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Biomedical subjects

G Motté

Publications and source records attributed to G Motté.

At least 37 records · Page 2Linked to original sources
PubMed1991

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↗
PubMed1991

Arrhythmogenic activities of antiarrhythmic drugs in conscious hypokalemic dogs with atrioventricular block: comparison between quinidine, lidocaine, flecainide, propranolol and sotalol.

In order to create and evaluate a model sensitive to QT-dependent proarrhythmic effects of drugs, a long QT syndrome was produced in chronically instrumented dogs with bradycardia and hypokalemia. Bradycardia (mean cycle length: 1495 +/- 78 msec) was provided by permanent atrioventricular block and hypokalemia (K+ = 2.6 +/- 0.05 mmol/l) by high doses of diuretics. To evaluate that model, six of these conscious dogs were subjected to quinidine, flecainide, lidocaine, propranolol and sotalol infusions. In crossover design, drugs were infused i.v. at rates allowing stable and nontoxic drug plasma levels during the experiment. Four-lead ECGs were recorded for arrhythmias for 30 min before (base line) and 75 min after onset of infusion. Ventricular cycle length was increased dramatically by sotalol, lidocaine and propranolol (+618 +/- 192, +388 +/- 125 and +329 +/- 114 msec, respectively) and QT interval was increased by sotalol, quinidine and flecainide (+56 +/- 8, +31 +/- 7.9 and +20 +/- 5.7 msec, respectively). Quinidine and sotalol, but not flecainide, propranolol or lidocaine, exhibited significant arrhythmogenic activities. During quinidine infusion, most dogs exhibited some ventricular arrhythmias whose most severe forms were runs of ventricular tachycardia. These arrhythmias were suppressed by pacing at high rates. During sotalol infusion, five out of six dogs exhibited typical "torsades de pointes." This incidence was not related to the slowing effects of sotalol on idioventricular pacemakers, because a similar incidence was obtained in five complementary dogs paced at 40 bpm. It could be related to dose, because torsades de pointes occurred only once in another group of five dogs receiving half the dose used in the controlled study. Only quinidine and sotalol, but not propranolol, flecainide or lidocaine, are clinically associated to torsades de pointes. They were also the only drugs associated with proarrhythmic events in the present study, a fact suggesting that QT-dependent arrhythmogenic effects of drugs can be reliably evaluated in conscious hypokalemic dogs with complete atrioventricular block.

Animals↗
PubMed1990

Effects of bepridil and diltiazem on ventricular repolarization in angina pectoris.

To examine the time-course and potential predictors of prolongation of ventricular repolarization with the calcium antagonist bepridil, the effects of bepridil (300 to 500 mg/day; n = 45) and diltiazem (180 to 300 mg/day; n = 42) on QT and QTc interval duration were analyzed in a randomized double-blind study in patients with angina pectoris. Electrocardiograms were recorded before and 14, 28, 70 and 112 days after treatment was begun. After 14 days, bepridil prolonged QT interval by 26 +/- 35 ms (range, -60 to 120 ms) and QTc (Bazett's formula) by 17 +/- 33 ms (range, -73 to 107 ms) compared to baseline (both p less than 0.05). QT or QTc did not significantly increase thereafter. However, among the 30 patients who had less than 40 ms QTc prolongation at day 14 compared with baseline, 13 (43%) exceeded this limit on at least 1 of the following visits. Diltiazem did not significantly alter QT or QTc intervals. The absolute change in QTc interval from baseline observed after 14 days of bepridil therapy was inversely proportional to the baseline QTc interval (r = -0.68; n = 42; p less than 0.001). The degree of bepridil-induced QTc prolongation on day 14 correlated with pretreatment RR interval (r = 0.36; n = 42; p less than 0.02). In conclusion, chronic administration of bepridil but not of diltiazem prolongs ventricular repolarization in patients with angina pectoris. The overall effects of bepridil therapy on QT and QTc intervals can be assessed by an electrocardiogram recorded after 14 days of treatment but subsequent measurements may be required in individual patients. A short baseline QTc interval and a slow initial heart rate may be potentially useful predictors of a greater QTc prolongation with bepridil.

Angina Pectoris↗
PubMed1990

[Treatment of arrhythmias in chronic cardiac insufficiency].

Arrhythmias are frequent and associated with a poor prognosis, especially when they arise from the ventricle. Although the correction of predisposing factors and improvement of hemodynamic conditions are essential, the use of antiarrhythmic drugs in this context poses problems. The treatment of even complex ventricular extrasystoles has not been shown to effectively prevent the serious arrhythmias responsible for sudden death. Depression of left ventricular function and: Or proarrhythmic effects of antiarrhythmic therapy in some patients, probably offset the benefits observed in others. The treatment of atrial arrhythmias remains traditional: reduction by drugs or electrotherapy and prevention of recurrences, or simply slowing the ventricular response. Sustained ventricular tachycardia and resuscitated ventricular fibrillation should be managed more aggressively, not by empirical antiarrhythmic treatment but by medical therapy guided by the results of electrophysiological studies, and, when this fails, by non-medical treatment: fulguration, implantable defibrillator, antiarrhythmic surgery, or even cardiac transplantation.

Adrenergic beta-Antagonists↗
PubMed1988

ECG gated thallium 201 myocardial images: value in detecting multivessel disease in patients on anti anginal therapy 1-3 months after myocardial infarction.

ECG gated 201Tl scintigraphy was compared to non gated images for detecting 2-3 vessel disease 1-3 months after a first uncomplicated myocardial infarction. In all, 111 patients on anti anginal treatment underwent coronary arteriography and stress thallium imaging; 39 showed single vessel disease (SVD), and 72 multivessel disease (MVD). Sensitivity of black and white analog images was 82% for SVD and 8% for MVD. Sensitivity of computerized colored static images was 87% for SVD and 33% for MVD. For gated images, sensitivity was 100% and 92% in patients with SVD and MVD respectively. Specificity for detecting MVD was 95% for black and white images, 77% for computerized colored static images, and 69% for ECG gated images. Thus, ECG gated exercise 201TL scintigraphy is useful for predicting the extent of coronary artery disease 1-3 months after myocardial infarction in patients on anti anginal therapy.

Angina Pectoris↗
PubMed1988

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↗
PubMed1987

[Cardiac metastases. Clinical arguments of the diagnosis].

The case reported here concerns an 80-year old man without history of coronary disease whose electrocardiogram showed localized and stable repolarization disorders, viz. elevated ST segment with isoelectric point J and negative T wave. This pattern suggested cardiac metastasis after chest examination had revealed a bronchial epidermoid carcinoma. Two-dimensional echocardiography showed that the lateral wall of the left ventricle was thickened, hyperechogenic and akinetic. The secondary cardiac lesions were confirmed at pathological examination. This case has prompted us to discuss the frequency of such secondary tumours of the heart, their mode of dissemination to the myocardium and their clinical and electrocardiographic aspects. It underlines the usefulness of echocardiography for the diagnosis of cardiac tumours.

Aged↗
PubMed1987

[Value of early vasodilator treatment with prazosin in chronic cardiac insufficiency].

The purpose of the present study was to find out whether the beneficial effect of prazosin in congestive heart failure persists after 2 and 6 months of treatment and whether the clinical and haemodynamic data obtained correlate with the response to treatment. Twenty-four patients of mean age 50.0 +/- 3.00 years presenting with congestive heart failure stage II (3 cases), stage III (18 cases) or stage IV (3 cases) in the NYHA functional classification were treated. All abstained from taking digitalis at least one week before treatment and were given prazosin 14.5 +/- 0.77 mg/day together with spironolactone 25 to 100 mg/day. The results of treatment were assessed by its effects on echocardiography, systolic time intervals, ejection fraction and cardiac index measured by the radioisotope method, and maximal duration of a 60-watt exercise on an ergometric bicycle. Treatment was discontinued before the 6th month in 9 out of 10 non-responders. The remaining 14 patients responded to treatment and their condition improved. Mean blood pressure rose in 6 months from 95.4 +/- 3.92 to 104 +/- 3.06 mmHg (p less than 0.05). The cardiothoracic ratio was reduced at 2 months (-0.05 +/- 0.01, p less than 0.01) and at 6 months (-0.08 +/- 0.02, p less than 0.01). Systolic time intervals were not significantly altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Danger of vasodilator therapy for pulmonary hypertension in patent foramen ovale.

A 23-year-old woman with systemic lupus erythematosus was found to have severe pulmonary hypertension with secondary patency of the foramen ovale. Infusion of hydralazine increased the basal right-to-left shunt and resulted in a dramatic fall in arterial oxygen pressure, with subsequent irreversible cardiovascular collapse. Vasodilator therapy appears to be hazardous in patients with severe pulmonary hypertension and patent foramen ovale.

Adult↗
PubMed1986

[Infranodal chronic auriculo-ventricular block in subjects under 50 years of age].

The aetiology and evolution of chronic infranodal atrioventricular block (AVB) of young patients are not well known: are they the first sign of subclinical myocardial disease which can only be diagnosed by long term follow-up or do they represent isolated degenerative disease of the conduction tissue (Lenegre's disease)? Eighteen patients (15 men, 3 women) aged 25 to 49 years (average 41.5 years) were followed up for periods of 2 to 20 years (average 7.33 years) after pacemaker implantation for syncopal AVB. Follow-up was focused on the evolution of the conduction defects and the cardiovascular status. The patients were divided into two groups at the initial assessment: Group I: 15 patients with documented AVB; Group II: 3 patients in whom all basal recordings showed sinus rhythm (SR). Apart from one patient with an early non-ischaemic dilated cardiomyopathy, there was no previous cardiovascular disease. There was no history of ischaemic heart disease, drug effects, infection or inflammation in favour of an acute AVB. Three patients had permanent AVB, either 2nd degree with bundle branch block (N = 2) or 3rd degree block (N = 1). The other 15 patients were in sinus rhythm with bundle branch block: left bundle branch block (LBBB) in 5 cases, right bundle branch block (RBBB) in 3 cases; RBBB with left anterior hemiblock in 5 cases, RBBB and left posterior hemiblock in 2 cases. Paroxysmal AVB was recorded in 12 of these 15 patients on at least one occasion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adams-Stokes Syndrome↗
PubMed1986

[Cardiac contusion with dissecting hematoma of the apex of the heart and interventricular communication].

The authors report the case of a post-traumatic ventricular septal defect diagnosed after the detection of a systolic murmur in a 39 year old man, 18 months after a car accident. Two-dimensional echocardiography and angioscintigraphy showed an abnormal cavity at the apex of the heart. At cardiac catheterisation there was a moderate left-to-right ventricular shunt through this cavity. There were no traumatic or atheromatous lesions of the coronary arteries. The operative appearances were of stunned myocardium which had caused a dissecting haematoma of the cardiac apex which ruptured into both ventricular cavities. The lesions were corrected surgically and the systolic murmur disappeared.

Accidents, Traffic↗