Biomedical subjects

P Dejode

Publications and source records attributed to P Dejode.

4 recordsLinked to original sources

PubMed2003

[Brugada syndrome].

The Brugada syndrome is characterised clinically by the occurrence of syncope or sudden death due to ventricular arrhythmias in patients with structurally normal hearts and electrocardiographic signs of right bundle branch block and ST elevation in the right precordial leads (V1 to V3). The transmission of the condition is autosomal dominant with variable penetration. Mutations have been identified in a gene coding for the alpha sub-unity of the sodium channel (SCN5A) on chromosome 3 in only 30% of cases. This mutation is responsible for a reduction of the density of the sodium current and explains the aggravation of the electrocardiographic anomalies by antiarrhythmic drugs which block the sodium channels. The prognosis is poor in symptomatic patients and depends on the prevention of sudden death by the implantation of an automatic defibrillator. The therapeutic decision is much more difficult in asymptomatic patients without a family history. The authors propose a decisional algorithm. The management may have to be modified in the months or years to come depending on advances in the understanding of this syndrome.

Algorithms↗

PubMed2003

[Bidirectional ventricular tachycardias].

Bidirectional tachycardias are rare arrhythmias. Nevertheless in the sixties and seventies these arrhythmias prompted much work relating to their mechanism. Discussions about the supposed supra-ventricular origin of certain bidirectional tachycardias essentially rested on presumptive arguments based on electrocardiographic analysis. All the electrophysiological investigations which could be performed in tachycardia showed a ventricular origin. The current hypotheses concerning the electrophysiological mechanism favour non-unifocal mechanisms as well as a very diverse aetiology: an automatic focus, or the triggered activities being associated with alternating conduction, or re-entry between the left hemibranches. Although the classic context is of excess digitalis with advanced cardiopathy, readily in atrial fibrillation with a poor prognosis as a corollary, the most recent description of catecholergic ventricular tachycardias with the very characteristic appearance of bidirectional tachycardias justifies updating the understanding of these unusual tachycardias.

Electrocardiography↗

PubMed1995

Spontaneous sequences of onset of torsade de pointes in patients with acquired prolonged repolarization: quantitative analysis of Holter recordings.

OBJECTIVES: This study investigated the cycle length changes preceding the spontaneous onset of torsade de pointes in patients with acquired prolonged ventricular repolarization. BACKGROUND: Torsade de pointes is a polymorphic ventricular tachycardia generally associated with prolonged ventricular repolarization. Because torsade de pointes is not inducible by programmed electrical stimulation, quantitative analysis of Holter recordings of spontaneous episodes may clarify the mechanisms favoring the onset of torsade de pointes in actual clinical conditions. METHODS: The digitized Holter recordings of 12 patients were analyzed by a computerized Holter system (ATREC). All arrhythmias were grouped according to three classes: 1) isolated premature ventricular beats (n = 47,147, mean/patient [+/- SD] 3,929 +/- 11,571); 2) salvos of 2 to 4 consecutive beats (n = 2,003, mean/patient 167 +/- 359); 3) torsade de pointes > or = 5 beats (n = 105, mean/patient 9 +/- 11). For each patient and class of arrhythmias, six variables were computed from the 10 min and the 10 cycles preceding the event onset. RESULTS: A significant heart rate increase in the last minute (p < 0.01) and typical oscillatory short-long-short cycle length sequences preceded the onset of arrhythmias, with greater oscillation preceding torsade de pointes than salvos and premature ventricular beats. The cycle lengths preceding the onset were highly correlated with the class of arrhythmias (r = 0.65, p < 0.005) and allowed the correct classification of 69% of events by discriminant analysis (p < 0.0001). A significant negative correlation was observed between the duration of torsade de pointes and the mean length of the initial cycles (r = -0.62, p < 0.001), indicating that longer torsade de pointes had a faster rate than that at onset. CONCLUSIONS: In patients with acquired prolonged repolarization, the spontaneous onset of ventricular arrhythmias was preceded by an increasing heart rate in the last minute and escalating oscillatory "short-long-short" cycle length patterns, with greater oscillations preceding torsade de pointes than salvos and isolated ventricular beats. These findings suggest that adrenergic- and pause-dependent mechanisms (possibly inducing afterdepolarizations and triggered activity) may have a synergetic role in the genesis of complex ventricular arrhythmias associated with delayed ventricular repolarization.

Aged↗

PubMed1993

[Effects of sublingual nifedipine on the velocity of pulse wave evaluated by Doppler echocardiography of the thoracic aorta].

Sublingual nifedipine has a rapid and powerful hypotensive effect. Its action on arterial distensibility can be assessed by measurement of pulse wave velocity (PWV) by Doppler echocardiography (DE). Ten patients were used to evaluate intra-observer reproducibility (Group 1). Fifteen hypertension patients (Group 2), not taking a calcium antagonist, 64 +/- 13 years-old, were studied by DE before and 15 minutes after 10 mg of SL nifedipine. The following were measured: systolic and diastolic blood pressures (SBP and DBP), heart rate (HR), echocardiographic shortening fraction (SF) and PWV, with sternal length (SL) taken as being identical to the length of the abdominal aorta between the isthmus and the coeliac region, and by measuring delta t: time interval for propagation of the pulsed Doppler velocimetric wave between the isthmic aorta and the coeliac aorta located by echocardiography: PWV = SL/delta t. Evidence was found in the nifedipine group (n = 15) of a fall in SBP (159.5 +/- 27.8 cf. 140.9 +/- 21 mmHg; p = 0.002); in DBP (88.6 +/- 13 cf. 79.6 +/- 8.3 mmHg; p = 0.005) and an increase in HR (72.3 +/- 10.7 cf. 76.8 +/- 12.9 bpm; p = 0.04). PWV decreased after nifedipine (10.5 +/- 3.9 cf. 7.15 +/- 12.9 bpm; p = 0.002). There was a linear correlation between the percentage reduction in PWV and left ventricular HR: y = 194x - 53; r = 0.56; p = 0.029.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Sublingual↗