Electrical activity of human atrial fibres at frequencies corresponding to atrial flutter.

Little information is available about rate dependent changes in electrical activity of human myocardial cells. We therefore studied, in vitro, the electrical activity of adult human atrial fibres driven at frequencies near that of atrial flutter by means of the standard microelectrode technique. Thirty two atrial samples exhibiting "normal" responses with fast upstroke were selected. At very high frequencies, the action potential (AP) upstroke arose from the repolarisation phase of the preceding AP in spite of marked frequency induced shortening of the plateau. As the stimulation rate was progressively increased, the take off potential (TOP) was less and less negative and the maximal rate of depolarisation (Vmax) decreased. Moreover, in most preparations, a clear alternation between two types of action potentials occurred. Calcium channel inhibitors cobalt (5 mM) or diltiazem (5 x 10(-6) M) shortened AP duration, increased Vmax and markedly reduced alternation. Sodium channel inhibitors, tetrodotoxin (7.5 10(-6) M) or lignocaine (10(-5) M) shortened AP duration and induced a transient increase in Vmax. Ouabain (10(-6) M) prolonged AP duration, decreased Vmax, enhanced alternation and finally suppressed the 1:1 capture of the atrial tissue. Our results show that, at high driving rates corresponding to the frequencies of atrial flutter, slight variations in action potential duration induced by drugs are associated with marked concomitant variations in Vmax and probably with consequent modifications of the conduction velocity.

Predictive value of hemostatic factors for sudden death in patients with stable angina pectoris.

To assess hemostatic risk factors for sudden death in patients with stable angina, 323 consecutive patients were recruited prospectively. Patients with clinical heart failure or recent myocardial infarction were excluded. The following clinical variables were recorded: age, gender, smoking habits, hypertension, previous myocardial infarction, left ventricular hypertrophy, and severe ventricular arrhythmia. Angiographic variables included coronary extent, assessed from Jenkins' and mean atherosclerotic scores, and left ventricular ejection fraction. Lipid variables included total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and apolipoproteins A-I and B. Hemostatic factors included fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2 antiplasmin, euglobulin clot lysis time, tissue plasminogen activator before and after venous occlusion, and plasminogen activator inhibitor. There were 34 deaths, 19 of which were sudden during the follow-up period (60 +/- 17 months). The association between each variable and the risk of sudden death was assessed by calculating the relative risk with the Cox univariate model. All significant predictors from the univariate analysis were then incorporated in a Cox multivariate model to select the independent predictors of sudden death. The independent predictors of sudden death were left ventricular hypertrophy (p < 0.04), lower left ventricular ejection fraction (p < 0.04), and shorter euglobulin clot lysis time after venous occlusion (p < 0.02), whereas fibrinogen (p < 0.07) and Jenkins' score (p < 0.08) were borderline. Determination of hemostatic variables, especially those pertaining to dynamic fibrinolysis, may thus be of value in assessing risk of sudden death.

Biological risk factors for sudden death in patients with coronary artery disease and without heart failure.

In a study of biological risk factors for sudden death in patients with coronary artery disease, 320 patients were, prospectively, recruited and followed-up over two years. None of the patients had heart failure or recent myocardial infarction. The following variables were recorded: previous acute myocardial infarction, hypertension, smoking habits, ventricular arrhythmia; the angiographic variables included: left ventricular ejection fraction, Jenkins' and mean atherosclerotic scores; lipid profile: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoproteins Al and B; hemostatic profile: fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2-antiplasmin, euglobulin clot lysis time and tissue plasminogen activator before and after venous occlusion, tissue plasminogen activator inhibitor, platelet factor 4, beta-thromboglobulin. During the follow-up period, 12 of the patients died suddenly. In these patients, ejection fraction was lower: 49 +/- 16% versus 61 +/- 14% for the other patients (P less than 0.02), fibrinogen higher: 3.9 +/- 0.8 g/l versus 3.5 +/- 0.8 for the living patients (P less than 0.05) and protein C lower: 89 +/- 39% versus 111 +/- 39% (P = 0.06) for the other patients. In multivariate analysis: lower ejection fraction (P less than 0.008), older age (P less than 0.03) and lower protein C (P less than 0.01) were correlated with sudden death. Among the patients with coronary artery disease, the raised fibrinogen and the decreased protein C appeared to be risk factors for sudden cardiac death. These alterations reflected a prothrombotic state which might increase the ischemic risk, due to an acute thrombosis, leading to the fatal ventricular arrhythmia. Determination of these hemostatic variables might be a useful adjunct for assessment of the vital prognosis of patients with coronary artery disease, especially the risk of sudden death in addition to other known clinical, electrocardiographic, hemodynamic risk factors. This would also guide both the instigation of complementary investigations and appropriate therapy in such high risk group of patients.

Intrapulmonary artery coiling of a permanent pacing lead.

Intrapulmonary artery displacement of a permanent ventricular lead is reported to be a severe form of lead coiling and is attributed to the failure of the fixation procedure. The lead instability indicated a need for surgical correction.

[Pharmacological treatment of ventricular tachycardia]. / Traitement pharmacologique des tachycardies ventriculaires.

Pharmacological antiarrhythmic therapy is the treatment of first intention for the prevention of ventricular tachycardia (VT). In sustained VT, electrophysiological investigations without treatment enable the induction of VT, the demonstration of its reproducibility, the confirmation of diagnosis (if necessary), the determination of its mechanism and the choice of treatment. In an effort to standardise the technique, a minimum acceptable protocol of stimulations was agreed upon: at least 2 cycles (600 milliseconds and 400 milliseconds) and 3 extrastimuli (S2, S3, S4). The percentage of inducibility (sensitivity) depends on the underlying heart disease and is of the order of 90-95% in coronary artery disease with a history of infarction. Serial electrophysiological studies show non-inducibility of VT with treatment in 20-60% of cases. This result is influenced by the ejection fraction, the type of ventricular arrhythmia (fibrillation or tachycardia) and the antiarrhythmic agent tested. A Class IA, then a Class IC antiarrhythmics or sotalol (if the ejection fraction is over 40%) are evaluated by this technique. Empiric therapy has no place in the management of malignant poorly tolerated arrhythmias. In recurrent, well tolerated arrhythmias which are non-inducible, treatment may be guided by the results of Holter monitoring, providing the patient has a sufficient number of extrasystoles. Exercise stress tests may be useful in effort or catecholamine-induced tachycardias. There is no consensus about the management of non-sustained VT. When these arrhythmias are associated with syncope or cardiac arrest, programmed ventricular stimulation seems indicated. The choice of antiarrhythmic drugs and their results are reviewed.

[Parkinson syndrome, a possible adverse effect of calcium inhibitors]. / Syndrome parkinsonien, effet indésirable possible des inhibiteurs calciques.

The effects of calcium inhibitors are not limited to the muscles and may affect other systems and cause varied side effects. Two cases of Parkinsonian syndrome occurring after starting therapy with calcium inhibitors (verapamil in one case and diltiazem in the other) are reported. Complete regression of the symptoms after withdrawing the drugs was strongly in favour of a causal relationship. The condition could be due to inhibition of the calcium channels in the central nervous system disturbing neurotransmission. This seems to be a rare side effect as there have only been three other reported cases of secondary extrapyramidal syndromes in the literature. However, a Parkinsonian syndrome is very invalidating and clinicians using this family of drugs should be aware of this possible complication.

[Percutaneous venoplasty for the implantation of a dual-chamber cardiac pacemaker]. / Veinoplastie percutanée pour permettre l'installation d'une stimulation cardiaque double chambre.

During reoperation for pacemaker implantation, venous catheterisation of the homolateral subclavian vein encountered obstruction at the brachiocephalic vein. Balloon angioplasty of the severe brachiocephalic stenosis was performed via the femoral vein. After repeat subclavian venous catheterisation two new pacing wires could be introduced without difficulty followed by active fixation in the atrium and passive fixation in the ventricular apex. The initial ventricular pacing wire was isolated and respected. The femoral vein approach gave simple and direct access to the site of dilatation at a distance to the operative field which was shielded from an infectious risk. The technique and results of percutaneous venous recanalisation have not been extensively analysed during reoperation for cardiac pacing. In chronic cardiac pacing, the success of homolateral operation despite venous occlusion or stenosis, ensures preservation of the venous capital.

[Atrioventricular block at nodal and infrahissian level during atrial tachycardia. Apropos of a case]. / Bloc auriculo-ventriculaire à l'étage nodal et infrahissien, au cours d'une tachycardie atriale. A propos d'un cas.

The authors report the case of a patient with atrial tachycardia and surface electrocardiographic signs of left anterior hemiblock and complete right bundle branch block with 10/3 atrioventricular block. The regularity of the RR intervals which were an exact multiple of the atrial cycle suggested the absence of a Wenckebach phenomenon. The sequence of atrioventricular conduction cannot be explained by classical models of intranodal conduction. Endocavitary recordings confirmed this hypothesis. They showed block at 2 levels: supra- and infrahisian. The suprahisian block functioned in the 2/1 mode and the infrahisian block in the 5/3 mode without incremental conduction distal to the His potential before the apparition of block. A double zone of intrahisian block could explain the observed sequence of atrioventricular conduction. The absence of Wenckebach phenomenon on the surface ECG during tachycardia could be a sign of infrahisian block. The authors suggest that the association of this sequence of atrioventricular conduction with intraventricular conduction defects is a formal indication for electrophysiological studies.

[Comparison of the efficacy of 2 delayed-action preparations of hydroquinidine and quinidine in the prevention of pacing induced ventricular tachycardia]. / Comparaison de l'efficacité de deux formes à libération prolongée d'hydroquinidine et de quinidine dans la prévention des tachycardies ventriculaires induites par stimulation.

The effects of two antiarrhythmic agents, hydroquinidine and quinidine on the prevention of pacing induced sustained ventricular tachycardia (VT) were studied in 14 patients. The underlying cardiac disease was old myocardial infarction (12 patients) or dilated cardiomyopathy (2 patients). Sustained monomorphic VT was induced in 14 patients during the initial electrophysiological study performed at least 48 hours after withdrawal of all antiarrhythmic therapy. The same stimulation protocol including 3 extrastimuli (S2 S3 S4) and 2 paced cycles (600 ms and 400 ms) was repeated at least 48 hours after the administration of 600 mg (2 gelules) per 24 hours of hydroquinidine or 1100 mg of quinidine arabogalactane sulphate, 3 to 4 hours after the last dose. This was an open, randomised, crossed over trial. Irrespective of the result observed with the first antiarrhythmic, used in an order attributed by a randomised table, the other antiarrhythmic was tested. Plasma concentrations were measured during the programmed stimulation test for both drugs. Induced VT was prevented by the two antiarrhythmics in 4 patients (28%). In one patient, VT was prevented by hydroquinidine but not by the quinidine compound, resulting in a prevention rate of 35% for the hydroquinidine. On the other hand, the quinidine compound was a total success in one patient in whom only a partial success was observed with hydroquinidine. VT remained inducible with both antiarrhythmics in 9 patients (64%).(ABSTRACT TRUNCATED AT 250 WORDS)

[Successful cardiac transplantation after 38 days of circulatory assistance with a heterotopic artificial heart]. / Succès d'une transplantation cardiaque après 38 jours d'assistance circulatoire par coeur artificiel en position hétérotopique.

The survival of a patient with irreversible cardiac failure on the cardiac transplantation waiting list was assured for 38 days by circulatory assistance with heterotopic Pierce Donachy prosthetic ventricles and followed by successful cardiac transplantation. This method of circulatory assistance is relatively simple to install from the technical point of view and provides a satisfactory haemodynamic result whilst waiting for a compatible donor organ. Several complications, some of them serious, were observed. Some were related to the patient's poor preoperative condition: acute renal failure, disorders of coagulation. These regressed slowly when the patient's haemodynamic status improved. On the other hand, septic problems and local haemorrhage were inherent to this technique. These are the commonest complications reported by other authors. Although the mortality rate during the period of circulatory assistance may appear to be high, this technique remains a valuable method of survival for selected patients and does not affect the chances of success of ulterior cardiac transplantation.