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Biomedical subjects

Y Grosgogeat

Publications and source records attributed to Y Grosgogeat.

At least 19 recordsLinked to original sources
PubMed1992

[Coronary pathology after heart transplantation].

Graft coronary disease is a frequent and devastating complication with rapid development after heart transplantation. Until now, non-invasive and invasive methods have proved to be insensitive in the prediction and detection of the early stages of this disease. Conventional arteriography is considered as the only reliable means of diagnosis, but it remains insensitive in the accurate evaluation of the severity of graft coronary lesions (obliterative, diffuse and distal lesions). Precise quantitation of coronary lumen changes may be a sensitive method for the accurate evaluation of graft coronary disease and help in the understanding of the natural course of development of this disease. The pathogenesis of the disease is still unclear. It is possible that graft coronary disease is a consequence of non-treated low-grade cellular rejections. In most cases, retransplantation must be considered as the unique solution.

Coronary Angiography↗
PubMed1992

Systemic embolism as a complication of percutaneous mitral valvuloplasty.

Systemic embolism is a potential and severe complication of percutaneous mitral valve dilatation. In our series of 80 cases, the incidence of systemic embolism was 3.75% (3 cases). Two cases occurred during the procedure itself. The cause of embolism was different in each case: cruoric thrombus formation occurred in 2 cases during or after dilatation, and was attributable to inappropriate heparinization, and catheter and guidewire thrombogenicity. In both cases heparin administration was delayed or given at a lower dosage. In the third case, calcific embolism occurred several days after valve dilatation. We think that the embolic calcified fragment was detached from the mitral leaflet at the time of or after balloon inflation. In these 3 cases, intraatrial thrombus mobilization was not the mechanism of systemic embolism. In 2 cases, transesophageal echocardiography had been performed before dilatation and excluded the presence of an atrial thrombus the day before the procedure. It is concluded that, together with mobilisation of left atrial thrombi, which can be adequately detected by transesophageal echocardiography, catheter-induced thrombi represent a significant cause of embolic complications and must be prevented by giving full-dose heparin during the total duration of the procedure. Calcific embolism may also occur, and may become more frequent if mitral valve balloon dilatation is proposed to a larger number of patients with valvular and subvalvular calcifications.

Aged↗
PubMed1992

Carotid stenosis is a powerful predictor of a positive exercise electrocardiogram in a large hyperlipidemic population.

Hypercholesterolemia is a major risk factor in coronary heart disease (CHD) and ischemic stroke. However, there is no general agreement on the usefulness of systematic screening of patients with hyperlipidemia by stress exercise electrocardiogram (ECG). The feasibility of this approach would depend on selecting patients with a high risk of CHD, since the sensitivity and specificity of the test depends on the prevalence of the disease. In view of the association of CHD and ischemic stroke, we undertook a study to determine whether the presence of atherosclerosis in the carotid arteries was predictive of a positive exercise ECG in a group of 778 asymptomatic patients referred to their hyperlipidemia. We a much higher percentage of positive exercise ECG in patients with carotid atherosclerosis in our ultrasonographic examinations. In a multiple regression analysis which included 13 parameters (age, sex, body mass index, arterial blood pressure, lipid parameters, serum level of glucose, smoking status and the severity of carotid lesions), the strongest predictors of a positive exercise ECG test were age (P = 0.014) and the degree of carotid atherosclerosis (P = 0.010). We therefore conclude that hyperlipidemic patients with atherosclerotic lesions on carotid arteries would benefit most from screening by the exercise ECG.

Adult↗
PubMed1992

Cardiomyopathy in Friedreich's ataxia: a Doppler-echocardiographic study.

Heart involvement is frequent in Friedreich's ataxia (FA), the most prevalent of the spino-cerebellar degenerative diseases, which is inherited with an autosomal recessive pattern. However, the pathophysiological link between cardiac and neurological disorders is not yet clearly established. We compared a group of 10 patients with FA to a control group (C) of 16 normal subjects, using Doppler-echocardiography. To see whether cardiac involvement was specific to FA, the data of patients with FA were also compared to those of patients with autosomal dominant olivo-ponto-cerebellar atrophia (OPCA), another spino-cerebellar degenerative disease. There was an increase in left ventricular mass index in FA (154 +/- 9 g.m-2 vs 99 +/- 7 g. m-2 in C, P < 0.001), systolic function was normal, the ejection fraction (EF) slope and E/A ratio were decreased (85 +/- 9 mm.s-1 vs 130 +/- 7 mm.s-1 in C, P < 0.001 and 1.5 +/- 0.1 vs 1.7 +/- 0.1 in C, P < 0.01, respectively), while the isovolumic relaxation period was increased (96 +/- 3 ms vs 92 +/- 2 ms in C, P < 0.01). Deceleration time and time-velocity integrals of A wave to total mitral flow were not modified. In OPCA only the E/A ratio was decreased (1.5 +/- 0.1 vs 1.7 +/- 0.1 in C, P < 0.05). These data show the presence of cardiomyopathy in FA with left ventricular hypertrophy and suggest the presence of diastolic function abnormalities. The cardiomyopathy seems specifically associated with FA and not to spino-cerebellar degenerative disease in general.

Adolescent↗
PubMed1992

Plasma calcitonin gene-related peptide decreases in chronic congestive heart failure.

To investigate the role of calcitonin gene-related peptide (CGRP) in cardiac failure, a sensitive and specific radioimmunoassay was developed to study plasma levels of CGRP in 37 normal subjects and 41 patients with heart failure (HF). The mean plasma levels of CGRP were 294.3 pg.ml-1 (SEM: 41.4) in normal subjects and 121.2 pg.ml-1 (SEM: 21.2) in HF patients. The significant decrease observed in HF patients suggests that CGRP is involved in the pathogenesis of heart failure via a direct effect or via modulation of sympathetic nervous activity.

Calcitonin Gene-Related Peptide↗
PubMed1992

Lack of platelet-activating factor release during reversible myocardial ischaemia.

Platelet-activating factor (PAF) is involved in experimental models of myocardial ischaemia, and PAF infusion can cause thromboxane release. Thromboxane is produced during brief episodes of reversible myocardial ischaemia in patients with coronary heart disease. To learn whether PAF synthesis is associated with thromboxane production in mild myocardial ischaemia, we performed rapid atrial pacing in four patients with angina pectoris which caused chest pain, ST segment depression (delta ST = -1.8 +/- 0.2 mm) and lactate excretion in the coronary sinus (percent lactate extraction decreased from 20 +/- 6% to -15 +/- 9%). Thromboxane B2 was produced causing a positive transmyocardial gradient (from 88 +/- 154 pg.ml-1 baseline to 1770 +/- 1407 pg.ml-1 at the peak) but there was no PAF release into coronary sinus blood. In four other patients we determined whether more pronounced ischaemia could be associated with PAF synthesis. Coronary sinus blood was sampled before and during balloon occlusion of a major coronary artery: PAF was not detected in coronary sinus, whereas percent lactate extraction decreased from 24 +/- 6% to -63 +/- 22% (n = 4). We conclude that PAF plays a minor role in short episodes of reversible ischaemia and does not participate in thromboxane production.

Angina Pectoris↗
PubMed1992

Comparison of DDD and 'VVI-R like' pacing during moderate exercise: echo-Doppler study.

The non-invasive haemodynamic comparisons of DDD and 'VVI-R like' pacing at rest and during moderate exercise by echo Doppler are reported. Twelve patients (six males, six females, mean age 48.2 years) with a dual chamber pacemaker were submitted to a series of two exercise tests in a semi-supine position, the first test in DDD mode and the second test in a 'VVI-R like' mode: VVT mode, during which pacing rate was externally increased by chest wall stimulation. During the second test, the workload profile was matched to that of the first test (66 watts and same exercise stages) and ventricular pacing rate was incremented via chest wall stimulation and reproduced exactly the heart rate profile of the first test in DDD mode. The heart rate averaged 81 beats.min-1 at rest and reached 116 beats.min-1 during exercise. At rest and throughout exercise tests, aortic blood flow velocity spectra were continuously recorded on video tape and analysed with the calculation program of the echocardiograph. At rest, ejection time, flow velocity integral, flow acceleration and stroke volume differed between DDD and 'VVI-R like' mode while other parameters did not. During exercise all but two parameters differed. DDD mode especially was associated with a larger stroke volume (81.9 vs 70.9 ml; P less than 0.001) and cardiac output (9.24 vs 8.011.min-1; P less than 0.001) than VVI-R mode.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Myocardial viability in patients with Q wave myocardial infarction and no residual ischemia.

BACKGROUND: Coronary revascularization in patients with persistent angina after myocardial infarction reduces the incidence of recurrent angina pectoris and myocardial infarction and improves left ventricular function. The results of revascularization after a Q wave myocardial infarction when there is no residual ischemia may depend on myocardial viability. METHODS AND RESULTS: To determine whether there was viable myocardium in the infarct area in the absence of clinical and scintigraphic evidence of myocardial ischemia, 15 asymptomatic patients with a Q wave myocardial infarction, no redistribution on stress 201Tl test, and single-vessel disease (greater than 70% stenosis) with persistent anterograde blood flow were randomized to percutaneous transluminal coronary artery angioplasty (PTCA) or conservative medical treatment. After 2 months of follow-up, mean coronary blood flow measured by Doppler catheter in the infarct-related artery was higher in the PTCA treatment group (33 +/- 6 ml/min, n = 8) than in the conservative treatment group (16 +/- 4 ml/min, n = 7; p less than 0.05 between groups). The 201Tl pathological-to-normal ratios measured on postexercise images did not change in patients treated conservatively during the follow-up period (delta = +1.1 +/- 2.2%; NS from baseline) but increased significantly in patients treated by PTCA (delta = +8.5 +/- 2.3%; p less than 0.01 from baseline; p less than 0.05 between groups). Segmental wall motion improved on left ventricular angiography 2 months after PTCA (delta = +11.5 +/- 2.2%; p less than 0.001 from baseline) significantly more than in the conservative treatment group (delta = +4.1 +/- 1.4%; p less than 0.05 between both groups). Improvements of 201Tl ratios and segmental wall motion indexes correlated significantly (r = 0.73, p = 0.002). The mild improvement of global left ventricular ejection fraction measured in the PTCA treatment group did not differ significantly from changes in the conservative treatment group. CONCLUSIONS: Successful angioplasty of the stenotic infarct artery in patients with a Q wave myocardial infarction and no residual ischemia improved coronary flow, 201Tl uptake in the infarct area, and regional wall motion. Therefore, myocardial viability may last several weeks, as long as residual blood flow persists in the infarct-related artery. Optimal assessment of viability by imaging techniques should identify patients who are most likely to benefit from revascularization.

Angioplasty, Balloon, Coronary↗
PubMed1992

[Right ventricular dysplasia].

Arrhythmogenic right ventricular dysplasia is responsible for ventricular tachycardia affecting an apparently healthy heart. It can sometimes lead to sudden death, which may be the presenting symptomatology of the disease. It results from fibro-adipose infiltration of the free wall of the right ventricle, and sometimes of the septum, possibly secondary to myocarditis. The prognosis depends upon the quality of the left ventricle. If it is healthy, the only risk is that of arrhythmia. Treatment using anti-arrhythmic drugs is most often effective and, with proper management, the prognosis is good and the risk of sudden death eliminated. If the left ventricle is abnormal, there is the risk that dysplasia associated with arrhythmia will progress to right then congestive cardiac failure in the context of a dilated idiopathic cardiomyopathy with ventricular tachycardias originating on the right side. Arrhythmogenic right ventricular dysplasia is a notable cause of sudden death in athletes. Routine screening of such individuals is justified, as is that of those with high risk occupations (locomotive and vehicle drivers, etc.).

Adolescent↗
PubMed1992

[VVI mode cardiac pacing: cause or risk factor of cerebral embolism?].

Epidemiological studies suggest that VVI pacing is associated with a higher risk of embolic complications than atrial or dual chamber pacing. However, no studies have been performed on pacemaker patients admitted to a neurological department with a cerebral embolism. The authors report the cases of 8 patients (6 men and 2 women) with an average age of 74 years and having the following characteristics: 1) a cerebral embolism, 2) a permanent cardiac pacemaker (7 VVI and 1 DDD mode). The average delay between implantation of the pacemaker and the neurological complication was 31 months. Cardiological investigations at the time of admission showed: a clinically evident cause of cardiac embolism in 3 cases (2 with VVI and 1 with DDD pacing); paroxysmal or permanent atrial fibrillation in 4 cases with VVI pacing at the time of the embolic event (in only one case at the time of implantation); various echocardiographic abnormalities in 6 of the 7 patients who underwent this examination, mainly left atrial dilatation (6/7), septal wall motion abnormalities in all related to ventricular pacing and unexplained left ventricular dilatation in 2 patients with VVI pacemakers. These results suggest that although the etiology of cerebral embolism was probably multifactorial in some patients, VVI packing probably a predisposing role, though not the only cause, and could be considered to be an embolic risk factor as suggested by previous epidemiological studies. These preliminary retrospective data should be interpreted cautiously taking into account the small population size. Prospective studies on pacemaker patients with cerebral embolism are required.

Aged↗
PubMed1992

[Ventricular tachycardia in a patient with rate-responsive cardiac pacemaker].

The authors report a case of syncopal ventricular tachycardia in a patient with a respiratory-dependent rate responsive pacemaker, followed-up for valvular heart disease with severe left ventricular dysfunction and sustained atrial and ventricular arrhythmias. The introduction of low dose betablocker therapy with reinforcement of the treatment of cardiac failure controlled the ventricular arrhythmia, after suppression of the data responsive function had been shown to be ineffective. The authors discuss the role of the rate responsive function in the triggering of the ventricular tachycardias.

Aged↗
PubMed1992

[Non invasive evaluation of cardiovascular effects of nebivolol in patients with cardiac insufficiency].

The results of several studies, mostly without controls, have suggested that betablockers, administered at progressively increasing doses, may be beneficial in cardiac failure. Based on this hypothesis, betablockers with a peripheral vasodilator effect, such as Nebivolol, could be particularly valuable in this indication. A preliminary study of its tolerance, haemodynamic and neurohormonal effects was carried out with a noninvasive methodology in 12 patients with cardiac failure in sinus rhythm, 8 men and 4 women (average age 53 +/- 12 years), all of whom had Class III or IV symptoms according to the NYHA Classification. The protocol had 2 phases: the first was an open phase during which Nebivolol was administered at a dose of 1 mg/day for 48 hours then 2.5 mg/day for 72 h. In the second phase, the patients were randomly separated into 2 groups, one to receive placebo and the other 2.5 mg for one week then 5 mg of Nebivolol for the 5 remaining weeks. The heart rate decreased significantly from 70 +/- 3 to 63 +/- 4 beats/min (p < 0.01) with Nebivolol 1 mg/day without further slowing at the 2.5 mg dosage. During the randomised phase, the heart rate remained stable in the Nebivolol group but increased to its initial value in the group given placebo. No aggravation of symptoms was observed in the Nebivolol group. No significant changes in cardiac output, parameters of cardiac loading or contractility could be demonstrated after 6 weeks' treatment. During submaximal exercise testing, plasma concentrations of catecholamines and atrial natriuretic factor tended to be higher with Nebivolol than with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1992

[Peripheral calcific embolism after percutaneous mitral valvuloplasty].

The authors report a case of calcific embolization after percutaneous mitral valvuloplasty. The nature of the embolism was confirmed by anatomopathological examination after popliteal embolectomy. This complication would appear to be extremely rare but represents an additional risk in patients with calcific mitral stenosis.

Adult↗
PubMed1992

[Experimental study of fulguration on a healthy ventricle. I. Acute lesions].

The effect of fulguration shocks applied to the healthy ventricular myocardium in 6 pigs weighing between 63 and 100 kg showed that for shocks with the same energy level as those used in clinical practice, the immediate effects of fulguration result in a hemorrhagic zone with a diameter of up to 15 mm. Histopathological examination revealed tearing of the cardiomyocytes which is probably related to barotraumatic phenomena. Deflagrating shocks of 90 Joules, with a short development time (non-self-inductive circuit) can lead to perforation of the myocardium in both the right and left ventricles. In this animal model, arrhythmia was rare and did not lead to sudden death in any case. No vascular damage was observed.

Acute Disease↗
PubMed1992

[Value of antimyosin monoclonal antibody scintigraphy in the diagnosis of acute myocardial infarction].

A 53 year old woman developed chest pain with transient anterior subepicardial ischaemic ECG changes and a mild increase in serum myocardial enzyme concentrations. She was admitted to hospital some time later but there were no electrocardiographic signs of infarction. Echocardiography was considered to be normal. Coronary angiography showed no significant stenosis and there were no segmental wall motion abnormalities on left ventriculography. The diagnosis of a non-Q wave infarct was confirmed by myocardial scintigraphy using antimyosin monoclonal antibodies labelled with Indium 111. The site and size of the necrosis were also determined by this non-invasive investigation.

Antibodies, Monoclonal↗
PubMed1992

[Experimental study of fulguration of healthy ventricle. II. Chronic lesions].

The effect of fulguration shocks was studied using healthy ventricular myocardium of 12 pigs weighing between 63 and 100 kg. With shocks of equal energy to those used clinically, lesions seen 24 hours after the session in two pigs showed the formation of loose fibrosis and of marked cellular infiltration as well as zones of hypercontraction with calcium precipitation. The size of chronic lesions seen during periods ranging from one week to 2 months was studied in 4 pigs. Transmural plaques with a diameter of 1.5 to 2 cm were seen in the right ventricle. For the same energy levels of 240 Joules delivered to left ventricular tissue, lesions were of the same size but were never transmural. Under certain conditions, lesions were disposed in the direction of the neutral electrode.

Acute Disease↗