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)

In a 45 year old male patient with a history of previous inferior myocardial infarction and unstable angina pectoris, coronary angiography revealed two-vessel disease: a 60-70% lesion in the middle third of the LAD, and a 90% lesion in the middle third of the very large RCA. There was only a small akinetic segment in the posterobasal region of the left ventricle. During angiography total occlusion of the RCA occurred followed the clinical and electrocardiographic signs of impending inferior reinfarction. Recanalization of the occluded vessel was accomplished by using a guide-wire, which was passed through a Sones catheter, placed in the RCA. The patient's symptoms subsided and the electrocardiographic signs of acute ischemia reverted within eight minutes. Aortocoronary bypass surgery with revascularization of the LAD and RCA was performed within 3 hours after recanalization. Postoperatively there was no evidence of major tissue loss by enzyme or electrocardiographic criteria. Control angiography, performed on the ninth day postoperatively, revealed the graft to the RCA to be widely patent. Left ventricular function was unchanged. It is concluded, that the combined approach of early transluminal recanalization of the acutely occluded RCA followed by successful construction of a graft to this vessel, has averted necrosis of a major portion of the left ventricle. However, general use of this technique does not seem advisable at the present time.
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PMID:Acute coronary occlusion with impending infarction as an angiographic complication relieved by a guide-wire recanalization. 31 53

This report described initiation of A-V nodal reentrant tachyycardia in a patient with acute inferior myocardial infarction. The onset of tachycardia was preceded by an abortive A-V nodal Wenckebach periodicity. A-V nodal ischemia with or without vagotonia was implicated as the cause of induction of critical functional dissociation between the two A-V nodal conduction pathways. Since the tachycardia manifested its rate between 95-110 beats/min during the evolutionary phase of acute inferior myocardial infarction, it simulated, electrocardiographically, an accelerated A-V junctional rhythm. Analysis of the onset of tachcardia was of diagnostic importance.
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PMID:A-V nodal reentrant tachycardia vs accelerated A-V junctional rhythm in acute inferior myocardial infarction. 73 96

We studied atrial arrhythmias during the first 12 h of admission to the hospital in 266 consecutive patients with acute myocardial infarction who subsequently underwent coronary angiography. Ten patients developed atrial fibrillation, one atrial flutter, and one supraventricular tachycardia. Another five developed sinus dysrhythmias. All of the above patients had an acute inferior myocardial infarction, and in 10 of the 12 patients with supraventricular arrhythmias and in four of five with sinus dysrhythmias, the origin of the sinus node artery started just after an occluded right coronary or left circumflex artery or was involved in the occlusion. Thus, ischemia of the sinus node due to coronary occlusion proximal to the origin of the sinus node artery was a likely cause of these arrhythmias.
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PMID:Early atrial arrhythmias in acute myocardial infarction. Role of the sinus node artery. 155 68

Assessments of the significance of precordial ST segment depression in acute inferior myocardial infarction (AIMI) have yielded conflicting results. Among 92 AIMI patients admitted within 6 hrs after the onset, 65 showed ST depression, and the remaining 27 showed no ST depression. These depressions were present in all of V1-4 (right type; 17), V2-5 (middle type; 10), V3-6 (left type; 13) and V1-6 (broad type; 25). The clinical severity was Forrester subset I in the majority (89%) of patients without ST change, while complications were prevalent in patients with ST depression, especially in the right type (44% were Forrester subset II-IV). Peak CK was 2,150 +/- 399 U/L in patients without ST depression, but it was elevated to 3,172 +/- 811 in patients with ST depression, especially in the right type (4,506 +/- 499). Wall motion evaluated by echocardiography and QRS scores on ECG also revealed greater abnormality in patients with ST change. The initial right coronary angiogram on admission revealed complete occlusion in 76% of these patients with ST depression of whom all of the right type had completely occluded artery. Abnormal motion of the anterior wall, which suggests remote ischemia associated with AIMI was proved neither by left ventriculography nor echocardiography. Hospital mortality in patients with ST depression (9.2%) was as twice as high as that in those without ST depression (4.6%). We concluded that ST depression in patients with acute inferior infarction may not be indicative of remote ischemia but manifests as a mirror image of a large infarction with a complicated clinical course.
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PMID:[Clinical characteristics of precordial ST-segment depression in acute inferior myocardial infarction]. 184 9

To study the predictive value of silent ischemia, a total of 132 patients with first transmural myocardial infarction were examined, 69 had anterior and 63 had inferior myocardial infarction. On days 8-12 of onset of the disease, all the patients underwent loading two-dimensional echocardiography along with transesophageal pacing, as well as polyposition coronary angiography. According to the echocardiographic findings, 3 groups of patients were identified: 1) 34 (25.8%) with painful ischemia; 2) 37 (28.0%) with silent ischemia; 3) 61 (46.2%) with a negative test. Ischemic alterations were more frequently seen in inferior (73%) than in anterior (36.2%) myocardial infarction. The patients with painful ischemia showed a lower threshold of ischemia occurrence, more severe and prolonged ST segment depression, and greater extent of an asynergic area than did the patients with silent ischemia. A 1-5-year (mean 2.4) follow-up revealed that in terms of the risk for postinfarction angina, recurrent myocardial infarction and fatal outcomes, patients with silent ischemia represent an intermediate group between those with painful ischemia and those who have a negative load test.
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PMID:[Prognostic significance of post-infarction "silent" ischemia]. 192 Nov 27

This communication describes the first successful Transluminal Coronary Angioplasty performed in the Republic of Panama. The patient was a 77 year old man who developed post-infarction angina twenty days after an acute inferior myocardial infarction. He had new manifestations of ischemia of the posterior-lateral left ventricular wall. Dilatation of a severe proximal lesion of a large right coronary artery, the culprit vessel, was accomplished without complications.
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PMID:[Coronary transluminal angioplasty. A reality in Panama]. 192 98

The electrocardiogram is the graphic representation against time of the difference in potential between points of the body caused by the current field of the heart. To examine the origin of this current field, a method of transforming body surface electrocardiographic data to the epicardial surface has been developed. The computed epicardial current density distributions in 219 patients with acute inferior myocardial infarction showed that, in 89% of patients, the current flow out of the heart during the ST segment came from two regions, not only from the infarction region but also from a region over the great vessels. This findings suggests that current flows from the ischemic region, through the low-resistance pathway provided by the intracavity blood, out the great vessels, and back to the epicardium. A similar pathway has been hypothesized when ischemia caused endocardial ST elevation, such as during a stress test or with unstable angina. To test this hypothesis, a group of patients with ST depression on the 12-lead electrocardiogram, not associated with ST elevation, was examined with body surface mapping. Ninety-four percent of patients had epicardial current density distributions that showed a region of current flow out of the heart and over the great vessels that was consistent with this hypothesis. This could explain the poor localization of coronary artery disease by electrocardiographic techniques when there is ST depression on the body surface.
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PMID:Importance of the great vessels in the genesis of the electrocardiogram. 186 Jan 91

Exercise electrocardiography with or without thallium-201 scintigraphy was performed (pre-hospital discharge) in 66 asymptomatic survivors of a first inferior myocardial infarction (IMI). Although coronary angiography revealed an 82% incidence of multivessel coronary artery disease (MV-CAD) in the total cohort, the sensitivity of exercise ECG for MV-CAD in the group with absent anterior ST-depression in the acute phase was low (11%). In contrast the presence of acute phase anterior ST-segment depression improved the yield for MV-CAD to 55%. Forty-six patients agreed to a symptom-limited exercise ECG plus/minus thallium imaging at 8-10 weeks post IMI. The sensitivity of detecting MV-CAD improved by 15% in patients with no acute phase anterior ST-segment depression and 16% in patients with acute phase anterior ST-segment depression. At each exercise protocol, thallium improved the sensitivity of exercise in detecting ischemia in the noninfarct zone. It is concluded that following IMI, a high percentage of asymptomatic patients whose acute phase ECG showed anterior ST-segment depression will have MV-CAD detected by heart-rate limited and, more so, by symptom-limited exercise ECG. The detection rate will double in patients with no anterior ST-segment depression if exercise testing is delayed until 8-10 weeks post IMI.
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PMID:Timing of stress testing in an asymptomatic survivor of inferior myocardial infarction. 233 45

To determine whether precordial ST segment depression during acute inferior myocardial infarction indicates posterolateral wall ischemia, anatomical predominance of coronary circulation was examined by coronary angiography and evaluated in 43 patients who experienced first acute inferior myocardial infarction. Among patients who underwent intracoronary thrombolysis within six hours from the onset of symptoms, the infarct-related artery was the right coronary artery (RCA) in 35. In addition, their early 12-lead electrocardiographic features were compared with those in eight patients having the infarct-related left circumflex coronary artery (group Cx). Thirty-five patients with RCA obstruction were categorized in four groups: Four patients with left predominant type (group L), 10 with balanced type (group B), five with right super-predominant type (group SR), and 16 with right intermediate type (group RI). Seventeen of the 21 patients in groups SR and RI demonstrated precordial ST segment depression, whereas it was present in only six of the 14 patients in groups L and B (p less than 0.05). Of the 29 patients in groups SR, Cx and RI, total ST segment depression in leads V1 through V4 (sigma ST) was greater in the 14 patients in groups L and B (p less than 0.05) than in other groups. Furthermore, in these 29, all patients in groups SR and Cx had greater sigma ST than did the patients in group RI (p less than 0.05). There was no significant difference in sigma ST between groups SR and Cx. Precordial ST segment depression did not correlate with concomitant disease of the left anterior descending artery and was not a mirror image of ST segment elevation in inferior leads. On thallium-201 scintigraphy, additional perfusion defects of the posterolateral wall were present in all eight patients in group Cx and in ten of the 21 patients in groups SR and RI. Thus, precordial ST segment depression during acute inferior myocardial infarction seemed to be affected by the pattern of coronary circulation. It was concluded that this ST depression represents more extensive involvement of the posterolateral wall in patients with right predominant coronary circulation as well as in those with left circumflex artery obstruction.
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PMID:[Precordial ST segment depression in acute inferior myocardial infarction: the importance of posterolateral wall infarction]. 263 23

It was hypothesized that in acute inferior wall myocardial infarction, an additional ischemic area in the subendocardium of the noninfarcting territory would produce a selective current dipole between the infarcting and ischemic regions. A resistance network model to calculate epicardial potentials from body surface electrocardiographic potentials was developed and used to examine the hypothesis in 219 patients with acute inferior myocardial infarction. In the learning set of 110 patients, two characteristic dipole patterns were observed, each associated with a high mortality rate in the ensuing 15 months when compared with that in the remaining patients. In the test set of 109 patients, a double-blind analysis of the patterns showed that the 34 patients with a dipole pattern had a collective mortality rate of 35% at 15 months compared with a 15 month rate of 5% in the remaining patients. In the total group of 219 patients, the magnitude of ST segment elevation and both the magnitude and integral of the area voltage of ST depression on the epicardium were significantly correlated with the mortality rate (p less than 0.0002 for all variables against death at 15 months). This study strongly suggests that ST depression due to ischemia can be differentiated from ST depression secondary to the ST elevation in acute inferior infarction by the examination of epicardial potential distributions.
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PMID:Derived epicardial potentials differentiate ischemic ST depression from ST depression secondary to ST elevation in acute inferior myocardial infarction in humans. 276 19


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