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Action potentials and ECGs were recorded from isolated guinea pig hearts during low flow (10% of control) and zero flow myocardial "ischaemia" and during subsequent reperfusion. During myocardial "ischaemia" ventricular tachycardia and ventricular fibrillation were significantly more frequent during low flow, than zero flow "ischaemia" (P less than 0.01). Reperfusion arrhythmias required a minimum ischaemic period of 10 to 15 min, were most frequent following 20 to 30 min of "ischaemia", being fewer following 60 min of "ischaemia" (P less than 0.05). The degree of "ischaemia" had little effect on reperfusion arrhythmias following 20 to 30 min of "ischaemia". Both types of "ischaemia" reduced action potential amplitude, Vmax, and duration, and increased conduction time. During low flow "ischaemia", electrophysiological change reached a nadir at 12 +/- 3 (mean +/- SEM) min, and in all cases spontaneous electrophysiological recovery in action potentials and conduction time preceded ventricular arrhythmias, which occurred at 18 +/- 3 min. In contrast during zero flow "ischaemia" electrophysiological changes were more marked and no recovery was observed. Refractory periods were initially prolonged by both forms of "ischaemia", followed by a marked shortening. The initial prolongation was more marked and subsequent shortening less during zero than low flow "ischaemia". Reperfusion induced electrophysiological recovery in all hearts; however reperfusion VF was preceded by further shortening of action potential duration and refractory period. These results indicate that residual flow during myocardial "ischaemia" is associated with spontaneous electrophysiological recovery and more frequent ventricular arrhythmias. The severity of "ischaemia" is less important than its duration for the development of reperfusion arrhythmias.
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PMID:Arrhythmias and cellular electrophysiological changes during myocardial "ischaemia" and reperfusion. 688 12

To define the utility of high-dose barbiturate therapy following an episode of complete global cerebral ischemia, we investigate the effects of 60 mg/kg of thiopental given to cats five minutes after resuscitation from 12, 14, or 16 min of electrically induced ventricular fibrillation (VF). All aspects of the arrest, resuscitation, with post-arrest care were carefully controlled, with the EEG becoming isoelectric 20-25 s after the onset mean resuscitation time of 2.5 +/- 0.2 (SEM) min. For any given duration of VF, there were no differences (control vs thiopental) in any pre- or post-arrest parameters (blood pressure, blood gases, electrolytes, etc.) A total of 68 resuscitated cats were entered into various treatment and control groups, and all but one group received 20-24 h of post-resuscitation paralysis, mechanical ventilation, and ICU support before being extubated. Cats received an additional six days of aggressive nursing care, and daily examinations were performed with the assignment of a neurologic deficit score (NDS) between 0 (normal) and (brain dead). Autopsies were performed to determine the cause of death in animals which died before the end of the seven-day observation period. The early post-arrest period was marked by the occurrence of repetitive, rhythmic bursts of high-frequency electroencephalographic (EEG) activity (? seizures) in 38 per cent of control animals (16/42, all arrest times combined). Ten of these animals died as a result of severe neurologic injuries. By contrast, only 12 per cent of treated cats (3/26) developed similar EEG patterns (P less than 0.05) and there were no neurologic deaths in the thiopental groups. The differences in the incidence of neurologic deaths (control vs. thiopental) was significant (P less than 0.02). The change in overall mortality did not quite reach significance (36 per cent vs. 21 per cent), and treatment had no effect on the incidence of deaths due to cardiovascular causes (e.g., myocardial infarctions). In spite of the effects on mortality, treatment had no effect on the neurologic function of survivors (assessed by NDS). These findings suggest that thiopental improved survival rates by suppressing an unusual post-arrest EEG pattern (? anticonvulsant effect), but had no additional cerebral protective effects.
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PMID:The neurologic effects of thiopental therapy following experimental cardiac arrest in cats. 709 47

The effects of carbocromene, 4 mg/kg intravenously, prior to coronary artery occlusion plus 40 microgram/kg/min during coronary artery occlusion and reperfusion on ventricular fibrillation threshold (VFT) were studied in pentobarbital-anesthetized open-chest dogs and compared to controls receiving saline. Coronary artery occlusion decreased VFT by 46 +/- 4% (mean +/- SEM, p less than 0.02) in controls and by 22+/-3% in drug-treated animals. Reperfusion of the occluded artery decreased VFT by 83+/-7% (p less than 0.01) in controls and by 47+/-5% in carbocromene-treated hearts (p less than 0.02). Hemodynamics did not change in the drug group during coronary artery occlusion. In controls, blood pressure and dP/dtmax decreased while heart rate, end-diastolic pressure and ST-T segments increased significantly during both coronary artery occlusion and reperfusion. The underperfused, ischemic region was assessed by staining with Evans blue and involved 34+/-3% of the left ventricular mass in controls but only 27+/-3% in carbocromene-treated hearts (p less than 0.05). These results indicate protective effects of carbocromene on ventricular vulnerability in canine hearts during coronary artery occlusion and subsequent reperfusion.
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PMID:Effects of carbocromene on ventricular fibrillation during acute myocardial ischemia in anesthetized dogs. 713 63

Isolated rabbit hearts undergo ventricular depolarization when exposed to 0.5 mM K--Krebs during 30 to 45 min. A ventricular tachyarrhythmia develops when these hearts are allowed to repolarize in 1.5 mM K--Krebs. Ventricular fibrillation usually follows. These arrhythmias do not cease spontaneously. Initially, perfusion with 0.5 mM K hyperpolarized the membrane to -100 +/- 1.2 mV (means +/- SEM), decreased the plateau level, greatly increased the action potential duration, and slowed down intraventricular conduction, despite the level of membrane polarization and a high rate of rise of the upstroke. After a delay of 15 to 30 min, a progressive depolarization occurred and a stable potential level of -61 +/- 1.9 mV was reached. The arrhythmia elicited by perfusion with 1.5 mM K was of ventricular origin but did not appear when the previous exposure to 0.5 mM K was reduced to 10 min. Addition of verapamil (1.0 microM) to the 1.5 mM K medium did not prevent the early appearance of the arrhythmia, but restored driven electrical activity after variable delays despite the persistence of alterations in the action potential configuration. Verapamil also abolished the slow depolarizing phase of the upstroke. It is proposed that the abnormal electrical activity arose in a partly depolarized Purkinje network and it may have been triggered by the electrical nonhomogeneity created by the repolarization of ventricular cells in an extracellular K+ concentration of 1.5 mM.
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PMID:Experimental arrhythmia elicited by low K perfusion. 716 50

Procaine hydrochloride was added to cardioplegia and studied for its efficacy in stabilizing the postischemic rhythm after aortic declamping in cardiac surgery. Fifty-six patients scheduled for coronary artery bypass grafting (CABG), were included in a randomized, double-blind study. The patients were anesthetized with isoflurane, low-dose fentanyl, diazepam, and pancuronium. In the study group (28 patients), St. Thomas' Hospital cardioplegic solution II (Plegisol) was prepared with 1 mM procaine. The control group (28 patients) was given the same cardioplegia with saline. Ventricular fibrillation (VF) occurring after declamping was treated with direct current (DC) shock (8-12-12-20 J). There were no significant differences with regard to demographic properties or anesthesiologic and surgical treatment. Two patients (7%) in the procaine group required DC shock for VF, compared to 28 (100%) in the control group (P < 0.001). The amount of lidocaine (mean +/- SEM) given for resistant dysrhythmias was 3.6 mg +/- 3.6 in the procaine group compared to 35.7 mg +/- 9.2 in the control group (P < 0.002). One patient in each group required temporary pacing. The number of synchronized DC shocks for conversion of atrial fibrillation was lower in the procaine group (P < 0.05). The enzyme release the first day after surgery was lower in the procaine group (P < 0.05). Procaine (1 mM) in cardioplegia stabilizes the postischemic rhythm in CABG surgery in humans without any observed adverse effects.
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PMID:Procaine is effective for minimizing postischemic ventricular fibrillation in cardiac surgery. 748 80

Acrivastine and terfenadine are second-generation antihistamines with similar pharmacologic profiles and comparable clinical efficacies for allergic rhinitis. However, terfenadine therapy has been associated with cardiovascular side effects that include prolonged QT interval, torsades de pointes, and ventricular fibrillation (VF). We examined the adverse effects induced by terfenadine on evoked action potentials (APs) in isolated canine cardiac Purkinje fibers and determined whether acrivastine causes similar disturbances in this preparation. Terfenadine produced a statistically significant decrease in the maximal rate of increase in the AP (dV/dt) at 10(-7) M, which corresponds to the highest plasma concentration observed clinically. The IC50 (mean +/- SEM) value for terfenadine-induced inhibition of dV/dt was 1.3 +/- 0.3 x 10(-6) M. The decrease in dV/dt caused by terfenadine became more pronounced with faster rates of stimulation. Acrivastine at a concentration of 10(-5) M, a value 10 times higher than plasma concentrations observed in clinical studies, caused no significant changes in AP duration (APD) or dV/dt. The IC50 (mean +/- SEM) value for the acrivastine-induced inhibition of dV/dt was estimated to be 8.0 +/- 3.7 x 10(-3) M. Terfenadine blocked the evoked AP at 3 x 10(-6) M, whereas no block was observed with acrivastine at 10(-3) M. The effective serum concentration of acrivastine is approximately 100 times higher than that of terfenadine. Because the IC50 value for inhibition of dV/dt for acrivastine is approximately 6,000 times greater than that for terfenadine, we estimate that acrivastine is approximately 60-fold less likely to cause disturbances in cardiac conduction than terfenadine.
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PMID:Terfenadine alters action potentials in isolated canine Purkinje fibers more than acrivastine. 750 35

We compared the effects of class I-IV antiarrhythmic agents on the ventricular fibrillation threshold (VFT) induced by electrical stimulation directly on the myocardium in anesthetized, open-chest guinea pigs. VFT was assessed by determining the intensity (mA) of electrical current required to induce ventricular fibrillation (VF) and is expressed as a percentage change of the baseline premedication value. The following antiarrhythmic agents or their solvent were administered intravenously (i.v.) to pentobarbital-anesthetized animals (n = 6-12 per group): class I antiarrhythmic agent encainide (1.5 mg/kg); class II antiarrhythmic agents atenolol (2.5 mg/kg), metoprolol (2.5 mg/kg), and nebivolol (2.5 mg/kg); class III antiarrhythmic agents dofetilide (0.08 mg/kg), terikalant (0.04 mg/kg), and DL-sotalolol (10 mg/kg); and class IV antiarrhythmic agent verapamil (0.16 mg/kg). The antiarrhythmic compounds or their solvents resulted in the following changes in the VFT at 15 min after treatment: saline control, 1 +/- 14% (mean +/- SEM) from its baseline value; 10% hydroxypropyl-beta-cyclodextrine (CD), 4 +/- 13%; encainide, 183 +/- 46% (p < 0.05 vs. saline); atenolol, 66 +/- 23% (p > 0.05 vs. saline); metoprolol, 89 +/- 25% (p > 0.05 vs. saline); nebivolol, 224 +/- 58% (p < 0.05 vs. 10% CD); DL-sotalol, 485 +/- 119% (p < 0.05 vs. saline); dofetilide, 357 +/- 69% (p < 0.05 vs. saline); terikalant, 487 +/- 183% (p < 0.05 vs. saline), and verapamil, -17 +/- 21% (p > 0.05 vs. saline). At the doses used, all compounds significantly reduced heart rate (HR).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antifibrillary action of class I-IV antiarrhythmic agents in the model of ventricular fibrillation threshold of anesthetized guinea pigs. 756 54

Low values of heart rate variability (HRV, a marker of vagal tone) and baroreflex sensitivity (BRS, a marker of vagal reflexes) identify patients at higher risk soon after myocardial infarction (MI). However, it is still unknown whether HRV and BRS correlate with malignant arrhythmias after the recovery from the transient post-MI autonomic disturbance. This study assessed whether HRV and BRS would differ in patients with malignant ventricular arrhythmias occurring long after MI compared with those in a control population. Twenty-eight patients entered the study: 14 patients with episodes of sustained ventricular tachycardia or ventricular fibrillation occurring more than 1 year after MI, age (mean +/- SEM) 64 +/- 2 years, and left ventricular ejection fraction 34% +/- 3% (VT/VF group) were compared with 14 similar patients with no ventricular tachycardia (control group). Mean RR interval was not different in the two groups (844 +/- 37 msec in VT/VF and 892 +/- 24 msec in control group). Also, no difference was found in any time- or frequency-domain measure of heart rate variability. However, patients in the VT/VF group had a significantly lower baroreflex sensitivity compared with patients in the control group (4.2 +/- 0.5 vs 8.0 +/- 1.1 msec/mm Hg, p = 0.008). Thus BRS but not HRV was reduced in patients with life-threatening ventricular arrhythmias occurring long after MI. A persistent depression of vagal reflexes may play a role in the occurrence of malignant arrhythmias, and analysis of BRS may potentially be helpful in the identification of patients at high risk long after myocardial infarction.
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PMID:Baroreflex sensitivity, but not heart rate variability, is reduced in patients with life-threatening ventricular arrhythmias long after myocardial infarction. 766 Oct 63

The effect of chronic angiotensin converting enzyme (ACE) inhibition on the incidence of fatal ventricular fibrillation during regional myocardial ischaemia and reperfusion is not known. A reduction in cardiac angiotensin II and/or a vagomimetic response may result in antiarrhythmic activity. Pigs pre-treated with the ACE inhibitor trandolapril 0.3 mg.kg-1 or placebo orally for 10 days were subjected to thoracotomy. The left anterior descending coronary artery was ligated (CAL) for 20 min and reperfused for 45 min. Trandolapril decreased cardiac ACE activity and prevented the fall in the ventricular fibrillation threshold (VFT) during ischaemia: after 5 min of ischaemia the VFT in the trandolapril group was 25.5 +/- 4.6 mA (mean +/- SEM) vs 13.1 +/- 2.2 mA in the placebo group (P < 0.05). Trandolapril also decreased the incidence of spontaneous ventricular fibrillation during reperfusion to 1/6 vs 6/7 in the placebo group (P < 0.05). Heart rate in the trandolapril group fell. During ischaemia, trandolapril increased blood flow in the non-ischaemic zone, but decreased blood flow in the central ischaemic zone of the left ventricle. Similarly it decreased tissue levels of phosphocreatine in this zone. During reperfusion trandolapril increased blood flow both in non-ischaemic and central ischaemic zones. Chronic oral pre-treatment with trandolapril resulted in marked antifibrillatory effects which were associated with inhibition of cardiac ACE activity and a decreased heart rate.
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PMID:Chronic oral pretreatment with the angiotensin converting enzyme inhibitor, trandolapril decreases ventricular fibrillation in acute ischaemia and reperfusion. 792 22

Predictors of survival and arrhythmia recurrence for patients with implanted defibrillators have been reported but patients with sustained, well-tolerated ventricular tachycardia were often excluded from these trials. Arrhythmia recurrence and survival in populations including these patients have been less well studied. The purpose of the present study was to examine predictors of spontaneous ventricular arrhythmias and mortality in patients who received a tiered therapy antitachycardia pacemaker/defibrillator for ventricular tachycardia, fibrillation, or both. Three hundred thirty-seven patients who received a Ventritex CADENCE tiered therapy antitachycardia device at one of 19 participating centers between July 11, 1989 and March 4, 1991 are included in this retrospective analysis. Diagnostic summary data and stored electrograms telemetered from the implanted device were assessed to determine characteristics of recurrent arrhythmias. Mean follow-up was 360 +/- 10 (SEM) days. Thirty-three patients died during follow-up. At least one recurrent ventricular arrhythmia was observed in 205 patients (61%). A total of 7,539 episodes were observed with a mean of 37 +/- 5 per patient. Patients with recurrent ventricular arrhythmias were slightly but significantly older (64 +/- 0.7 vs 59 +/- 1.2 years; P < 0.001) but were not distinguished by gender or underlying structural disease. Patients whose presenting arrhythmia was monomorphic ventricular tachycardia were more likely to experience recurrent ventricular arrhythmias (69% recurrence rate) than patients presenting with ventricular fibrillation or polymorphic ventricular tachycardia (46% recurrence rate; P < 0.001). Cycle length of spontaneous tachycardia was also a predictor of arrhythmia recurrence. Patients having slower ventricular arrhythmias were less likely to remain recurrence free. Mean left ventricular ejection fraction was similar for patients with and without recurrences. Younger age and absence of arrhythmia recurrence but not presenting arrhythmia were predictors of survival. We conclude that age and presentation with monomorphic ventricular tachycardia are important predictors of arrhythmia recurrence for this patient population. Exclusion of patients with monomorphic ventricular tachycardia underestimates the rate of recurrent ventricular arrhythmias and utilization of device therapy.
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PMID:Predictors of device activation for ventricular arrhythmias and survival in patients with implantable pacemakers/defibrillators. CADENCE Investigators. 799 19


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