuclide studies were performed during the recovery periods on the first, 7th-14th, and 30th hospital day. Fifteen of the 25 patients initially had decreased right ventricular ejection fractions (evidence of right ventricular infarction). The mean value was 28 +/- 8% on the initial day, but 7-14 days and 30 days after the acute attack, it improved markedly to 36 +/- 9% and 39 +/- 9%, respectively. Regional wall motion abnormality resolved in 10 of the 15 patients on the 30th hospital day. In 25 patients with old myocardial infarction or with angina pectoris, RNV was performed at rest and during supine exercise to determine the influence or right coronary artery disease. Right ventricular ejection fraction was changed by exercise from 42 +/- 7% to 44 +/- 10% in patients with proximal artery lesions, and from 45 +/- 7% to 50 +/- 10% in patients with distal artery lesions. Right ventricular ejection fraction increased in patients with isolated right coronary artery disease (rest: 44 +/- 8%, exercise: 49 +/- 9%), decreased in patients with combined left anterior descending artery disease (rest: 40 +/- 6%, exercise: 38 +/- 11%) and increased in patients with combined circumflex artery disease (rest: 43 +/- 5%, exercise: 47 +/- 6%). We concluded that right ventricular infarction is a frequent complication in patients with inferior myocardial infarction. However, right ventricular ejection fraction and right ventricular regional wall motion abnormality improve dramatically within one month. Stress-induced ischemia would be rare in patients with isolated right coronary artery disease. The above findings support the notion that the right ventricular myocardium has peculiar coronary perfusions.
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PMID:[Right ventricular ischemia evaluated by radionuclide ventriculography]. 349 9

This study was designed to evaluate the effects of metaraminol (Aramine) in six patients with evolving acute inferior wall myocardial infarction accompanied by hypotension and warm limbs. There were 16 episodes of acute inferior wall ischemia, and the response to therapy was judged by evaluating blood pressure and ST segment and T wave abnormalities. Three patients received intravenous isosorbide dinitrate and two received streptokinase as the initial therapy. The mean ST segment elevation was significantly reduced (from 4.94 +/- 1 to 0.5 +/- 0.7 [p less than 0.0001]) after metaraminol infusion was initiated. The average T wave height also decreased (from 6.8 +/- 2 to -1.3 +/- 2.5 mm [p less than 0.0005]). The average heart rate decreased from 82 +/- 11 to 69 +/- 9 beats/min (p less than 0.05) and the mean arterial blood pressure increased from 81 +/- 12 mm Hg before metaraminol treatment to 126 +/- 8 mm Hg after treatment. All these changes occurred within a few minutes after metaraminol therapy was instituted. In 12 episodes, accelerated idioventricular rhythm appeared concomitantly with the resolution of ST segment elevation. Coronary angiography performed between 4 and 10 days after admission demonstrated significant obstruction in all infarct-related arteries, but none was totally occluded. Left ventricular function was normal in three patients and slightly hypokinetic in the inferior wall in two. These results indicate that in a selected group of patients with acute inferior myocardial infarction, metaraminol administration (in certain hemodynamic circumstances) can alleviate acute ischemia within a few minutes and thereby reduce ischemic injury.
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PMID:Effect of metaraminol during acute inferior wall myocardial infarction accompanied by hypotension: preliminary study. 366 8

Limitations of the standard 12-lead electrocardiogram in sensitivity, specificity and information content on the effort induced ischemic process might be partly due to an inadequate sampling of cardiac electrical events. An extensive array of electrodes is an effective way to verify this hypothesis. Actually body surface mapping provides: a 10-15% increase in diagnostic yield mainly in patients with mild coronary artery disease and elusive signs of ischemia in standard leads a very approximate indication of the extent of coronary artery disease a substantial contribution to the identification of the site of ischemia. Regarding the last point, preliminary results of an ongoing study are reported. One hundred and three patients with recent myocardial infarction have been studied by exercise test with simultaneous recording of surface map and Thallium 201 scan. So far in the subset with inferior myocardial infarction (76 patients) three different map patterns corresponding to different ischemic regions (anterior, inferior and posterior) have been identified. In anterior myocardial infarction (27 patients) a characteristic map pattern for exercise-induced myocardial ischemia has been observed, apparently able to discriminate between ischemia and the changes of early repolarization induced by the dyskinesia of the infarcted ventricular wall. In conclusion, electrocardiographic mapping makes a practical contribution to the understanding of ischemia-induced cardiac electrical events.
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PMID:Can body surface mapping improve the diagnostic power of standard electrocardiography in effort myocardial ischemia? 375 6

Mechanisms responsible for atrioventricular (AV) block during acute inferior myocardial infarction are only partially understood. Increased parasympathetic tone is the factor usually postulated; however, persistence of AV block after atropine administration is frequently observed. Adenosine, an endogenous ischemic metabolite, has well established depressant effects on AV node conduction. In this report, an episode of atropine-resistant AV block was reversed by aminophylline, a competitive adenosine antagonist, in a patient with an acute inferior myocardial infarction. This observation suggests a role for adenosine in the mediation of ischemia-induced AV node block.
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PMID:Mechanism of atropine-resistant atrioventricular block during inferior myocardial infarction: possible role of adenosine. 376 Mar 93

19 patients with transitory ST-segment depression in the wall opposite the infarcted territory during acute transmural myocardial infarction (AMI) were studied. We investigated the reproducibility of this reciprocal ST depression induced by stress testing and correlated the ECG changes with coronary angiographic evaluation of arteries supplying the remote area. We tried to derive criteria for detection of simple mirror image. 3 different groups were defined according to ECG evolution: Group 1 consisted of 7 anterior and 3 inferior AMI where reciprocal ECG changes disappeared appeared within 24 to 48 hours independently of the ECG changes in the infarcted area. These ST depressions were reproduced by stress testing one to two months later, and correlated angiographically with an anatomic lesion. 7 out of 10 patients later had bypass graft surgery. Group 2 consisted of 7 patients in whom posterior wall extension of an inferior AMI made the diagnosis of anterior ischemia impossible. In another two patients (one anterior and one inferior AMI) reciprocal ST depression and infarcted area ECG changes showed a simultaneous evolution. The reciprocal ST depression could not be reproduced during stress testing and did not correlate with any angiographic lesion. It is concluded that reciprocal ST depression during the acute phase of transmural anterior or purely inferior myocardial infarction is correlated with multivessel coronary disease if their regression is not strictly simultaneous to the infarction-related ECG changes. Further investigations are indicated in these patients.
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PMID:[Significance of reciprocal ST-segment depression in the acute stage of transmural myocardial infarct]. 382 17


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