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Biomedical subjects

L Fermont

Publications and source records attributed to L Fermont.

At least 73 records · Page 4Linked to original sources

[Acute infectious myocarditis (author's transl)].

Among the primary myocardiopathies resulting from a known cause, acute infectious myocarditis plays an important part. This condition, usually interstitial myocarditis of viral etiology, occurs predominantly in the infant under two years of age. They are characterized by a hypotrophic hypokinetic myocardiopathy which is very hard to differentiate from endocardial fibroelastosis. Fibroelastosis is probably only one possible result of the course of certain myocarditis'. However, on the whole, prognosis is good and the children recover. Typhoid fever and diphtheria may also compromise myocardial function.

Acute Disease↗

[Myocardiopathies secondary to cardiovascular diseases: systolic strain and diastolic overload (author's transl)].

All cardiovascular malformations compromise ventricular function and lead to alterations in the myocardial structure. Most of these are adaptive reactions. However, in some cases, this reaction overreaches its object and leads to an authentic myocardiopathy. This myocardiopathy is usually hypertrophic in obstacles which result in systolic overload of the left ventricle (coarctation peri-orificial stenosis of the aorta, systemic hypertension) or of the right ventricle (pulmonic stenosis), or congestive in diastolic overload by left-to-right shunts or valvular insufficiency. These myocardiopathies may prevent recognition of the signs of the underlying heart disease thereby leading to diagnostic errors and delay in therapy. They may constitute the main factor of an operative decision.

Aortic Coarctation↗

[Treatment of ventricular tachycardia in infancy and childhood with amiodarone].

Ventricular tachycardia, especially in its apparently primary form, is rare in children and difficult to treat, often requiring aggressive methods of reduction or antiarrhythmic drugs unsuited for paediatric practice. Therefore, we investigated the use of amiodarone whose efficacity in the treatment of resistant ventricular tachycardia and good tolerance in children have been established. Three infants, aged from 9 to 15 months, and two children aged 6 and 7 years with apparently primary VT were selected. Etiological investigations were negative in four cases but in one of the older children a left ventricular fibroma was diagnosed and removed surgically. Amiodarone was administered orally at a dose of 500 mg/m2/24 hrs for 5 to 15 days, and then 250 mg/m2/24 hrs for one month in the surgical patient and for 9 to 39 months in the four "idiopathic" cases. Reduction of VT was obtained in all cases 8 to 48 hours after the first dose. There was only one recurrence, attributed to an over-rapid reducing in dosage; it quickly regressed after returning to the initial dosage. Stable sinus rhythm was maintained at long-term: 18 months, 2 years and 5 years after tailing off a course of 20, 40 and 1 month's treatment in 3 children. These cases are considered to be cured, but in one of these children two courses of amiodarone were required, the second for a relapse 3 months after stopping a 9 month's course of therapy. The other two children are still under treatment after 9 and 15 months with no recurrences. There were no hemodynamic, ocular or thyroid side effects. On the other hand, three cases of photosensitivity, two minor and one major requiring termination of therapy after a 20 months course, were observed. In conclusion, amiodarone would appear to be the treatment of choice for ventricular tachycardia in children, reduction of the arrhythmia being obtained in all cases even by oral administration within reasonable limits: its prophylactic value is excellent and clinical tolerance very satisfactory: a definitive cure can be hoped for an idiopathic VT providing that maintenance therapy has been sufficiently prolonged (2 years).

Amiodarone↗

["Straddling" tricuspid valve across an isolated ventricular septal defect. Apropos of 4 cases].

Four cases of children from 10 months to 3 years of age with isolated ventricular septal defects and straddling tricuspid valve are reported. Three patients underwent surgery (mean age: 24 months). The lesion was diagnosed during operation in 2 cases. The VSD was a perimembranous defect with extension to the ventricular inlet in 2 cases, and in the other it was entirely muscular. The straddling involved all the septal leaflet of the tricuspid valve in 1 case. In two cases, there was doubling of the segment with one part crossing the VSD. The left ventricular attachment was a type B in 2 patients and type C in 1 patient. The tricuspid ring was normally situated in all patients (no overriding). In 2 patients, the diagnosis was made with the aid of complementary investigations, and, in particular, 2D echocardiography. One of these patients has not yet undergone surgery as the lesion is well tolerated and because of associated mitral regurgitation. In 3 patients, surgery consisted of repairing the ventricular septal defect, leaving the abnormal part of the tricuspid valve in the left ventricle. All patients survived; there were no cases of post-operative atrioventricular block or signs of tricuspid incompetence. With reference to these three cases, the authors review the main anatomical lesions, the diagnostic signs and different methods of treatment of this condition. Straddling tricuspid valve may present as a simple ventricular septal defect. This diagnosis should be considered in all cases of posterior ventricular septal defects.

Angiography↗

[Prolonged Q-T interval with functional A-V block in neonates and young infants (author's transl)].

A prolonged Q-T interval (0.56 to 0.70 s.) with second degree A-V block was present in 5 children. Auscultation in utero (2 cases) or at birth (1 case) and syncopal attacks at 15 days and 2 months of life led to the discovery of the arrhythmia which was complicated with torsades de pointes. One patient died at 1 month of age; another is treated with propranolol and an internal pacemaker; the last 3 recovered, either spontaneously or with propranolol. The originality of this syndrome of unknown etiology is due to the A-V block, secondary to delayed repolarization (prolonged Q-T interval). Torsades de pointes and ventricular fibrillation are the main risks. Treatment includes beta adrenergic blocking agents associated with a temporarily implanted pacemaker. In a few cases, the internal pacemaker has to be left permanently.

Adrenergic beta-Antagonists↗

[Importance of echocardiography in the evaluation of surgical results in the tetralogy of Fallot].

M mode echocardiography was performed one year after surgical correction of Fallot's tetralogy in 32 patients (average age: 2, 7 years). All patients were asymptomatic without treatment and the average cardiothoracic ratio was 0,56 +/- 0,03. Echocardiographic indices of left ventricular function distinguished 4 patients with myocardial dysfunction (2 cases of poor myocardial protection and 2 double Blalock-Taussig anastomoses). Right ventricular diastolic internal dimensions were increased in 75 % cases. The ratio of right to left ventricular internal dimension was used to classify patients into three groups: Group I (ratio Less Than 0,70) 17 patients; Group II (ratio 0,70 Greater Than 0,80) 4 patients, and Group III (ratio Greater Than 0,80) 11 patients. This ratio was not related to the age of the patient of surgery or to the type of patch used on the right ventricular outflow tract but was related to the pressures recorded at operation after correction. A ratio Greater Than 0,80 was strongly suggestive of a significant residual abnormality which was often curable. Echocardiography has become an essential investigation in the follow up of Fallot's tetralogy after surgical correction: a right: left ventricular ratio Less Than 0,70 obviates the need of control catheterisation. On the other hand, a ratio Greater Than 0,80 is a strong indication for cardiac catheterisation even in the absence of clinical abnormalities.

Child↗

[Anatomic correction of transposition of the great vessels with interventricular communication. A series of 24 consecutive operations].

The results of surgical correction at arterial level in 24 cases of transposition of the great arteries with ventricular septal defect are reported. The majority of children (19/24) had undergone previous pulmonary artery bonding between the ages of fifteen days and 3 months (average 1,5 months). Surgical correction was performed on average 14 months later. This consisted of repair of the ventricular septal defect and arterial shift to reestablish ventriculoarterial concordance with reimplantation of the coronary arteries. In the last 9 cases no prosthetic materials were used on the right outflow tract. The operative mortality was 9/24 (6 of the first 12, and 3 of the last 12 cases). The cause of death was due to associated lesions, congenital (coarctation of the aorta, mitral valve malformation), or iatrogenic related to previous surgery (stenosis of the right ventricular infundibulum). Left ventricular failure was common despite preparation with pulmonary artery banding and merited systematic treatment mainly with arterial vasodilator therapy and prolonged ventilatory assistance. The surviving children are asymptomatic without treatment. Control catheter studies did not show any significant abnormality except in one case of pulmonary hypertension. The exceptional quality of these results, the absence of prosthetic material and the hope of reducing avoidable mortality justify this approach to surgical cure of the malformation. Preparation by pulmonary artery banding and the use of this method in "simple" forms of transposition are questions which remain open to discussion.

Child, Preschool↗