[Complete atrioventricular block of the young adult... do not forget sarcoidosis]. / Bloc auriculoventriculaire complet du sujet jeune... Penser à la sarcoïdose.

The authors report the case of a 27 years old athletic patient, without any antecedents, presenting with a recent complete atrioventricular (AV block, disclosed by an effort dyspnoea and syncope. The electrophysiological exploration showed a nodal AV block. The magnetic resonance imaging revealed the existence of a septal hypersignal in T1 mode enhanced after Gadolinium injection, and left ventricular function normality. It also revealed the existence of a pulmonary parenchyma infiltrate, confirmed by thoracic scanner. Pathological examination of transbronchial biopsies showed noncaseating granuloma, consistent with sarcoidosis. Programmed electrical stimulation induced no ventricular arrhythmia. A dual chamber pace-maker was implanted because of the AV block permanence and the poor clinical tolerance, associated with steroid therapy (prednisolone 1 mg/kg/j). After a 18 months follow-up, the patient remains asymptomatic, and the 12-lead ECG shows a normal AV conduction. The authors discuss the different aetiologies of AVB, and emphasize to realize an exhaustive assessment in young adults. The cardiac localization disclosing sarcoïdosis and the complete AV block disappearance under therapy make that observation original. The occurrence of a complete AV block complicating sarcoidosis poses a management and prognosis problem.

[Heart failure due to non-infectious causes in developing countries: etiologic approach and therapeutic principles]. / Insuffisance cardiaque d'origine non infectieuse en zone tropicale: approche étiologique et principes thérapeutiques.

Cardiovascular disease is a major worldwide health problem with a growing impact in developing countries. Heart failure is the clinical manifestation of many advanced cardiac disorders. It can have numerous etiologies and the incidence of non-infectious causes is increasing with socio-economic development, thus illustrating the global nature of this epidemiologic transition. Several of the numerous non-infectious causes of heart failure involve cardiac diseases specific to tropical areas including dilated cardiomyopathy, endomyocardial fibrosis, and peripartum cardiomyopathy. Other widespread disorders are becoming more common as a result of the epidemiologic transition. Cardiovascular risk factors are changing particularly with regard to the incidence of coronary artery disease, ischemic cardiomyopathy, and hypertension-related complications. The purpose of this article is to provide an overview of non-infectious causes of heart failure in terms of frequency, onset, and therapeutic requirements. Symptomatic treatment of heart failure is same as in developing countries but is often delayed due to shortcomings in the care system.

[Left ventricular noncompaction: a cardiomyopathy in young individuals. Description of first cases in Africa]. / La non compaction du ventricule gauche, une cardiomyopathie du sujet jeune: premieres observations Africaines.

Left ventricular noncompaction (LVNC) is a recently identified and probably rare congenital cardiomyopathy characterized by changes in the structure of the myocardium secondary to incomplete embryogenesis. The purpose of this report is to describe three cases of LVNC involving African patients. To our knowledge these are the first cases described in Africa. All three patients in this series were men from sub-Saharan Africa ranging in age from 23 to 45 years. The first patient in whom cardiomegaly was recognized on a routine chest x-ray was asymptomatic. The second who presented with exertional dyspnea developed left bundle branch block. The third was admitted to the hospital for acute pulmonary edema. In all three cases transthoracic echocardiography suggested diagnosis. The left ventricle was dilated and hypokinetic and the myocardium exhibited a spongy aspect in association with the presence of prominent trabeculations separated by crypts located at the apex and lateral wall. Color Doppler demonstrated that intratrabecular recesses were filled by intraventricular blood flow. Magnetic resonance imaging (MRI) specifically confirmed this morphological feature. Sudden death due to arrhythmia, cardiac insufficiency, and systemic emboli are the main complications of LVNC. The incidence of LVNC, which is certainly underestimated, is highest in young adults but it can be diagnosed at any age. Echocardiography and MRI are effective tools for detection of the morphologic diagnostic criteria. Recent evidence suggests that LVNC is of genetic origin and the data reported here shows that the underlying mutations are present in sub-Saharan populations. Family screening in African populations is still difficult. Therapeutic management is currently based on symptomatic treatment of cardiac insufficiency and can require techniques not readily available in tropical settings.

[Thoracic aortic dissection revealed by systemic cholesterol embolism]. / Dissection de l'aorte thoracique révélée par des embolies systémiques de cristaux de cholesterol.

Systemic cholesterol embolism is a rare complication of atherosclerosis, and has various presentations. Arterial catheterisms are a common cause. However, the association with an aortic dissection has been exceptionally reported. We report the observation of a 70 year-old man, with coronary artery disease, hypertension, diabetes and dyslipidemia. Six months before hospitalization, a coronary angioplasty was performed due to recurrent angina. The association of purpuric lesions on the feet, with acute renal failure confirmed cholesterol embolism syndrome. Transoesophageal echocardiography showed a dissection of the descending thoracic aorta associated with complex atheroma. The evolution was marked by the pulpar necrosis of a toe and by a worsening of the renal failure, requiring definitive hemodialysis. Further echographic control highlighted the rupture of the intimal veil of the dissection. Cholesterol embolism syndrome may reveal an aortic dissection in patients without thoracic symptoms. In such cases, transoesophageal echocardiography is a useful and non-invasive examination.

[Acute myocarditis and eosinophilic pneumonia: good outcome after medical treatment and long-term follow-up]. / Myocardite aiguë et pneumopathie à éosinophiles: évolution favorable après traitement médical et suivi à long terme. A propos d'un cas.

The authors report a case of acute eosinophilic myocarditis (AEM) with acute left ventricular failure preceded by an acute hypoxaemic eosinophilic pneumonia. The diagnosis of myocarditis was confirmed histologically. That of the eosinophilic pneumonia was base on the abundance of eosinophilic polynuclear cells in the bronchoalveolar lavage and appearances on computerised tomography. The pulmonary lesions rapidly and definitely regressed and complete recovery of left ventricular function was obtained by long-term steroid therapy. This favourable outcome has been sustained after 11 years of follow-up despite the presence of chronic mild hypereosinophilia. In the absence of specific clinical and paraclinical data, the diagnosis of AEM was based on the demonstration of an inflammatory infiltrate rich in polynuclear eosinophils and necrotic myocardial lesions. This histological signature may be obtained in vivo by endomyocardial biopsy, the indication of which must be rapidly recognised. Only the instauration of early and intensive steroid therapy seems to influence the outcome which is frequently poor. The synthesis of the anatomo-clinical and experimental data suggests a myocardial aggression by cytotoxic effects of granular protein components released during activation of polynuclear eosinophils. The role of AEM is discussed in the different aspects of cardiac hypereosinophilia.

[Diagnosis of cardiac sarcoidosis and follow-up of 24 consecutive patients]. / Diagnosis de localisations cardiaques et suivi longitudinal de 24 sarcoïdoses.

PURPOSE: Cardiac sarcoidosis is responsible for 50% of deaths which mainly occur by ventricular arrhythmia or conduction disorders. The aim of this study is to determine the value of cardiac explorations for an early diagnosis of these localizations, which are often underestimated and can cause sudden death. PATIENTS AND METHODS: We prospectively studied 24 consecutive patients, aged 33 +/-10 years, presenting with a sarcoidosis. Nine (38%) were asymptomatic and had no treatment. Fifteen (62%) were symptomatic: two (8%) had only pulmonary lesions and 13 (54%) had a polyvisceral disease. Seven (30%) were treated. Thirteen (54%) had an elevation of the disease activity markers. The patients had a 12-lead ECG, an echocardiography (TTE), a Holter ECG and a Magnetic Resonance Imaging (MRI) at inclusion. RESULTS: Realization rate was: 100% ECG (24), 83% TTE (20), 75% Holter ECG (18) and 62% MRI (15). Only two patients (8%) had a cardiac involvement. The first one had a polyvisceral sarcoidosis presenting with a hypokinetic cardiomyopathy and a complete AV block and the second one presented with a complete AV block which revealed sarcoidosis. Both patients had a MRI septal hypersignal and disease activity markers. They were treated with cardiac stimulation and corticotherapy: the first patient died suddenly, the second one remains asymptomatic after a 14 months follow-up. The 22 patients (92%) with normal explorations did not present any cardiac involvement during the follow-up (3.7 +/-1.6 years). CONCLUSIONS: This study confirms the rarity of cardiac involvement in sarcoidosis. An exhaustive cardiac check-up does not seem very productive even for patients presenting with polyvisceral disease or an elevation of disease markers. A systematic 12-lead ECG seems to be the most useful and simple tool for the early diagnosis of cardiac sarcoidosis. The other explorations will be realized according to clinical data. The absence of abnormal findings seems to have a good negative predictive value allowing to rule out a cardiac problem.

[Cardiac extension of a non-Hodgkin lymphoma revealed by an atrial flutter]. / Flutter atrial révélateur de l'extension cardiaque d'un lymphome malin non hodgkinien.

Primary or secondary cardiac lymphomas are not frequent. Their clinical expression is unusual and the diagnosis is rarely made during the patient's life. Our case report, which is a slow atrial flutter with a pericardial effusion, is an uncommon discovery mode for a malignant lymphoma. Their diagnosis and the mechanism of the arythmia were allowed by non-invasive cardiac imagery (transesophageal echography and magnetic resonance imaging), which showed a tumour-like infiltration of the right atrium, of the right ventricle posterior wall, and of the atrioventricular junction. The diagnosis of a high grade B cell malignant non-hodgkin lymphoma, involving the bone marrow, the liver and the kidneys was made by biopsies of lymph nodes, histological analysis of the bone marrow, and a body CT scan. Throughout the first chemotherapy sequence, we observed a spontaneous return to a sinusal rhythm, and the cardiac MRI showed a regression of the myocardial infiltration and of the pericardial effusion; moreover, the patient's state improved and the peripheral lymph nodes shrank back to a normal size. However, the patient passed away, due to neurological complications 13 months after the diagnosis of lymphoma, without recurrence of cardiac involvement.

Gastrin and pepsinogen changes during an Ostertagia ostertagi challenge infection in calves.

Daily changes in serum gastrin and pepsinogen concentration have been studied during two types of infection with Ostertagia ostertagi in calves. In a first experiment two calves were trickle infected (10 times 10,000 L3 Ostertagia) and two animals received a single infection of 100,000 L3 Ostertagia. Gastrin and pepsinogen changes are discussed in relation to adult wormburdens. The second experiment involved 8 calves and was designed to investigate pepsinogen and gastrin changes following a challenge infection in previously sensitized calves. The high dosed group was infected with 5,000 L3 O. ostertagi during 30 days, the low dosed group received 500 L3 O. ostertagi and group 3 served as uninfected control. At day 41 post infection all animals were treated with oxfendazole and on day 61 challenged with 100,000 L3 O. ostertagi. Only in the high dosed group a distinct pepsinogen and gastrin reaction was noticed. Both parameters dropped to almost preinfection levels after treatment. Two days post challenge a moderate rise (+/- 1,000 mU tyr) of the pepsinogen concentration was observed in the previously infected animals and gastrin showed a temporary slight increase in several animals 8 to 10 days post challenge. The effect of treatment and challenge infection is discussed in relation to gastrin and pepsinogen changes and immunity.