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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The antiarrhythmic and antifibrillatory actions of bepridil, an antianginal agent with cardiac fast and slow channel-blocking activities, were evaluated in conscious dogs 3 to 7 days after anterior myocardial infarction. The i.v. administration of 5.0 mg/kg of bepridil prevented the initiation of ventricular tachycardia in four of 12 postinfarction dogs tested and slightly but significantly prolonged the effective refractory period determined at the right ventricular outflow tract. The i.v. administration of 10.0 mg/kg of bepridil prevented ventricular tachycardia induction in seven of 13 dogs tested and significantly reduced the rate of the induced tachycardia in the remaining six dogs. Significant increases in ventricular activation times measured in both normal and infarcted areas of myocardium, as well as a modest prolongation in ventricular refractoriness, accompanied administration of 10.0 mg/kg of bepridil. Acute pretreatment with 5.0 and 10.0 mg/kg of bepridil produced a dose-dependent and significant (10.0 mg/kg) delay in the development of ventricular fibrillation in response to ischemia at a site remote from previous myocardial infarction, as well as suggestive increases in survival 24 hr after the development of ischemia. These results suggest that bepridil may possess antiarrhythmic properties useful in the management of recurrent ventricular tachycardia in the setting of myocardial infarction and in the suppression of early ischemia-mediated ventricular fibrillation in the presence of previous myocardial injury.
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PMID:Antiarrhythmic and electrophysiologic effects of bepridil in chronically infarcted conscious dogs. 387 85

The influence of the duration of ischemia on infarct size and left ventricular function (LV) was assessed in 30 patients with a first anterior myocardial infarction (MI) and intracoronary thrombolysis (ICTL) on admission. The occlusion time of the left anterior descending coronary artery (LAD) was 4 hours or less in 11 patients (group I), 4-10 hours in 11 (group II) and 10 hours or more in eight (group III). Serial measurements of serum creatine kinase-MB were carried out during the acute phase. Four weeks after the procedure, electrocardiographic pathological Q waves on 34-lead precordial mapping were scored, viable left ventricular myocardial volume and the ratio of infarcted to total left ventricular myocardial volume was estimated by myocardial emission computed tomography (ECT) with thallium-201. In the acute phase enzymatic estimation of infarct size showed a significant difference between group I and the other two groups but not between groups II and III; there were no significant differences in the degree of left ventricular asynergy among the three groups. In the chronic phase infarct sizes evaluated by both Q wave mapping and ECT were smaller in group I than those in group II, which were smaller than those in group III; there were significant differences in the degree of LV asynergy among the three groups (group I less than II less than III). LV function was nearly normal in group I, moderately impaired in group II, but severely depressed in group III 4 weeks later. The present study indicates that infarct size extends and LV function deteriorates with the duration of occlusion of the LAD and that not only early (less than or equal to 4 hours) but also later (4-10 hours) reperfusion is beneficial to prevent the extension of MI and deterioration of LV function in patients with anterior MI.
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PMID:Effects of intracoronary thrombolysis on infarct size and left ventricular function in patients with anterior myocardial infarction--enzymatic, electrocardiographic, radionuclide and hemodynamic evaluations. 387 37

The antiarrhythmic and antifibrillatory actions of the dextrorotatory isomer of sotalol, administered in a multiple-dose regimen, were evaluated in conscious dogs 3 to 5 days after anterior myocardial infarction. The intravenous administration of d-sotalol, four 8 mg/kg doses over a 24-hour treatment period, suppressed the induction of ventricular tachycardia by programmed electrical stimulation in six of nine dogs tested, slowed the rate of the induced tachyarrhythmia in two of the remaining three dogs, and provided significant protection (5 of 8 d-sotalol vs 0 of 8 vehicle control) against the development of ventricular fibrillation in response to ischemia at a site distant to a previous myocardial infarction. Increases in ventricular myocardial refractoriness and in QTc and paced QT intervals suggest that class III electrophysiologic actions contribute to the antiarrhythmic properties of dextrorotatory sotalol in this animal model. The degree of beta-adrenergic receptor blockade produced by d-sotalol in this dose regimen was negligible. These findings suggest the potential utility of d-sotalol in the prevention of ventricular tachycardia and ventricular fibrillation in the setting of myocardial infarction, particularly when beta-adrenergic receptor blockade is undesirable or contraindicated.
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PMID:Prevention of ventricular fibrillation by dextrorotatory sotalol in a conscious canine model of sudden coronary death. 399 29

We initiated a retrospective study to determine whether ST segment depression seen in inferior leads (II, III, and aVF) during acute anterior myocardial infarction (MI) is a reciprocal change or an independent sign of ischemia of additional myocardium. We selected 20 patients with anterior MI and attempted to compare findings of subsequent cardiac catheterization and the clinical course of 14 patients with ST segment depression (group A) and six without ST segment depression (group B). Patients in group A had a higher prevalence of right coronary artery disease (13 vs 0, P less than .01), multivessel disease (14 vs two, P less than .01), inferior wall motion abnormalities (seven vs 0, P less than .01), and ejection fraction of less than .50 (ten vs two, P greater than .05) than those in group B. A greater number of patients in group A had serious in-hospital and follow-up complications (12 vs two, P less than .05). We conclude that ST depression in leads II, III and aVF during acute anterior MI is not "reciprocal change" but a high-risk indicator.
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PMID:ST segment depression in acute anterior myocardial infarction. 400 99

The efficacy of verapamil and lidocaine for treating ischemia-induced arrhythmias was determined in a conscious canine model with a previous myocardial infarction remote from the ischemic area. Temporary (up to 5.5 minutes) occlusion of the circumflex coronary artery was made in eight conscious dogs that had sustained an anterior myocardial infarction 13 to 35 days previously. Each dog served as its own control. Ventricular arrhythmias were observed in 100% of control experiments but in only 25% of experiments after verapamil pretreatment at 0.4 mg/kg body weight. Repetitive ventricular complexes, defined as two or more consecutive ventricular complexes terminating spontaneously in sinus rhythm, were seen in 88% of control experiments and 13% of verapamil experiments, whereas ventricular fibrillation was seen in 6% of control experiments but in no verapamil experiment. Thus, verapamil abolished arrhythmias or reduced the grade of arrhythmias in all dogs. Six of the eight dogs were also tested with lidocaine pretreatment at one or two doses resulting in mean plasma levels of 3.8 +/- 2.0 micrograms/ml. Ventricular arrhythmias were seen in 92% of control experiments and 100% of lidocaine experiments. The incidence of ventricular fibrillation increased from 8% in control to 60% in lidocaine experiments. It is concluded that verapamil may prevent severe ischemia-induced arrhythmias after a recent myocardial infarction, whereas lidocaine may in some cases aggravate arrhythmias.
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PMID:Effects of verapamil and lidocaine in a canine model of sudden coronary death. 403 Dec 80

The electrocardiographic responses to programmed ventricular stimulation and acute posterolateral myocardial ischemia were studied in conscious dogs treated with the resolved optical isomers of sotalol. Studies were conducted 3-7 days after anterior myocardial infarction to determine the relative contributions of beta-adrenergic receptor blockade and direct Class III electrophysiologic actions in the antiarrhythmic and antifibrillatory actions of the isomers. With cumulative i.v. administration of up to 8 mg/kg, both the beta-blocking levorotatory isomer and the dextrorotatory isomer suppressed the induction of ventricular tachyarrhythmias by programmed stimulation in at least 50% of dogs tested. Both isomers produced equivalent 15-20% increases in normal zone ventricular refractoriness, thereby preventing propagation of programmed ventricular extrastimuli of sufficient prematurity to elicit tachyarrhythmias. The levorotatory isomer of sotalol prolonged the PR interval; the administration of the dextrorotatory isomer increased QTc and, in several dogs, was associated with the development of ventricular ectopy. The prior administration of 8 mg/kg of either optical isomer of sotalol prevented the immediate spontaneous development of ventricular fibrillation in response to ischemia at a distance from the previous site of infarction. These results suggest that alterations in ventricular refractoriness may underlie the antiarrhythmic and antifibrillatory actions of the optical isomers of sotalol and of racemic sotalol.
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PMID:Antiarrhythmic and antifibrillatory actions of the levo- and dextrorotatory isomers of sotalol. 608 71

Two patients with complete heart block complicating extensive anterior myocardial infarction underwent late (greater than 40 hours) coronary reperfusion with angioplasty. One to one atrioventricular conduction was restored within minutes of reperfusion despite a lack of measurable ventricular muscle salvage as demonstrated by ventriculography 1 week later. The evidence favors reversible ischemia rather than extensive necrosis of the proximal conduction system as the mechanism of heart block in this subgroup of patients.
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PMID:Effects of reperfusion on complete heart block complicating anterior myocardial infarction. 623 90

The purpose of this study was to evaluate the detectability of stress-induced ischemic lesion in patients with previous myocardial infarction using single photon emission computed tomography (SPECT) producing thallium-201 (T1-201) myocardial perfusion imagings (MPI). Seventy patients underwent stress SPECT by symptom-limited graded bicycle ergometer exercise using a dual-headed rotating gamma camera (Toshiba GCA70A) equipped with a computer system (GMS90). After intravenous administration of 2.5 mCi of T1-201, stress SPECT data at 10 minutes and delayed SPECT data at 3 hours after the injection were collected in the 64 X 64 matrix form covering 360 degrees directions by camera sweep of 180 degrees in 6 minutes, which were immediately followed by conventional planar imagings (PL). Transaxial tomographic image reconstruction was performed by convolution method using a Shepp-Logan's filter. Thereafter, sagittal and coronal tomographic images were reconstructed for about 2 minutes. Image interpretation was assessed visually. The results were as follows: Sensitivity and specificity in detecting the affected vessel with more than 75% stenosis by segmental analysis of myocardial images were higher by SPECT than by PL (LAD 89% and 65%, LCX 68% and 56%, RCA 89% and 76% in sensitivity and LAD 94% and LCX 75%, 92% and 94%, RCA 81% and 59% in specificity, respectively). Sensitivity in detecting both single (82%) and multivessel disease (76%) was fairly high. Detectability of stress-induced ischemia (i.e. occurrence of a new defect in patients with previous myocardial infarction and ST-segment depression in ECG) was significantly higher in SPECT (67%) than in PL (39%, p less than 0.005) and in ECG (39%, p less than 0.005). A perfusion defect in the extensive anterior wall, marked left ventricular dilatation and the widening of the angle toward the apex composed of septal and anterolateral walls in transaxial images were the findings characteristic of anterior myocardial infarction with severe dyskinesis. We conclude that stress SPECT is a useful noninvasive technique for the documentation of the number of vessels affected and severe wall motion abnormality of the LV and for the detection of stress-induced ischemia in previous myocardial infarction.
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PMID:[Detectability of stress-induced ischemic lesion in previous myocardial infarction using 201T1 myocardial single photon emission computed tomography]. 633 58

This study was performed to determine whether inferior ST segment depression during early stages of acute transmural anterior myocardial infarction identifies patients with multivessel coronary artery disease and additional inferior ischemia. Coronary and left ventricular angiography were performed within 3.4 months in 33 patients with acute transmural anterior infarction. Initial electrocardiograms, 2 to 5 hours after onset of chest pain, revealed significant ST segment depression (greater than or equal to 0.1 mV) in at least two of leads II, III and a VF in 15 patients (45%) (group B); in 18 patients (group A) this finding was absent. Compared with group A, patients in group B had greater anterior ST elevation (1.2 versus 0.7 mV, p less than 0.025); higher serum peak creatine kinase (2,475 versus 1,147 IU/liter, p less than 0.005); higher Killip scores (2.1 versus 1.3, p less than 0.001); more in-hospital complications (60 versus 17%, p less than 0.05); lower mean left ventricular ejection fraction (34 versus 55%, p less than 0.001); more frequent regional left ventricular dysfunction in anterolateral (91 versus 44%, p less than 0.05), posterolateral (36 versus 0%, p less than 0.05) and inferior (100 versus 6%, p less than 0.005) regions; greater wall motion abnormality scores (10.0 versus 5.5, p less than 0.005); higher frequency of concomitant left circumflex or right coronary artery disease, or both (80 versus 28%, p less than 0.01); more frequent postinfarction angina (100 versus 39%, p less than 0.001) and lower New York Heart Association functional classification scores (1.7 versus 2.4, p less than 0.05) at 6 month follow-up. The time course of inferior ST depression differed from that of anterior ST elevation. Thus, inferior ST depression was maximal in the first 48 hours and decreased (p less than 0.05) thereafter. In contrast, ST elevation in leads V1 to V6 and I appeared to decrease (p = NS) between days 4 and 7. However, inferior ST depression "mirrored" ST elevation in lead aVL, which also decreased (p less than 0.05) after 48 hours. Thus, inferior ST depression during anterior infarction is associated with more extensive infarction, greater morbidity and higher frequency of multivessel coronary disease. Such inferior ST depression might reflect not only "reciprocal change," but also ischemia in adjacent lateral and remote inferior regions.
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PMID:Inferior ST segment depression during acute anterior myocardial infarction: clinical and angiographic correlations. 647 Mar 25


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