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Biomedical subjects

A Balaud

Publications and source records attributed to A Balaud.

11 recordsLinked to original sources
PubMed1989

[Survival in primary dilated cardiomyopathy as a function of tobacco smoking. A retrospective study].

In order to determine the influence of tobacco smoking on the course and long-term prognosis of idiopathic dilated cardiomyopathy, we conducted a retrospective study of 111 patients (95 men and 16 women, mean age 45.5 +/- 8.1 years) who had undergone cardiac catheterization between January 1970 and December 1979 and had been followed up for 6 to 16 years. The criteria of inclusion was diffuse hypokinesia of the left ventricle with an ejection fraction of 50 per cent or less, normal coronary arteriography and cardiomyopathy of unknown origin. The overall mortality rates at 1, 5 and 10 years were 10, 50 and 66 per cent respectively, and the main predictive factor was the left ventricular ejection fraction. Forty-six per cent of these patients were smokers, 19 per cent were non-smokers and 35 per cent had undetermined smoking habits. A univariate analysis showed a favourable predictive effect of smoking on survival (P less than 0.01), and this was confirmed by the statistical hypothesis of maximum bias for patients with undetermined smoking habits. On multivariate analysis, this predictive effect was superseded by the left ventricular ejection fraction, but after stratification of the sample according to the mean value of ejection fraction (30 per cent), the predictive value of smoking reappeared clearly in the group with a less than 30 per cent ejection fraction (P less than 0.003).

Adult↗
PubMed1988

Dilated cardiomyopathy: long-term follow-up and predictors of survival.

To determine long-term survival and the prognostic factors of dilated cardiomyopathy, we retrospectively studied a consecutive series of 111 patients (95 men, 16 women, mean age: 45.5 +/- 8.1 years) undergoing cardiac catheterization and diagnostic coronary angiography from January 1970 to December 1979. The inclusion criteria were: normal coronary angiography, diffuse hypokinesia of the left ventricle and left ventricular ejection fraction less than 50%. Base-line clinical data were collected from the hospital records and follow-up data were obtained from the general practitioners and cardiologists. A questionnaire was sent to all living patients. The length of follow-up ranged from 6 to 16 years. Six patients (5%) were lost to follow-up. At the time of catheterization, a majority of the patients had dyspnea and were in New York Heart Association (NYHA) classes II (41%) and III (31%). Clinical history revealed an excessive alcohol consumption in 56% of the patients. During follow-up, 66 patients (63%) died (heart failure: 37%; sudden death: 19%; non-cardiac death: 15%; unknown cause: 27%). Actuarial survival was 90, 50, and 33% at 1, 5, and 10 years, respectively. Univariate analysis revealed that 10-year mortality was related to: left ventricular ejection fraction less than 30%; left ventricular end-diastolic pressure greater than 10 mm Hg; cardiothoracic ratio greater than 54%; episodes of heart failure; left ventricular end-diastolic volume greater than 200 ml/m2, dyspnea of NYHA class III or IV; absence of smoking; absence of moderate systemic hypertension; electrocardiographic evidence of left ventricular hypertrophy and mean systemic arterial pressure greater than 95 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Correlation between late surface potentials and inducible ventricular arrhythmias. Apropos of 115 cases].

Programmed ventricular stimulation and a search for late surface potentials (LP) by means of signal-averaging and quantification by Simson's method were performed in 115 patients divided into five groups: group I (n = 50) with no myocardial infarction (MI) and no clinical or induced ventricular tachycardia (VT); group II (n = 28) with MI and no clinical or induced VT; group III (n = 8) with MI, no clinical VT but induced non sustained VT (NSVT); group IV (n = 19) with MI, no clinical VT but induced sustained VT (SVT); group V (n = 15) with clinical and induced VT. The terminal portion of the averaged signal (AS) was analyzed by three parameters: duration of AS terminal portion less than 40 microvolts (Dur TP), AS amplitude 50 and 40 ms before its end (Amp 50, Amp 40). The presence of TP was defined in two ways: criterion A = Amp 40 less than 25 mcv, criterion B = at least two sub-criteria: Dur TP greater than 40 ms, Amp 50 less than 25 mcv, Amp 40 less than 15 mcv. Compared to groups I and II, the AS of group V was characterized by a prolonged and low amplitude terminal portion (p less than 0.001). Groups III and IV were intermediate. The incidence of TP in groups I to V was 20, 28, 37, 56 and 80% respectively with criterion A, and 4, 4, 0, 28 and 66% respectively with criterion B. The lower incidence of TP in group IV as compared to group V was probably due to the induction of purely artefactual SVT's, notably those with rapid cycle (greater than 270 cps/min) which are remarkable on several accounts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Spasm in a single coronary artery].

A 52 year old man presented with effort and resting angina with positive exercise stress testing and myocardial scintigraphy. The initial coronary angiogram showed a single coronary vessel arising from the right coronary ostium dividing into a right coronary artery with a normal trajectory lined with a few non stenotic atheromatous plaques and a left coronary artery which passed between the aorta and pulmonary artery to reach the left atrioventricular groove. At first, it was suggested that the angina was due to compression of the left coronary vessel by the great arteries during effort, but this mechanism could not explain attacks of resting angina and the failure of betablocker therapy. An ergometrine test performed during repeat coronary angiography induced almost complete occlusion of the right coronary vessel and Prinzmetal diaphragmatic ischaemia. The anginal attacks were completely suppressed by Calcium antagonist drugs. The association of coronary spasm and a single coronary artery is rare; only one case has been previously reported. We do not believe that there was a relationship between the two phenomena in our case: the spasm occurred at a distance from the aberrant course of the vessel. The authors emphasise the diagnostic problems and the potential danger of this association.

Coronary Vasospasm↗
PubMed1985

[Sudden death in mitral valve prolapse. Apropos of 2 cases].

Two cases of sudden death are reported in patients with mitral valve prolapse with mitral insufficiency. Both had significant impairment of left ventricular function. Irreversible ventricular fibrillation occurred in one patient one-half hour preceding a catheterization, whereas the other patient died during sleep. Review of the literature revealed 42 cases of sudden death in patients with prolapse. Occasionally left ventricular dysfunction or medication overdosage can explain or favor development of the terminal arrhythmia, but usually no precipitating factor other than prolapse can be identified. It appears impossible to identify actual subgroups at risk, although sudden death does occur more frequently in patients with a large amount of prolapse of both valves, previous syncopal episodes, and ECG abnormalities at rest. Complex ventricular arrhythmias are also reported, but their predictive importance is difficult to evaluate. Sudden death is a rare complication of mitral prolapse, fact which should conservatively influence indications for further supplementary testing and treatment in these patients.

Adult↗