[Contribution of cardiac MRI in the initial evaluation and follow-up of myocarditis mimicking acute coronary syndrome: a series of 43 patients]. / Apport de l'IRM cardiaque dans l'évaluation initiale et le suivi des myocardites mimant un syndrome coronaire aigu : à propos d'une série de 43 patients.

AIMS: The diagnosis of acute myocarditis is complex, especially when the clinical presentation mimics an acute coronary syndrome. This condition may promote the progression to dilated cardiomyopathy and the occurrence of severe arrhythmias. A reassessment integrating a cardiac MRI at three months after the acute episode could help identify patients with a poor prognosis. PATIENTS AND RESULTS: This prospective series of 43 consecutive patients hospitalised for acute myocarditis included 36 men and seven women, with a mean age of 32 years, with no indication of heart failure. All patients presented elevated levels of troponin I. Echocardiography showed moderate left ventricular dysfunction in six cases and segmental wall motion abnormalities in 22 cases. After gadolinium injection, a subepicardial late enhancement was observed in 39 cases. Three months after the acute episode, all patients were asymptomatic. The echocardiography and laboratory tests were normal. In 23 cases, the MRI showed persistence of the late enhancement without segmental wall motion abnormality. After a mean follow-up of three years, one patient was lost to follow-up and only one suffered a heart failure revealing a dilated cardiomyopathy complicated by ventricular arrhythmias. CONCLUSION: On admission, the subepicardial localisation of late enhancement in the cardiac MRI is reliable criteria for the diagnosis of acute myocarditis, enabling to rule out an acute coronary syndrome. During follow-up, the persistence of late enhancement has no impact on prognosis. In this series, after a mean follow-up of three years, it was not associated with clinical or paraclinical abnormalities, except in one patient.

[Pulmonary vein leiomyosarcoma extending into the left atrium]. / Léiomyosarcome de la veine pulmonaire avec extension dans l'oreillette gauche.

In this paper, the authors report the case of a 28-year-old man with pulmonary vein leiomyosarcoma presenting subacute respiratory distress. Thoracic computed tomography and transoesophagal ultrasonographic examination of the heart suggested the diagnosis of a heart tumour revealed by the obstruction of the mitral valve and pulmonary oedema. Emergency cardiac surgery revealed the mass to be a leiomyosarcoma, probably extending from the right inferior pulmonary vein and extending into the left atrium. The clinical evolution was complicated because of a sudden local relapse. The patient underwent a second cardiac intervention involving lower right lobectomy followed by adjuvant chemotherapy with an ifosfamide-adriamycin combination. This treatment failed to control the disease and a third cardiac intervention was necessary with second-line gemcitabine-paclitaxel adjuvant chemotherapy. Further recurrences were observed with metastases first in the scalp and then in the spine and adrenal glands leading to the death of the patient 2 years after the diagnosis.

[Cardiac damage due to scorpion envenomation: case involving atrial flutter]. / Envenimation scorpionique avec atteinte cardiaque: à propos d'une observation de flutter atrial.

The purpose of this report is to describe a case of scorpion envenomation observed in northern Chad in a 24-year-old-man with no medical history. The victim rapidly developed supraventricular arrhythmia due to catecholaminergic storm induced by the neurotoxic activity of the venom. Cardiomyopathy that can lead to fatal acute heart failure is a risk after scorpion envenomation. Heart damage is observed in 1% of scorpion envenomation cases and can result from several mechanisms, i.e., adrenergic myocarditis (as in the patient herein), toxic myocarditis or myocardial ischemia. Few articles describing supraventricular arrhythmia following scorpion envenomation have been published. It is paroxystic and regresses spontaneously in case of transient catecholaminergic storm. Occurrence of atrial flutter, even if not associated with heart failure, is an indication of severe scorpion envenomation and requires close patient monitoring and symptomatic treatment using betablocking drugs. The efficacy of specific treatment for scorpion envenomation, i.e., immunotherapy, remains controversial.

[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.

Evaluation of heart failure management in a Military Hospital.

PURPOSE: Evaluate heart failure management in a Military Hospital in 2005. METHODS: Retrospective audit of 46 case records of patients hospitalised with heart failure within the framework of an accreditation procedure. RESULTS: The left ventricular ejection fraction was evaluated in 85% of cases during the reference hospital stay. Systolic heart failure was detected in 63% of cases. At least one NT-proBNP assay was performed for each patient. A global assessment was systematically performed, except for the mini mental state examination in patients aged over 75 years who represented 80% of patients. Initial therapeutic education was provided for 50% of systolic heart failure patients. Prescription rates in systolic heart failure were 76% for angiotensin-converting enzyme inhibitors, 7% for angiotensin receptor antagonists; 84% for at least one medicinal product in the above 2 classes; 68% for beta-blockers and 32% for spironolactone. A hospital discharge report was available for 93% of the patients. Elective re-admissions to hospital for uptitration of treatment concerned 10% of systolic heart failure patients. Emergency hospital re-admissions after a cardiovascular event (usually decompensation), concerned 35% of patients, after an average duration of one year of follow-up. These latter re-admissions, often repeated, led to 4% of additional hospital deaths. The initial hospital mortality rate was 13%. CONCLUSION: Therapeutic patient education is under development. Medication may still be optimised, both qualitatively and quantitatively. Surveillance is planned with a yearly audit.

[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.

La non compaction du ventricule gauche; une cardiomyopathie du sujet jeune : premieres observations africaines

La non compaction du ventricule gauche (NCVG) est une cardiomyopathie congenitale de description recente et probablement rare; caracterisee par une alteration de la structure du myocarde secondaire a une embryogenese incomplete. Les auteurs rapportent trois observations de patients africains porteurs d'une NCVG; jusqu'a present et a notre connaissance jamais decrite dans cette population. Il s'agit d'une serie de trois hommes ages de 23 a 45 ans et originaires d'Afrique subsaharienne. Le premier presentant une cardiomegalie sur un cliche thoracique de realisation systematique etait asymptomatique. Le second; dyspneique a l'effort; etait porteur d'un bloc de branche gauche. Le troisieme etait hospitalise pour un oedeme aigu du poumon. Dans les trois cas; l'echocardiographie trans-thoracique a permis d'evoquer le diagnostic. Le ventri- cule gauche etait dilate et hypokinetique avec un aspect spongieux du myocarde; revelant la presence de trabeculations saillantes separees par des cryptes; localisees a l'apex et a la paroi laterale. Le Doppler couleur permettait de visualiser le remplissage inter-trabeculaire par le flux sanguin. L'IRMcardiaque a confirme cet aspect morpholo- gique specifique. Lamort subite d'origine rythmique; l'insuffisance cardiaque et les accidents emboliques constituent les principales complications de la NCVG. Cette pathologie dont la frequence est certainement sous estimee; se revele volontiers chez l'adulte jeune mais peut etre diagnostiquee a tout age. L'echocardiographie et l' IRM permettent la mise en evidence des criteres morphologiques qui affirment le diagnostic. L'origine genetique de la NCVG a ete recemment rapportee; et les presentes obser-vations demontrent que les mutations responsables sont presentes dans la population d'Afrique subsaharienne. Le depistage familial dans les populations africaines peut s'averer difficile a realiser. La prise en charge therapeutique actuelle est fondee sur le traitement symptomatique de l'insuffisance cardiaque; et peut mettre en oeuvre des techniques parfois peu accessibles en milieu tropical.MOTS-CLeS Non compaction du ventricule gauche - Cardiomyopathie - Echocardiographie

La non compaction du ventricule gauche; une cardiomyopathie du sujet jeune : premieres observations africaines

La non compaction du ventricule gauche (NCVG) est une cardiomyopathie congenitale de description recente et probablement rare; caracterisee par une alteration de la structure du myocarde secondaire a une embryogenese incomplete. Les auteurs rapportent trois observations de patients africains porteurs d'une NCVG; jusqu'a present et a notre connaissance jamais decrite dans cette population. Il s'agit d'une serie de trois hommes ages de 23 a 45 ans et originaires d'Afrique subsaharienne. Le premier presentant une cardiomegalie sur un cliche thoracique de realisation systematique etait asymptomatique. Le second; dyspneique a l'effort; etait porteur d'un bloc de branche gauche. Le troisieme etait hospitalise pour un oedeme aigu du poumon. Dans les trois cas; l'echocardiographie trans-thoracique a permis d'evoquer le diagnostic. Le ventricule gauche etait dilate et hypokinetique avec un aspect spongieux du myocarde; revelant la presence de trabeculations saillantes separees par des cryptes; localisees a l'apex et a la paroi laterale. Le Doppler couleur permettait de visualiser le remplissage inter-trabeculaire par le flux sanguin. L'IRMcardiaque a confirme cet aspectmorphologique specifique. Lamort subite d'origine rythmique; l'insuffisance cardiaque et les accidents emboliques constituent les principales complications de la NCVG. Cette pathologie dont la frequence est certainement sous estimee; se revele volontiers chez l'adulte jeune mais peut etre diagnostiquee a tout age. L'echocardiographie et l'IRMpermettent la mise en evidence des criteres morphologiques qui affirment le diagnostic. L'origine genetique de la NCVG a ete recemment rapportee; et les presentes observations demontrent que les mutations responsables sont presentes dans la population d'Afrique subsaharienne. Le depistage familial dans les populations africaines peut s'averer difficile a realiser. La prise en charge therapeutique actuelle est fondee sur le traitement symptomatique de l'insuffisance cardiaque; et peut mettre en oeuvre des techniques parfois peu accessibles en milieu tropical

[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.

[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.

[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.

The effects of antimalarial drugs on ventricular repolarization.

Cardiotoxicity has become a major concern during treatment with antimalarial drugs. Lengthening of the QTc and severe cardiac arrhythmia have been observed, particularly after treatment with halofantrine for chloroquine-resistant Plasmodium falciparum malaria. The purpose of this prospective study was to evaluate whether antimalarial agents alter dispersion of the QTc and ventricular repolarization dynamicity. Sixty patients with uncomplicated falciparum malaria were randomly allocated in four groups of 15 patients and treated with quinine, mefloquine, artemether, or halofantrine at recommended doses. Patients in treatment groups were compared with a group including 15 healthy controls with no history of malaria and/or febrile illness within the last month. QTc dispersion was measured on surface electrocardiograms. Repolarization dynamicity was analyzed from Holter recordings, which allow automatic beat-to-beat measurement of QT and RR intervals. Plasma drug concentration was determined by reversed-phase high-performance liquid chromatography. No change in QTc dispersion was observed after treatment with quinine, mefloquine, or artemether. Treatment with halofantrine was followed by a significant increase in QTc dispersion at 9 hours (P < 0.0001) and 24 hours (P < 0.01). Assessment of QT heart rate variability by QT/RR nychtohemeral regression slope demonstrated no significant difference between the artemether (mean +/- SEM = 0.170 +/- 0.048), mefloquine (0.145 +/- 0.044), and the control groups (0.172 +/- 0.039). A significant decrease in the Q-eT/RR slope was observed in the quinine group compared with the control and artemether groups (0.135 +/- 0.057; P < 0.04). With halofantrine, a significant increase in the QT/RR regression slope (0.289 +/- 0.118) was observed (P < 0.0002). QTc interval, QT dispersion, and QT regression slope were significantly correlated with halofantrine and quinine plasma concentration. Mefloquine and artemether did not alter ventricular repolarization. Quinine induced a significant decrease in QT/RR slope of the same order of magnitude as those previously observed with quinidine. Both QTc dispersion and QT/RR slope were significantly modified by halofantrine. These repolarization changes were related to a class-III antiarrhythmic drug effect and may explain the occurrence of ventricular arrhythmia and/or sudden deaths reported after halofantrine intake.

[Buerger's disease and coronary disease]. / Maladie de Buerger et atteinte coronaire.

The authors report the case of a 33 year old man with distal occlusive arterial disease diagnosed as Buerger's disease, with two previous transient ischaemic attacks and coronary disease resulting in myocardial infarction. Coronary angiography showed narrowing of the second segment of the left anterior descending artery, occluded distally and not suitable for revascularisation. The observation of coronary artery disease is very rare in Buerger's disease and data of coronary angiography are very sparse in this context. The occurrence of myocardial infarction and the angiographic appearances of the left anterior descending artery raise the question of coronary involvement of Buerger's disease.

[Salmonella aortic valve endocarditis presenting with rupture of a femoral artery mycotic aneurysm]. / Anévrisme mycotique fémoral rompu, révélateur d'une endocardite aortique à salmonelle.

The incidence of Salmonella enteritidis infections has greatly increased over the last few years. Cardiovascular are amongst the most severe extra-digestive complications. The authors report a case of Salmonella enteritidis presenting with rupture of a femoral artery mycotic aneurysm in a chronic alcoholic patient. Salmonella enteritidis was isolated from blood cultures and the operation specimen after the obligatory limb amputation. The outcome was finally favourable after appropriate antibiotic therapy with a residual, stable grade 3 aortic regurgitation. This rare condition is generally observed in immuno-compromised subjects and carries a high mortality (40 to 70% of cases). The initial infectious signs may be masked, and, in these cases, rupture of an aneurysm is often the mode of presentation. Rapid treatment is essential with, ideally, resection of the aneurysm with reestablishment of arterial continuity and adapted, prolonged antibiotic therapy.