Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042510 (ventricular fibrillation)
 10,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MDL 11,939 (alpha-phenyl-1-[2-phenylethyl]-4-piperidine-methanol) is a new class III antiarrhythmic agent that was evaluated for antiarrhythmic activity in anesthetized dogs. Intravenous (i.v.) administration of MDL 11,939 (1, 3, and 10 mg/kg) increased left ventricular effective refractory periods. Q-T interval, and Q-Tc in a dose-related way. The effects of MDL 11,939 on ventricular refractoriness were similar to those observed with administration of identical doses of d-sotalol, with the exception that those produced by MDL 11,939 lasted longer. Intraduodenal administration of 10 mg/kg MDL 11,939 also increased left ventricular effective refractory period (LV ERP). The increase in left ventricular refractoriness produced by MDL 11,939 occurred without a significant increase in QRS duration. MDL 11,939 (10 mg/kg i.v.) also protected against induction of ventricular tachycardia (VT) and ventricular fibrillation (VF) induced with programmed electrical stimulation (PES) in anesthetized dogs with chronic 4- to 7-day myocardial infarctions. In comparison, antiarrhythmic effects of bretylium (10 mg/kg i.v.) against PES-induced ventricular arrhythmias were dependent on additional administration of propranolol (0.1 mg/kg i.v.), whereas propranolol alone (0.1 mg/kg i.v.) was ineffective. The results observed with MDL 11,939 are consistent with its in vitro class III antiarrhythmic action and suggest utility for this agent in treatment of VT and VF.
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PMID:Antiarrhythmic and electrophysiologic effects of MDL 11,939, a novel class III antiarrhythmic agent in anesthetized dogs. 170 Feb 8

Glibenclamide (Gli) 0.3, 1, 3 mg.kg-1 and tolbutamide (Tol) 3, 10, 30 mg.kg-1 iv 10 min before ischemia or ouabain infusion prevented ventricular fibrillation induced by ischemia in rat and arrhythmias induced by ouabain in guinea pig. Gli 10 mumol.L-1 and Tol 1 mmol.L-1 increased APD and ERP in rat ventricular muscle. Gli 0.1, 1, 10 mumol.L-1 and Tol 0.01, 0.1, 1 mmol.L-1 prevented and reversed the shortening of APD and ERP induced by hypoxia in guinea pig ventricular muscle. These effects of Gli and Tol were dose-dependent. The results confirmed that Gli and Tol were effective on arrhythmias induced by ischemia and ouabain by blocking ATP-sensitive potassium channel.
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PMID:Effects of glibenclamide and tolbutamide on ischemia- and ouabain-induced arrhythmias and membrane potentials of ventricular myocardium from rat and guinea pig. 181 92

To examine the influence of sympathetic nerve activity on ventricular arrhythmogenicity in the dog with chronic hypokalemia, an electrophysiologic study was performed before and after bilateral stellectomy (BS) in 10 dogs with chronic hypokalemia (2.8 +/- 0.1 mEq/L), which was created by feeding a low-potassium diet and by administering furosemide over a four-week period, and the results were compared with those obtained from 10 dogs with normokalemia (4.7 +/- 0.3 mEq/L) from being fed an ordinary diet over a four-week period. Before BS the incidence of electrically induced ventricular arrhythmias was higher in the hypokalemic than in the normokalemic dogs. After BS it was decreased considerably in the hypokalemic but not in the normokalemic dogs. Heterogeneity of effective refractory period (delta ERP), which was determined as the difference between the longest and shortest effective refractory periods in three sites of the right and left ventricles, was greater in the hypokalemic than in the normokalemic dogs before BS. The delta ERP decreased slightly in the two groups both before and after BS. There was, however, no significant difference in delta ERP in the two groups both before and after BS. Ventricular fibrillation threshold (VFT) was significantly lower in the hypokalemic dogs than in the normokalemic dogs before BS (p less than 0.005). VFT was elevated in the two groups after BS. Percent increase in VFT after BS was significantly greater in the hypokalemic than in the normokalemic dogs. In conclusion, sympathetic nerve activity may play an important role in the increase in ventricular arrhythmogenicity in the presence of chronic hypokalemia.
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PMID:Influence of sympathetic nerve activity on ventricular arrhythmogenicity in the dog with chronic hypokalemia. 195 75

Paroxysmal atrial fibrillation (PAF) in patients with manifest WPW syndrome can be a life-threatening arrhythmia by deterioration into ventricular fibrillation. In patients with asymptomatic WPW pattern, the first PAF may lead to ventricular fibrillation or sudden death. Therefore, the purpose of this study was to predict a fatal PAF in patients with asymptomatic WPW pattern. The patient population was divided into two groups: (1) 145 patients with manifest WPW syndrome, excluding intermittent ones (32 with an episode of PAF, 49 with AV reciprocating tachycardia alone, and 64 without any episode of paroxysmal tachyarrhythmia), and (2) mixed group of patients with and without WPW syndrome (36 with an episode of PAF and 66 without PAF). The results were as follows: (1) (a) out of 32 patients with WPW syndrome and PAF, 8 patients were observed to have both the shortest preexcited R-R interval of less than 200 msec during PAF and the shortest antegrade effective refractory period of the accessory pathway (ERP-AP) of less than 250 msec, 7 of whom had dizziness or syncope during PAF and 2 died suddenly during the follow-up period; (b) 21 (32.8%) out of 64 patients with asymptomatic WPW pattern showed the shortest antegrade ERP-AP less than 250 msec; (2) patients with PAF had a higher tendency to develop repetitive atrial firing (RAF), as well as fragmented atrial activity (FAA), which were induced using programmed atrial stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prediction of a fatal atrial fibrillation in patients with asymptomatic Wolff-Parkinson-White pattern. 227 12

Seventy-two patients with sustained ventricular tachycardia or syncope of unknown origin underwent electrophysiologic evaluation before and after therapy with flecainide (200-300 mg day-1). In all patients, sustained ventricular tachycardia or ventricular fibrillation was inducible during control electrophysiologic study. During flecainide therapy, sustained ventricular tachycardia (VT) was no longer inducible in 18 patients (25%) whereas in 54 patients, VT was still inducible. In five of the latter patients, VT became more difficult to induce (overall efficacy 32%). The rate of VT decreased from 214 +/- 49 beats min-1 during the control electrophysiologic study to 178 +/- 48 beats min-1 during flecainide (P less than 0.01). The ERP of the right ventricle increased from 251 +/- 27 ms during the control study to 267 +/- 34 ms on flecainide (P less than 0.01). Mean ejection fraction and mean LVEDP did not differ between responders and non-responders, yet the presence of a left ventricular aneurysm correlated with a lack of antiarrhythmic response to flecainide. VT rate as well as VT morphology during the control study discriminated between responders and non-responders; 11% of patients with VT-rate less than or equal to 230 beats min-1 responded to oral flecainide compared with 31% with a VT rate greater than 230 beats min-1 at control. 26% with induced monomorphic VT responded, compared with 100% with induced VF during the control study. 18 of 23 responders were discharged on flecainide. During a mean follow-up of 26 +/- 18 months, two patients experienced a recurrence of VT and in one patient, flecainide had to be discontinued due to side-effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Efficacy of flecainide in pacing-induced sustained ventricular tachyarrhythmias: correlation to clinical parameters and tachycardia-characteristics. 251 4

1. In a placebo-controlled study of the antiarrhythmic and electrophysiological properties of atenolol and mexiletine, programmed electrical stimulation (PES) was performed in three groups of six conscious greyhounds, 7-30 days after coronary artery ligation. 2. In the placebo group, repeated PES challenge resulted in the consistent induction of ventricular tachycardias (VT) in 4/6 dogs and ventricular fibrillation in 2/6. Atenolol prevented arrhythmia induction in 4/6 dogs, one continued to demonstrate a VT and one died (P less than 0.05 compared with placebo). In the mexiletine group 5/6 dogs continued to demonstrate a VT and one died. 3. Electrocardiographic parameters were not affected by any treatment. There was no change in blood pressure in any group but when compared with placebo, heart rate fell (P less than 0.05) after atenolol (256 micrograms kg-1) and increased (P less than 0.05) after mexiletine (16 mg kg-1). Effective (ERP) and functional (FRP) refractory periods did not change after mexiletine, but ERP was prolonged (P less than 0.05) after atenolol. 4. The results indicate that atenolol but not mexiletine is effective in preventing re-entrant arrhythmias in this conscious canine model. Antiarrhythmic efficacy may be related to a fall in heart rate and/or a prolongation of refractoriness.
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PMID:Atenolol, but not mexiletine, protects against stimulus-induced ventricular tachycardia in a chronic canine model. 292 74

In our earlier experiments administration of the stable PGI2 analogue: 7-oxo-PGI2-ephedrine salt to dogs resulted in a late-appearing and long-lasting protection from coronary ligation induced ischaemia as well as from postocclusion and reperfusion arrhythmias. Objective of the present study was to evaluate the extent and duration of antiischaemic and antiarrhythmic action induced by a single dose 50 ug/kg i.m. 7-oxo-PGI2 in dogs subjected to myocardial ischaemia evoked by left anterior descending coronary artery (LAD) ligation at different intervals (2, 6, 24, 48, 72 hours and 2 weeks) after treatment. After anaesthesia and thoracotomy the electrophysiological parameters - sinus cycle length (SCL), corrected sinus node recovery time (CSNRT), atrial and ventricular functional refractory period (AFRP, VFRP), and atrio-ventricular effective refractory period (A-V ERP) - were determined by means of computer controlled programmed electrical stimulation. Then the animals were subjected to LAD occlusion for 25 minutes and subsequent reperfusion. 7-oxo-PGI2 pretreatment considerably protected against myocardial ischaemia i.e. there was significant reduction in ST-segment elevation, the number of extrasystoles (ES) and the incidence of ventricular fibrillation (VF). The antiischaemic action started 2 or 6 hours after the drug administration, however, the maximal protection - indicated by the diminution of ischaemic epicardial ST-segment elevation - as well as the most striking reduction in postocclusion and reperfusion arrhythmias could be observed 48 hours after the single dose of 7-oxo-PGI2 and in case of two weeks treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:7-oxo-PGI2 induced late appearing and long lasting antiischaemic and antiarrhythmic action in dogs. 307 67

Electrophysiologic properties of the left ventricle, vulnerability to ventricular arrhythmias and regional myocardial blood flow (RMBF) of the left ventricle were examined during superposition of acute ischemia on a healed myocardial infarction. The left circumflex coronary artery (LCX) was ligated in 13 dogs with a 28-day-old anteroapical infarction. Six (46%) of 13 dogs had reproducible ventricular tachycardia in response to programmed ventricular stimulation before LCX ligation. Ventricular fibrillation could be induced in 2 of these 6 dogs. After LCX ligation, 11 (85%) of 13 dogs had ventricular arrhythmias induced by ventricular stimulation. Nine of 13 dogs had ventricular tachycardia and 7 of 13 dogs had ventricular fibrillation. The heterogeneity of the effective refractory period (delta ERP) and the local intraventricular conduction time (LIVCT) in the border and the infarct zones of the left ventricle increased significantly after LCX ligation. RMBF in the border and the infarct zones were markedly decreased by LCX ligation. The magnitude of reduction of RMBF was correlated significantly with the prolongation of LIVCT. In conclusion, acute critical reduction of the collateral blood supply causes a more heterogeneous refractory period and conduction delay in the preexisting ischemic area of the heart, increasing the vulnerability to lethal ventricular arrhythmias.
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PMID:Influence of collateral flow reduction on electrophysiologic properties of preexisting ischemic area and inducibility of ventricular arrhythmias in the dog. 344 40

Electrophysiologic investigations have been performed in 13 patients with symptomatic WPW syndrome. The effective refractory periods of the right atrium (AERP), the antegrade effective refractory periods of the accessory pathway (AP-ERP) during sinus rhythm and at different cycle length, the shortest RR-intervals with preexcitation during atrial fibrillation (RR-AF) and the appearance of block in the AP during incremental atrial pacing have been measured. The data collected during sinus rythm (SR) and at different pacing rates were analyzed and compared. During SR (cycle length 851 +/- 157 ms) AERP measured 263 +/- 56 ms and AP-ERP 309 +/- 55 ms. At a cycle length of 450-550 ms, AERP measured 221 +/- 36 ms and AP-ERP 250 +/- 35 ms, and at a cycle length of 400-450 ms AERP was 213 +/- 35 ms and AP-ERP 230 +/- 42 ms. The mean RR-AF was 253 +/- 35 ms. A significant correlation was found between AERP and AP-RP at a cycle length of 400-450 ms (r = 0.92), but not between AP-ERP and RR-AF at any cycle length. Block in the AP occurred at a mean pacing cycle length of 280 +/- 42 ms. The electrophysiologic measurements of patients with syncope did not differ from patients without syncope in our group. The data show that in patients with a long AP-ERP (greater than 290 ms) during SR an increase of the heart rate leads to a significant shortening of the AP-ERP. No relevant correlation was found between AP-ERP and mean RR-AF. Patients with AP-ERP shorter than RR-AF appear to be a high-risk subgroup for ventricular fibrillation during AF.
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PMID:[Effect of heart rate on the refractory period of the accessory atrioventricular pathway in Wolff-Parkinson-White syndrome]. 408 83

The pathomechanism of arrhythmias consecutive to a prolonged electrical systole --the long QT syndrome--was studied by local hypothermia in the heart. Local increase in the QT-interval (long QT with unhomogeneous repolarisation) was induced at a circumscribed area of the right ventricle by perfusion of the mid- and end-sections of the right coronary with cooled blood. The effect of local prolongation of QT on the arrhythmic susceptibility of the heart was studied by means of programmed electrical stimulation. Induced local hypothermia of the heart was found to increase the QT-interval of the ECG-tracings, also if QT had been corrected for heart rate. The local ECG tracings showed a considerable increase of the QT-interval at the selected right ventricular area under the effect of induced hypothermia but in relation to QT (ERP/QT) it diminished. The long QT in association with an unhomogeneous repolarization went hand in hand with an increased irritability of the heart. Early ventricular impulses were found to elicit extrasystolic runs, ventricular tachycardia or ventricular fibrillation. The results indicate that the cause of tachyarrhythmias consecutive to the long QT-syndrome may be ascribed to the inhomogeneity of repolarization on the one hand, and to the shortness of ERP in relation to the QT-duration on the other.
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PMID:Increased susceptibility of the heart to arrhythmia in response to QT-prolongation associated with unhomogeneous repolarization: further data concerning the pathomechanism of arrhythmias associated with long QT-syndrome. 718 48


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