Non-contact mapping to guide catheter ablation of untolerated ventricular tachycardia.

AIMS: The role of a novel non-contact mapping system (ESI 3000, Endocardial Solutions) to guide radiofrequency catheter ablation of untolerated ventricular tachycardia was investigated in 17 patients; 11 with prior myocardial infarction, three with arrhythmogenic right ventricular dysplasia, and three with idiopathic dilated cardiomyopathy. METHODS: Twenty-seven monomorphic ventricular tachycardias were induced (mean cycle 320+/-60 ms, range 230-450 ms), mapped for 15-20 s, and terminated by overdrive pacing or DC shock. Off-line analysis of isopotential activation mapping was performed to identify the diastolic pathway and/or the exit point of the ventricular tachycardia reentry circuit. Radiofrequency current was applied to create a line of block across the diastolic pathway or around the exit point. RESULTS: All 27 ventricular tachycardias were mapped with the non-contact system. The endocardial exit point (-7+/-15 ms before QRS onset) was defined in 21/21 postinfarction ventricular tachycardias, in 3/3 arrhythmogenic right ventricular dysplasia and in 1/3 idiopathic dilated cardiomyopathy ventricular tachycardias, respectively. The diastolic pathway (earliest endocardial diastolic activity: -65+/-49 ms before QRS onset) was identified in 17/21 postinfarction ventricular tachycardias, in 1/3 arrhythmogenic right ventricular dysplasia and in 1/3 idiopathic dilated cardiomyopathy ventricular tachycardias, respectively. Catheter ablation was performed in 25/27 ventricular tachycardias (93%) in 15/17 patients (88%): 16/25 ventricular tachycardias (64%) were successfully ablated in 10/17 patients (59%). Catheter ablation was not performed in two patients or proved unsuccessful in five patients. At a follow-up of 15+/-5 months, there was no recurrence of documented ventricular tachycardia in all 10 patients with successful catheter ablation; in two of them a previously non-documented ventricular tachycardia occurred. A high recurrence of ventricular tachycardia was observed in patients with a failed procedure (5/7: 71%). No major complication or death occurred. CONCLUSIONS: Non-contact mapping can be effectively used to map and guide radiofrequency catheter ablation of untolerated ventricular tachycardias. Given the favourable acute and clinical long-term results, this approach proves to be more effective in patients with postinfarction ventricular tachycardias, in comparison to patients with arrhythmogenic right ventricular dysplasia and idiopathic dilated cardiomyopathy.

Electrophysiological characteristics and outcome in patients with idiopathic right ventricular arrhythmia compared with arrhythmogenic right ventricular dysplasia.

BACKGROUND: Idiopathic right ventricular arrhythmias (IRVA) are responsive to medical and ablative treatment and have a benign prognosis. Arrhythmias caused by right ventricular dysplasia (ARVD) are refractory to treatment and may cause sudden death. It is difficult to distinguish between these two types of arrhythmia. OBJECTIVE: To differentiate patients with IRVA and ARVD by a conventional electrophysiological study. METHODS: 56 patients with a right ventricular arrhythmia were studied. They had no history or signs of any cardiac disease other than right ventricular dysplasia. They were classified as having IRVA (n = 41) or ARVD (n = 15) on the basis of family history, ECG characteristics, and various imaging techniques. They were further investigated by standard diagnostic electrophysiology. RESULTS: The two groups were clearly distinguished by the electrophysiological study in the following ways: inducibility of ventricular tachycardia by programmed electrical stimulation with ventricular extrastimuli (IRVA 3% v ARVD 93%, p < 0.0001); presence of more than one ECG morphology during tachycardia (IRVA 0% v ARVD 73%, p < 0.0001); and fragmented diastolic potentials during ventricular arrhythmia (IRVA 0% v ARVD 93%, p < 0.0001). Data from the clinical follow up in these patients supported the diagnosis derived from the electrophysiological study. CONCLUSIONS: Patients with IRVA or ARVD can be distinguished by specific electrophysiological criteria. A diagnosis of ARVD can be made reliably on the basis of clinical presentation, imaging techniques, and an electrophysiological study.

[Effectiveness of long-term ACE-inhibition on pulmonary diffusion and ventilation-perfusion ratio in chronic heart failure: correlation with physical performance]. / Efficacia a lungo termine dell'ACE-inibizione su diffusione polmonare e accoppiamento ventilazione-perfusione nell'insufficienza cardiaca cronica: relazione con la performance fisica.

Pulmonary dysfunction contributes to exercise intolerance in patients with chronic heart failure, and ACE-inhibition improves the functional capacity of these subjects. In this study, we investigated whether and how ACE-inhibitors affect pulmonary function and ventilatory response during exercise in chronic heart failure. Twenty patients with idiopathic dilated cardiomyopathy and left ventricular ejection fraction < 35% underwent pulmonary function tests and exercise evaluation with analysis of expired gases before and after 1 year of treatment with enalapril (10 mg bid). To explore whether or not the respiratory influence of ACE-inhibitors is peculiar to the syndrome of cardiac failure, we also studied 19 subjects with mild, untreated primary hypertension who followed the same protocol. In this group, enalapril exerted a neutral effect on pulmonary function. In chronic heart failure patients, lung volumes were abnormal and did not improve after enalapril treatment; on the contrary, alveolar diffusing capacity for carbon monoxide increased towards normal values. Exercise tolerance time, peak exercise oxygen consumption, ventilation, and tidal volume also improved and the dead space to tidal volume ratio was reduced at the peak exercise and intermediate exercise phases (20, 60 W). Changes in carbon monoxide diffusion were positively correlated to those occurring during peak exercise oxygen consumption. A negative correlation was found between the variations in oxygen consumption and those in dead space to tidal volume ratio at peak exercise. We conclude that in patients with chronic heart failure, ACE-inhibition restores diffusing lung properties and improves ventilation-perfusion matching during exercise. In this syndrome, sustained reduction in gas exchange resistance is a fundamental therapeutic property of this class of drugs.

[A failed improvement in pulmonary function and exercise capacity with carvedilol in congestive heart failure despite an excellent effect on left ventricular function]. / Mancato miglioramento della funzione polmonare e della capacità di esercizio con carvedilolo nello scompenso cardiaco congestizio, nonostante un eccellente effetto sulla funzione ventricolare sinistra.

This study was aimed at investigating in chronic heart failure (CHF) the effects that beta-blockade with carvedilol may have on lung function, and their relationship with left ventricular (LV) performance and peak exercise oxygen uptake (VO2p). CHF causes disturbances in ventilation and pulmonary gas transfer (stress failure of alveolar-capillary membrane) that participate in limiting VO2p. Carvedilol improves LV function and not VO2p. Twenty-one NYHA functional class II-III patients were randomized (2 to 1) to carvedilol (25 mg bid., 14 patients) or placebo (7 patients) for 6 months. Rest forced expiratory volume (FEV1), vital capacity (VC), total lung capacity (TLC), carbon monoxide diffusing capacity (DLCO), its alveolar-capillary membrane component (DM), pulmonary venous and transmitral flows (for monitoring changes in LV end-diastolic pressure, EDP), LV diastolic (EDD) and systolic (ESD) dimensions, stroke volume (SV), ejection fraction (EF), fiber shortening velocity (VCF) were measured at baseline and at 3 and 6 months. VO2p, peak ratio of dead space to tidal volume (VD/VTp), ventilatory equivalent for CO2 production (VE/VCO2), VO2 at anaerobic threshold (VO2at) were also determined. FEV1, VC, TLC, DLCO, DM were impaired in CHF compared to 14 volunteers, and did not vary with treatment. Carvedilol reduced EDP, EDD, ESD, and increased EF, SV, VCF, without affecting VO2p, VO2at, VD/VTp, VE/VCO2, at 3 and 6 months. Placebo was ineffective. In CHF, carvedilol exerts neutral effects on ventilation and pulmonary gas transfer and ameliorates LV function at rest. This proves that antifailure treatment may not be similarly effective on cardiac and pulmonary function; and does not contradict the possibility that persistence of lung impairment may contribute to lack of improvement in exercise performance with carvedilol.