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Biomedical subjects

G Motté

Publications and source records attributed to G Motté.

At least 55 records · Page 3Linked to original sources
PubMed1984

Physiopathology of ventricular tachyarrhythmias.

Ventricular arrhythmias may be the result of three mechanisms: abnormal automaticity, triggered activity complicating early or late after-depolarizations, and reentry by circular pathway or by reflection. These three fundamental mechanisms have been observed in the intact heart in experimental models of myocardial ischemia and digitalis intoxication. In man, the arguments in favor of a given mechanism are indirect and may be determined by their response to stimulation. It may be possible to state the following conclusions: (1) reentry is at the origin of ventricular fibrillation, certain ventricular tachycardias of bundle branch reentry and probably most chronic sustained ventricular tachycardias that are easily inducible; (2) the mechanism of certain other ventricular arrhythmias sustained remains unknown; (3) even when arrhythmias are associated with reentry, the triggering extrasystole can arise from a focal origin.

Action Potentials↗
PubMed1984

[Arrhythmia caused by potassium deficiency].

Although experimental hypokalaemia leads to a wide range of arrhythmias and conduction defects, the only significant clinical result of potassium depletion (with or without hypokalaemia) is observed at ventricular level: ventricular extrasystoles, typical forms of ventricular tachycardia or, more commonly, the form suggesting torsades de pointe . The mechanism of these ventricular arrhythmias is obscure and may involve either reentry phenomena favored by the heterogenicity of the refractory periods at the Purkinje-ventricular junction or automaticity related to the increase in the slope of diastolic depolarisation or with the appearance of early post-potentials in series. Although arrhythmias are rare in isolated hypokalaemia and a healthy heart, they are common and serious if hypokalaemia complicates organic cardiac disease, especially when associated with another factor of cellular desynchronisation such as bradycardia or myocardial impregnation by certain antiarrhythmic drugs. The increased toxicity of digitalis in hypokalaemia is a well known example. Treatment is based essentially on compensating the potassium depletion, bearing in mind the risks of massive supplements administered too rapidly, and on the administration of potassium-sparing drugs (spironolactone and others). Rapid cardiac pacing is often useful in preventing recurrence of torsades de pointe while waiting for adequate potassium repletion.

Animals↗
PubMed1983

Determination of the left bundle branch refractoriness by distal His bundle pacing in patients with left bundle branch block.

Electrophysiological studies were carried out in two patients with an idiopathic left bundle branch block. Consistent distal His bundle pacing resulted in the normalization of the QRS complex in both patients. Extrastimulation during basic distal His pacing at several cycle lengths was carried out successfully. Using this technique, the refractory periods of the left bundle branches were measured and found to be within the normal range. In addition, they decreased with the shortening of the basic cycle length. These results demonstrated the possibility of determining the refractoriness of the left bundle branch by His bundle pacing in patients with left bundle branch block. Hypotheses are postulated about the presumed location of the lesion responsible for the left bundle branch block.

Adult↗
PubMed1983

[Reciprocating tachycardia and anterograde conduction by a nodoventricular pathway].

Two patients were investigated for paroxysmal regular tachycardia with left bundle branch block centrifugation. A right-sided nodo-ventricular accessory pathway was demonstrated in both cases at electrophysiological investigation with His bundle recording and atrial and ventricular programd pacing techniques. However, the function of this pathway was different in the two cases. In the first case, there were no signs of an accessory pathway on the surface ECG in sinus rhythm but it could be unmasked by simple right atrial pacing at the same rhythm (widening of the QRS and shortening of HV from 40 to 25 ms). The tachycardias could be only initiated by ventricular extrastimulus. They showed major pre-excitation with left sided delay and a 1/1 atrio-ventricular response. There was no His potential before the ventriculogramme which retained the same configuration throughout the attack. The investigations also suggested the presence of a dual nodal pathway with the accessory pathway connected to the slow pathway. In the second case, the presence of an accessory pathway could be suspected from the appearance of the QRS complex in sinus rhythms. Tachycardia was initiated by an atrial extrastimulus with initially a first complex showing slightly more marked pre-excitation and a distinct His potential before the QRS but with a shorter HV interval than in sinus rhythm. Then the reciprocating tachycardia had appearances of major pre-excitation, left-sided delay and a 1/1 atrio-ventricular response. However, in contrast to the first case, all ventricular complexes were preceded by a His potential and the degree of pre-excitation was variable with a HV interval ranging from 0 to 15 ms. These two cases merit attention because of: --their points in common: nodal duality and an accessory pathway which was not atrio-ventricular (decremental conduction) but nodo-right ventricular, conducting well in the anterograde direction but more or less masked in sinus rhythm; the presence of the accessory pathway was clearly visible during reciprocating tachycardia; --the differences: in the first case the nodo-ventricular pathway formed part of the circuit of the reciprocating tachycardia which was antidromic: descending limb, the slow nodal pathway and then the accessory nodo-ventricular pathway; ascending limb, the His bundle and then the rapid nodal pathway. In the second case, the reciprocating tachycardia was entirely intranodal, the accessory pathway not being involved in the circuit but connected to it in parallel with the normal Hisian pathway.

Adult↗
PubMed1982

[Changes in the physical properties of the arterial system and left ventricular performance with age and in permanent arterial hypertension: their interrelation].

The purpose of this work was to study interactions between physical properties of the arterial system and left ventricular performance during aging in normal and in hypertensive patients. 50 patients were studied; 28 normal patients (age range 22 to 68 years) and 22 patients with essential hypertension (age range 23 to 63 years). In hypertensive patients, the end systolic pressure-volume ratio (ESP/ESV), modulus of chamber stiffness (kp), left ventricular wall thickness (h), mass (m), m/LVEDV ratio (LVEDV: left ventricular end diastolic volume), systemic arterial resistance (SAR), pulse wave velocity (C) and characteristic impedance of the ascending aorta (Zc) were increased compared to normal subjects of similar age. The ejection fraction (EF), the mean velocity of fiber shortening (VCF) and dp/dt max were unchanged. In normal patients: the ESP/ESV ratio, kp, h, m, m/LVEDV ratio, SAR, C and Zc increased with age; there were no age related changes in EF, VCF or dp/dt max. In both groups, there was a close relationship between the m/LVEDV ratio and Zc, the characteristic impedance of the ascending aorta. These results suggest that: 1. aging and arterial hypertension lead to similar changes in the physical properties of the arterial system and in left ventricular performance; 2. in both cases, the development of concentric cardiac hypertrophy is closely related to the physical properties of the arterial system.

Adult↗
PubMed1981

[Fragmenting of the His potential after atrial stimulation].

Splitting of the His potential (H) in sinus rhythm is generally considered to be pathological but its significance during programmed atrial stimulation is not clear. This phenomenon was observed in 10 out of 53 patients aged between 19 and 45 years (average 31.8 years) not suspected of having paroxysmal intranodal block (asymptomatic, sinus rhythm without bundle branch block). Under basal conditions the H and the HV interval (35 to 50 ms; average 41 ms) were normal. Split H was observed with pacing periods of 680 to 885 ms (average 754 ms) and H1 H2 intervals of 325 to 450 ms (average 395 ms). The maximal interval between the split potentials ranged from 80 to 130 ms (average 100 ms). Splitting disappeared at the shortest periods when variable pacing cycles were used. The response to regular atrial pacing up to 150 bpm (10 cases) and to Ajmaline (1 mg/Kg) (4 cases) was normal. All patients but one were followed up to 10 to 41 months (average 21.4 months); the clinical and ECG parameters remained stable during this period. The presence of fragmented potentials between the atrial and ventricular complexes during programmed atrial stimulation may pose a difficult diagnosis problem, especially with respect to delayed atrial potentials. Splitting of the H is generally attributed to dispersion of the depolarisation wave front in the His bundle due to the persistence of the functional refractory state. Other mechanisms, especially longitudinal dissociation of the His bundle, may be discussed. From a prognostic point of view, this finding does not seem to carry more serious implications than simple lengthening of the HV interval or intranodal conduction delay, phenomena usually considered to be non-pathological.

Adolescent↗
PubMed1981

[Double Wenckebach phenomenon at nodal and His levels. Electrophysiological demonstration in slow and irregular flutter].

The authors describe the analysis of a case of atrial flutter with a slow ventricular response, the block being 9:2 with a first RR interval measuring between 3 and 4 PP intervals and a second RR interval between 5 and 6 PP intervals, the second of the 2 RR intervals being exactly 9 PP intervals. The only possible explanation of this sequence is firstly a 3:1 intranodal block (Wenckebach 3:2 in the central zone N of the node and 2:1 block at the nodo-hisian junction) followed by a 3:2 infra- or intra-hisian Wenckebach phenomenon. The His bundle recordings during flutter confirmed this hypothesis with the recording of a 3:2 block after the H potential. When sinus rhythm was restored at atrial level, the intrahisian conduction defect persisted (2:1 or 3:2 Wenckebach block).

Aged↗
PubMed1981

[Atrioventricular block disclosing an isolated congenital aneurysm of the sinus of Valsalva, extending into the septum and not ruptured].

A case of a congenital aneurysm of the right anterior sinus of Valsalva (ASV) extending into the septum is reported. The patient, a 20 year old male Central-African, presented with syncopal complete atrioventricular block (AVB) or recent onset. There were no clinical or radiological signs of associated cardiac disease. After implantation of a pacemaker, the diagnosis of an ASV extending into the septum was suggested on routine M mode echocardiography. It was confirmed by two-dimensional echocardiography and aortography. These investigations provided data on its size, its relationship to the cardiac chambers and also showed absence of rupture. The neck of the aneurysm was closed by an endo-aortic approach. There was moderate postoperative aortic regurgitation. This case underlines the value of systematic echocardiography in young patients with AVB of recent onset and obscure origin.

Adult↗