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

The relationship between activity of the autonomic nervous system, myocardial ischemia, and malignant arrhythmias has been investigated in a new experimental preparation for sudden death. Fifty-seven dogs were chronically instrumented and studied under control conditions (n = 15) and 1 month after production of an anterior myocardial infarction (n = 42). The protocol consisted in occluding the left circumflex coronary artery for 2 min, commencing at the last minute of an exercise stress test and extending through the first minute after cessation of exercise. With this protocol, ventricular fibrillation was observed in 40% of normal dogs and 66% of dogs with infarction. In 14 dogs with infarction, left stellectomy reduced the incidence of ventricular fibrillation to zero (p less than .001). The reflex changes in heart rate elicited within the first minute of ischemia during exercise in the animals that survived (from 204 +/- 14 to 198 +/- 31 beats/min, -6) were opposite those in animals that had ventricular fibrillation (from 208 +/- 24 to 229 +/- 30 beats/min, +21) (p less than .05). The ischemia-induced reduction in heart rate despite continuation of exercise suggests the presence in the dogs that survived of active vagal reflexes that may have played an important role in the maintenance of cardiac electrical stability. This preparation has the potential to induce ventricular fibrillation consistently in conscious animals by the interaction of a few clinically relevant factors (acute myocardial ischemia, submaximal exercise and its cessation, sympathetic and vagal reflexes, and heart rate) and offers the possibility of acquiring further insights into the mechanisms of malignant arrhythmias and evaluating novel strategies for targeted prevention.
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PMID:Autonomic mechanisms in ventricular fibrillation induced by myocardial ischemia during exercise in dogs with healed myocardial infarction. An experimental preparation for sudden cardiac death. 669 63

This study tests the hypothesis that myocardial ischemia is responsible for exercise-induced S-T segment elevation in patients with previous anterior myocardial infarction (MI). Exercise stress testing in conjunction with thallium imaging of the myocardium was performed in 28 patients with previously documented anterior MI. Thallium images were analyzed by computer for the presence of initial uptake defects and evidence of abnormal clearance of the isotope from the myocardium (that is, imaging evidence of ischemia). Total S-T segment elevation (sigma ST) in precordial leads V1 to V6 at rest was subtracted from sigma ST at peak stress in order to quantitate the extent of S-T elevation induced by stress (delta ST). Two groups of patients were identified; 1 with stress-induced S-T elevation (Group I, delta ST greater than or equal to 4.0 mm) and 1 without this abnormality (Group II, delta ST less than 4.0 mm). Evidence of abnormal thallium washout from myocardial scan segments occurred in 12 of 15 Group I patients versus 9 of 13 Group II patients (difference not significant). In addition, abnormal tracer washout from anterolateral or septal scan segments occurred in 5 patients in each group. Likewise, abnormal thallium clearance from inferior or posterior scan segments occurred in 8 of 15 Group I patients versus 7 of 13 Group II patients (difference not significant). The patient with the greatest amount of stress-induced S-T elevation (S-T 11.5 mm) had no evidence of ischemia during the stress test. However, Group I patients did have larger anterolateral plus septal initial thallium uptake defect scores than did those of Group II (10 of 15 with defect score greater than or equal to 350 in Group I versus 1 of 13 in Group II, p less than 0.002). Similarly, resting left ventricular ejection fraction greater than or equal to 30% was present in only 4 of 15 Group I patients versus 13 of 13 in Group II (p less than 0.001). Finally, multiple stepwise linear regression analysis demonstrated that delta ST correlated best with the extent of initial anterolateral plus septal thallium uptake defect score (F = 17.3, p less than 0.001) and to a lesser extent with resting ejection fraction (F = 5.2, p less than 0.05) and change in heart rate from rest to peak stress (F = 8.1, p less than 0.01; corrected multiple correlation coefficient = 0.76, p less than 0.001). Thus, in patients with previous anterior MI (1) exercise-induced myocardial ischemia occurs as often with as without S-T segment elevation, (2) myocardial ischemia is not required for the production of stress-induced S-T segment elevation, and (3) stress-induced S-T elevation primarily reflects the extent of previous anterior wall damage and to a lesser extent an increase in heart rate between rest and peak stress.
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PMID:Role of myocardial ischemia in the genesis of stress-induced S-T segment elevation in previous anterior myocardial infarction. 684 56

The prevalence rate of exercise- S-T segment elevation of 0.1 mV or greater in symptomatic patients is 3.0 to 6.5 percent in most studies. S-T segment elevation is associated with a more severe degree of myocardial ischemia than depression and frequently implies a high grade coronary stenosis in the vessel that supplies the site of ischemia. Leads V4 to V6 and bipolar lead CM5 have been found to be relatively insensitive in detecting exercise-induced S-T segment elevation. The pathogenesis of S-T segment elevation is different in three clinical patient subsets reviewed. In patients afer infarction, the largest of the three subgroups, exercise-induced S-T segment elevation usually appears in leads with Q waves, is more common after anterior myocardial infarction and implies underlying akinetic of dyskinetic wall motion. Of patients with variant angina, 10 to 30 percent have during exercise S-T segment elevation that is most likely provoked by coronary arterial spasm. The natural history of variant angina is cyclic, and clinical observations and laboratory findings are dependent on particular phases in the disease process and treatment. Finally, 0.2 to 1.7 percent of symptomatic patients without infarction or variant angina have exercise-induced S-T segment elevation. Although most of the latter have fixed high grade coronary arterial stenoses at angiography, the exact pathogenetic mechanism of S-T segment shift in this patient group is not yet fully understood.
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PMID:S-T segment elevation and coronary spasm in response to exercise. 701 17

A 34-year old woman, with a 3 yr history of severe seropositive rheumatoid arthritis (RA) with lupus anticoagulant and anticardiolipin antibodies, developed a massive anterior myocardial infarction and ischemia of the lower extremities, with disseminated intravascular coagulation resulting from extensive tissue damage. Seven days after admission, she died of severe heart failure complicated by ventricular fibrillation. To our knowledge, this is the first documented case of fatal acute antiphospholipid syndrome in RA.
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PMID:Catastrophic antiphospholipid syndrome with fatal acute course in rheumatoid arthritis. 747 89

The electrophysiologic and antifibrillatory properties of NE-10064 were studied in vivo in a conscious canine model of sudden cardiac death. Purpose bred male mongrel dogs weighing 14.5-21.5 kg were anesthetized, and surgical anterior myocardial infarction (MI) was induced by a 2-h occlusion, with reperfusion, of the left anterior descending coronary artery (LAD). Three to 5 days after induction of anterior wall MI, animals were subjected to testing by programmed electrical stimulation (PES). As compared with predrug incidence (12 of 12), NE-10064 (10 mg/kg intravenously, i.v.) reduced (p < 0.05) the incidence (8 of 12) of PES-induced ventricular tachycardia (VT). All but 1 control animal remained inducible after vehicle (5% dextrose in water). The cycle length of induced VT was not prolonged by NE-10064 (0.245 +/- 0.046 s predrug vs. 0.301 +/- 0.060 s postdrug). NE-10064 increased ventricular effective refractory period (VERP 166 +/- 5 ms predrug vs. 194 +/- 13 ms postdrug, p = 0.013), prolonged QTc interval (310 +/- 12 ms predrug vs. 350 +/- 16 ms postdrug, p = 0.004) and prolonged the effective refractory period (ERP) of noninfarcted myocardium (p = 0.045). The drug did not affect ECG-indexes of conduction velocity: QRS and P-R intervals were not affected, nor were activation delay and conduction time of noninfarcted and infarcted myocardium. In the sudden cardiac death protocol, NE-10064 protected (p = 0.018) against ischemia-induced ventricular fibrillation (VF, 75% survival with drug vs. 25% survival without drug). NE-10064 afforded protection (p = 0.040) throughout 14 h posterolateral ischemia in the presence of the previous anterior infarct.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protection against programmed electrical stimulation-induced ventricular tachycardia and sudden cardiac death by NE-10064, a class III antiarrhythmic drug. 750 98

Ventricular arrhythmias (VAs) that occur following an acute extensive anterior myocardial infarction (MI) usually respond to conventional antiarrhythmic regimes of treatment. Rarely, the VA may prove intractable to therapy. This report is of three patients who presented at varying time frames (3 h to 10 weeks) following an anterior MI. They exhibited sustained monomorphic ventricular tachycardia and hemodynamic instability despite multiple antiarrhythmic drug therapy, intravenous magnesium, direct-current cardioversion (DCCV), overdrive pacing (in one case), and intra-aortic balloon counterpulsation (IABP). Although there was no clinical evidence of continuing ischemia and although coronary angiography that was done in each case showed the infarct-related artery (IRA) to subtend akinetic areas on left ventricular (LV) angiogram, percutaneous transluminal coronary angioplasty (PTCA) of the IRA was done in all three cases. Reestablishing patency of the IRA helped in controlling the VA dramatically with average therapeutic doses of antiarrhythmic drugs. All three patients showed this control to have been maintained over a follow-up period of more than 1 year, with partial improvement in LV function and signal-averaged electrocardiogram negative for late potentials. Thus, in patients with extensive infarction and intractable VA, PTCA of the IRA may provide control of VA even in the absence of clinical signs of active ischemia or viable muscle mass.
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PMID:Coronary angioplasty for the control of intractable ventricular arrhythmia. 758 68

Thrombolytic therapy markedly reduces mortality and improves left ventricular function in patients with acute myocardial infarction. Improvement may be even more substantial with adjuvant therapy. Aspirin has proved to be effective adjuvant therapy to thrombolysis. Other antiplatelet agents that may be even more effective or have an additive effect with aspirin are being studied. The role of antithrombotic agents, especially heparin, as adjuvant therapy remains unclear. Immediate cardiac catheterization with angioplasty has been used as adjunct therapy, but its routine use is not recommended. Instead, elective angioplasty (cardiac catheterization, with revascularization as indicated) should be undertaken in patients with recurrent ischemia. Angioplasty as an alternative to thrombolysis may be advantageous in certain patients, such as those presenting in cardiogenic shock or with contraindications to thrombolysis. The role of primary angioplasty in other groups (eg, the elderly, those with anterior myocardial infarction) remains unclear, and further trials are necessary before it can be recommended over thrombolytic therapy. Equipment needed for angioplasty limits its practicality, whereas thrombolytic therapy can be administered at most US hospitals.
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PMID:Adjuvants to thrombolysis after acute myocardial infarction. Does adding antiplatelet agents, antithrombotics, or angioplasty make a difference? 799 77

Fatty acid scintigraphy is an interesting new technique for assessing the extent of myocardial infarction. We studied 19 patients with electrocardiographically verified first anterior myocardial infarction using radioiodinated phenylpentadecanoic acid and single photon emission computed tomography (SPECT). Besides the expected lesions in the territory of the left ascending coronary artery, a total of nine patients (47%) had severe (uptake < 50% of maximum) defects in the presumptive territory of the right coronary artery at rest. A link between the size of anterior injury and the occurrence of inferoposterior lesions was established. Over 20% paradoxical relative filling-in was seen in four of these inferoposterior defects in the subsequent exercise imaging, but only once anteriorly. Exercise-induced ischaemia (reduction in relative uptake > 20%) was demonstrated in 11 cases (58%). Ischaemia occurred most frequently in patients with small infarcts, and it did not coincide with the reversed redistribution. We conclude that the inferoposterior rest defects are unlikely to have been caused by technical artefacts or local injury, and should perhaps rather be linked with general strain in the left ventricle during the early phase of myocardial remodeling after anterior infarction. In any case, our results indicate that shortly after infarction myocardial viability should be evaluated very cautiously.
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PMID:False inferoposterior fatty acid uptake rest defects in patients with first anterior myocardial infarction. 804 18

Rapid reperfusion of the occluded coronary artery is essential for the reduction of mortality and complications of acute myocardial infarctions. Intravenous thrombolytic therapy using various thrombolytic substances has proven to be effective and easy to perform and has gained widespread acceptance for treatment of acute myocardial infarction. Because of several contraindications, as well as failure to achieve patency of the infarcted vessel in 25-30% of patients, severe bleeding complications, a time interval of 6 or more hours after suspected onset of myocardial infarction, and a high rate of recurrent ischemia, this treatment is currently limited to a small percentage of patients with acute myocardial infarction. Immediate percutaneous transluminal coronary angioplasty (PTCA) can be applied to nearly every patient presenting with acute myocardial infarction. Therefore, we offer immediate PTCA as the primary treatment to all of our patients presenting with acute myocardial infarction. Between January 1987 and December 1991, immediate PTCA was performed in 785 of 903 (87%) consecutive patients (aged 23-86 years, mean 61 +/- 10). 82% (640/785) of the patients were men. Anterior myocardial infarction was present in 372 patients (47%), inferior infarction in 413 patients (53%). 245 patients (31%) had 1-vessel disease, 221 patients (28%) two-vessel disease and 319 patients (41%) had three-vessel disease. 97 patients (12%) were in cardiogenic shock. In 675/785 patients (86%) the infarct related vessel was occluded (TIMI < or = 1). 86% of patients had a patent infarct related vessel (TIMI > or = 2) leaving the catheterization laboratory. The overall in-hospital mortality was 6.9% (54/785 patients), after exclusion of high-risk patients (age > 75 years, cardiogenic shock, PTCA under cardiopulmonary resuscitation) mortality decreased to 2.5%. Recurrent ischemia necessitated immediate repeat PTCA in 4.4% of the patients, in 8.1% of patients another elective PTCA was performed during hospitalization and 9.7% of patients were sent to surgery (4.0% on an emergency basis). 87% of all patients presenting with acute myocardial infarction could be treated successfully with immediate PTCA. With respect to the severely ill group of patients the primary success rate is high, the rate of reocclusion is low, and the overall mortality is extremely low. From our data, it is obvious that immediate PTCA compared to thrombolytic therapy is the superior treatment of myocardial infarction.
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PMID:[PTCA in the acute state of myocardial infarct: hospital course of 785 consecutive patients]. 806 43

The purpose of this study was to examine the relationship between the presence or absence of ST segment depression in inferior leads (II, III, and aVF) and ST segment elevation in lateral (I and aVL) or left precordial (V5 and V6) leads with the amount and location of myocardium at risk for infarction in patients with acute anterior myocardial infarction. Forty-three patients with anterior infarctions were injected with technetium 99m-sestamibi when they were first seen and underwent tomographic imaging to measure the amount and location of myocardium at risk. Patients with inferior ST depression (n = 10) compared with those without ST depression (n = 33) had perfusion defects that extended significantly further into the lateral wall (47 degrees vs 20 degrees, p = 0.04) and larger anterior injury vectors (6.47 vs 4.92, p = 0.008). There was no significant association with the percentage of myocardium at risk, disease of the right coronary artery, the presence of an inferior perfusion defect, or the size of the inferior injury vector. Among the patients with ST elevation in lateral leads (n = 16) compared with those without (n = 27), there was a significantly more lateral defect border (47 degrees vs 25 degrees, p = 0.007) and a larger anterior injury vector (6.07 vs 4.81, p = 0.01). There was no significant correlation with the percentage of myocardium at risk. A significant relationship could not be demonstrated between the presence of ST elevation in the left precordial leads and any measure of the amount or location of myocardium at risk. These data support the theory that inferior ST depression in patients with transmural anterior ischemia is a "reciprocal" finding and does not represent inferior ischemia. The presence of inferior ST depression or lateral ST elevation is associated with a more lateral perfusion defect. Neither of these ECG findings is associated with the amount of myocardium at risk for infarction.
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PMID:The relationship of inferior ST depression, lateral ST elevation, and left precordial ST elevation to myocardium at risk in acute anterior myocardial infarction. 836 5


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