Outcomes after cryoablation vs. radiofrequency in patients with paroxysmal atrial fibrillation: impact of pulmonary veins anatomy.

AIMS: Pulmonary vein isolation is the mainstay of treatment in catheter ablation of paroxysmal atrial fibrillation (AF). Cryoballoon ablation has been introduced more recently than radiofrequency ablation, the standard technique in most centres. Pulmonary veins frequently display anatomical variants, which may compromise the results of cryoballoon ablation. We aimed to evaluate the mid-term outcomes of cryoballoon ablation in an unselected population with paroxysmal AF from an anatomical viewpoint. METHODS AND RESULTS: Consecutive patients with paroxysmal AF who underwent a first procedure of cryoballoon ablation or radiofrequency were enrolled in this single-centre study. All patients underwent systematic standardized follow-up. Comparisons between radiofrequency and cryoballoon ablation (Arctic Front™ or Arctic Front Advance™) were performed regarding safety and efficacy endpoints, according to pulmonary vein (PV) anatomical variants. A total of 687 patients were enrolled (376 radiofrequency and 311 cryoballoon ablation). Baseline characteristics and distribution of PV anatomical variants were generally similar in the groups. After a mean follow-up of 14 ± 8 months, there was no difference in the incidence of relapse (17.0% cryoballoon ablation vs. 14.1% radiofrequency, P = 0.25). We observed no interaction of PV anatomical variants on mid-term procedural success. CONCLUSION: Our findings suggest that mid-term outcomes of cryoballoon ablation for paroxysmal AF ablation are similar to those of radiofrequency, regardless of PV anatomy. The presence of anatomical variants of PVs should not discourage the referral of patients with paroxysmal AF for cryoballoon ablation.

[Risks of pulmonary vein isolation by radiofrequency for the treatment of paroxysmal atrial fibrillation: a single centre experience of the first 200 patients]. / Risques liés a l'isolement par radiofréquence des veines pulmonaires pour le traitement de la fibrillation auriculaire paroxystique: expérience monocentrique des 200 premiers patients.

The authors report the initial experience of an electrophysiological laboratory starting ablation for atrial fibrillation, a promising technique which is not yet widely practiced because of the risks related to the procedure. The incidence of severe complications (tamponade, pulmonary vein stenosis, ischaemic events) did not appear to be different in the first 100 procedures compared with the next 100 procedures: 3% in the two groups. The selection of patients, strict perioperative management and the initial support by confirmed operators seem to be the factors which minimise the complications rate of the procedure.

Lack of haemodynamic effects of nitric oxide on post-capillary pulmonary hypertension induced by acute sino-aortic denervation.

1. The aims of the present experiments were to define a new experimental model of pulmonary hypertension induced by a post-capillary mechanism and to assess the haemodynamic effects of nitric oxide on post-capillary pulmonary hypertension. 2. Cardiopulmonary variables of 28 male beagle dogs, anaesthetized with chloralose, 16 spontaneous breathing and 12 with assisted ventilation, were studied before and after sino-aortic denervation (SAD). The haemodynamic effects of inhaled nitric oxide (25 p.p.m., 10 min). N(omega)-nitro-L-arginine methyl ester (20 mg kg-1, i.v.), urapidil (0.5 mg kg-1-, i.v.) and propranolol (300 micrograms kg-1, i.v.) were studied after SAD. 3. SAD induced an acute and transient pulmonary hypertension, more marked in spontaneous breathing dogs. This pulmonary hypertension involved a post-capillary mechanism, secondary to the left ventricular haemodynamic effects of the acute increase of left ventricular after-load induced by systemic hypertension. In fact, the increase of mean pulmonary arterial pressure after SAD and the decrease of this parameter after urapidil or propranolol were strongly correlated with the variations of pulmonary capillary wedge pressure. Furthermore, no significant change in pulmonary vascular resistance was found after SAD or administration of alpha or beta-adrenoceptor antagonists. 4. Inhaled nitric oxide did not reverse pulmonary hypertension induced by SAD. N(omega)-nitro-L-arginine methyl ester had no significant haemodynamic effect of pulmonary circulation. 5. In conclusion, the lack of effect of inhaled nitric oxide and nitric synthase inhibitor on pulmonary circulation parameters SAD suggest that endothelium-derived oxide is not involved in the mechanisms leading to post-capillary pulmonary hypertension.

[Therapeutic choices in silent ischemia]. / Choix thérapeutiques dans l'ischémie silencieuse.

Silent or painless myocardial ischaemia is a common presentation of coronary insufficiency. Repeated episodes lead to anatomical and functional myocardial changes and are associated with the risk of ischemic cardiomyopathy, infarction, arrhythmias and sudden death. The physiopathology is complex and involves transient changes in coronary flow secondary to abnormalities of coronary vasomotricity. It is commonly observed in association with symptomatic angina, in unstable angina and after acute myocardial infarction. In all cases, appropriate treatment is required, the aim being to decrease and suppress not only pain but also ischaemia. Treatment is guided by the ischemic episodes. "Isolated" silent myocardial ischaemia as the only sign of coronary insufficiency justifies accurate evaluation of the coronary status, risk factors and a therapeutic trial, followed by systematic coronary angiography if the ischaemia persists. Silent myocardial ischaemia has modified classical therapeutic attitudes in which the choice of treatment is based on the severity of functional impairment. Priority should now be given to treating the severity of the ischaemia and of the anatomical lesions.

[Inferior wall myocardial infarction and atrioventricular block; angiography and prognosis]. / Infarctus inférieurs et blocs auriculo-ventriculaires; données angiographiques et pronostic.

This study was based on 42 cases of 2nd or 3rd degree atrioventricular block out of 292 cases of inferior wall myocardial infarction. The criteria of selection were monitoring in the intensive care unit during the acute phase, selective coronary angiography in the first 48 hours to 5 days, and regular clinical follow-up during the first year after infarction. The conduction defect was either immediately recorded on the first ECG, delayed (between the 12th and 24th hour) or late (after the 3rd day). These 42 inferior wall infarcts with atrioventricular block (incomplete in 14 and complete in 28 cases) differed from inferior infarction without block by: - the severity of the clinical signs during the acute phase (35% with cardiac failure, 19% with cardiogenic shock); - the severity of the coronary lesions (71.4% with triple vessel disease in infarction with atrioventricular block compared with 32% in those without block, p < 0.02); - the prevalence of the association of > 70% stenosis of the right coronary and left anterior descending arteries; - the alteration of left ventricular function (53% patients with atrioventricular block had ejection fraction of under 30%); - the severity of these infarcts was not related to the atrioventricular block which regressed in 95% of cases but to the severity of the coronary disease, the left ventricular dysfunction and the advanced age of the patients (72.3 +/- 8 years).

[Simplified approach to ablation in atrial flutter using a single catheter electrode. Based on 70 cases]. / Approche simplifiée de l'ablation du flutter auriculaire par un seul cathéter muni d'électrodes. A propos de 70 observations.

The object of this study was to assess the feasibility, efficacy and risks of ablation of common atrial flutter using a single catheter electrode. Recent studies have shown that radiofrequency ablation is effective for interrupting atrial flutter but with a variable rate of recurrence. Therefore, the search for a conduction block in the isthmic region has become the reference method for reducing the incidence of recurrence but this requires the use of costly material. The necessity of single usage has incited research to find a less costly method without compromising efficacy. The authors reviewed the results in 70 consecutive patients with common atrial flutter resistant to anti-arrhythmic medication. The site of ablation was located using anatomical landmarks and electrophysiological criteria. The anatomic site was situated either on a lateral isthmus or, to a variable degree, a septal isthmus; the electrophysiological criterion was an endocavitary auriculogramme, the amplitude of which had to decrease by more than 2/3 after application of the radiofrequency. The technique was interrupted not after the interruption of the flutter but after obtaining a microvoltage atrial activity along the isthmus. Radiofrequency energy of 10 to 50 W was delivered at each site for 90 seconds. Atrial flutter was interrupted in all 70 patients (100%). The average number of applications to interrupt the flutter was 12.67 and to create a microvoltage barrier 14.58. The average duration of the radiofrequency procedure was 50.43 minutes. After an average of six months' follow-up, the recurrence rate was 13%: 9 patients, 5 of whom underwent a second session of radiofrequency ablation. There were no immediate complications after this method of ablation.

[Hypertensive cardiopathy and ventricular late potentials]. / Cardiopathie hypertensive et potentiels tardifs ventriculaires.

Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The aim of this work is to study the incidence of ventricular late potentials (LP) and their relation to ventricular arrhythmias in 148 hypertensive patients, 87 men and 55 women, without evidence of a coronaropathy. For each patient we carried out a signal-averaged electrocardiography, an echocardiogram to determine the LV mass index (LVMI) and the LV end-diastolic dimension (EDD), and 24 hours Holter monitoring to record ventricular arrhythmias filed according to Lown's classification. LP were considered present if the root-mean-square voltage during the last 40 ms of the QRS was: < 20 uV in absence of bundle branch block, or < or = 17 uV in presence of bundle branch block. [table: see text] The frequency of LP appears exceptional in hypertensive patients without LVH (5%) and remains uncommon in patients with concentric LVH (13%). The incidence of LP is only frequent at the end stage of hypertensive cardiopathy with eccentric LVH (48%). The severity of ventricular arrhythmias is only correlated to the presence of LP in patients with concentric LVH (p < 0.02).

[Correlation between QT interval dispersion and ventricular arrhythmia in hypertension]. / Corrélation entre la dispersion de l'intervalle QT et les arythmies ventriculaires dans l'hypertension artérielle.

OBJECTIVE: To evaluate the correlation between QT interval dispersion (QTd) and ventricular arrhythmias in hypertensive patients (pts) with or without left ventricular hypertrophy (LVH). A secondary aim was to investigate correlations of QTd with other markers of arrythmogenic propensity: ventricular late potentials (LP) and heart rate variability (HRV). METHODS: We retrospectively measured the QTd on the 12 standard surface ECG leads in 230 hypertensive pts (94F, 136M; 59.6 +/- 12.7 years old). A 24 hours ECG Holter recording was performed in 218 pts and ventricular arrhythmias were appreciated using the Lown classification. Left ventricular mass was determined by echocardiography (LVM-Devereux formula) and left ventricular mass index (LVMI) were determined in 202 subjects. LP (122 pts) and HRV (55 pts) were investigated. RESULTS: The QTd varied between 20 and 160 msec (57.8 +/- 32.7 msec). The distribution of pts classified using Lown criteria was: 29 pts (13.3%) class O; 106 pts (48.6%) class I; 8 pts (3.6%) class II; 13 pts (6%) class III; 29 pts (13.3%) class IVa; 33 pts (15.1%) class IVb; 116 pts (69.5%) had LVH determined by echocardiography. The QTd was strongly correlated with the Lown classes (p < 0.0001). The QTd was significantly broader in Lown classes III, IVa and IVb compared to classes O, I and II cumulated (p < 0.002); there was no difference concerning QTd between Lown classes III, IVa and IVb. The QTd was also correlated with the absolute number of premature ventricular depolarizations/24 hours (p = 0.02; r = 0.16). The 75 pts with an increased LVMI had significantly elevated QTd compared to pts without it (p < 0.0001). Qtd was correlated with LVMI (r = 0.37; p < 0.0001). There was no correlation between QTd and the existence of LP (which were correlated with the Lown classes; p < 0.03) and HRV parameters. CONCLUSION: Elevated QT interval dispersion is associated with more severe ventricular arrhythmias in hypertensive subjects with LVH. The mechanism of an increased inhomogeneity of repolarisation is probably related to the anatomic modifications induced by LVH. No significant correlation between QTd, LP and HRV was observed.

[Absence of the effect of nitric oxide on pulmonary and systemic hypertension induced by sino-aortic denervation]. / Absence d'effet du monoxyde d'azote sur l'hypertension artérielle pulmonaire et systémique induite par la défrénation sino-aortique.

Inhaled nitric oxide, a selective pulmonary vasodilator, reverses hypoxic pulmonary vasoconstriction and is an effective treatment in some cases of human pulmonary hypertension. Localization of nitric oxide synthase had indicated a neural role for nitric oxide. Thus, we studied the interactions between inhaled nitric oxide and systemic and pulmonary vascular reactivity in acute neurogenic hypertension. In 6 male beagle dogs (mean weight: 15 +/- 1 kg), anesthetized by chloralose (8 cg/kg) and in spontaneous ventilation, the hemodynamic effects on systemic and pulmonary circulation of inhaled nitric oxide (12 ppm) were studied before and after acute sino-aortic denervation. The hemodynamic effects of intravenous propranolol (300 micrograms/kg) were studied after denervation. Mean arterial pressure (MAP), pulmonary capillary pressure (PCP), mean arterial pulmonary pressure (MAPP), cardiac input (CI) and oxygen venous saturation (SvO2) were measured. [table: see text] Sino-aortic denervation causes an acute and transitory pulmonary hypertension due to a double mechanism: a post-capillary hypertension (increase PCP) secondary to an increase left ventricular post-charge by systemic hypertension and a precapillary hypertension. In fact, vascular pulmonary resistances increase from 1.8 +/- 0.1 to 3.4 +/- 0.8 uW after denervation (p < 0.05). Change in pulmonary vascular reactivity induced by catecholamines is probably involved. Propranolol but not inhaled nitric oxide reverse pulmonary hypertension due to sino-aortic denervation.

[Myocardial infarction in non-menopausal women. Coronary lesions and prognosis]. / Infarctus du myocarde chez des femmes non ménopausées. Lésions coronaires et pronostic.

Between 1977 and 1990, 64 premenopausal women, under 50 years of age (42 +/- 5.6 years), were admitted for typical acute myocardial infarction with pathological Q waves. Twenty one patients had attempted myocardial revascularisation either by intravenous thrombolysis or primary angioplasty (n = 3). All patients underwent coronary angiography with selective left ventriculography during their hospital admission. This group of 64 women was characterised by the association of coronary risk factors (2.8 per patient): smoking (89%), hyperlipidaemia (67%), diabetes (45%) and oral contraception (35%). Coronary angiography showed single vessel occlusion in 86% of patients receiving oral contraception, multiple vessel disease in 36.5% and single or double vessel disease in 31.7% of the other patients. There were 3 deaths during the hospital period (4.6%), 12 cases of left ventricular failure, 2 ventricular aneurysms, 2 operated ischaemic mitral regurgitations and 9 recurrences of pain treated by angioplasty. During follow-up (36.5 +/- 4 months), 22 patients were readmitted to hospital and there were 3 further deaths, 12 cases of persistent cardiac failure, 10 cases of latent ventricular dysfunction and 9 ischaemic reoccurrences treated by angioplasty or surgery. The results in this group of patients suffering from myocardial infarction at an unusually early age for women showed that although the mortality was similar to that observed in men of the same age (9%) there was a very high morbidity and a high risk of cardiac failure. The prognosis of myocardial infarction in women, though better than 10 years ago, should improve with immediate revascularisation, the correction of cardiovascular risk factors and the rapid application of all techniques of modern cardiology.

[Prophylactic value of automatic implantable defibrillators: a case report of a patient with asymptomatic Brugada syndrome]. / Intérêt prophylactique du défibrillateur automatique implantable: à propos d'une observation de patient ayant un syndrome de Brugada asymptomatique.

The authors report the case of an asymptomatic 32 year old man with no family history of sudden death but with ECG changes suggesting Brugada's syndrome. He underwent implantation of an automatic defibrillator after inducible syncope ventricular fibrillation had been demonstrated during electrophysiological investigation. The later occurrence of three episodes of ventricular fibrillation treated by the defibrillator confirmed a posteriori the logic of this therapeutic approach.

[Brugada syndrome and supraventricular arrhythmias]. / Syndrome de Brugada et arythmies supraventriculaires. A propos d'une observation clinique.

The author reports the case of a 46-year old patient diagnosed with idiopathic ventricular fibrillation (Brugada syndrome) further to induction of class Ic antiarrhythmic therapy for the management of paroxystic ventricular fibrillation. It would appear that this diagnosis is increasingly frequent in young patients with Brugada syndrome shown to be minimal or intermittent on electrocardiograms. Atrial arrhythmia was the only rhythmic pathology objectively evidenced in this patient and the author was consequently led to reconsider its prevalence in patients presenting this syndrome both in the literature and according to his personal experience.

[Prognosis of silent myocardial ischemia]. / Le pronostic de l'ischémie myocardique silencieuse.

Asymptomatic or silent myocardial ischemia (SI) is frequent in coronary heart disease and its prognostic value is controversial. The aim of our study is to compare coronary atherosclerosis, left ventricular function and clinical out come of 110 patients with S.I. (A group) and 210 patients with stable angina (B group). The 320 patients were submitted: to symptom limited exercise stress-test with permanent electrocardiographic control by a Case 12-15 digitalized system with ST segment depression interpretation. A test was considered positive for ischemia if there was ST depression of > 1 mv in magnitude from baseline, persisting for 0.08 sec or exercise angina and ischemia: to selective coronarography by Seldinger technic, with left ventricular cineangiography in 2 incidences. A significant coronary stenosis was defined as > 50% reduction of luminal diameter; to medical treatment with betablockers (87.5% of patients), calcium inhibitors (12.5%), aspirin (90%) and nitrates; to regular medical surveillance. During the follow-up (42.4 +/- 5 months in mean) the number of deaths, myocardial infarctions, heart failure, unstable angina and revascularizations were analyzed. Patients of A group with S.I. had a high percentage of risks factors (diabetes mellitus 55%, nicotinism 85%, dyslipidemia 22.5%) and history of previous myocardial infarction in 33% of cases. There are not significant differences between severity and extension of coronary disease, or ventricular dysfunction in patients of A group or B. The percentages of deaths (2.10 versus 3%), acute myocardial infarctions (9.5 versus 8.5%), heart failures (2.72 versus 3%), surgical indications (14.7 versus 15.7%) are not significantly different between the 2 groups. In A group, 34% of patients were treated by angioplasty versus 40% of patients in group B (p < 0.02). S.I. has a bad prognostic and the clinical out come of coronary heart disease is not dependent of presence of angina during exercise testing and daily activities.

[How to evaluate sudden cardiac death risk after myocardial infarction?]. / Comment évaluer le risque de mort subite dans les suites d'un infarctus du myocarde ?

Sudden cardiac death is the mode of death of more than half of coronary heart disease patients. Preventing sudden cardiac death involves prevention of ventricular arrhythmias occurrence as well as the treatment by an implantable cardioverter defibrillator. The evaluation of sudden cardiac death risk should consider the underlying cardiopathy, the associated coronary risk factors and all pharmacological treatment efficient to reduce ventricular remodeling and myocardial ischemia. Only significant low ejection fraction and positive ventricular testing in some cases are now considered are now considered by the current French recommendations for cardioverter defibrillator implantation in primary prevention. However, other noninvasive markers such as heart rate variability and T wave alternans are of interest in sudden cardiac death risk stratification after myocardial infarction.

[Rhythm control - cardioversion]. / Contrôle du rythme sinusal - Cardioversion.

In case of persistent and symptomatic atrial fibrillation, a pharmacological cardioversion under effective anticoagulation treatment may be performed according to current guidelines. In the absence of return to sinus rhythm, a Direct-Current cardioversion can be performed. After returning to sinus rhythm will arise the question of anticoagulation and antiarrhythmic drugs treatments that will be most often long-term pursued.

Prognostic value of arrhythmogenic markers in systemic hypertension.

OBJECTIVE: To evaluate the prognostic value of arrhythmogenic markers in hypertensive patients. DESIGN: Two hundred and fourteen hypertensive patients without symptomatic coronary disease, systolic dysfunction, electrolyte disturbances or anti-arrhythmic therapy were included. Recordings were made of 12-lead standard ECGs with calculations of QT interval dispersion, 24 h Holter ECGs (204 patients), echocardiography (187 patients) and signal-averaged ECGs (125 patients). BASELINE DATA: echocardiographic left ventricular hypertrophy was found in 63 patients (33.7%), non-sustained ventricular tachycardia (Lown class IV b) in 33 patients (16.2%), ventricular late potentials in 27 patients (21.6%). Mortality: after a mean follow-up of 42.4 +/- 26.8 months, global mortality was 11.2% (24 patients), cardiac mortality 7.9% (17 patients), sudden death 4.2% (nine patients). Univariate analysis: predictors of global, cardiac and sudden death were age > or = 65 years, ECG strain pattern, Lown class IV b and QT interval dispersion > 80 ms (P < or = 0.01). Left ventricular mass index was closely related to cardiac mortality (P = 0.002). Multivariate analysis: only Lown class IV b was an independent predictor of global (RR 2.6, 95% CI 1.2-6.0) and cardiac mortality (RR 3.5, 95% CI 1.2-9.7). CONCLUSION: In hypertensive patients, non-sustained ventricular tachycardia has a prognostic value.

Prognostic value of late potentials in patients with congestive heart failure.

To investigate whether detection of ventricular late potentials could provide prognostic information in patients with congestive heart failure with or without bundle branch block, we prospectively obtained a signal-averaged ECG from 151 patients with congestive heart failure, using specific criteria in 57 patients with bundle branch block. Late potentials were detected in 49 patients (32.5%); their incidence was not significantly different in patients without (31%; 29 patients) or with bundle branch block (35%; 20 patients). Late potentials were present in 25 of 73 patients (34%) with idiopathic dilated cardiomyopathy, in 20 of 57 patients (35%) with ischaemic cardiomyopathy and in four of 21 patients (19%) with hypertensive heart disease (ns). Age, NYHA class, ejection fraction and use of amiodarone were not statistically different among patients with or without late potentials. In contrast, patients with late potentials had more past episodes of sustained ventricular tachycardia (8.2%; four patients) than those without late potentials (1.9%; two patients). Twenty four hour ambulatory ECGs were obtained in 135 patients (89%). Non-sustained ventricular tachycardia was not correlated with the presence of late potentials found in 45 of 88 patients (51%) without late potentials and in 29 of 47 patients (62%) with late potentials (ns). The mean follow-up was 27 +/- 12 months; 51 patients died, 31 from progressive congestive heart failure and 13 suddenly; seven prospectively had sustained ventricular tachycardia. The total mortality rate, the cardiac mortality rate and sudden death risk were not significantly related to the presence of late potentials; their incidence were respectively 35% (36 patients), 32% (33 patients) and 10% (10 patients) in patients without late potentials and 31% (15 patients), 23% (11 patients) and 6% (three patients) in those without late potentials. The incidence of sustained ventricular tachycardia during follow-up was 2% (two patients) in patients without late potentials and 10% (five patients) in those with late potentials. The incidence of sustained ventricular tachycardia experienced by the patients before the study or seen during follow-up was significantly increased in the presence of late potentials: 18% (nine patients) vs 2% (two patients) in the absence of late potentials (P < 0.001). Removal from the study of data from patients with bundle branch block, patients with severe congestive heart failure (NYHA 3 or 4) or patients taking amiodarone did not alter these results. Thus, signal-averaged ECG results only improved risk stratification for sustained ventricular tachycardia in patients with congestive heart failure and failed to identify patients at high risk for sudden death.