[Intracavitary cardiac electric fulguration in the treatment of ventricular tachycardias].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Brugada.
Explore the source record for details and available documents.
The possibility that an asynchronous increase in the ventricular monophasic action potential duration is the basis of the quinidine-induced torsade de pointes, has led us to study the electrophysiological effects of increasing doses of intravenous quinidine. We measured the monophasic action potential duration and the ventricular effective refractory period at several right ventricular myocardial sites in the anaesthetized dog. Our results showed that quinidine induces a dose-dependent prolongation in ventricular effective refractory period and in ventricular monophasic action potential duration. These increases were uniform throughout the right ventricle. No variations in repolarization or in refractoriness were observed between the four ventricular sites studied. The results suggest that quinidine does not have a direct effect on dispersion of repolarization, and that mechanisms other than its direct electrophysiological action are involved in the development of torsade de pointes.
The purpose of this study was to find out whether non-invasive transoesophageal pacing could effectively replace right intra-atrial pacing for the indirect evaluation of sinus node and atrioventricular (AV) node function. In a population of 17 patients the corrected sinus node recovery time (CSRT), the atrio-sinu-atrial conduction time (ASACT) and Wenckebach's point (W) were calculated by intracavitary pacing, then by transoesophageal pacing. There was no significant difference between the two methods in pre-pacing sinus cycle. With right intra-atrial pacing, mean CSRT value was 365 +/- 54 ms (with 5 values greater than 520 ms), mean ASACT value was 229 +/- 29 ms (with 8 values greater than 220 ms), and W occurred at a mean cycle length of 425 +/- 29 ms. With transoesophageal pacing, mean CSRT value was 406 +/- 87 ms (with 5 values greater than 520 ms), mean ASACT value was 222 +/- 17 ms (with 8 values greater than 220 ms), and W occurred at a mean cycle length of 408 +/- 26 ms. The two methods correlated very closely for CSRT and W (r = 0.97) and relatively well for ASACT (r = 0.84). The number of CSRT and ASACT values regarded as prolonged was the same with the two methods; 84% of recorded (i.e. maximal) CSRT values occurred with the same length of pacing cycle. There was no statistically significant difference between the two methods in the calculation of CSRT and ASACT, but W occurred at a slightly shorter cycle (p less than 0.05) with transoesophageal pacing. Thus, transoesophageal pacins is a non-invasive, easy to perform method for indirect exploration of sinus node and AV node function in patients who do not require subnodal conduction studies.
Following acute myocardial infarction, fragments of human cardiac myosin can be detected in plasma by means of monoclonal antibodies to myosin heavy chains from the left human ventricle. The cumulative amounts of myosin released during the first 9 post-infarction days are proportional to the size of the infarct (Tao Ming et al., in the press). The purpose of our study was to evaluate the effectiveness of a fibrinolytic treatment administered in the acute phase of myocardial infarction by measuring in the plasma, the circulating fragments of human cardiac myosin. Three groups of patients with acute myocardial infarction were investigated: 13 patients (group A) received a conventional treatment; 8 patients (group B) were treated with intravenous streptokinase without success, i.e. with persistence of the coronary occlusion; 9 patients (group C) were successfully treated with intravenous streptokinase, resulting in recanalization of the coronary artery. We found that the cumulative amount of myosin released during the first 9 post-infarction days was significantly lower in patients successfully treated with streptokinase [group C: (3.8 +/- 2.3) 10(3) ng/ml/day]. There was no difference in cumulative release of myosin between control patients [group A: (7.0 +/- 3.3) 10(3) ng/ml/day] and patients with unsuccessful fibrinolytic treatment [group B: (10.0 +/- 4.1) 10(3) ng/ml/day]. These results were unrelated to the localisation of the infarct. It is concluded that measuring the cumulative amounts of myosin released is a means of evaluating the effectiveness of fibrinolytic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
The cardiac electrophysiological effects of Penticainide, a new antiarrhythmic agent, were studied by means of intracardiac electrodes in the anaesthetized dog. Intravenous administration of 5 mg/kg of Penticainide reduced the sinus rate and prolonged the sinus node recovery time. Atrial refractory periods increased. Anterograde intranodal conduction slowed and nodal refractoriness increased. Conduction time in the His-Purkinje tissue and ventricle increased, as did the ventricular refractory periods. Monophasic action potential duration was not altered by the drug in the atrium or the ventricle. The mechanism of action of Penticainide as an antiarrhythmic drug seems to be correlated to its membrane effects: inhibition of the fast-inward current, responsible for the marked effects on His-Purkinje and ventricular tissues; and inhibition of the slow-inward current, suggested by its effects on sinus node and atrio-ventricular node.
In anesthetized dogs, it has already been shown that cibenzoline (4 mg/kg i.v.) possesses class 1 anti-arrhythmic properties. In this work, the cardiac electrophysiologic effects of cibenzoline (1 mg/kg i.v.) were studied before and after propranolol (0.2 mg/kg i.v.) treatment. Cibenzoline caused a slight tachycardia, a reduction of conduction velocity in the His-Purkinje system and in the ventricle, but no significant effects in the atria and the atrioventricular node were detected. On the contrary, when dogs were given the beta-adrenoceptor blocking agent propranolol, cibenzoline produced major effects in the slow response structures, especially in the sinus node and the atrioventricular node (bradycardia and depression of the atrioventricular nodal conduction). No further effects were observed on the His-Purkinje system and ventricle as compared to administration of cibenzoline alone. In dogs, cibenzoline given i.v., had no effects on the slow response systems, probably because of sympathetic nervous system intervention since the class 4 effects of cibenzoline appeared after beta-adrenoceptor blockade.
Radiofrequency catheter ablation has been established as a non-surgical curative treatment modality for the management of patients with paroxismal supraventricular tachycardia. Success rates for atrioventricular node reentrant tachycardia and accessory pathway-mediated macroreentrant tachycardia exceed 95%. Results in patients with atrial flutter and atrial tachycardia are encouraging, with success rates exceeding 75%.
Brugada's syndrome is one of the main causes of sudden death in young adults without a structural heart disease. This is an electrical cardiac illness secondary to a mutation of SCN5A gene of chromosome 3 that has a dominant autosomic transmission pattern. This mutation implies the dysfunction of the sodium channel that increases the Ito, loosing the dome of the epicardiac action potential phase two. An "all or none" repolarization pattern ensues and gives rise to a phase two reentry. This kind of reentry is responsible for the initiation and perpetuation of malignant ventricular arrhythmias among these patients. The clinical characteristics of the syndrome are the right bundle branch block, ST segment elevation from V1 to V3 leads and sudden death or syncope. In some patients, a pharmacological test must be done with ajmaline or procainamide to unmask the electrocardiographic changes. At present, the only effective treatment is the implantable cardioverter defibrillator (ICD). This device has the capability to reduce mortality from 40% annually to 0% at ten years. Pharmacological treatment is not useful.
The effects of increasing plasma levels of bupivacaine on sinus node, atrial tissue, atrio-ventricular node, His-Purkinje system and ventricular tissue were evaluated in 16 thiopental-anesthetized dogs. A bolus of bupivacaine administered over 3 min was followed by an infusion over 60 min. Three dosages were administered: 1 mg/kg followed by 0.5 mg/kg/hr in 4 dogs, 2 mg/kg followed by 1 mg/kg/hr in 6 dogs and 4 mg/kg followed by 2 mg/kg/hr in 6 dogs. Electrophysiological parameters of sino-atrial node, atria, atrioventricular node, His-Purkinje system and ventricle and mean aortic pressure were recorded before the administration of bupivacaine (control) and 5, 15, 30, 45 and 60 min after the initial bolus. Blood samples were taken at the same time. On the basis of plasma bupivacaine concentrations, the dogs were divided in 6 groups: group 0 (control), group I (less than 1 microgram/ml), group III (1.5 to 2 micrograms/ml), group IV (2 to 3 micrograms/ml) and group V (greater than 3 micrograms/ml). At plasma concentrations less than 1.5 micrograms/ml bupivacaine prolonged conduction times over the His-Purkinje system and ventricle. At plasma levels greater than 1.5 microgram/ml it depressed also the sinus node and the atrioventricular node functions. No statistically significant difference was found between the control group and the other groups for mean aortic pressure, pH, PaCO2, PaO2 and kalemia. In conclusion, it is suggested that bupivacaine behaves as a class I antiarrhythmic drug at the lower plasma concentrations and as a class I and class IV antiarrhythmic drug at higher plasma concentrations.
Explore the source record for details and available documents.