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

Acute myocardial ischemia is a serious complication of percutaneous transluminal coronary angioplasty (PTCA). Between September 1981 and September 1985, 240 patients underwent 260 PTCAs at the Hadassah University Hospital. Thirteen patients (5%) developed signs of acute ischemia during or immediately after the procedure. In 10 patients (4.2%) emergency coronary artery bypass grafting was performed. The left anterior descending artery in nine cases and the right coronary artery in one case were occluded. In eight patients intraaortic balloon counterpulsation (IAB) was begun prior to surgery. On the average 1.8 grafts per patient were performed. Two patients who were transferred to surgery while being resuscitated died from myocardial rupture, one during surgery and the other 4 days postoperatively. Perioperative infarction rate was 50% (5/10). Six patients are angina-free 3 to 46 months postoperatively. Better patient selection, performance by an experienced team, early use of IAB, and immediate surgery might reduce the current periprocedure morbidity and mortality rate of PTCA.
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PMID:Emergency coronary artery bypass for acute myocardial ischemia following percutaneous transluminal coronary angioplasty. 294 76

A 52-year-old man had longstanding hypertension and asymemtric septal hypertrophy and normal major coronary arteries. His acute anterior wall ischemia gave rise to transient Q waves and septoapical dyskinesia, complicated by mural thrombus formation. Follow-up revealed a gradual and complete recovery of echocardiographic left ventricular function with total disappearance of mural thrombi and of electrocardiographic Q waves. Acute myocardial ischemia can cause prolonged electrical and mechanical stunning which can lead to mural thrombus formation.
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PMID:Acute myocardial ischemia with prolonged left ventricular dyskinesia and mural thrombus formation in asymmetric septal hypertrophy. 334 53

Acute myocardial ischemia followed by protracted asynergy and subsequent resolution was defined as reversible ischemic myocardial damage. The purpose of this study was to confirm the existence of this entity and to illustrate the clinical features. The subjects consisted of 26 patients with typical acute myocardial ischemia who satisfied the above definition, and serial changes in left ventricular wall motion were observed by two-dimensional echocardiography. The left ventricle was divided into 11 segments and the movement was scored according to the dynamic behavior of each segment by five points ranging from normal (0) to dyskinesis (4), and evaluated semiquantitatively using the total score sum as the total asynergy score. Compared to the initial value, this score decreased to 57% after one week, 38% in two weeks, 22% in three weeks and 17% in four weeks. The asynergy persisted 23.7 +/- 13.5 days and ranged from two days to three months. The peak CPK ranged from 32 to 561 IU (mean 212 +/- 157 IU). Coronary arteriography revealed undisturbed flow of the responsible artery in both acute and chronic phases including four cases of successful PTCR. Comparison of the electrocardiographic changes and asynergy showed that diminished R wave amplitude, ST segment elevation and inverted T waves are frequently associated with persistence of asynergy, extensive asynergy can even occur in cases without a diminished R wave or abnormal Q wave and when asynergy resolves, ST segments tend to return to the baseline, but T wave inversion commonly persists. A transient Q wave was observed in 38% of the patients examined. The electrocardiogram became normal in an average of 111.3 +/- 75 days. In conclusion, there is a subgroup of reversible asynergy among cases of unstable angina pectoris or subendocardial infarction. The mechanism for this may be myocardial "stunning" following transient transmural ischemia. Recognition of this fact seems very important in the diagnosis and treatment of acute myocardial ischemia.
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PMID:[Reversible ischemic myocardial damage: clinical observation using two-dimensional echocardiography]. 365 11

To evaluate whether myocardial texture changes resulting from acute ischemia can be visualized with satisfactory spatial resolution, short axis compound echo images (CEI) (B-scan) were obtained from 12 excised canine hearts in vitro. Seven had myocardial ischemia produced by open chest ligation of the left anterior descending coronary artery (LAD) for 15-30 min prior to excision. The CEI were constructed by compounding 60 simple linear B-scans. Hearts were sectioned after scanning, and gross morphological changes were recorded. Microscopic comparison between grossly abnormal and normal regions were recorded. The CEI from the ischemic group revealed altered myocardial texture seen as bright coarsely granular echoes in the regions normally perfused by the ligated LAD artery. Corresponding anatomic sections revealed increased redness in these regions. Microscopically these regions revealed interstitial and intercellular edema as compared to the normal regions. Acute myocardial ischemia can be visualized in CEI and these regions have significantly increased backscatter, decreased attenuation, and decreased speed of ultrasound relative to normal regions in the same hearts. Myocardial edema is probably responsible for these changes.
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PMID:Echocardiographic visualization of acute myocardial ischemia--in vitro study. 379 86

Acute myocardial ischemia is a serious complication of percutaneous transluminal coronary angioplasty, often requiring emergency myocardial revascularization. Since our initial report of 17 such patients, we have encountered an additional 32 patients requiring emergency myocardial revascularization since September, 1981. The indication for emergency myocardial revascularization was ischemic chest pain in all 32 patients. Percutaneous transluminal coronary angioplasty resulted in injury to the right coronary artery in 11 patients, the left anterior descending artery in 19 patients, and the left main artery in two patients. The onset of ischemia was immediate in 26 patients but delayed up to 22 hours in six patients. Chest pain was associated with ST-segment elevation in 21 patients, hypotension in 7 patients, and cardiac arrest in 6 patients. Immediate intra-aortic balloon pumping was instituted in the angioplasty suite in 16 patients. The mean time from onset of ischemia to completed revascularization was 156 minutes with a mean of 1.6 grafts performed per patient. Seventeen patients (53%) had enzyme evidence of myocardial infarction postoperatively, with a significantly higher (p less than 0.01) incidence of myocardial infarction in those patients with preoperative ST elevation (76% versus 9%). In the 21 patients with ST-segment elevation, the incidence of Q wave infarction was 20% (3/15) with balloon pumping and 50% (3/6) without balloon pumping. Complications associated with intra-aortic balloon pumping occurred in one patient (6%). There were no hospital or late deaths with follow-up extending 16 months. The spectrum of injury resulting from percutaneous transluminal coronary angioplasty extends from chest pain alone to severe transmural ischemia with hypotension or cardiac arrest. Presentation may be immediate or delayed. Urgent emergency myocardial revascularization remains the accepted therapy for this complication. Immediate preoperative intra-aortic balloon pumping is a useful adjunct to emergency myocardial revascularization in the group of patients with acute ischemia and ST-segment elevation.
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PMID:Surgical management of acute myocardial ischemia following percutaneous transluminal coronary angioplasty. Role of the intra-aortic balloon pump. 623 Apr 89

Changes in conduction times induced by ischemia (delta CT) have been shown to be quantitatively related to genesis of spontaneous ischemic ventricular fibrillation (VF). We studied conduction delay encountered by premature impulses in epicardium and endocardium in both anterograde and retrograde directions during ischemia and reperfusion in eight control and in eight verapamil treated dogs. Acute myocardial ischemia was produced by single-stage ligation of left anterior descending artery below second diagonal initially, and 30 minutes later below first diagonal branch. In treated dogs, verapamil was given, 0.15 mg/kg intravenous bolus, immediately after first ligation and was followed by an infusion of 7.5 micrograms/kg/min. Thus post-treated segment and pretreated segment were obtained in the same animal. delta CT was compared between control and treated dogs in four myocardial zones: (1) normal, (2) ischemic including pre- and post-treated segments, (3) reperfused, and (4) border of reperfusion or ischemia. Results showed that ischemia-induced conduction delay was significantly less in verapamil treated dogs throughout period of ischemia and reperfusion, both in epicardium and endocardium. In addition, in the border of ischemia retrograded conduction showed significantly less depression during ischemia and reperfusion. The protective effect of verapamil was impressive both in pretreated and post-treated segments of ischemic myocardium. We conclude that verapamil offers significant protective action with regard to ischemia-induced conduction delay. Since delta CT is quantitatively related to ischemic VF, verapamil can be antiventricular fibrillatory in myocardial ischemia.
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PMID:Effect of verapamil on conduction delay produced by myocardial ischemia and reperfusion. 626 20

Acute myocardial ischemia reduces tolerance of the heart to arrhythmogenic actions of digitalis glycosides. Because both ischemia and the glycoside produce profound changes in activity of the autonomic nervous system and because sympathetic discharge or catecholamines enhance toxic actions of the cardiac glycosides, the possibility that alterations in digitalis sensitivity of ischemic heart involve changes in sympathetic nerve activity was examined using alpha-chloralose-anesthetized cats. Left anterior descending coronary artery (LAD) was completely occluded by ligation and, 40 min later, a slow i.v. infusion of digoxin was started at a rate of 1 microgram/kg/min. LAD ligation alone did not produce arrhythmias in that condition, but shortened the time to onset of digoxin-induced arrhythmias and thereby reduced the amount of digoxin required to produce the toxic manifestation. Concomitantly, digoxin concentration in plasma and nonischemic areas of the heart were lower in LAD-ligated cats at the onset of arrhythmias than those in sham-operated cats. Myocardial digoxin content in the ischemic area of the LAD-occluded heart was lower than that in nonischemic areas of the same heart. At the onset of digoxin-induced arrhythmias, Na,K-adenosine triphosphatase activity of ischemic myocardium was significantly higher than that in the nonischemic area, reflecting a lower digoxin occupancy of the glycoside binding sites on the sodium pump. Spinal cord (C1) transection or propranolol treatment prolonged the time to arrhythmias in both control and LAD-ligated cats, but failed to abolish the effect of LAD ligation to augment digoxin toxicity. Bilateral vagotomy also did not alter the enhancement of digoxin toxicity caused by ligation of LAD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of sympathetic nervous system in ischemia-induced reduction of digoxin tolerance in anesthetized cats. 632 71

Acute myocardial ischemia is accompanied by a marked decrease in the oxidation of fatty acids. Whether similar changes occur during chronic ischemia was studied in 13 beagles. In 10 dogs, an ameroid constrictor was implanted about the left circumflex artery; 3 others served as sham-operated controls. Mitochondrial and peroxisomal fatty acid oxidation of (1-14C)oleate were measured and compared in affected (posterobasal left ventricular endocardial [posterior LV endo]) and unaffected (anteroapical LV epicardial [anterior LV epi]) tissues of control and experimental dogs. Five experimental and 3 control dogs were killed after 3 weeks. The posterior LV endo sections of experimental dogs at 3 weeks showed increased fatty acid oxidation due to peroxisomal (KCN-insensitive) beta oxidation (p less than 0.01). The anterior LV epi sections showed no difference in fatty acid oxidation between sham-operated and experimental dogs. Five dogs were studied after 3 months; fatty acid oxidation of the posterior LV endo section was normal. Thus, under a slowly evolving state of myocardial ischemia, highly localized and reversible adaptive changes in fatty acid oxidation occur that enable the affected tissue to cope with a fatty acid load. When collateralization is accomplished, fatty acid metabolism reverts to normal.
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PMID:Reversible, highly localized alterations in fatty acid metabolism in the chronically ischemic canine myocardium. 646 25

Acute myocardial ischemia induced by coronary occlusion in dogs is most severe in the subendocardial region, whereas more collateral blood flow is often present in the subepicardial region. Initially, all ischemic myocytes are reversibly injured, but beginning at 15 to 20 minutes after the onset, and continuing for 3 to 6 hours, there is a wave front of cell death from the subendocardial region to the less ischemic subepicardial region, such that by 6 hours, the final transmural extent of the infarct is established. Thus, ischemic myocardium cannot be salvaged by reperfusion after greater than or equal to 6 hours of coronary occlusion in open-chest anesthetized dogs. In the severely ischemic subendocardial region, most of the creatine phosphate is lost within the first 3 minutes of ischemia in vivo, and adenosine triphosphate (ATP) is depleted to 35% of control by 15 minutes (when cellular injury is still reversible), and to less than 10% of control at 40 minutes (when injury is irreversible). Tissue ATP content and other indexes of subcellular damage have also been compared after different periods of ischemia using a model of total myocardial ischemia in vitro. As long as the ATP of the tissue was not depleted below 5 mumols/g dry weight, incubated slices of injured myocardium resynthesized high-energy phosphates and excluded inulin. However, lower tissue ATP was associated with depressed high-energy phosphate resynthesis and failure of cell volume regulation. Overt membrane damage, as measured by an increased inulin-diffusible space, was detected only after the tissue ATP decreased to less than 2.0 mumols/g of dry weight. Thus, marked ATP depletion is associated with the onset of structural and functional indexes of irreversible injury. However, whether irreversibility is caused by the marked ATP depletion or by other concomitant metabolic consequences of ischemia is not known. Myocardial ischemic cellular injury is reversible despite depletion of 70% of the control ATP. Nevertheless, when myocyte injury is reversible, there is slow repletion of adenine nucleotides. This slow metabolic recovery may explain the delayed recovery of contractile function observed after reperfusion of ischemic myocardium.
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PMID:Pathobiology of acute myocardial ischemia: metabolic, functional and ultrastructural studies. 686 59

Effects of calcium antagonists and lidocaine on the conduction delay observed in the ischemic myocardium were studied in 24 open-chest anesthetized dogs. Acute myocardial ischemia was produced by complete occlusion of the left anterior descending coronary artery (LAD) for 5 to 10 minutes. The conduction time was measured from the initial deflection of V waves on the His bundle electrograms to the major deflection of the bipolar electrograms recorded from the ischemic and non-ischemic subepicardium under a constant atrial pacing. LAD occlusion produced conduction delay in the ischemic zone (14.3 +/- 2.3 msec, p less than 0.001) with no effect on the normal zone. This ischemia-induced conduction delay was reversible and rate-dependently increased. Administration of lidocaine (2 mg/kg bolus, 4.3 mg/kg/hr constant infusion) prior to the second occlusion increased conduction delay by 12.9 +/- 1.9 msec (p less than 0.001) whereas diltiazem (0.4 mg/kg i.v.) and verapamil (0.3 mg/kg i.v.) reduced the ischemia-induced conduction delay by 12.7 +/- 4.9 msec (p less than 0.05) and 8.4 +/- 1.8 msec (p less than 0.001), respectively. These results indicate that slow channel blocking agents reduce the conduction delay induced by the myocardial ischemia, in contrast with the prolonging effect of lidocaine.
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PMID:Effects of calcium antagonists and lidocaine on conduction delay induced by acute myocardial ischemia in dogs. 720 68


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