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

The antiarrhythmic and antifibrillatory actions of the alpha 1-adrenoceptor antagonist prazosin were evaluated in conscious dogs 4-7 days after anterior myocardial infarction. Both the intravenous (i.v.) low single dose administration of 100 micrograms/kg and the higher multiple dose administration of 500 micrograms/kg every 6 h for 24 h failed to alter electrocardiographic intervals, ventricular effective refractory periods, or the induction of ventricular tachycardia (VT) by programmed ventricular stimulation. During the first 30 min of a subsequent episode of acute posterolateral ischemia, the incidence of ventricular fibrillation (VF) was reduced from 13 of 16 (81%) in vehicle-pretreated control animals to 2 of 8 (25%, p less than 0.05) in animals pretreated with 100 micrograms/kg prazosin and 3 of 8 (37%, p less than 0.05) in animals pretreated with 500 micrograms/kg prazosin every 6 h for 24 h. The continued administration of prazosin in the higher dose regimen, every 6 h for 24 h, significantly enhanced survival at 24 h after the onset of posterolateral ischemia in postinfarction dogs relative to the vehicle group [24-h survival: 1 of 16 (6%) vehicle v 4 of 8 (50%) in higher dose prazosin group, p less than 0.05]. These findings suggest that the blockade of alpha 1-adrenoceptor stimulation may be efficacious in preventing lethal ventricular arrhythmias associated with acute ischemia, despite the lack of effect on electrophysiologic parameters and induction of VT in the postinfarction setting.
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PMID:Alpha-adrenergic influences in canine ischemic sudden death: effects of alpha 1-adrenoceptor blockade with prazosin. 244 Nov 61

Recently, this laboratory has demonstrated an enhanced susceptibility toward the development of lethal ventricular arrhythmias occurring in response to acute posterolateral ischemia in dogs with previous anterior myocardial infarction in the presence of therapeutic serum concentrations of digoxin. In the present study, acute posterolateral myocardial ischemia was produced in the absence of previous myocardial infarction in 15 digoxin-pretreated (1.19 +/- 0.21 ng/ml serum digoxin, 5-7 days pretreatment) and 11 vehicle-pretreated dogs. The incidences of sudden ventricular fibrillation and of 24 h arrhythmic mortality in response to posterolateral ischemia were 4/15 (27%) vs. 1/11 (9%) (p = 0.23) and 7/15 (47%) vs. 4/11 (36%) (p = 0.27) for digoxin- vs. vehicle-pretreated dogs, respectively. Ventricular ectopic activity at 24 and 48 h after the onset of posterolateral ischemia was reduced significantly by both intravenous lidocaine (1.0-5.0 mg/kg) and verapamil (50.0-500.0 micrograms/kg) in the vehicle-pretreated dogs, whereas neither antiarrhythmic agent significantly suppressed ventricular ectopy in the digoxin-pretreated dogs. The mean sizes for developing posterolateral myocardial infarctions (percentage of left ventricle) were greater for the digoxin-pretreatment group (31.9 +/- 2.8%) vs. vehicle-pretreatment group (14.8 +/- 2.0%, p less than 0.001). These findings suggest that uncomplicated acute myocardial ischemia in the presence of serum concentrations of digoxin that are considered clinically therapeutic may result in the development of larger areas of developing myocardial infarction and in the occurrence of ventricular arrhythmias that are less sensitive to suppression with conventional antiarrhythmic agents.
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PMID:Effect of digoxin on the extent of injury and the severity of arrhythmias during acute myocardial ischemia and infarction in the dog. 245 14

Recently, this laboratory has demonstrated an enhanced susceptibility toward the development of ischemia-related lethal ventricular arrhythmias in the presence of therapeutic serum concentrations of digoxin in conscious dogs after myocardial infarction. The present study was performed to assess the effect of the interruption of cardiac sympathetic influences, via subacute left stellate ganglionectomy (LSGX), on digitalis-mediated ischemic ventricular arrhythmias. Commencing 4-5 days after anterior myocardial infarction, 11 dogs with LSGX and 14 sham controls were administered digoxin (0.0125 mg/kg/day i.v.) for 5-7 consecutive days. At baseline testing, programmed ventricular stimulation failed to initiate ventricular tachycardia in any postinfarction dog entered into this evaluation. After treatment, 11/11 digoxin + LSGX (1.33 +/- 0.10 ng/ml serum digoxin) and 14/14 digoxin-treated sham (1.23 +/- 0.14 ng/ml serum digoxin) dogs remained nonresponsive to programmed stimulation testing. The incidence of arrhythmic mortality in response to subsequent ischemia at a site remote from the infarcted anterior region was greater in the digoxin-treated sham group (1.22 +/- 0.21 ng/ml serum digoxin) than in the digoxin + LSGX group (1.33 +/- 0.10 ng/ml serum digoxin); mortality was 6/10 (60%) digoxin sham vs. 1/10 (10%) digoxin + LSGX, p less than 0.005. The underlying anterior myocardial infarct sizes (% of left ventricle: 6.8 +/- 2.3 vs. 6.6 +/- 1.1) did not differ between the digoxin sham and digoxin + LSGX groups. However, the digoxin sham controls developed larger posterolateral myocardial infarctions than did the digoxin + LSGX animals (% of left ventricle: 27.4 +/- 3.0 vs. 16.7 +/- 2.7, p less than 0.05). Norepinephrine concentrations in posterolateral through posteroseptal ventricular sections were not altered by LSGX in a separate group of digoxin-treated postinfarct dogs. The results suggest that left stellate ganglionectomy may reduce the incidence of digitalis-mediated malignant ventricular arrhythmias during ischemia, possibly due to a reduction in the severity of ischemic injury.
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PMID:Antiarrhythmic actions of left stellectomy in digitalis-mediated malignant ventricular arrhythmias in the postinfarcted canine heart. 245 51

To evaluate the usefulness of exercise Tl-201 myocardial scintigraphy, we performed positron emission tomography and conventional exercise Tl-201 emission computed tomography (ECT) in 33 patients with old anterior myocardial infarction (Q-MI: 24, non Q-MI: 9). N-13 ammonia was used as a blood flow tracer, and imaging was performed at rest and after multistage, symptom-limited ergometer exercise. After the administration of F-18 deoxyglucose (FDG) at rest in the fasting state, metabolic imagings were performed to evaluate regional exogenous glucose utilization. Tl-ECT showed fixed defects in 19 of the 33 patients, redistribution of the tracer in nine and no defects in five. All patients having partial or complete redistribution on Tl-ECT showed exercise-induced ischemia on PET with N-13 ammonia and an increased uptake of FDG in the hypoperfused region, suggesting the presence of ischemic but potentially salvageable tissues. In addition, PET with N-13 ammonia detected periinfarct ischemia in nine of the 19 with fixed defects on Tl-ECT, and increased uptakes of FDG were observed in eight of the 19. These results indicate that Tl-ECT may underestimate myocardial viability in clinically infarcted regions. Further studies are needed to determine whether restoring coronary flow improves wall motion in regions with fixed defects on Tl-ECT.
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PMID:[Usefulness of exercise Tl-201 myocardial scintigraphy: comparison with positron emission tomography]. 248 26

The in-hospital course of 500 consecutive patients treated with coronary angioplasty for acute myocardial infarction was reviewed in relation to their clinical and angiographic presentation and angioplasty outcome to determine which patients benefit most from successful angioplasty in this setting. Patient age was 56 +/- 11 years (mean +/- SD) and 78% were men; 46% had anterior myocardial infarction, 49% received concomitant intravenous thrombolytic therapy, left ventricular ejection fraction was 47 +/- 11% and median time to angioplasty was 4.7 h (range 1 to 24). Angioplasty was successful in 78% of patients and partially successful in 7% of patients; the overall in-hospital mortality rate was 10.2%. Multivariate analysis found six independent correlates (p less than 0.05) of in-hospital mortality: left ventricular ejection fraction less than or equal to 30%, lack of postangioplasty infarct artery patency, age greater than 65 years, recurrent ischemia after successful angioplasty, emergency bypass surgery and arterial pressure on admission to the catheterization laboratory less than 100 mm Hg. After consideration of these predictors of survival in multivariate analyses, angioplasty success still was independently correlated with improved in-hospital survival for patients with cardiogenic shock (p = 0.002) and anterior myocardial infarction (p = 0.007). A trend toward an independent beneficial effect of successful angioplasty on survival was also noted in patients with inferior wall infarction and precordial ST segment depression (p = 0.063) and for all patients who were hypotensive on admission to the catheterization laboratory, regardless of the infarct site (p = 0.057).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Implications for patient triage from survival and left ventricular functional recovery analyses in 500 patients treated with coronary angioplasty for acute myocardial infarction. 252 54

A patient admitted in a Coronary Care Unit with an acute anterior myocardial infarction, is presented. He had initially normal left ventricular function and, on the 11th day he had, suddenly, an acute pulmonary edema. The reason for this episode was detected through imaging techniques--echocardiography and isotopic studies, and consisted on infarct expansion with early evolution for apical aneurysm. Contrast angiography confirmed the presence of a huge aneurysm and two vessels disease. Tallium Scintigraphy showed reversible ischemia beyond necrotic areas. The patient was submitted to aneurysmectomy and received three aorto-coronary bypass. He is now doing well, in class I, NYHA. The discussion emphasizes the actual role of imaging techniques in the diagnosis of infarct expansion and early functional aneurysm. We discuss the prognostic of infarct expansion and the importance of perfusion studies on defining areas of myocardium in jeopardy, enabling a better surgical approach.
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PMID:[Early left ventricular dysfunction in acute myocardial infarct. Evaluation using imaging methods]. 263 14

We studied the efficacy of coronary angioplasty (PTCA) of the infarct-related artery in 29 patients with prior myocardial infarction by stress thallium scan. Twenty-seven patients had anterior myocardial infarction (single LAD disease), one had inferior (single RCA disease) and one had posterior (single LCX disease). According to the stress-redistribution thallium scintigraphic finding before PTCA, the patients were classified in 4 groups; (A): three patients with complete redistribution. (B): fourteen patients with incomplete redistribution. (C): seven patients with partial redistribution. (D): five patients with no redistribution. After PTCA, the parameters of residual ischemia in the infarct area (% RD and Thallium ischemic score = TIS) were improved significantly but those of infarct size (RD% uptake and Defect Score = DS) were improved slightly in group A. In group B and C, % RD, TIS, RD% uptake and DS were all improved significantly. In group D, TIS was improved slightly and DS was improved slowly 3 months after PTCA. Group A had high probability of viable muscle and group D had high probability of scar at the infarct zone. Group B and C showed intermediate type between group A and D. The change of infarct area after PTCA was variable in 4 groups but both residual ischemia and infarct size decreased in all groups. Thus, PTCA of infarct-related coronary artery is useful even in the patients with prior myocardial infarction.
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PMID:[Usefulness of coronary angioplasty (PTCA) of the infarct-related artery in patients with prior myocardial infarction--follow up of infarct zone pre- and post-angioplasty by stress thallium scan]. 281 Sep 2

The antiarrhythmic and antifibrillatory actions of dilevalol, the R,R-isomer of labetalol, were evaluated in conscious dogs 4 to 6 days after anterior myocardial infarction. The administration of dilevalol in a lower dose of 0.3 mg/kg i.v. q 8 hr or a higher dose of 3.0 mg/kg i.v. q 8 hr over a period of 24 hr failed to alter electrophysiologic parameters or significantly suppress the induction of ventricular tachycardia by programmed ventricular stimulation (incidence of ventricular tachycardia suppression: 4 of 25 [16%] dilevalol vs. 1 of 14 [7%] vehicle). Pretreatment with dilevalol failed to reduce arrhythmic death in response to the subsequent development of ischemia at a site distant to the area of previous infarction (mortality: 8 of 10 [80%] dilevalol vs. 14 of 14 [100%] vehicle), but did alter the nature of the lethal ischemic arrhythmia from ventricular fibrillation (incidence of ventricular fibrillation: 14 of 14 [100%] vehicle vs. 2 of 8 [25%] dilevalol, P less than .05) to bradyarrhythmia with eventual sinoatrial arrest (6 of 8 [75%] dilevalol). The administration of methylscopolamine, 0.01 mg/kg both i.v. and i.m., to postinfarction animals pretreated with dilevalol, 3.0 mg/kg i.v. q 8 hr for 24 hr, reduced significantly mortality in response to subsequent posterolateral ischemia (mortality: 4 of 10 [40%] dilevalol plus methylscopolamine vs. 14 of 14 [100%] vehicle, P less than .05). However, methylscopolamine alone failed to suppress the development of ischemic ventricular fibrillation in 5 of 6 (83%) postinfarction dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antifibrillatory efficacy of concomitant beta adrenergic receptor blockade with dilevalol, the R,R-isomer of labetalol, and muscarinic receptor blockade with methylscopolamine. 288 7

Environmental studies suggested that exposure to carbon monoxide (CO) increases cardiovascular mortality among patients with coronary artery disease. We investigated whether, in dogs with a healed anterior myocardial infarction at low and high risk for ventricular fibrillation, acute exposure to CO has adverse effects during acute myocardial ischemia combined with exercise. One month after myocardial infarction, 17 dogs had ventricular fibrillation and 16 survived during the combined exercise and ischemia test. These tests were then repeated in all dogs with different concentrations of carboxyhemoglobin (COHb) (from 5% to 15%). With 15% COHb, heart rate (HR) at rest and during exercise was higher (p less than 0.05) than in the control tests. Surprisingly, the reflex HR response to acute ischemia was also altered; namely, the HR reduction characteristic of the low-risk animals was anticipated and accentuated (-31 +/- 25 versus 2 +/- 30 beats/min, p less than 0.05). Conversely, the HR increase characteristic of the high-risk group was reduced by CO (44 +/- 52 versus 72 +/- 43 beats/min, p less than 0.05). With 15% COHb, malignant arrhythmias occurred in two of the low-risk dogs and in none of the high-risk dogs. In the latter, CO was tested with a combination of exercise work load and myocardial ischemia duration not associated with ventricular fibrillation (VF) in the control condition. This study demonstrated that brief exposure to CO (1) profoundly alters the reflex HR response to exercise and to acute myocardial ischemia and (2) does not enhance the occurrence of malignant arrhythmias in conscious dogs with a healed myocardial infarction.
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PMID:Carbon monoxide and lethal arrhythmias in conscious dogs with a healed myocardial infarction. 291 9

This study quantitatively evaluated the change in myocardial blood flow resulting from medical revascularization in patients with acute anterior myocardial infarction. Changes in great cardiac vein flow were measured using a thermodilution technique in 13 patients with acute infarction; 3 received intracoronary streptokinase and 10 percutaneous transluminal angioplasty. Average great cardiac vein flow during left anterior descending coronary artery occlusion was 62 +/- 6 ml/min and increased to 70 +/- 7 ml/min (p = 0.039) after arterial recanalization. There was significant individual variability in the great cardiac vein flow increments that was highly predictive of functional recovery as expressed by the change in ejection fraction at 7 to 10 days (r = 0.93, p = 0.0008). Incremental great cardiac vein flow was inversely correlated with the degree of residual stenosis and the duration of ischemia (r = 0.88, p = 0.0007). Patients with residual stenosis less than or equal to 50% had a significantly larger increase in great cardiac vein flow (14 +/- 5 ml/min) than did those with residual stenosis greater than 50% (0 +/- 2 ml/min, p = 0.026). Neither preinterventional left ventricular ejection fraction, hemodynamics nor age predicted incremental great cardiac vein flow. Therefore, quantitative measurements of great cardiac vein flow during medical revascularization in patients with an acute anterior myocardial infarction demonstrate variable reflow that is physiologically significant. A high grade residual stenosis and prolonged period of ischemia limit large increases in flow and prevent functional recovery. This study emphasizes the fact that recanalization in itself cannot be used as an indicator of the success of interventions designed to produce myocardial reperfusion.
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PMID:Quantitative measurement of coronary flow during medical revascularization (thrombolysis or angioplasty) in patients with acute infarction. 295 24


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