PubMed Health⌕ Search

Biomedical subjects

A Belin

Publications and source records attributed to A Belin.

10 recordsLinked to original sources
PubMed2001

[Programmed left ventricular stimulation in non-sustained ventricular arrhythmias].

The presence of nonsustained ventricular arrhythmia (NSVA) is an independent factor of sudden rhythmic death. The primary objective of our study was to evaluate the correlation between inducibility during programmed ventricular stimulation (PVS) and the presence of ventricular late potentials, the ejection fraction, the grade of arrhythmia, and the underlying cardiopathy. The secondary objective was to evaluate the interest of PVS in patients with NSVA. Ninety eight patients with NSVA have been tested by PVS and 14 were inducible. During the mean follow up of 24 months, 8 patients died, 3 of them suddenly. A significative statistical correlation was found between ventricular late potentials and inducibility (negative predictive value = 91%; p = 0.03). No correlation was found between the ejection fraction, the grade of arrhythmia, the cardiopathy and inducibility. In patients with ischaemic cardiopathy, PVS has allowed to identify a subgroup of patients with high risk of sudden death. In this subgroup, serial PVS for drug testing has contributed to choose the therapeutic regimen supposed to be more effective for prevention of fatal arrhythmia. Multiple factors explain sudden death, even though the initial treatment has been chosen by electrophysiologic studies. For non inducible patients, empiric treatment is not proven to be reliable, and the best therapeutic regimen is still unidentified, especially in the subgroup of patients with low ejection fraction. In this subgroup, the implantable cardioverter defibrillator vives better protection against sudden rhythmic death.

Adolescent↗
PubMed2000

Improvement of cardiac neuronal function after carvedilol treatment in dilated cardiomyopathy: a 123I-MIBG scintigraphic study.

UNLABELLED: Carvedilol can induce important clinical and hemodynamic improvements in patients with chronic heart failure resulting from severe left ventricular (LV) dysfunction. This study examines the impact of carvedilol on cardiac neuronal function using 123I-metaiodobenzylguanidine (MIBG) scintigraphy in dilated cardiomyopathy. METHODS: Twenty-two patients with chronic heart failure (19 men, 3 women; mean age, 54 y; age range, 34-64 y) assessed as New York Hospital Association (NYHA) class II or III and with initial resting radionuclide LV ejection fractions (LVEF) < 0.40 were enrolled in the study. Patients had long histories of symptomatic LV dysfunction despite optimal diuretics and angiotensin-converting enzyme inhibitor treatment. Over a 6-mo period, 50 mg/day carvedilol was administered to these patients. Planar 123I-MIBG scintigraphy provided measurements of cardiac neuronal uptake (as heart-to-mediastinum count activity ratio [HMR]), 4h after intravenous injection of 185 MBq MIBG. Hemodynamic, clinical, radionuclide LVEF and HMR data measured at the outset and after 6 mo of carvedilol were compared. RESULTS: Resting heart rate decreased from 81 +/- 13 to 71 +/- 9 bpm (P = 0.003). After carvedilol therapy NYHA functional classification for these patients improved from 2.6 +/- 0.5 to 2.3 +/-0.5 (P = 0.04), LVEF improved from 22% +/- 9% to 30% +/- 13% (P = 0.005), and HMR improved from 145% +/- 23% to 170% +/- 25% (P = 0.0001). CONCLUSION: Carvedilol induces improvements of clinical symptoms and cardiac neuronal and systolic functions in patients with dilated cardiomyopathy and chronic optimal treatment.

3-Iodobenzylguanidine↗
PubMed1998

Impact of exercise rehabilitation on cardiac neuronal function in heart failure: an iodine-123 metaiodobenzylguanidine scintigraphy study.

Exercise training can induce important haemodynamic and metabolic adaptations in patients with chronic heart failure due to severe left ventricular dysfunction. This study examined the impact of exercise rehabilitation on cardiac neuronal function using iodine-123 metaiodobenzylguanidine (MIBG) scintigraphy, Fourteen patients (11 men, 3 women; mean age 48 years; range: 36-66 years) with stable chronic heart failure of NYHA class II-III and an initial resting radionuclide left ventricular ejection fraction (LVEF) < 50% were enrolled in the study. Patients underwent progressive, supervised endurance training (treadmill test, Bruce protocol) during a 6-month period (60 sessions, 3 sessions per week) at a cardiac rehabilitation referral centre in order to measure exercise parameters. Planar 123I-MIBG scintigraphy provided measurements of cardiac neuronal uptake (heart-mediastinum ratio activity, 4 h after intravenous injection of 185 MBq of MIBG). Radionuclide LVEF was also assessed at the outset and after 6 months of exercise training. Workload (801 +/- 428 vs 1229 +/- 245 kpm.min-1, P = 0.001), exercise duration (504 +/- 190 vs 649 +/- 125 s, P = 0.02), and myocardial MIBG uptake (135% +/- 19% vs 156% +/- 25%, P = 0.02) increased significantly after rehabilitation. However, LVEF did not change significantly (23% +/- 9% vs 21% +/- 10%, p = NS). It is concluded that exercise rehabilitation induces improvement of cardiac neuronal function without having negative effects on cardiac contractility in patients with stable chronic heart failure.

3-Iodobenzylguanidine↗
PubMed1995

[Proarrhythmic effects of anti-arrhythmia agents].

Antiarrhythmic medications are widely used either at the ventricular or supraventricular level. However, those drugs can induce severe side effects. Actually, antiarrhythmic drugs are paradoxically able to favour the occurrence of new arrhythmias or aggravate the preexisting arrhythmia for which they were indicated. These proarrhythmic effects have been found in 10 to 20% of patients, as evidenced by literature. Moreover, the CAST study showed a significant increase in mortality in patients with non sustained ventricular arrhythmias after myocardial infarction who were treated with either flecainide or encainide, compared to the placebo group. This overmortality seems to be due, in large, to the proarrhythmic effects of antiarrhythmic drugs. Several mechanisms have been evoked, related to the type of antiarrhythmic drug and to the presenting arrhythmia: early post-depolarization due to slow calcium and sodium inward currents in the case of torsades de pointes, facilitation of intraventricular reentries in the case of class 1c antiarrhythmic drugs, facilitation of the ventricular response of atrial arrhythmias. These deleterious effects, that can be very serious, are unpredictable, not toxicity-related and all antiarrhythmic drugs are involved. Their detection appears to be difficult and is based upon ECG, Holter monitoring, treadmill test and possibly electrophysiologic study. The use of antiarrhythmic drugs requires the knowledge of their proarrhythmic effects, the analysis of the benefit-risk ratio--particularly if left ventricular function is impaired--and careful monitoring.

Anti-Arrhythmia Agents↗
PubMed1995

[Comparative study of verapamil LI 120 mg 3 times a day and verapamil LP 120 mg twice a day in stable exertion-induced angina. A multicenter study].

A multicentre, open, crossover study in 27 patients with exertional angina compared the efficacy of verapamil LP 120 mg twice a day (VP LP 120) with that of verapamil LI 120 mg 3 times a day (VP LI 120) by means of stress tests. The study procedure was as follows: 7-day selection period during which the patient received placebo, and two 21-day treatment periods by VP LI 120 or VP LP 120 according to the crossover principle. At the end of each treatment phase, a stress test was performed at the trough serum concentration for each substance. VP LP 120 mg and VP LI 120 mg both improved exercise capacity compared to placebo. Comparison of VP LP 120 and VP LI 120 did not reveal any significant difference for stress test parameters (total duration of effort: 12 +/- 3.2 min with placebo, 13.3 +/- 3.7 min for the VP LI phase, 13.9 +/- 3.2 min for the VP LP phase; % FMT reached: 87.2% +/- 7.2 for VP LI, 89% +/- 7.3 for VP LP; time to onset of significant ST depression: 10 min +/- 2.9 for VP LI, 11 min 3.6 for VP LP). The efficacy of VP LP 120 in exertional angina is therefore identical to that of VP LI 120, despite a reduction of the total dose and serum levels.

Administration, Oral↗
PubMed1992

[Correlations between the different criteria of late potentials and results of programmed ventricular stimulation after myocardial infarction].

Five to ten per cent of survivors of acute myocardial infarction die within two years. The majority of these deaths are sudden and are attributed to a lethal ventricular arrhythmia. This is usually ventricular tachycardia degenerating to ventricular fibrillation. These post-infarction tachycardias are generally due to reentry. They require an anatomic arrhythmogenic substrate, a zone of delayed conduction. This can be detected as late potentials on signal averaged ECG. The triggering of a significant ventricular arrhythmia by ventricular stimulation is closely correlated to the occurrence of a severe ventricular arrhythmia in the months following infarction. Programmed ventricular stimulation could, therefore, help to identify patients requiring close follow-up and/or preventive antiarrhythmic therapy, but cannot be offered to all patients because of its invasive nature. Seventy nine post-infarction patients were studied prospectively. All underwent coronary angiography, signal averaging electrocardiography, and programmed ventricular stimulation at least 15 days after infarction. Fifty five patients had at least one criterion of late potentials (QRS duration > or = 110 ms and/or amplitude of the last 40 ms < 27 microV and/or duration of potentials of under 40 microV > 37 ms). Twenty four patients had no late potentials. The results of programmed stimulation were estimated to be positive when sustained or unsustained monomorphic ventricular tachycardia was triggered, and negative when ventricular fibrillation, ventricular flutter unsustained polymorphic ventricular tachycardia or no arrhythmia could be induced. Programmed ventricular pacing triggered 15 significant events, 17 unsustained polymorphic ventricular tachycardias, 13 ventricular flutters and 11 ventricular fibrillations. The exploration was negative in 23 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

[Comparison of the efficacy of verapamil and diltiazem in stable exercise angina. A double-blind and crossover study].

Calcium channel blockers are now recommended for the treatment of stable angina but few studies have been carried out comparing the efficacy of verapamil and diltiazem in this indication. The short-term efficacy of these two drugs was compared in a double-blind crossover trial in 12 patients. The following protocol was used, 24 hour selection period followed by two crossover treatment periods versus double placebo. Exercise stress tests were performed 2 hours after the last dose at the end of each treatment period. Each patient underwent 3 stress tests: the first during the selection period whilst taking verapamil and diltiazem placebo (ET0), the second after the first treatment period at day 7 (ET1) and the third after the second treatment period at day 14 (ET2). A comparison of exercise capacity (ET0 to ET1 and ET2) showed improved effort tolerance and an increase in the ischaemic threshold with calcium blocker therapy. The duration of effort, the maximum sustained load, the rate-pressure product and the time to ST depression were all significantly increased. On the other hand, there were no significant changes in the percentage theoretical maximum heart rate attained, the heart rate at which ST depression occurred, the maximum ST depression and the incidence of angina. A comparison between ET1 and ET2 did not show any difference in the parameters of maximum effort or of the appearance of myocardial ischaemia. The comparison of exercise stress tests performed after treatment with verapamil and after diltiazem showed that the total duration of exercise, the maximum sustained load (in watts) and the rate-pressure product were identical.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

[Myocardial metabolism in angina with angiographically normal coronary arteries].

Myocardial metabolism was studied during rapid atrial pacing in 22 patients with angina and angiographically normal coronary arteries. Pyruvate, non esterified fatty acid and lactate levels were measured in the coronary arteries and veins under basal conditions, at the peak of atrial pacing and during the recovery phase. A control group of 8 patients had neither angina, ST depression, or lactate production during atrial pacing. A correlation was observed between the coronary arterio-venous difference and arterial pyruvate and non esterified fatty acid levels in the 22 patients during the 3 periods of study. The control patients did not differ significantly from the rest of the population. There was a correlation between the coronary arterio-venous difference and arterial lactate levels under basal conditions in all of the study and control groups. This correlation remained significant during atrial pacing and the recovery period only in the control group. It was possible to distinguish a group of 14 patients (64 p. 100) (Group A) with a correlation coefficient of lactate production similar to the control group (+/- 2 standard deviations) during atrial pacing, from a second group of 8 patients (36 p. 100) (Group B) with abnormal myocardial metabolism. The arterial lactate concentrations were similar in both groups in the 3 periods of study. A coefficient of lactate extraction less than 10 p. 100 was observed in 2 patients in Group A and in 7 patients in Group B (88 p. 100, p less than 0.01). One patient in Group B had a coefficient of lactate extraction greater than 10 p. 100 (+ 13 p. 100).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Value of cardiac scintigraphy with I123 meta-iodobenzylguanidine in congestive heart failure. A review].

Heart failure is accompanied by major disturbances of the functioning of the sympathetic nervous system: global overactivation and local modifications of the adrenergic system. 123I-MIBG cardiac scintigraphy is an isotope technique investigating presynaptic adrenergic function. The cardiac uptake of MIBG is decreased during heart failure, reflecting a reduction of norepinephrine reuptake by cardiac presynaptic nerve endings. Alteration of presynaptic function occurs early and plays an important role in the pathogenesis of the deterioration of heart failure. 123I-MIBG cardiac scintigraphy allows in vivo assessment of the myocardial adrenergic reserves of patients with congestive heart failure. It should be proposed in all patients with severe ventricular dysfunction to help define the indications for heart transplantation.

3-Iodobenzylguanidine↗