Factors associated with early atrial fibrillation after ablation of common atrial flutter. A single centre prospective study.

BACKGROUND: The occurrence of early atrial fibrillation (< or = 6 months) after ablation of common atrial flutter is of clinical significance. Variables predicting this evolution in ablated patients without a previous atrial fibrillation history have not been fully investigated. OBJECTIVES: The aim of the present study was: (1) to identify predictive factors of early atrial fibrillation (< or = 6 months) in the overall population following atrial flutter catheter ablation; (2) to identify predictive variables of early atrial fibrillation following (< or = 6 months) atrial flutter catheter ablation within a subgroup of patients without documented prior atrial fibrillation. METHODS: This study prospectively included 96 consecutive patients (age 65 +/- 13 years; 18 women) over a 12-month period. Their counterclockwise flutter was ablated by radiofrequency, by the same operator, with an 8-mm-tip catheter. Clinical, electrophysiological and echocardiographic data were collected and 27 variables were retained for analysis: age; gender; type of atrial flutter (permanent vs paroxysmal); symptom duration (months +/- SD); pre-ablation history of atrial fibrillation; structural heart disease; left ventricular ejection fraction (%); left atrial size (mm); cava--tricuspid isthmus dimension; septal isthmus dimension; systolic pulmonary pressure > or < or = 30 mmHg; right atrial area; left atrial area; isthmus block; number of radiofrequency applications (+/- SD); antiarrhythmic drugs at discharge; left ventricular diastolic diameter; left ventricular systolic diameter; left ventricular telediastolic volume; left ventricular telesystolic volume; A-wave velocity (cm . s(-1)); E-wave velocity (cm . s(-1)); E/A; isovolumetric relaxation time; E-wave deceleration time; significant mitral regurgitation and flutter cycle length (ms). RESULTS: Of the 96 consecutive ablated patients, early atrial fibrillation was documented in 16 patients (17%). Atrial fibrillation occurred 30 +/- 46 days (range 1 to 171 days) after ablation. Univariate analysis associated an early occurrence of atrial fibrillation with: atrial fibrillation history, left ventricular ejection fraction, left atrial size, left ventricular telesystolic volume, A-wave velocity, significant mitral regurgitation and flutter cycle length. Multivariate analysis using a Cox model found that the only independent predictors of early atrial fibrillation were left ventricular ejection fraction and pre-ablation history of atrial fibrillation. In the subgroup without prior atrial fibrillation history (n=63; 66%), the only independent predictor of early atrial fibrillation was the presence of a significant mitral regurgitation. CONCLUSIONS: In a subgroup of patients without atrial fibrillation history, 8% of patients revealed an early atrial fibrillation. Mitral regurgitation is a strong predictive factor of early atrial fibrillation occurrence with 80% sensitivity, 78% specificity and 98% negative predictive value. These data should be considered in post-ablation management.

Clinical characteristics, aetiological factors and long-term prognosis of myocardial infarction with an absolutely normal coronary angiogram; a 3-year follow-up study of 91 patients.

OBJECTIVES: The purpose of this study was to evaluate the clinical outcome of a large cohort of patients who suffered an acute myocardial infarction with absolutely normal epicardial coronary arteries at the post-myocardial infarction coronary angiogram. The aetiological and prognostic factors in this population were also analysed. BACKGROUND: Few data exist concerning the outcome, and aetiological and prognostic factors, of patients with myocardial infarction and angiographically absolutely normal coronary arteries. METHODS: Ninety-one patients (34 females/57 males; mean age 50+/-13 years, range 24--78 years) admitted with an acute myocardial infarction had absolutely normal coronary arteries at the angiogram performed 6.2+/-4 days (range 1--15 days) after the myocardial infarction, defined by smooth contours and no focal reduction (NC). Of the 91 NC patients, 71 were evaluated prospectively, alongside a systematic search of all aetiological factors reported in the literature. The NC patients were matched for age, sex, and the same period of myocardial infarction onset with a group of 91 patients with coronary artery stenosis (>50% diameter stenosis) at the angiogram performed 7.3+/-4 days (range 1--15 days) after the myocardial infarction (SC). RESULTS: The percent of smokers was similar between the two groups; higher prevalence rates of coronary heart disease family history, obesity, hypertension, hypercholesterolaemia and diabetes mellitus were found in SC (P=0.043 to 0.0001). In NC, coronary spasm was found in 15.5%, congenital coagulation disorders in 12.8%, collagen tissue disorders in 2.2%, embolization in 2.2%, and oral contraceptive use in 1.1%. Left ventricular ejection fraction at hospital discharge was higher in NC (60%+/-13%) than in SC (55%+/-13%, P=0.04). The mean follow-up was 35 months (range 1--100 months). Kaplan-Meier event-free survival, with the combined end-point defined as death, reinfarction, heart failure and stroke was 75% in NC vs 50% in SC (P<0.0001). Survival rate was 94.5% in NC compared to 92% in SC (ns). Univariate predictors of events in NC were left ventricular ejection fraction (P=0.03), age (P=0.02), diabetes (P=0.01), and smoking (P=0.03). Using Cox multivariate analysis, independent predictors of long-term outcome in NC patients were left ventricular ejection fraction (P=0.003) and diabetes (P=0.004). CONCLUSION: Aetiological factors, predominantly coronary spasm and inherited coagulation disorder, can be detected in only one third of the patients with myocardial infarction and absolutely normal coronary angiograms despite a systematic search in a prospective population. Mortality rates are similar but morbidity is lower in myocardial infarction patients with absolutely normal coronary angiography compared with those with coronary artery stenosis. The only two independent factors predictive of poor outcome in myocardial infarction patients with normal coronary arteries are left ventricular function and diabetes.

[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.

[The heart and the eosinophil]. / Le coeur et l'eosinophile.

The beneficial effects of polynuclear eosinophils (PE) are well known. However, under certain circumstances, PE can be harmful. The heart is a prime target for PE toxicity which is due to release of basic proteins by eosinophils including major basic protein, cationic protein, and peroxidase. The most common manifestation of PE toxicity is chronic parietal endocarditis (CPE) which regroups two entities: Loeffler's fibroplastic endocarditis and Davies' endomyocardial fibrosis. Loeffler's fibroplastic endocarditis occurs mainly in temperate climates. Patients present high, persistent eosinophil levels similar to those observed in essential hypereosinophilic syndrome (EHS) or Chusid syndrome. Davies' endomyocardial fibrosis occurs in tropical countries where eosinophilic helminthiasis are endemic. The incidence of eosinophilic myocarditis (EM) is low but probably underestimated. EM can be observed in any case involving PE and has been described in many cases of drug-induced atopy, in Churg and Strauss syndrome, and in EHS. The most common cause of death is short-term occurrence of cardiogenic shock or dilated hypokinetic cardiomyopathy. Some patients have been successfully treated by early, intensive corticosteroid therapy and/or heart transplantation. The nosological classification of EM and CPE remains controversial. The two disorders may form a continuum with CPE as the second phase. Other authors have suggested that EM and CPE result from the action of PE on two distinct targets, i.e. endothelial cells for EM and myocytes for CPE. In the future, it may be possible to identify subjects with a predisposition to PE-induced heart disease by studying of genes coding for interleukins (IL-5, IL-4, IL-3) and GM-CSF in the 5q31-q33 region of chromosome 5.

[Acute eosinophilic myocarditis: a diagnostic and therapeutic emergency]. / La myocardite aigue a eosinophiles: une urgence diagnostique et therapeutique.

This report describes three histologically documented cases of acute eosinophilic myocarditis. These three cases illustrate the different clinical and therapeutic outcomes of this disease which can range from full recovery under prolonged corticosteroid treatment to requirement for emergency heart transplantation or death due to intractable cardiac insufficiency. In absence of specific clinical or laboratory data, diagnosis must be established in vivo by endomyocardial biopsy demonstrating eosinophil-rich inflammatory infiltration and necrotic lesions. Rapid decision-making is necessary to allow early initiation of intensive corticosteroid treatment without which the most likely outcome is death. Clinicopathological and experimental evidence suggests that acute eosinophilic myocarditis is caused by the cytotoxic effects of granule components (mainly major basic protein) released by activated polynuclear eosinophils.