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Biomedical subjects

J Brugada

Publications and source records attributed to J Brugada.

At least 109 records · Page 6Linked to original sources
PubMed1993

The complexity of mechanisms in ventricular tachycardia.

Several pathophysiological substrates may be responsible for ventricular tachycardia (VT) occurring in the chronic phase of a myocardial infarction. Reentrant circuits can have anatomical or functional characteristics. Macroreentrant or microreentrant circuits have been described. Activation maps have shown that the circuit can be represented as a single loop or as a figure-of-eight reentrant pattern. All these different substrates have in common that they result in sustained monomorphic VT. The adequate treatment will probably be different for each one of them. In this article, some possible pathophysiological substrates of VT occurring in the chronic phase of a myocardial infarction are reviewed. Finally, we speculate on how catheter ablation may modify each one of the substrates.

Catheter Ablation↗
PubMed1993

Regional entrainment of atrial fibrillation studied by high-resolution mapping in open-chest dogs.

BACKGROUND: It recently has been demonstrated that during atrial fibrillation, a short and variable excitable gap exists, allowing regional control of atrial fibrillation by local stimulation. In the present study, we visualized the process of excitation during regional entrainment of atrial fibrillation by rapid pacing. METHODS AND RESULTS: In six open-chest dogs, the excitation of the left atrial free wall was mapped using a spoon-shaped mapping electrode (248 points). Episodes of atrial fibrillation were induced by burst pacing (50 Hz, 2 seconds). During atrial fibrillation, the electrograms showed rapid irregular activity with a median cycle length of 98 +/- 16 ms (mean +/- SD, n = 6). Rapid pacing in the center of the mapping electrode at intervals slightly shorter or longer than the median atrial fibrillation interval resulted in regional capture of atrial fibrillation. The window of entrainment was 16 +/- 5 ms. Mapping of atrial fibrillation showed that the left atrium was activated by fibrillatory wavelets coming from different directions. During entrainment, a relatively large area with a diameter of about 4 cm was activated by uniform wave fronts propagating away from the site of stimulation. The area of entrainment was limited by intra-atrial conduction block and by collision with fibrillation waves. Regional control of atrial fibrillation was lost by pacing either too slowly or too rapidly. In the first case, retrograde invasion of the area of entrainment by fibrillatory waves resulted in depolarization of the pacing site prior to the stimulus. Pacing too rapidly caused acceleration of atrial fibrillation by induction of local intra-atrial reentry circuits with a revolution time shorter than the pacing interval. CONCLUSIONS: During atrial fibrillation, an area with a diameter of about 4 cm can be entrained by local pacing. The resulting reduction in fibrillating tissue mass was not sufficient to terminate atrial fibrillation. Extension of the area of entrainment was limited by intra-atrial conduction block, whereas entrainment at a too high rate resulted in acceleration of atrial fibrillation by induction of local microreentry.

Animals↗
PubMed1993

Entrainment of reentrant ventricular tachycardia in anisotropic rings of rabbit myocardium. Mechanisms of termination, changes in morphology, and acceleration.

BACKGROUND: Entrainment of ventricular tachycardia can either terminate or change the rate and/or morphology of ventricular tachycardia. The purpose of this study was to elucidate the underlying mechanisms by mapping of entrainment of ventricular tachycardia. METHODS AND RESULTS: In 10 Langendorff-perfused rings of anisotropic rabbit left ventricular epicardium created by a cryoprocedure, ventricular tachycardia with a cycle length of 167 +/- 17 milliseconds was induced by incremental pacing. During transient entrainment (10 stimuli), the circulating wave was extinguished by collision with the paced antidromic wave, whereas ventricular tachycardia was reset by the paced orthodromic wave. At shorter pacing intervals, the site of collision shifted deeper into the circuit. Entrainment at high rates (104 +/- 11 milliseconds) resulted in either termination (n = 54), a change in morphology (n = 8), or acceleration (n = 6) of ventricular tachycardia. Termination of ventricular tachycardia was due to complete (84%) or partial (16%) block of the paced orthodromic wave. Partial block induced microreentry within the circuit, resulting in a reflected echo wave that terminated ventricular tachycardia. A change in morphology of ventricular tachycardia was due to reversion of the direction of propagation of the circulating wave around the obstacle. Acceleration of ventricular tachycardia was caused by double-wave reentry induced by block of the paced antidromic wave. In 28 cases, the sequence of activation during entrainment was not stable but changed from beat to beat due to varying arcs of conduction block. Block occurred predominantly (86%) during slow transverse propagation. Before termination, local oscillations in interval occurred, resulting in a shortening of the last local interval at the site of block by 10 +/- 6 milliseconds. CONCLUSIONS: Termination of ventricular tachycardia by entrainment was due either to complete orthodromic block or to a reflected echo wave. A change in morphology occurred when the direction of the circulating wave reversed. Acceleration of ventricular tachycardia was due to initiation of double-wave reentry. All changes were preceded by conduction block during one or more stimuli at one or multiple sites in the circuit. Block occurred predominantly during slow transverse propagation and was preceded by local oscillations in interval at the site of block.

Animals↗
PubMed1993

[Cardiotoxicity of local anesthetics].

The intravascular administration and the high blood resorption of local anesthetic agents are known to induce neurotoxic accidents. However, the use of potent local anesthetic drugs such as bupivacaine is responsible for serious cardiotoxic accidents with a mortality of about 50%. Indeed, bupivacaine induces both electrophysiologic and haemodynamic disturbances with the occurrence of conduction blocks, arrhythmias and cardiovascular collapse. Moreover, cardiotoxicity is worsened by: bupivacaine-induced sympathetic activation which facilitates tachycardia and arrhythmias, metabolic abnormalities such as hypoxia, acidosis, hyperkaliemia and hypothermia, pregnancy, diazepam pretreatment, and the antiarrhythmic drugs. In case of cardiac arrest, CPR must be made. In the other cases, the first treatment is to oxygenate, to intubate the trachea and to ventilate the lungs, and then to stop convulsions. Specific cardiac resuscitation remains controversial because it is based principally on experimental results. We demonstrated that the combination of clonidine and dobutamine is efficient to reverse both haemodynamic and electrophysiologic impairments induced by a large dose of bupivacaine in anesthetized dogs. Whatever the efficiency of specific resuscitation, it must be emphasized that prevention of toxic accident must always include: the best choice of local anesthetic drug (e.g.: lidocaine+alpha-2 agonist vs bupivacaine), test dose, aspiration and slow administration. Finally, the monitoring of regional anaesthesia must be similar to that in use for general anaesthesia and drugs and devices for resuscitation must be ready.

Anesthetics, Local↗
PubMed1992

Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report.

OBJECTIVES: The objectives of this study were to present data on eight patients with recurrent episodes of aborted sudden death unexplainable by currently known diseases whose common clinical and electrocardiographic (ECG) features define them as having a distinct syndrome different from idiopathic ventricular fibrillation. BACKGROUND: Among patients with ventricular arrhythmias who have no structural heart disease, several subgroups have been defined. The present patients constitute an additional subgroup with these findings. METHODS: The study group consisted of eight patients, six male and two female, with recurrent episodes of aborted sudden death. Clinical and laboratory data and results of electrocardiography, electrophysiology, echocardiography, angiography, histologic study and exercise testing were available in most cases. RESULTS: The ECG during sinus rhythm showed right bundle branch block, normal QT interval and persistent ST segment elevation in precordial leads V1 to V2-V3 not explainable by electrolyte disturbances, ischemia or structural heart disease. No histologic abnormalities were found in the four patients in whom ventricular biopsies were performed. The arrhythmia leading to (aborted) sudden death was a rapid polymorphic ventricular tachycardia initiating after a short coupled ventricular extrasystole. A similar arrhythmia was initiated by two to three ventricular extrastimuli in four of the seven patients studied by programmed electrical stimulation. Four patients had a prolonged HV interval during sinus rhythm. One patient receiving amiodarone died suddenly during implantation of a demand ventricular pacemaker. The arrhythmia of two patients was controlled with a beta-adrenergic blocking agent. Four patients received an implantable defibrillator that was subsequently used by one of them, and all four are alive. The remaining patient received a demand ventricular pacemaker and his arrhythmia is controlled with amiodarone and diphenylhydantoin. CONCLUSIONS: Common clinical and ECG features define a distinct syndrome in this group of patients. Its causes remain unknown.

Adult↗
PubMed1992

Which ventricular tachycardia is dangerous?

The treatment of ventricular arrhythmias remains a major challenge in cardiology. Several very helpful pieces of information can be obtained from the clinical history. The left ventricular function and the hemodynamic effects of a ventricular tachycardia are the two main factors affecting survival. Therefore, if a patient with sustained ventricular tachycardia presents with syncope or cardiac arrest, or if his functional class for dyspnea is III-IV (NYHA classification), he is a candidate for an implantable defibrillator while otherwise medical therapy is advised.

Decision Trees↗
PubMed1992

The electrocardiographic, clinical, and electrophysiologic spectrum of idiopathic monomorphic ventricular tachycardia.

Clinical, ECG, and electrophysiologic data from 47 patients who had episodes of sustained or nonsustained monomorphic VT with no evidence of structural heart disease were reviewed. According to the QRS configuration during tachycardia, four groups were distinguished. Nine patients had a right bundle branch block configuration and superior frontal plane QRS axis (group 1). Nine patients had a right bundle branch block configuration but an intermediate or right QRS axis (group 2). Group 3 consisted of five patients with a left bundle branch block configuration and a left axis deviation, and in group 4 there were 24 patients who had a left bundle branch block configuration with an intermediate or right frontal axis. Patients in group 1 had dizziness during tachycardia less frequently, but they needed cardioversion to terminate their arrhythmias more often. They experienced tachycardia during exercise less often, and tachycardia was not initiated during exercise testing. They had fewer ventricular premature beats according to the Holter recording. During the electrophysiologic study, VT was induced and terminated by pacing more often in this group. Patients with idiopathic VT with a right bundle branch block configuration and a superior axis seem to be a unique group of patients with idiopathic VT, and reentry seems to be the most likely arrhythmia mechanism in this group. The other ECG configurations share the same clinical and electrophysiologic characteristics, which suggest that the underlying arrhythmia mechanism is the same.

Adult↗
PubMed1992

Radiofrequency ablation of symptomatic but benign ventricular arrhythmias.

Two cases are presented where ablation of severely symptomatic ventricular arrhythmias not responding to medical therapy was accomplished with radiofrequency current application. After a routine programmed stimulation protocol, a quadripolar ablation catheter with a 4-mm tip was advanced percutaneously into the left ventricle in one case and into the right ventricle in the second case; and after precise pace mapping, the arrhythmogenic focus was successfully ablated using radiofrequency current. The postablation ambulatory recording revealed virtual eradication of ventricular ectopy in both cases. In conclusion, in severely symptomatic cases of "benign" ventricular arrhythmias, radiofrequency ablation offers an effective therapeutic alternative.

Adult↗
PubMed1992

Echo-wave termination of ventricular tachycardia. A common mechanism of termination of reentrant arrhythmias by various pharmacological interventions.

BACKGROUND: Based on epicardial mapping, different mechanisms of termination of reentrant ventricular tachycardia by various pharmacological interventions are described. METHODS AND RESULTS: In 40 Langendorff-perfused rabbit hearts, rings of anisotropic left ventricular epicardium were made by a cryoprocedure. Sustained monomorphic ventricular tachycardia based on continuous circus movement of the impulse around the ring was induced by programmed stimulation. Increasing doses of heptanol (n = 10), potassium (n = 10), tetrodotoxin (n = 6), RP62719 (a new class III drug) (n = 4), flecainide (n = 5), and propafenone (n = 5) were administered to terminate ventricular tachycardia. Epicardial mapping (248 points) was used to study the mechanism of termination of ventricular tachycardia. In 28 of 40 hearts, ventricular tachycardia terminated because the drugs produced complete conduction block of the impulse in a segment of the reentrant pathway. In the remaining 12 hearts (heptanol, n = 2; potassium, n = 3; tetrodotoxin, n = 2; RP62719, n = 2; flecainide, n = 1; and propafenone, n = 2), termination of ventricular tachycardia occurred by collision of the circulating impulse with a spontaneous antidromic wave front reflected within the circuit. This phenomenon occurred when the circulating impulse encountered an arc of functional conduction block that did not extend along the whole width of the ring. As a result, the impulse dissociated into a continuing orthodromic circulating wave and a returning antidromic echo-wave caused by microreentry within the ring. CONCLUSIONS: Independent of their mechanisms of action, sodium channel blockers, electrical uncouplers, and class III drugs terminate reentrant ventricular tachycardia either by complete conduction block or by collision of the impulse with an echo-wave.

Animals↗
PubMed1992

RP 58866 and its active enantiomer RP 62719 (terikalant): blockers of the inward rectifier K+ current acting as pure class III antiarrhythmic agents.

The present article presents an overview of the pharmacologic profile of the benzopyran derivative RP 58866, a racemic mixture, and of RP 62719 (terikalant), its active enantiomer. In normal cardiac tissues studied in vitro, both drugs dose-dependently prolonged the atrial and ventricular action potential but affected neither the upstroke of the action potential nor the diastolic potential. Patch-clamp experiments demonstrated that the prolongation of the action potential induced by the drugs is due to a specific blockade of the inward rectifier K+ current. In vivo, intravenous administration to anesthetized dogs of low doses of RP 62719 consistently induced bradycardia and prolonged the atrial, nodal, and ventricular refractory periods, but did not affect the conduction velocity. Because of these properties, RP 58866 and RP 62719 exert potent antiarrhythmic and antifibrillatory actions both at the atrial and ventricular levels in various experimental models of arrhythmia. Our results demonstrate that RP 58866 and RP 62719 are K(+)-channel blockers acting as pure class III antiarrhythmic drugs.

Action Potentials↗
PubMed1992

Reversal of electrophysiologic and hemodynamic effects induced by high dose of bupivacaine by the combination of clonidine and dobutamine in anesthetized dogs.

The ability of clonidine and dobutamine to correct bupivacaine-induced cardiac electrophysiologic and hemodynamic impairment was evaluated in an experimental electrophysiologic model on closed-chest dogs. Five groups (n = 6) of pentobarbital-anesthetized dogs were given atropine (0.2 mg/kg IV). Group 1 was given a saline solution; all other dogs were given bupivacaine (4 mg/kg IV) over a 10-s period. Group 2 was given only bupivacaine. Group 3 was given clonidine (0.01 mg/kg IV) over a 1-min period. Group 4 was given a dobutamine infusion at 5 micrograms.kg-1.min-1. Group 5 was given the combination of clonidine and dobutamine. Bupivacaine induced bradycardia, prolonged atrioventricular conduction time (PR interval), atrioventricular node conduction time (AH interval), His-Purkinje conduction time (HV interval), and QRS duration. Bupivacaine decreased left ventricular (LV) dP/dt max and increased LV end-diastolic pressure (LVEDP). Clonidine improved QRS duration and HV interval but enhanced AH interval, bradycardia, and hemodynamic depression induced by bupivacaine. Dobutamine infusion improved LV dP/dt max but did not modify bupivacaine-induced ventricular electrophysiologic impairment. The combination of clonidine and dobutamine corrected not only the electrophysiologic impairment induced by bupivacaine but also the hemodynamic depression. As the HV interval and the QRS duration could be correlated with ventricular conduction velocities, we conclude that (a) clonidine reversed the slowing of ventricular conduction velocities induced by bupivacaine, and (b) the combination of clonidine and dobutamine was able to correct the cardiac disturbances induced by bupivacaine in anesthetized dogs.

Animals↗
PubMed1992

Electrophysiologic and arrhythmogenic effects of bupivacaine. A study with high-resolution ventricular epicardial mapping in rabbit hearts.

It has been shown that administration of toxic doses of bupivacaine may induce ventricular dysrhythmias. However, the mechanism of these dysrhythmias is still unknown. The present study was designed to test the hypothesis that bupivacaine facilitates the occurrence of reentrant ventricular dysrhythmias. High-resolution ventricular epicardial mapping was used to study the effects of 0.2, 0.5, 1.0, and 5.0 micrograms/ml bupivacaine in 11 Langendorff-perfused rabbit hearts. Five hearts were kept intact (intact heart). In six other hearts, a thin layer of epicardium was obtained by an endocardial cryotechnique (frozen heart). Bupivacaine induced ventricular dysrhythmias in 3 of 5 intact hearts at 5.0 micrograms/ml. In 3 of 6 frozen hearts, 0.2 micrograms/ml bupivacaine facilitated the induction of ventricular tachycardia by programmed electrical stimulation. Epicardial mapping showed that all tachycardias were based on reentry of the impulse around an arc of functional conduction block. Moreover, bupivacaine significantly prolonged the ventricular effective refractory period and slowed longitudinal and transverse conduction velocity in a dose- and use-dependent manner. It is concluded that bupivacaine facilitates induction of reentrant ventricular dysrhythmias in isolated rabbit heart.

Animals↗
PubMed1991

Clinical and electrophysiologic characteristics of exercise-related idiopathic ventricular tachycardia.

In 37 (70%) of 53 patients with idiopathic ventricular tachycardia (VT), episodes were mainly related to exercise (group 1). These patients were younger (33 +/- 14 vs 44 +/- 18 years, p = 0.015) and more often had dizziness during VT (71 vs 40%, p = 0.003) than the 16 patients in whom VT was not exercise-related (group 2). Patients in group 1 needed cardioversion less often to terminate the arrhythmia (4 (11%) vs 6 (40%), group 2 [p = 0.04]). VT was initiated during exercise testing in 62% of patients in group 1 but in only 1 patient in group 2 (p = 0.0004). Induction of clinical VT during programmed stimulation was observed in a similar percentage in group 1 (49%) and group 2 (50%) patients. Isoproterenol infusion facilitated the induction of VT in 9 of 20 (45%) group 1 and in 2 of 8 (25%) group 2 patients (p = not significant). After a mean follow-up of 2.9 +/- 2.5 years, 8 (22%) group 1 patients and 5 (31%) group 2 had at least 1 episode of symptomatic VT. Only 1 patient died suddenly. Class III drugs were the most useful in preventing recurrences. Beta-blocking agents were of little value in both groups. Patients with VT and a structurally normal heart have a good prognosis despite recurrences of their arrhythmia. The relation of the arrhythmia to exercise has no prognostic implications.

Adult↗
PubMed1991

Longitudinal dissociation of atrioventricular accessory pathways.

Unusual properties of atrioventricular (AV) accessory pathways were found during electrophysiologic investigations in four patients (three men and one woman). Anterograde longitudinal dissociation of the accessory pathway was observed in two patients and retrograde longitudinal dissociation in two others. Two patients had an accessory pathway with a slow conduction time, one in anterograde direction and one in retrograde direction. These observations further expand our knowledge of the spectrum of electrophysiologic properties of accessory AV pathways.

Adult↗
PubMed1991

Clinical presentation and prognosis of left main coronary artery disease in the 1980s.

Clinical presentation and course were studied in 127 consecutive patients with angiographically proven left main coronary artery disease. Mean age was 62 (37-79) years. Thirteen patients (10%) had no history of chest pain, seven (5%) had atypical chest pain, and the remaining 107 (85%) typical angina pectoris. Eighty-two patients (65%) had unstable angina, 73 had suffered a myocardial infarction (MI) in the past, and 50 (68%) had post MI angina pectoris. The electrocardiogram was analysed in 102/125 patients during an episode of chest pain and also when they were without chest pain. Outside an episode of chest pain the ST segment was normal in 42 patients (32%), the T wave was normal in 50 patients (38%) and both the ST and T were normal in 33 patients (25%). During chest pain all patients had an abnormal ECG, the most frequent pattern being ST segment depression in leads V3, V4 and V5 (with maximal depression in V4), and ST segment elevation in leads V1 and aVR. The average number of leads with ST-T abnormalities was 6.4. A symptom-limited exercise test on a treadmill with 12-lead ECG monitoring was performed in 89 patients. The exercise test was abnormal in 88 patients (99%), most of whom (74 patients) were already in the first or second stage of the Bruce protocol. The most frequently observed abnormality was ST segment depression of 2 mm or more in leads V4, V5, and V6, and ST segment elevation in leads V1 and aVR. The systolic blood pressure during exercise fell or remained at the same level in 38 patients (43%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗