Biomedical subjects

M Viallet

Publications and source records attributed to M Viallet.

11 recordsLinked to original sources

PubMed2000

Predictive factors of ventricular fibrillation triggered by pause-dependent torsades de pointes associated with acquired long QT interval: role of QT dispersion and left ventricular function.

INTRODUCTION: Death due to acquired torsades de pointes usually is caused by ventricular fibrillation (VF), but the contributing factors to VF triggered by pause-dependent torsades de pointes are not understood. METHODS AND RESULTS: We evaluated 91 patients who fulfilled four criteria: (1) pause-dependent torsades de pointes; (2) prolonged QT interval and/or corrected QT (QTc) (>0.44 sec); (3) long-short initiation sequence; and (4) conditions known to induce pause-dependent torsades de pointes. There were 38 patients with a documented VF (group I) and 53 without VF (group II). Absolute and relative dispersions of QT and QTc were calculated based on the 12-lead standard ECG. Group I differed from group II with regard to myocardial infarction history (32% vs 13%; P = 0.035), left ventricular ejection fraction (44% +/- 14% vs 65% +/- 9%; P < 0.0001), presence of structural heart disease (100% vs 20.8%; P < 0.0001), QT mean (591 +/- 73 msec vs 514 +/- 78 msec; P < 0.0001), QTc mean (563 +/- 76 msec vs 508 +/- 90 msec; P = 0.002), absolute QT dispersion (166 +/- 56 msec vs 84 +/- 49 msec; P < 0.0001), relative QT dispersion (9.9% +/- 3.5% vs 6.3% +/- 3.2%; P < 0.0001), absolute QTc dispersion (158 +/- 57 msec vs 81 +/- 44 msec; P < 0.0001), and relative QTc dispersion (9.9% +/- 3.6% vs 6.2% +/- 3%; P < 0.0001). Multiple regression analysis showed that ejection fraction (P = 0.0001), presence of structural heart disease (P < 0.0001), and relative QTc dispersion (P = 0.038) were the only independent predictors of VF. CONCLUSION: Left ventricular function, presence of structural heart disease, and QTc relative dispersion should be evaluated carefully in patients with conditions susceptible to inducing torsades de pointes.

Aged↗

PubMed1998

Double postinfarction cardiac rupture of left ventricular free wall and papillary muscle documented by transthoracic echocardiography.

A 70-year-old man presented with a posteroinferolateral acute myocardial infarction complicated by rupture of the left ventricular inferior wall and partial rupture of the posteromedial papillary muscle. Transthoracic echocardiography documented both of these complications and led to prompt and successful surgical repair.

Aged↗

PubMed1983

Comparison of short-term efficacy of diltiazem and propranolol in unstable angina at rest--a randomized trial in 70 patients.

The short-term efficacy of diltiazem (D) has been compared to that of propranolol (P), in a group of 70 patients hospitalized in the Coronary Care Unit for unstable angina, defined as recent (less than one month) appearance or aggravation of spontaneous chest pains. Among the 70 patients, 24 had angina only at rest. The patients have been divided into two groups according to ST-T changes during chest pain: 29 with ST elevation (group A) and 41 with other repolarization abnormalities (group B). Treatment was then randomized in each group. Treatment Treatment was considered successful only if spontaneous chest pains disappeared completely. Thirty-four patients were treated with D (282 +/- 102 mg/day) and 36 with P (158 +/- 81 mg/day). In the whole group and in groups A and B considered individually, responses to D and P did not differ. Among the 24 patients with angina exclusively at rest, nine successes and four failures were observed with D. There was no symptomatic relief among the 11 patients treated by P (P = 0.001). Moreover, the number of episodes of angina was decreased by D and unchanged by P, while eight out of the 11 failures with P were immediate successes when treatment was replaced with D. These results suggest that D is preferable to P for management of unstable angina in patients with angina which is exclusively spontaneous.

Adult↗

PubMed1981

[Acute cardiac liver. Diagnostic problems in 4 cases (author's transl)].

Four personal cases with histological examination of the liver and a review of 70 cases collected from the literature have enabled the authors to develop the diagnostic problems involved in acute cardiac liver. An accurate diagnosis of this condition, which consists of acute hepatic cytolysis on a background of heart failure, can only be based on its course and/or on the presence of histological changes in the liver.

Acute Disease↗

PubMed1981

Pharmacokinetics and bioavailability of diacetolol, the main metabolite of acebutolol.

The pharmacokinetics and bioavailability of diacetolol, the principal metabolite of acebutolol, were studied in 6 healthy subjects. Plasma concentrations were determined following a single intravenous injection of diacetolol 100 mg and three oral doses of diacetolol 100, 400 and 800 mg, in random order. The average oral bioavailability of diacetolol was F: 0.302 +/- 0.052 (100 mg), 0.363 +/- 0.052 (400 mg) and 0.426 +/- 0.068 (800 mg); the differences are not significant. The mean plasma half-life of the terminal phase, 7.94 +/- 0.26 h after intravenous administration, was significantly higher than after oral administration 12.27 +/- 1.00 h (100 mg), 12.82 +/- 1.59 h (400 mg) and 13.05 +/- 13.05 +/- 1.22 h (800 mg) (p less than 0.02 to 0.05); the mean urine half-lives of the terminal phase were not significantly different. Renal clearance of diacetolol 10.2 +/- 0.81 . h-1 represented about wo-thirds of total body clearance 15.9 +/- 1.21 . h-1. The results suggest either a first-pass effect or incomplete absorption of diacetolol after oral administration.

Acebutolol↗

PubMed1978

[The myocardiopathies of systemic lupus erythematosus].

Myocardial involvement in lupus erythematosis takes the form of an interstitial myocarditis with cellular infiltration and fibrinoid necrosis. The most lesions are perivascular, and involve the arterioles. The myocardial fibres are involved secondarily to the vascular lesions, or by grossly, damaging sclerosis. The clinical features are variable:--no clinical features, but haemodynamic evidence of abnormal ventricular function, and perhaps sudden death;--arrhythmias and disorders of atrio-ventricular conduction;--cardiac failure, which may be due to a genuine cardiomyopathy (a part may be played by hypertension, pulmonary hypertension, renal failure, constrictive pericarditis or haemodynamically major valve disorders);--abnormalities of the coronary trunk in a certain number of cases. If anti-nuclear antibodies are present in a cardiomyopathy, the presence of DLE or of a drug-induced lupus syndrome must be suspected. There remain some awkward cases which defy classification, and which systematic use of echocardiography and pericardial and myocardial biopsy may be able to define more accurately.

Antibodies, Antinuclear↗

PubMed1974