[Giant left ventricular false aneurysme revealing a silent myocardial infarction]. / Volumineux faux anévrisme de la pointe du ventricule gauche révélant un infarctus du myocarde silencieux.

Left ventricular false aneurysms are rare. They are secondary to a myocardial rupture which is contained by adherent pericardium and scar tissue. LV pseudoaneurysm contains no endocardium or myocardium unlike left ventricular true aneurysm. Most cases of LV pseudoaneurysm are related to acute myocardial infarction in inferior or posterior wall. We report a case of a 56-year-old man with a medical history of chronic cigarette smoking, dyslipidemia, and obesity. The patient had no myocardial infarction before. He was admitted for evaluation of important shortness of breath at effort without chest pain for 5 months. Physical exam find an enlarged left ventricular. The electrocardiogram revealed Q waves and ST segment elevation in leads V1 to V6. Transthoracic echocardiogram showed a large thrombosed apical left ventricular false aneurysm, severe left ventricular dysfunction, which were confirmed by cardiac magnetic resonance imaging, this exam also showed no viability in the mid left anterior descending coronary artery territory. The coronary angiography showed an occlusion of the mid left anterior descending coronary artery and a stenosis of the first diagonal artery. The patient was offered a surgical aneurysectomy with coronary artery bypass. The surgery was successful with amelioration of symptoms. We present a rare case of a giant false left ventricular aneurysm complicating a silent myocardial infarction in the anterior wall. The diagnosis is made by cardiac echocardiogram and cardiac magnetic resonance imaging. Because of the important risk of rupture, the surgical treatment is required.

[Arrhythmogenic right ventricular dysplasia. Report of 4 cases]. / La dysplasie ventriculaire droite arythmogene. A propos de 4 cas.

Arythmogenic right ventricular dysplasia (ARVD) was supposed to be a part of VHL diseases; ARVD is in fact a well defined anatomo-pathological entity, originally described by Fontaine and Frank in 1977. The authors report 4 new cases of ARVD were desmitted at the department of cardio A. The disease was announced by the usual rhythmic disorders. The diagnostics of ARVD was based upon a bundle of electrical, echocardiographic and histological arguments. The rhythmic stability was obtained in three cases with medical treatment, the endocavity ablation was necessary in one case. A study of the diagnostic and therapeutic forms is performed from a literature review.

Third-degree atrioventricular block in a patient under chloroquine therapy.

The first case of chronic cardiac toxicity due to an antimalarial agent was reported in 1971 and since then several cases of heart failure, restrictive cardiomyopathy or atrioventricular block have been ascribed to this family of drugs. We report the case of a 43-year-old woman who developed juvenile chronic arthritis at the age of ten, followed in adulthood by sero-positive rheumatoid arthritis. In 1980 she was put under chloroquine sulfate (hydroxychloroquine was not available) in a dose of 200 mg/d (152.66 mg of chloroquine), with 10 mg/day of prednisone. She developed myalgia and increased skin pigmentation, but disregarded recommendations that these symptoms required discontinuation of chloroquine therapy. She was lost to follow-up, but continued the chloroquine therapy of her own accord. In December 1993, she developed a third-degree atrioventricular block with syncopes requiring implantation of a pacemaker. The rare but well-documented myopathy induced by antimalarial agents can produce early severe lesions of the cardiac muscle, which may have a predilection for the interventricular septum, explaining the risk of atrioventricular block. Although histologic studies were not performed in our patient, the clinical evidence of toxicity, absence of underlying heart disease and fairly young age of the patient pointed to chloroquine toxicity. Periodic cardiac investigations including electrocardiography may be warranted in patients under antimalarial therapy.

[Treatment of ventricular tachycardia by endocardial fulguration. Apropos of 86 cases]. / Le traitement des tachycardies ventriculaires par la fulguration endocavitaire. A propos de 86 cas.

Between 1983 and 1991, 86 cases of ventricular tachycardia (VT) resistant to antiarrhythmic therapy were treated by endocardious catheter fulguration: there were 21 cases of right ventricular dysplasia (RVD), 35 chronic myocardial infarctions (MI), 11 dilated cardiomyopathies (DCM), 10 bundle branch VT, 5 idiopathic septal VT, 3 operated Fallot procedures, 1 Ebstein's anomaly. There were 69 men and 17 women aged 14 to 76 years (average 45 +/- 18 years). The ejection fraction was under 30% in 37 cases. Forty-five VTs were permanent or recurred several times daily; 6 were inducible despite drug therapy and 35 patients had monthly recurrences. A total of 141 different forms of VT were treated in 133 procedures. One session was sufficient in 49 cases; 2 sessions were required in 29 cases; 3 sessions in 6 cases and 4 sessions in 2 cases. A total of 480 DC shocks were delivered with energies of 160 to 300 joules. The CPK-MB levels were 37 +/- 30 i.u./l. The following complications were observed: 7 perioperative deaths, 2 cardiac tamponades requiring surgical drainage, 1 permanent AV block, 5 reversible left ventricular failures. Follow up concerned 79 patients: 5 were followed up for less than 3 months with death occurring from cardiac failure which had been present before the ablation procedure without recurrence of VT. Seventy-four patients were followed up from 3 to 111 months (56 +/- 33 months). Thirty-two patients were without any antiarrhythmic therapy and had no recurrence of VT. Two of these patients developed a different form of VT 2 and 6 years after the catheter ablation.(ABSTRACT TRUNCATED AT 250 WORDS)