High-risk accessory pathway radiofrequency ablation in a transplanted donor heart: a case report.
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Adolescent↗
Biomedical subjects
C Sebag
Publications and source records attributed to C Sebag.
[Electrocardiographic aspects of atrial fibrillations].
The electrocardiographic analysis of atrial fibrillation is usually easy. However, some cases may be difficult to interpret: the organisation and voltage of the fibrillation waves can be very variable leading to appearances of atypical flutter in cases with large "f" waves or, conversely, in cases with low voltage fibrillation, to those of sinus mode dysfunction. The ventricular response may be slow: the conduction is usually delayed in the atrioventricular node where concealed conduction plays an important role in determining the ventricular response. Regular ventriculogrammes correspond to a junctional or ventricular escape rhythms. Aberrant conduction in the His-Purkinje system may sometimes be observed after long diastoles (phase 4 block) but often terminates short, preceded by long cycles (phase 3 block). It is usually easy to differentiate them from ventricular ectopics or preexcitation by careful examination and application of classical diagnostic criteria.
Atrial Fibrillation↗
[Radiofrequency catheter ablation: theoretical and technical aspects].
Radiofrequency currents produce circumscribed tissue necrosis by progressive and localised heating. Endocardial application via the percutaneous approach with a specific electrophysiological catheter enables destruction of the anatomical substrate of many cardiac arrhythmias. The technique is well tolerated due to the absence of barometric phenomena and general anaesthesia, and the possibility of modulating the energy delivered, which explains why it has supplanted fulguration in most indications. The technological evolution aims to increase the lesional power and decrease the number of complications. This implies the development of catheters capable of delivering greater currents without the risk of thrombus formation and of generators dependent on electrical or thermal parameters. The low incidence of complications reported by centres using the technique is based on an excellent understanding of the technique, the use of appropriate material, the surveillance of parameters which allow detection of unwanted effects and the respect of a strict operation protocol. In the absence of these precautions, the wide diffusion of this technique, favored by its low cost and relative simplicity, may be associated with an increase in the number of side effects which could be lethal. This cannot be accepted in a technique with such wide indications, including arrhythmias with a usually benign long-term prognosis.
Animals↗
[Electrophysiological mechanisms of ventricular arrhythmia in myocardial infarction].
In experimental models of coronary occlusion, the physiopathology of ventricular arrhythmias varies with its timing, there being three main phases: early, late and chronic. The early phase covers the first 30 minutes and is dominated by tachycardias and fibrillations resulting from multiple micro-reentry circuits which are the consequence of major changes in conduction and excitability created by acute ischaemia. These arrhythmias may be triggered by extrasystoles which have a different mechanism related to the injury current generated in the border zone between ischaemic and healthy cells. The late phase lasts about 72 hours: it is characterised by polymorphic ventricular extrasystoles and bursts of relatively slow ventricular tachycardia. Much more rapid tachycardia can be induced by stimulation. The origin of these arrhythmias is usually in the surviving Purkinje fibres of the subendocardium. The mechanisms are variable: abnormal automaticity, reentry or activity triggered by delayed after depolarisations. During the chronic phase, reentrant tachycardia is possible but only when induced by stimulation. Delayed conduction is the consequence of non-uniform antisotropism related to the disorientation of the myocardial fibres caused by fibrosis. In the clinical situation, most research has been centered on sustained monomorphic ventricular tachycardias of the chronic phase. Their mechanism is almost exclusively reentry (the circuits usually being located in the subendocardium) as suggested by the triggering and interruption of clinical tachycardias by stimulation, the recording of fragmented activation or prepotentials at the site of emergence of the tachycardia and the phenomena of pacing.
Arrhythmias, Cardiac↗
Cardiopulmonary response during exercise of a beta 1-selective beta-blocker (atenolol) and a calcium-channel blocker (diltiazem) in untrained subjects with hypertension.
The effects of beta-blockers and calcium-channel blockers on cardiopulmonary response during exercise are not well characterized. Sixteen sedentary patients with essential hypertension underwent a randomized, double-blind, cross-over study comparing atenolol and diltiazem sustained-release 300 mg, each administered during 6 weeks, after a 15-day run-in placebo period. Neither atenolol nor diltiazem significantly affected maximal exercise duration, maximal oxygen uptake, ventilatory threshold, or any of the ventilatory parameters during exercise. With atenolol, the maximal oxygen pulse was significantly increased and compensated for the decrease in heart rate during exercise. Atenolol and diltiazem do not limit maximal exercise tolerance in untrained hypertensive subjects, but the circulatory profile is more preserved with diltiazem.
Adult↗
[Drug treatment of chronic ventricular arrhythmia].
The treatment of chronic ventricular arrhythmias depends on the severity and tolerance of the arrhythmia. Extrasystoles, even repetitive, in the healthy heart, are usually respected when asymptomatic or treated with betablockers in first intention when symptomatic. These drugs should also be proposed for patients with ischemic heart disease and non-sustained ventricular tachycardia, a situation in which Class I antiarrhythmics should be avoided. The prevention of sustained ventricular tachycardial may be empirical, with betablockers and/or amiodarone, or guided by the results of pharmacological tests during endocavitary electrophysiological studies.
Adrenergic beta-Antagonists↗
[How to evaluate the arrhythmogenic risk after myocardial infarction?].
The risk of sudden arrhythmic death after myocardial infarction is high, especially during the first months. The evaluation of this risk should be performed before hospital discharge in the same way as residual ischaemia and left ventricular function, which are independent risk factors for arrhythmia, are assessed. Holter monitoring provides information not only about ventricular hyperexcitability (especially the detection of unsustained ventricular tachycardia) but also about the activity of the autonomic nervous system by analysis of variations of the sinus rhythm, the decrease of which carries a poor prognosis. The search for an arrhythmogenic substrate requires signal averaged electrocardiography, but although the absence of late potentials carries a good prognosis, the positive predictive value of this investigation is very low. The association of non-invasive indices of poor prognosis greatly increases the probability of a major arrhythmic event; this may require consideration of programmed ventricular pacing, another method of substrate and risk assessment, which has the added advantage of sometimes indicating the most appropriate therapy.
Arrhythmias, Cardiac↗
[Percutaneous ablation of atrioventricular junction by radiofrequency current in resistant atrial arrhythmia. Results of a series of 24 patients].
Catheter ablation of the atrioventricular junction may be proposed for the treatment of certain atrial arrhythmias resistant to antiarrhythmic therapy. One of the methods currently being evaluated uses radio-frequency energy which has certain advantages compared with direct current ablation because of the progressive and limited lesions it produces. This technique was used in 24 patients with atrial arrhythmias resistant to antiarrhythmic therapy. The radio-frequency energy was delivered without general anaesthesia with HAT 100 and 200 (OSYPKA) generators in the unipolar mode (average 17.4 watts) for an average period of 22.3 +/- 8 seconds. The catheter (8F USCI suction catheter in the first 18 patients and a 7F Polaris Mansfield, deflectable catheter with a large distal electrode in the remainder) was positioned at the nodo-hisian junction at a point where the two distal electrodes recorded a large atrial deflection and the smallest possible hisian potential. The conduction defects induced during the acute phase generally remain stable in cases of complete atrioventricular block and tend to regress in cases of incomplete atrioventricular block despite initial control of atrioventricular conduction. During follow-up (21 +/- 16 months), 14 patients (58%) remained in complete atrioventricular block, 4 patients (17%) had controlled atrioventricular conduction with an acceptable ventricular rate with associated previously ineffective antiarrhythmic therapy. Radio-frequency ablation was a failure in 6 patients (25%). There were no haemodynamic, rhythmic or ischaemic complications during the acute phase or during follow-up. These results suggest radio-frequency energy is a seductive alternative to direct current ablation for percutaneous modification of atrioventricular conduction in patients with refractory atrial arrhythmias. However, simple modulation of atrioventricular conduction gives aleatory results due to the tendency to regression during follow-up. On the other hand, complete atrioventricular blocks created by radio-frequency energy are generally definitive and are associated with a junctional escape rhythm which is usually stable.
Adult↗
Complete atrioventricular block following mediastinal irradiation: a report of six cases.
Complete atrioventricular block (AVB) following radiotherapy has been reported rarely, usually after high dose mediastinal irradiation for Hodgkin's disease or lung or breast carcinoma. We report six new cases of episodic complete infranodal AVB, requiring permanent pacemaker implantation. The mean age was 48-years old (ranging from 25-60) at the first Adams Stokes attack, mean delay was 12 years after irradiation (10-18), and mean radiation dose was 5,200 rads (4,000-6,500). All patients had abnormal interval electrocardiograms (right bundle branch block in two, left bundle branch block in three, alternating left and right bundle branch block in one). Electrocardiograms during the episode of AVB or Holter recordings were consistent with infranodal block in all patients; electrophysiological study performed in five patients confirmed infranodal AVB in four, and one was normal. Pericardial disease was constant, which included pericardial constriction in four patients. Two patients died after failure of pericardiectomy to improve congestive heart failure, due to epicardial, myocardial, and endocardial involvement. Noncardiac mediastinal lesions were present in four cases. Since this delayed complication may occur in patients of such age that the relation between the AVB and the chest irradiation is questionable, we propose the following etiologic criteria; high radiation dose (over 4,000 rads); delay of 10 years or more; abnormal interval tracings; pericardial involvement; and associated cardiac or mediastinal radiation-induced lesions.
Adult↗
Predictive value of electrophysiologic studies during treatment of ventricular tachycardia with the beta-blocking agent nadolol. The Working Group on Arrhythmias of the French Society of Cardiology.
Sixty patients with recurrent inducible sustained ventricular tachycardia were prospectively treated with nadolol (40 or 80 mg/day). Old myocardial infarction was present in 43 patients and dilated cardiomyopathy in 12. In group I (n = 36), nadolol was given alone, whereas in group II (n = 24), previously ineffective treatment with amiodarone was continued in combination with nadolol. Left ventricular ejection fraction was higher in patients in group I (0.40 +/- 0.12) than in group II (0.30 +/- 0.10, p less than 0.01) patients. Electrophysiologic study was repeated after short-term treatment with nadolol, which was continued regardless of the results of this test, according to the scheme of the parallel approach. Recurrence of spontaneous tachycardia or sudden death occurred in 21 patients after 10 +/- 9.2 months; sustained tachycardia was inducible in 19 on nadolol therapy. The remaining 39 patients (of whom 21 had inducible tachycardia while taking the drug) have had no recurrence of tachycardia after 27.8 +/- 9.3 months of follow-up study. Sensitivity, specificity and predictive value of a positive and negative test were 90.5%, 46%, 47.5% and 90%, respectively. The results differ between group I and group II patients, the latter having a high percent of false positive responses. This difference is even more obvious with respect to left ventricular ejection fraction: the predictive value of a positive test was 86% when ejection fraction was greater than 0.40 and 39% when it was less than 0.40.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Clinical electrophysiologic properties of magnesium and correlations with its anti-arrhythmia efficacy in acquired torsade de pointes].
Recently, intravenous administration of low doses of magnesium has proved remarkably effective in the treatment of acquired torsade de pointe, but its electrophysiologic effects remain poorly understood. Three clinical cases are reported in three distinct situations (quinidine treatment, hypokalemia, bradycardia with complete atrioventricular block). These cases confirm the efficacy of magnesium, which acts without notable modification of ventricular cycles or the duration of repolarization. In ten patients undergoing intracavitary exploration, the electrophysiologic parameters were analyzed before and after injection of magnesium sulfate (35 mg/kg). Only three parameters were significantly altered; the corrected sinusal recovery time (increase from 245 +/- 92 ms to 296 +/- 96 ms), the effective nodal refractory period (increase from 333 +/- 98 ms to 346 +/- 93 ms), and the Wenckebache period (decrease from 157 +/- 28/min to 144 +/- 21/min). No changes were noted in other parameters, notably ventricular (QT interval, QRS duration, HV interval, and effective ventricular refractory period). The arrhythmic action on the ventricle is therefore remarkable and is not accompanied by patent electrophysiologic effects. The efficacy of magnesium in torsade de pointe may suggest action on calcium currents.
Aged↗
Rupture of the stomach and the esophagus after attempted transcatheter ablation of an accessory pathway by direct current shock.
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Aged↗
Reduced sensitivity of human platelets to PAF-acether following ticlopidine intake.
We investigated in 9 patients the effect of a 7-day treatment by Ticlopidine (250 mg b.i.d.) on washed platelets activation by PAF-acether in comparison with adenosine 5'-diphosphate (ADP) and arachidonic acid (AA). Aggregations induced by ADP were totally suppressed upon drug administration. AA-induced aggregations were partly but significantly inhibited (p less than 0.05). Responses of platelets to PAF-acether before treatment differed from patient to patient. A paired Student's test and a two-way analysis of variance showed a significant inhibitory effect of Ticlopidine treatment on PAF-acether-induced aggregation. The inhibitory effect of Ticlopidine or its metabolite(s) was evidenced after platelet washing procedure, suggesting a persistent effect of this drug on platelet after administration of the drug has been stopped.
Adenosine Diphosphate↗
[Calcium antagonists and cardiac rhythm disorders].
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Arrhythmias, Cardiac↗
Effect of diltiazem on myocardial infarct size estimated by enzyme release, serial thallium-201 single-photon emission computed tomography and radionuclide angiography.
Diltiazem is a calcium antagonist with demonstrated experimental cardioprotective effects. Its effects on myocardial infarct size were studied in 34 patients admitted within 6 hours after the first symptoms of acute myocardial infarction. These patients were randomized, double-blind to placebo or diltiazem (10-mg intravenous bolus followed by 15 mg/hr intravenous infusion during 72 hours, followed by 4 X 60 mg during 21 days). Myocardial infarct size was assessed by plasma creatine kinase and creatine kinase-MB indexes, perfusion defect scores using single-photon emission computed tomography with thallium-201 and left ventricular ejection fraction measured by radionuclide angiography. Tomographic and angiographic scanning was performed serially before randomization, after 48 hours and 21 days later. Groups were comparable in terms of age, sex, inclusion time and baseline infarct location and size. Results showed no difference in creatine kinase and creatine kinase-MB data between controls and treated patients, a significant decrease in the perfusion defect scores in the diltiazem group (+0.1 +/- 3.0 placebo vs -2.2 +/- 1.9 diltiazem, p less than 0.02) and a better ejection fraction recovery in the diltiazem group (-4.2 +/- 7.4 placebo vs +7.7 +/- 11.2 diltiazem, p less than 0.05). Myocardial infarct size estimates from perfusion defect scores and enzyme data were closely correlated. These preliminary results suggest that diltiazem may reduce ischemic injury in acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
Clinical Enzyme Tests↗
Mode of action of antiarrhythmic drugs and the implicated arrhythmogenic risk.
The mode of antiarrhythmic action of drugs usually cannot be extrapolated from their electrophysiologic properties despite extensive in vitro and in vivo assessment: in most cases, the mechanism of arrhythmias remains uncertain and cannot be established by clinical evaluation including electrophysiologic study; in specific cases where the arrhythmia substrate is fully described, the exact origin of antiarrhythmic action is unknown, especially when chronic preventive treatment is considered where triggering events are probably important. Nevertheless, the profound electrophysiologic changes resulting from antiarrhythmic drugs alter several delicate balances, at the cellular level (repolarizing and depolarizing currents) and at the tissue level (refractory period/conduction time ratio). Some afterdepolarizations can be elicited, especially when repolarization is delayed by long cycle lengths and K+ current inhibition; reentry is enhanced when conduction impairment occurs without similar change in refractoriness. Proarrhythmic effects of drugs seem to relate to these alterations and caution should be exerted when ECG shows drug-induced QT or QRS prolongations.
Animals↗
Phase mapping of radionuclide gated biventriculograms in patients with sustained ventricular tachycardia or Wolff-Parkinson-White syndrome.
Accuracy of Fourier phase mapping of radionuclide gated biventriculograms in detecting the origin of abnormal ventricular activation was studied during ventricular tachycardia or preexcitation. Group I included six patients suffering from clinical recurrent VT; 3 gated blood pool studies were acquired for each patient: during sinus rhythm, right ventricular pacing, and induced sustained VT-Group II included seven patients with Wolff-Parkinson-White syndrome and recurrent paroxysmal tachycardia; 3 gated blood pool studies were acquired for each patient: during sinus rhythm, right atrial pacing and orthodromic reciprocating tachycardia. Each acquisition lasted 5 min, in 30 degrees-40 degrees left anterior oblique projection. In Group I, the Fourier phase mapping was consistent with QRS morphology and axis during VT (5/6), except in one patient with LV aneurysm and LBBB electrical pattern during VT. Origin of VT on phase mapping was located in the right ventricle (n = 2) or in left ventricle (n = 4), at the border of wall motion abnormalities each time they existed (5/6). In Group II, the phase advance correlated with the location of the accessory pathway determined by ECG and endocardial mapping (n = 6) and per-operative epicardial mapping (n = 1). Discrimination between anterior and posterior localisation of paraseptal pathways and location of intermittent preexcitation was not possible. We conclude that Fourier phase mapping is an accurate method for locating the origin of VT and determining its etiology. It can help locate the site of ventricular preexcitation in patients with only one accessory pathway; its accuracy in locating multiple accessory pathways remains unknown.
Adult↗
Ventricular tachycardia revealing a hydatid cyst.
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Aged↗