[Chemotherapy and cardiotoxicity]. / Chimiothérapie et cardiotoxicité.

Among the various anticancer drugs, used alone or in combination during courses of chemotherapy, anthracyclines (leader: doxorubicin) are responsible for direct myocardial toxicity, which can exceptionally be acute, but more often chronic with a delayed onset. This cardiotoxicity is directly proportional to the cumulative dose administered and the recommended total dose for doxorubicin is 550 mg/m2. The risk factors able to potentiate cardiotoxicity must be analysed before starting chemotherapy and follow-up by ultrasonography and/or isotope ejection fraction must be repeated before each course. The treatment of anthracycline-induced heart failure consists of digitalis alkaloids combined with angiotensin converting enzyme inhibitors. The cardiac toxicity of 5FU is currently explained by the theory of coronary spasm, based on clinical findings such as chest pain associated with ischaemic electrical modifications. The incidence of this toxicity is low, but it can be fatal. Exceptional examples include the cardiotoxicity induced by high-dose cyclophosphamide responsible for acute haemorrhagic myocarditis, potentiation of the cardiotoxic effect of anthracyclines by dacarbazine and plicamycin, and serious ventricular and supraventricular arrhythmias induced by amsacrine. Among the various cytokines used in oncology, interferon is responsible for heart failure, reversible after stopping treatment, but also for ventricular arrhythmias, or even sudden death, the pathophysiology of which still remains unclear.

[Significance of lymphoplasmocytic infiltration in arrhythmogenic right ventricular dysplasia. Apropos of 3 own cases and review of the literature]. / Signification des infiltrats lymphoplasmocytaires dans la dysplasie ventriculaire droite arythmogène. A propos de 3 cas personnels et d'une revue de la littérature.

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.

[Outcome of arrhythmogenic right ventricular dysplasia. Apropos of 4 cases]. / Modalités évolutives de la dysplasie ventriculaire droite arythmogène. A propos de 4 observations.

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.