Biomedical subjects

S Dinanian

Publications and source records attributed to S Dinanian.

8 recordsLinked to original sources

PubMed1996

Initial and long-term evaluation of escape rhythm after radiofrequency ablation of the AV junction in 50 patients.

Between 1986 and 1994, 50 patients (mean age 63 +/- 13 years), 25 of whom had organic heart disease and presenting with atrial arrhythmias refractory to 5.6 +/- 1.6 antiarrhythmic drugs, underwent radiofrequency ablation (5 +/- 3 pulses by procedure; duration of pulses 50.5 +/- 32 s) of the proximal AV junction to create complete and permanent AV block. The escape rhythm was studied immediately after the procedure and during long-term follow-up. Immediately after the procedure, an escape rhythm was observed in 80% of the patients (junctional in 92%). Over a mean follow-up of 36 +/- 16 months in 47 patients (2 patients died before assessment of escape rhythm and 1 was lost to follow-up), an escape rhythm was present in 39 patients (83%) and absent in the remaining 8 (17%). The only significant difference between the two groups was the initial presence of an escape rhythm (P = 0.008). However, three patients with an initial escape rhythm had none during long-term follow-up. The initial presence of an escape rhythm as a predictive factor of its presence during follow-up had a sensitivity of 87%, specificity of 63%, positive predictive value of 92%, and negative predictive value of 50%. Thus, the absence of an escape rhythm during long-term follow-up causing pacemaker dependency was noted in 1 of 6 patients. This represents a limitation to this palliative treatment, which should be reserved for patients suffering from supraventricular tachycardias refractory to other treatments.

Adult↗

PubMed1995

[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↗

PubMed1995

[Double responses].

Double response is a rare electrocardiographic phenomenon requiring two atrioventricular conduction pathways with very different electrophysiological properties. Double ventricular responses are the usual manifestation: an atrial depolarisation (spontaneous or provoked, anticipated or not) is followed by a first ventricular response dependent on an accessory pathway or a rapid nodal pathway and then a second response resulting from sufficiently delayed transmission through a nodal pathway for the ventricles to have recovered their excitability when the second wave of activation reaches them. A simple curiosity when isolated and occurring under unusual conditions, particularly during electrophysiological investigation of the Wolff-Parkinson-White syndrome, the double response may initiate symptomatic non-reentrant junctional tachycardia when associated with nodal duality and repeating from atria in sinus rhythm. The functional incapacity and resistance to antiarrhythmic therapy may require referral for ablation of the slow pathway.

Atrioventricular Node↗

PubMed1994

[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↗

PubMed1993

[Diagnosis of ventricular tachycardia by electrocardiography].

In monomorphic wide QRS complex tachycardia, it is important to differentiate ventricular tachycardia from supraventricular tachycardia with aberration or preexcitation both from the prognostic and therapeutic view points. Atrioventricular dissociation with fusion complexes allows diagnosis of ventricular tachycardia but the negative predictive value of these criteria is low. Extreme QRS axis deviation, concordant morphological criteria in leads V1-V2 and V6 and analysis of the RS complexes in the precordial leads, nearly always enable supraventricular tachycardia with aberration. The distinction with other causes of wide QRS complex tachycardias (supraventricular tachycardia with preexcitation or with non-systematized intraventricular conduction defects) is much more difficult in the absence of a reference recording and depends more on the clinical context than ECG analysis.

Diagnosis, Differential↗

PubMed1992

[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↗

PubMed1992

[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↗

PubMed1992

[Double-blind clinical and echocardiographic study of oral enoximone versus placebo in severe cardiac insufficiency].

The effect of enoximone was assessed by a randomised double blind trial versus placebo. The clinical status of the patients was evaluated by the NYHA classification and quality of life score. Inotropic state was estimated from the maximum acceleration of aortic and pulmonary blood flow recorded by Doppler echocardiography. Thirty patients with severe cardiac failure, aged 66.4 +/- 14 years, symptomatic despite maximal therapy associating diuretics, digitalis, nitrate derivatives and angiotensin converting enzyme inhibitors, were included. Fifteen patients were given enoximone 100 mg three times a day orally (Group E) and the other 15 were given a placebo (Group P). The NYHA class and quality of life scores were assessed at D0, D4 and D31. Doppler echocardiography and Holter recordings were performed on D0 and D31. The two groups were comparable at D0. Ten patients abandoned the trial, 3 from Group E (including 1 death) and 7 from Group P (including 3 deaths). At D4, 13 patients from Group E and 8 from Group P were clinically improved (p < 0.05). At D31, the clinical state was stable or improved in 10 of the 12 patients in Group E and 6 of the 8 patients in Group P (NS). No secondary effects were severe enough to warrant the withdrawal of treatment: the frequency of ventricular extrasystoles was comparable in the two groups at D0 and D31. At D31 the maximal aortic acceleration had increased by 20% compared with D0 (p < 0.05) and the maximal pulmonary acceleration by 31% (p < 0.05) in Group E. The same parameters showed no significant change in Group P (-6% and +5% respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗