Flecainide acetate in the prevention of paroxysmal atrial fibrillation: a nine-month follow-up of more than 500 patients.

In order to assess efficacy, safety, and long-term tolerance of flecainide for the prevention of paroxysmal atrial fibrillation (PAF), 944 patients (555 male) were enrolled in an open multicenter study. All patients had had greater than or equal to 1 episodes of atrial fibrillation and were in sinus rhythm at the time of entry. The mean age was 65.3 +/- 11 years, and 43% of patients had no detectable heart disease. The mean daily dose of flecainide was 190 +/- 34 mg. Clinical examination, electrocardiogram (ECG) and 24-hour Holter monitoring were performed at entry into the study and on months 3, 6, and 9. Of the patients, 189 were lost to follow-up. Of the remaining 755 patients, 562 (74%) continued the treatment during the 9-month period and 193 (26%) dropped out. A total of 84 adverse effects were reported in 7.6% enrolled patients and in 9% of patients during follow-up, with treatment interruption in 50% of the cases. There were only 3 minor cardiovascular side effects, all leading to treatment discontinuation. No deaths in patients with recurrent PAF and no proarrhythmic events were reported. Flecainide appears to be effective in preventing PAF, with 65% of patients being arrhythmia-free after 9 months of treatment at a mean daily dose of 200 mg. Side effects were common, but clinically significant adverse events were infrequent.

[von Willebrand's disease and coronary atherosclerosis. Apropos of 3 cases]. / Maladie de Willebrand et athérosclérose coronarienne. A propos de trois cas.

The von Willebrand factor (VWF) is a link in the platelet-vessel wall interaction which plays an essential role in the response of the vessel wall to an atherosclerosis-including aggression. However, can von Willebrand's disease really prevent the development of atherosclerosis? The authors report 3 cases of young men aged 36, 40 and 51 years with atherogenic risk factors and von Willebrand's disease (two mild and one severe form). The three patients developed both atherosclerotic lesions and thrombosis. This would suggest that VWF deficiency does not protect humans from atherosclerosis.

[Left ventricular hypertrophy and arrhythmia. An aspect of hypertensive cardiomyopathy]. / Hypertrophie ventriculaire gauche et troubles du rythme cardiaque. Un aspect de la cardiopathie hypertensive.

Epidemiological data has established a relationship between left ventricular hypertrophy (LVH) and sudden cardiac death. This relationship is independent. The search for ventricular and atrial arrhythmias in hypertensives confirms a greater prevalence of these arrhythmias in patients with LVH. The mechanism of these arrhythmias is multifactorial: ischemia, subendocardial fibrosis, increased sympathetic tone, electrolyte disturbances, age, and hemodynamic changes may be arrhythmogenic substrates both at the ventricular and auricular levels. The relationship between LVH (marker or cause) and the detected arrhythmias remain obscure. The most sensitive markers of severity seem to be the ECG parameters (LVH with overload), echocardiographic mass (greater than + 20%) and septal thickness (greater than 12 mm). The evolution of arrhythmias with regression of LVH is unknown. Respect of electrolyte equilibrium would seem to be the only unquestioned therapeutic intervention.

[Predictive factors of the therapeutic result in the prevention of auricular fibrillation. Role of electrophysiological studies]. / Eléments prédictifs du résultat thérapeutique dans la prévention des fibrillations auriculaires. Rôle de l'étude électrophysiologique.

A population of 50 patients suffering from paroxysmal attacks of atrial fibrillation was studied prospectively to evaluate the prognostic value of 20 variables: 6 clinical variables: sex, age, cardiopathy, number of arrhythmic attacks, "vagal" triggering, failure of class IA antiarrhythmic agents; 3 echocardiographic variables: left ventricular diastolic diameter and percentage of fibre shortening, left atrial diameter; 6 basic electrophysiological data: threshold, refractory periods at 110 and 150/min, modalities of induction of a sustained arrhythmia; 4 results observed with an infusion of flecainide in doses of 2 mg/kg: arrest or persistence of the arrhythmia, whether or not it could be reinduced and value of refractory periods; doses of flecainide administered orally. With a mean +/- SD follow-up period of 7.7 +/- 7.3 months, preventive treatment with flecainide 233 +/- 7 mg failed in 16 patients (32 per cent) and succeeded in 34 patients (68 per cent). Analysis of Kaplan-Meier curves and use of Cox's multidimensional model showed that two electrophysiological data were of prognostic value: atrial effective refractory period, and non-inducibility of the arrhythmia after intravenous administration of flecainide. Thus, the probability of failure increases with the refractory period value and decreases with the non-inducibility of the arrhythmia.

[Study and value of high amplification atrial signal in arterial hypertension]. / Etude et intérêt du signal auriculaire haute amplification dans l'hypertension artérielle.

The aim is the analysis of the P wave on the signal averaged ECG in 31 pts: 12 control pts (6 M, 6 W, 40 +/- 10 y) 12 HTA (9 M, 3 W, 60 +/- 7 y), 7 pts (5 M, 2W, 48 +/- 7 y) with sustained paroxystic atrial fibrillation (AF) without organic heart disease, without antiarrhythmic drugs. We measured the filtered P wave duration (Ad), the integral of Ad, the root mean square voltage of Ad for the last 10, 20, 30, 40, 60 msec and the duration of P wave on the ECG in lead II (P II) and the echocardiographic dimensions of the atria (LAd). HTA Ad (132 +/- 12 msec)* et > control Ad (116 +/- 10 msec) HTA LAd (38 +/- 3 mm) et > control LAd (31 +/- 0.7 mm) HTA PII (120 +/- 1.5 mm)* et > control PII (88 +/- 10 mm). The difference between HTA Ad (132 +/- 12 msec) and AF Ad (129 +/- 7 msec) is not significant. The linear regression tests don't show correlation between P II and Ad and between LAd and Ad in HTA group. There is a correlation between Ad and LAF in AF group (r = 0.83, p 0.02). HTA RMS 2o (2.2 + 0.6 microV), control RMS 2o (3.9 + 1.8 V) but HTA RMS 2o and AF RMS 2o (2.4 +/- 0.6 microV) are not significantly different and are not correlated with LAd and PII. A long duration of P filtered P wave and a low RMS 2o observed in HTA group and AF group would be a criteria of atrial vulnerability. p < 0.05.

[Antihypertensive treatment and remission of left ventricular hypertrophy. Critical study]. / Traitement antihypertenseur et régression de l'hypertrophie ventriculaire gauche. Etude critique.

Left ventricular hypertrophy which is the adaptive mechanism of the heart to hypertension may become a cardiovascular risk factor independent of the hypertension which induced it: the regression of left ventricular hypertrophy therefore constitutes one of the medium-term objectives of antihypertensive therapy. Some antihypertensive drugs make the left ventricular hypertrophy regress early and permanently: methyldopa, betablockers, converting enzyme inhibitors, calcium antagonists. The reduction of myocardial mass is slight or debatable with diuretics and absent or inconstant with vasodilator therapy. The regression of left ventricular hypertrophy in hypertension raises several problems: the reliability of methods of measurement; inter-individual and inter-drug variations; the beneficial nature of this regression; the preventive effect of regression of left ventricular hypertrophy on cardiovascular complications. In the light of recent trials, early treatment of hypertension may prevent the development of left ventricular hypertrophy.

[An evaluation of the therapeutic trials aimed at regression of ventricular hypertrophy in arterial hypertension]. / Bilan des essais thérapeutiques visant à faire régresser l'hypertrophie ventriculaire gauche dans l'hypertension artérielle.

Left ventricular hypertrophy (LVH) which is a mechanism of adaptation of the heart to hypertension (HT) may become a cardiovascular risk factor independent of the HT which has caused it. Causing the regression of LVH is thus one of the mid-term aims of antihypertensive therapy. Certain antihypertensive drugs are capable of producing an early and durable regression of LVH: methyldopa, beta-blockers, ACEI, calcium blockers. The effect of mass reduction is moderate or doubtful with diuretics, while it is nil or inconstant with vasodilators. The regression of LVH in HT raises various problems: 1) reliability of the measurement technique, 2) inter-individual and inter-drug variations, 3) favourable nature of regression, 4) preventive effect of regression against cardiovascular complications. Finally, in the light of recent studies it appears that early treatment of HT may prevent the onset of LVH.

[Indications and limitations of anticoagulant treatment in elderly patients]. / Indications et limites des traitements anticoagulants chez les personnes âgées.

Anticoagulants constitute the rational treatment of thromboembolic accidents occurring in elderly people, but they are often not prescribed because of the risk of haemorrhage. The chronological age by itself is not a contra-indication, the limitations being the diseases associated with ageing. Anticoagulants may be used as curative treatment in atrial fibrillation with dilated left atrium (greater than 45 mm at echocardiography), in myocardial infarction, embolic strokes and complicated arteritis. They may also be used as preventive and curative treatment in phlebitis and pulmonary embolism. The complications of anticoagulant therapy will be better prevented by using the international normalized ratio and by prescribing doses that are adequate for each indication.