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Biomedical subjects

F Fontaliran

Publications and source records attributed to F Fontaliran.

At least 37 records · Page 2Linked to original sources
PubMed1996

[Right precordial leads and sudden death. Relation with arrhythmogenic right ventricular dysplasia].

Non-coronary ST-segment elevation during right sided chest pain has been described in subjects with episodes of ventricular fibrillation at rest. This syndrome has been attributed to functional phenomena or to structural myocardial changes. A personal case has features belonging to two categories: ST-segment elevation observed before, during and after episodes of arrhythmia was compared to 11 previously recorded ECG recordings. Right ventricular dysplasia was shown by electrocardiography, electrophysiology and echocardiography. In addition, ST-segment elevation is classified in 3 categories: triangular and dome-shaped are the most commonly observed forms during the arrhythmias: the third form with "saddle"-shaped appearances has not been previously described and would seem to be a minor equivalent observed during intercritical periods. This form is found in 30% of clinically documented cases of arrhythmogenic right ventricular dysplasia.

Arrhythmias, Cardiac↗
PubMed1995

The arrhythmogenic right ventricle. Dysplasia versus cardiomyopathy.

Twenty-four patients presenting with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ventricular tachycardia of right ventricular origin associated with structural abnormalities of the right ventricle) were divided into two groups with left ventricular ejection fraction (LVEF) above or below 45%. The distribution of LVEF in the group with LVEF below 45% was comparable with the distribution in 6 patients with idiopathic dilated cardiomyopathy who had ventricular tachycardia originating in the left ventricle (P = 0.2). They also had the same unfavorable long-term prognosis. Therefore, it is suggested that the term, arrhythmogenic right ventricular cardiomyopathy (ARVC), be restricted to patients with a LVEF below 45%. Histological data obtained in the ARVC group showed signs of acute or chronic myocarditis (in the right and left ventricles). It can be hypothesized that patients with arrhythmogenic right ventricular dysplasia (ARVD) may be prone to develop infectious myocarditis. In patients in whom an abnormal host immune response had been seen, progressive deterioration of right and left ventricular function could be observed. This pattern may be superimposed on the genetically determined background of ARVD. This could explain the wide spectrum of clinical presentation observed in patients with tachycardia originating in an abnormal right ventricle.

Adolescent↗
PubMed1995

[Significance of lymphoplasmocytic infiltration in arrhythmogenic right ventricular dysplasia. Apropos of 3 own cases and review of the literature].

Three patients with typical histological signs of arrhythmogenic right ventricular dysplasia progressed to fulminating heart failure in 1 case and unexplained sudden death in the other two. There were signs of superacute myocarditis in the first case, previous healed pericarditis in the second and chronic myocarditis in the third case. These cases suggested the presence of an inflammatory process complicating the substrate of the dysplasia. Arrhythmogenic right ventricular dysplasia seems to be a developmental defect which is complicated in 50 to 70% of patients, according to a review of 74 cases reported in the literature, by a varying degree of myocarditis suggesting particular susceptibility of these patients to infection and explaining the presence of unusual amounts of fibrous tissue in some and the so called "progressive" nature of the disease in other patients.

Adult↗
PubMed1995

[Outcome of arrhythmogenic right ventricular dysplasia. Apropos of 4 cases].

The authors propose a classification of the outcome of arrhythmogenic right ventricular dysplasia with reference to 4 selected cases with a follow-up period of over 9 years. In type I, the left ventricular ejection fraction is normal (EF > 50%) and the risk, exclusively arrhythmic, can be controlled by appropriate antiarrhythmic therapy. This is the commonest form of arrhythmogenic right ventricular dysplasia with different varieties according to the degree of dilatation of the right ventricle. In type II, there is a variable degree of left ventricular involvement (30 < EF < 50%) either by extension of a comparable disease process as observed in the right ventricle or by an isolated or superimposed phenomenon of myocarditis. This form is stable and may remain stable for many years providing the arrhythmias are correctly treated. In type III, progressive degradation of the myocardium is observed over a period of about 10 years with a clinical presentation comparable to that of certain arrhythmogenic dilated cardiomyopathies which are often hereditary. In this case, the patients have an arrhythmic risk associated with that of cardiac failure which becomes progressively irreversible. The histology shows interstitial fibrosis with biventricular lymphocytic infiltration suggesting an autoimmune phenomenon. Therefore, the classification of cases of arrhythmogenic right ventricular dysplasia depends on the potential evolutivity of the lesions. When the patient is seen in the early stages of the disease, the prognosis should be garded, especially in a hereditary form.

Adult↗
PubMed1995

[Arrhythmogenic right ventricle: dysplasia or cardiomyopathy? Value of left ventricle ejection fraction].

The left ventricular ejection fraction (LVEF) of 76 patients suffering from arrhythmogenic dysplasia or cardiomyopathy of the right ventricle (ventricular tachycardia associated with structural abnormalities of the right ventricle) demonstrated two subgroups situated above and below 45%. Values of LVEF less than 45% were similar to those of a control population of 6 cases of idiopathic dilated cardiomyopathy with ventricular tachycardia of left ventricular origin (p = 0.2). These patients also have the same unfavourable long-term prognosis. Histological data obtained from four cases belonging to the group of patients with dysplasia or cardiomyopathy of the right ventricle with a low ejection fraction demonstrated the presence of signs of myocarditis involving both ventricles. This suggests that these patients may suffer from an infectious phenomenon superimposed on a specific histological substrate, which may lead to deterioration of their myocardial function. These results are in line with those of the literature. The term arrhythmogenic cardiomyopathy of the right ventricle should therefore be reserved to the subgroup of patients with an LVEF less than 45%. Finally, arrhythmogenic cardiomyopathy of the right ventricle appears to be a complication of dysplasia following the development of a myocarditic phenomenon. This may explain the wide range of clinical forms observed in patients with ventricular tachycardia of right ventricular origin associated with structural abnormalities of the right ventricle.

Adolescent↗
PubMed1994

Long-term effects of dynamic aortomyoplasty.

Aortomyoplasty consists of wrapping the latissimus dorsi muscle (LDM) around the ascending aorta and electrostimulating it during diastole. The ascending aorta will act as an ectopic neo-ventricle compressed during diastole, thus reproducing the effects of long-term diastolic counterpulsation. In 5 goats, the right LDM was transferred to the thoracic cavity after removal of the second rib. The ascending aorta was enlarged by a pericardial patch and wrapped with the LDM. Postoperative electrostimulation was delivered in a counterpulsating manner. Hemodynamic studies were performed at 12 and 24 months postoperatively. Percent increase in the subendocardial viability index (diastolic pressure-time index/systolic tension-time index) was calculated using unassisted and assisted cardiac cycles with the stimulator off versus the stimulator on at a 1:1 ratio in the basal state and after acute heart failure was induced by the administration of high doses of propranolol hydrochloride. Diastolic counterpulsation of the ascending aorta resulted in significant improvement in the subendocardial viability index long term, both in basal state conditions and after induced cardiac failure. During heart failure, aortomyoplasty increased the cardiac output and decreased systemic vascular resistance. Histopathologic studies up to 24 months showed preservation of the histologic structure of the aortic wall and no evidence of thromboembolism. Tight adhesions developed between the aortic wall (including the pericardial patch) and the LDM. The diameters of the enlarged aortas showed no significant differences compared with diameters immediately postoperatively. In conclusion, aortomyoplasty produces chronic diastolic augmentation with preservation of aortic structure. After induction of heart failure, aortomyoplasty offers efficient circulatory support.

Animals↗
PubMed1993

[Holter and sudden death: value in a case of arrhythmogenic right ventricular dysplasia].

The authors report the first case of arrhythmogenic right ventricular dysplasia presenting with a sudden death due to primary ventricular fibrillation (ventricular fibrillation not preceded by ventricular tachycardia) recorded by the Holter method. The patient was a 56 year old man whose only complaint was near syncopal case is the fact that it is the first documented case of ventricular fibrillation revealing arrhythmogenic right ventricular dysplasia, the diagnosis of which was made at autopsy. In addition, the Holter recording showed the factors which triggered the arrhythmia: the "trigger" of 4 monomorphic ventricular extrasystoles during the minute preceding the ventricular fibrillation; the arrhythmogenic substrate giving rise to late ventricular potentials and, finally, the analysis of the R-R intervals suggesting a role of the sympathetic and parasympathetic nervous systems. Holter recordings could help identify subjects at high risk of severe ventricular arrhythmias.

Adipose Tissue↗
PubMed1993

[Arrhythmogenic right ventricular dysplasia. A new clinical entity].

Arrhythmogenic right ventricular dysplasia has been identified in 1977. It affects the right ventricle and its etiology is unknown. It has been recently included in the group of cardiomyopathies since it affects mainly the right ventricular muscle. It is found in young adults, frequently sportsmen who have a nearly normal cardiac physical examination. Ventricular arrhythmias could lead to palpitations, syncopes or even sudden death. This accident could be the first presenting sign of the disease. Two physiopathogenic mechanisms have been considered: heredo-familial origin or the result of a burned out myocarditis which could be the result of an abnormal immunological response. Its treatment mainly involves antiarrhythmic drugs. In the resistant cases ablative techniques, implantable defibrillator or surgery and even cardiac transplantation could be considered. Correctly treated, ARVD has a good prognosis. More extensive studies are necessary both on the clinical as well as the basic science standpoints.

Adolescent↗
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

[Focal junctional tachycardia in adults. Anatomo-electrophysiological aspects apropos of a case].

The authors report the case of a 65 year old patient with focal junctional tachycardia complicating infectious myocarditis which had a fatal outcome. The ECG recordings showed episodes of tachycardia alternating with junctional rhythm at 90/min. There were signs of retrograde conduction. The anatomopathological findings were typical of acquired myocarditic lesions in the lower part of the atrioventricular node with congenital abnormalities, in particular a bifid node and His bundle with an accessory paraseptal atrioventricular bundle. This is the first description, to the best of the authors's knowledge, of junctional tachycardia associated with a latent pre-excitation.

Aged↗
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

[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↗
PubMed1991

Comparative anatomy and histology of the radial artery and the internal thoracic artery. Implication for coronary artery bypass.

Anatomical characteristics of the radial a. were compared to those of the internal thoracic a., considered as a gold standard in coronary surgery. The length, the diameter, the collateral distribution and the wall thickness of these two arteries were studied comparatively. In addition, a comparative histological analysis was carried out. Anatomical and histological characteristics of these two arteries have important implications for coronary artery bypass.

Angiography↗