Notes: The high R-R variability in permanent atrial fibrillation (AF) is stable. Its behavior in paroxysmal AF is unknown. The aim of this study was to examine heart rate variability behavior during paroxysmal AF and its relationship with clinical characteristics by using time-domain indices and scatterplot analysis.〈section xml:id="abs1-2"〉〈title type="main"〉MethodsIn 43 patients, R-R variability was assessed by time-domain indices and graphical measurements of scattering area (SA) on scatterplot for each sample of 150-second ventricular rhythms extracted at the onset, the middle, and before termination of AF episodes recorded on Holter monitoring. Results were compared between the three time periods, and a nested procedure assessed the components of the SA variance.〈section xml:id="abs1-3"〉〈title type="main"〉ResultsIn 110 episodes lasting 89 ± 130 minutes with a mean of 2.5 ± 3 (1–12) per patient, mean R-R interval did not significantly change while time-domain indices and SA significantly decreased between the three time periods (P 〈 0.05 for SD and CV, P 〈 10−2 for rMSSD and pNN50, P 〈 10−4 for SA, ANOVA 1). The magnitude of the decrease in SA was not related to any episode characteristic; in addition, there was no variation from episode to episode within patient (1% of SA variance), and the high variation between patients (70%, P 〈 10−4) was not related to any clinical parameter.〈section xml:id="abs1-4"〉〈title type="main"〉ConclusionsHeart rate variability decreases gradually during paroxysmal AF. This decrease is peculiar to each patient, unrelated to clinical status. A.N.E. 1999; 4(2):144–151

Notes: Changes in QT interval durations on 24-hour ambulatory ECGs reflect circadian variations in ventricular repolarization. However, the reproducibility of such measurements is unknown.〈section xml:id="abs1-2"〉〈title type="main"〉MethodsTwo 24-hour Holter recordings were obtained in 9 healthy volunteers, and in 15 post-myocardial infarction (Ml) patients. First, automated measurements of QT apex and QT end were compared with manual measurements. Second, automated measurements of QT intervals were compared for each subject between the first and second Holter recordings. The coefficient of reproducibility was calculated as twice the standard deviation of differences between paired measurements.〈section xml:id="abs1-3"〉〈title type="main"〉ResultsThe coefficient of reproducibility for the comparison of manual and automated measurements of QT apex was 9 ms in healthy volunteers and 12 ms in post-MI patients. This coefficient was 12 ms in both healthy volunteers and post-MI patients for the comparison of manual and automated measurements of QT end. The coefficient of reproducibility for the comparison of automated measures of QT apex in the two Holter recordings was 16 ms in healthy volunteers and 18 ms in post-MI patients. These coefficients were 19 ms and 23 ms, respectively, for the comparison of automated measures of QT end.〈section xml:id="abs1-4"〉〈title type="main"〉ConclusionsAutomated and manual measurements of QT intervals obtained from 24-hour ambulatory ECGs provide similar results. Short-term reproducibility of automated measurements of QT intervals is acceptable.

Notes: Introduction: Mechanisms for thromboembolic complications during complex ablation procedures in left atrium (LA) have not been defined. The aim of this study was to determine the effect of the perfusion rate of the transseptal sheath on the incidence of thromboembolic complications during catheter ablation for atrial fibrillation (AF) or LA macroreentrant tachycardia. Methods and Results: We analyzed clinical and procedural data from 86 consecutive patients (153 procedures) referred for catheter ablation of AF (74 patients) or LA macroreentrant tachycardia (12 patients). The transseptal sheath was continuously perfused at a low flow rate (3 mL/hour) for the first 32 patients and at a high flow rate (180 mL/hour) for the subsequent 54 patients. Ablation was mainly performed using map-guided isolation of pulmonary veins for AF and three-dimensional electroanatomic mapping for LA macroreentrant tachycardia. Five patients (6% of patients and 3.5% of procedures) developed a cerebral thromboembolic complication, all during procedures using low-flow perfusion. Sheath perfusion rate and total procedure duration were the two variables significantly associated with the occurrence of stroke (P = 0.013 and 0.001, respectively). After adjustment in a multivariable analysis, sheath perfusion rate remained the only risk factor for stroke. The risk was 17 times higher using low-flow than high-flow perfusion (odds ratio 17.26, 95% confidence interval 1.14–260.81, P = 0.04). No other clinical or procedural parameters had any significant effect. Conclusion: Sheath perfusion rate is an important determinant of the risk factor for stroke during complex LA ablation procedures. Continuous high-flow perfusion appears to be effective in preventing this complication. (J Cardiovasc Electrophysiol, Vol. 15, pp. 276-283, March 2004)

Notes: Objectives: Mitral valve prolapse (MVP) is associated with arrhythmias and sudden death. Some studies suggest that abnormalities of the autonomic nervous system (ANS) may contribute to these arrhythmias. In a family investigation with genetic analysis of patients carrying a MVP, we performed a Holter study to define the autonomic profile of MVP. Methods and Results: A 24-hour digitized 3-lead Holter ECG was recorded in 30 patients with MVP and in two control groups, a group of 30 healthy relatives and a group of 31 healthy volunteers. We studied especially heart rate variability (HRV) and QT dynamicity. The slope of the relationship between ventricular repolarization and heart rate was studied separately during day and night. There was no difference in HRV (SDNN, rMSSD) among the three groups. On the contrary, QT interval duration was increased in patients with MVP as compared to healthy relatives (QT end: 409 ± 52 ms vs 372 ± 23 ms, P 〈 0.05; QT apex: 319 ± 42 ms vs 286 ± 23 ms, P 〈 0.01) and to healthy volunteers (QT end: 409 ± 52 ms vs 376 ± 25 ms, P = 0.004; QT apex: 319 ± 42 ms vs 289 ± 23 ms, P 〈 0.01). Nocturnal ventricular repolarization rate dependence was increased in MVP as compared to healthy relatives (0.16 ± 0.06 vs 0.13 ± 0.04, P 〈 0.05) and to healthy volunteers (0.16 ± 0.06 vs 0.11 ± 0.06, P 〈 0.001) whereas the 24-hour and diurnal QT–R-R slope was not disturbed. Conclusion: In MVP, QT is increased and the circadian modulation of QT end/RR slope is disturbed with an increased nocturnal rate dependence. These abnormalities of ventricular repolarization might explain the risk of arrhythmic events in MVP.

Notes: This study was performed to examine precursors of ventricular tachyarrhythmias in patients who experienced a sustained ventricular tachyarrhythmia and received appropriate therapy by ICD. From an overall consecutive population of 77 patients, 18 patients (1 woman, mean age 61.7 ± 10.8 years ) were selected for having experienced a sustained ventricular tachyarrhythmia and received at least one appropriate ICD therapy preceded by 20 minutes of internal information. The number of premature ventricular complexes (PVCs)/min for each of the 20 minutes preceding the onset of ventricular tachyarrhythmia, the shortest coupling intervals between PVC and normal sinus beat, and the presence of short-long-short (SLS) interval sequences were examined. Data were stratified according to underlying disease, left ventricular ejection fraction, rate of ventricular tachyarrhythmia, and antiarrhythmic therapy. One hundred twenty-eight episodes of spontaneous ventricular tachyarrhythmia were retrieved. Rapid ventricular tachyarrhythmia (〉160 beats/min) were preceded by a significantly greater mean number (3.71 ± 6.36) of PVCs than slower ventricular tachyarrhythmia (≤160 beats/min) (0.63 ± 0.88, P = 0.0004) . The mean shortest PVC coupling interval was significantly shorter in patients with (588 ± 99 ms) versus without (643 ± 111 ms, P = 0.03) ischemic heart disease, before episodes of rapid (527 ± 55 ms) versus slower (636 ± 105 ms, P = 0.0001) ventricular tachyarrhythmia, and in the absence (538 ± 80 ms) versus the presence (620 ± 105 ms, P = 0.006) of amiodarone. SLS sequences preceded 29% of rapid ventricular tachyarrhythmic episodes, versus 8% of the slower ventricular tachyarrhythmia (P 〈 0.01) . Significant differences were found in the characteristics of PVCs preceding ventricular tachyarrhythmic episodes in accordance to their rate and the underlying cardiomyopathy. Though insufficient in isolation, these findings may be helpful when combined with other observations to develop preventive algorithms, or to refine the programming of implantable devices. (PACE 2003; 26[Pt. I]:1454–1460)

Notes: TOUSSAINT, J-F., et al.: Ventricular Coupling of Electrical and Mechanical Dyssynchronization in Heart Failure Patients. We studied the relationships of electrical and mechanical synchronization in patients with heart failure (CHF) and various degree of ventricular conduction delays. Ninety-two CHF patients (60 ± 13 years old, LVEF 〈 45%), NYHA II-III-IV, and 35 age-matched control subjects were studied with angioscintigraphic phase analysis. We measured ejection fractions (LVEF, RVEF) and calculated the total activation time for the left (TtLV) and right ventricle (TtRV), and the synchronization time between right and left ventricle (TRVLV), and between LV apex and base (Tab). Patients were divided into three groups according to QRS duration: group 1 〈 120 ms (n = 28), group 2 〈 150 ms (n = 23), group 3 ≥ 150 ms (n = 41). In group 1: LVEF = 31.1 ± 10.9%, RVEF = 30.1 ± 12.6%, TtLV = 204 ± 70 ms, TtRV = 183 ± 61 ms, TRVLV = 7 ± 33 ms, Tab = 29 ± 23 ms. In group 2, these were: 27.8 ± 9.1%, 27.8 ± 8.8%, 227 ± 95 ms, 248 ± 137 ms, 35 ± 42 ms*, and 39 ± 53 ms respectively. In group 3: LVEF = 20.5 ± 9.5%†, RVEF = 28.4 ± 16.1%, TtLV = 304 ± 155 ms†, TtRV = 234 ± 106 ms†, TRVLV = 64 ± 42 ms†, and Tab = 67 ± 48 ms*, all P 〈 0.001 versus controls *P 〈 0.05 versus G1, †P ≤ 0.01 versus G1. A significant relation links QRS to both inter- and intraventricular asynchrony (TRVLV: r = 0.65; TtLL: r = 0.70, Tab: r = 0.60), and to LV function (r = 0.72); while LVEF relates more closely to intraventricular asynchrony: TtLV (r = 0.52), TtLL (r = 0.67), than to interventricular asynchrony: TRVLV (r = 0.48); P 〈 0.01, P ≤ 0.001. In CHF patients, electromechanical and contractile alterations are coupled; regional activation may be an early parameter allowing the detection of ventricular dyssynchronization.

Notes: Despite the demonstrated efficacy of implantable cardioverter defibrillators (ICDs) in reducing sudden and total mortality in selected populations, their implantation rates vary greatly between countries. The aim of our study was to analyze temporal and geographical trends in ICD implantations in countries with similar health related expenditure in Western Europe. A total of 2,257 patients from ten European evaluation studies of Medtronic defibrillators and defibrillation electrodes, conducted between 1993 and 1998, representing 12 countries, was included in this analysis. Rates of implantation and clinical characteristics were compared between countries and years of implantation. Rates of implantation differed greatly between Western European countries and did not correlate with indices of health related expenditure (i.e., number of patients per physician and number of patients per hospital bed). However, there was a strong and statistically significant negative correlation between the use of amiodarone and the rates of implantation (r =−0.66, P = 0.02). Temporal trends showed a significant increase in the age of the patients receiving an ICD between 1993 and 1998(57 ± 14 vs 61 ± 12years, mean ± SD, P 〈 0.001). There was also a temporal trend towards an increased incidence of coronary artery disease and a significant decrease in the incidence of cardiomyopathy. There was a temporal increase in implantations in patients with a history of ventricular tachycardia. Despite a general scientific agreement that ICDs are a first line treatment for patients at high risk of sudden cardiac death, their acceptance remains low in several developed countries. This low acceptance may not be entirely related to budget constraint but may also be related to their perceived efficacy by physicians and health authorities.

Notes: BÉCANE, H.–M., et al.: High Incidence of Sudden Death with Conduction System and Myocardial Disease Due to Lamins A and C Gene Mutation. We studied 54 living relatives from a large French kindred, among which 17 members presented with a cardiomyopathy transmitted on an autosomal dominant mode. Five of these individuals had clinical manifestations of muscle disease phenotypically consistent with Emery-Dreifuss muscular dystrophy. Genetic analysis of this kindred had demonstrated a nonsense mutation in the LMNA gene located on chromosome 1q11–q23. This gene encodes lamins A and C, proteins of the nuclear lamina located on the inner face of the nuclear envelope. We retrospectively determined the cause of death of 15 deceased family members, 8 of whom had died suddenly, 2 as a first and single manifestation of the disease. The six other cases had histories of arrhythmias and left ventricular dysfunction before dying suddenly, and three of them died despite the prior implantation of a permanent pacemaker. The mean age of onset of cardiac symptoms among affected living family members was 33 years (range 15–47 years), and the first symptoms were due to marked atrioventricular conduction defects or sinus dysfunction, requiring the implantation of permanent pacemakers in seven cases. Myocardial dysfunction accompanied by ventricular arrhythmias developed rapidly in the course of the disease and resulted in severe dilated cardiomyopathy requiring cardiac transplantation in three cases. In conclusion, in patients presenting a life-threatening familial or sporadic cardiac restricted phenotype similar to that described here, mutations in the lamins A and C gene should be looked for. In the genotypically affected individuals, cardiological and electrophysiological follow-up should be performed to prevent sudden death that could occur rapidly in the evolution of such disease.

Notes: The lack of specificity of VT detection is a significant shortcoming of current ICDs. In a French multicenter study, 18 patients underwent implantation of the Defender 9001 (ELA Medical), an ICD utilizing dual chamber pacing and arrhythmia detection. Over a mean follow-up period of 7.1 ± 4.5 months, 176 tachycardia episodes recorded in the device memory were analyzed, and physician diagnosis was compared with that by the device. All 122 VT/VF episodes were correctly diagnosed, as were 51 of 53 supraventricular tachyarrhythmias. Two episodes of AF with rapid regular ventricular rates were treated as VT, and a third episode, treated as VT, could not be diagnosed with certainty. A dual chamber pacemaker defibrillator offers improved diagnostic specificity without loss of sensitivity, in addition to the hemodynamic benefit of dual chamber pacing. (PACE 1997;20

Notes: Background: In dilated cardiomyopathy (DCM) patients (pts) with cardiac resynchronization therapy (CRT) for ventricular dyssynchrony, long-term predictors of mortality and morbidity remain poorly investigated. Method and Results: We reviewed data of 102 pts, 68 ± 10 years, NYHA Class II–IV (14 Class II, 67 Class III, 21 Class IV), who benefited from CRT (69 CRT, 33 CRT-ICD). Fifty-two patients had an ischemic DCM, 36 a previously implanted conventional PM/ICD, 29 a permanent atrial fibrillation, and 19 needed dobutamine in the month preceding implant. QRS duration was 187 ± 35 ms, left ventricular end-diastolic diameter 72 ± 10 mm, mitral regurgitation severity 1.9 ± 0.8, echographic aorto-pulmonary electromechanical delay 61.5 ± 25 ms and septo-lateral left intraventricular delay 86 ± 56 ms, pulmonary artery pressure (PAP) 43 ± 11 mmHg, angioscintigraphic left ventricular ejection fraction (EF) 20 ± 9%, and right ventricular EF 30.5 ± 14%. Over a mean follow-up of 23 ± 20 months, 26 pts died (18 heart failures (HFs), 1 arrhythmic storm, 7 noncardiac deaths). Positive univariate predictors of death from any cause were NYHA Class IV (P 〈 0.001), and need for dobutamine the month preceding CRT (P 〈 0.008), while use of β-blocking agents (P 〈 0.08) and left ventricular EF (P 〈 0.09) were negative ones. NYHA Class IV was the only independent predictor at multivariate analysis (P 〈 0.01). Survival at 24 months was 85% in Class II, 80% in Class III, and 37% in Class IV (II vs III, P = ns; III vs IV, P 〈 0.001). When using a composite endpoint of death from any cause and unplanned rehospitalization for a major cardiovascular event, there were 48 events (14 HF deaths, 3 noncardiac deaths, 26 HF rehospitalizations, 2 paroxysmal atrial fibrillation, 2 sustained ventricular tachycardia, 1 nonfatal pulmonary embolism). Predictors of death from any cause/unplanned rehospitalization for a major cardiovascular event in the follow-up were NYHA Class IV (P 〈 0.001), need for dobutamine during the month preceding CRT (P 〈 0.002), and PAP (〈0.02). NYHA Class IV was the only independent predictor at multivariate analysis (P 〈 0.05). Event-free proportion at 24 months was 70% in Class II, 64% in Class III, and 37% in Class IV (II vs III, P = ns; III vs IV, P 〈 0.01). When considering determinants of mortality only in NYHA Class IV patients, no variable was significantly correlated to mortality. Need for dobutamine during the last month preceding CRT did not add an adjunctive mortality risk. Conclusion: Baseline NYHA Class IV at implantation appears as the most important determinant of a poor clinical outcome in terms of both mortality and morbidity. No predictive criteria seem available for NYHA Class IV patients, in order to discriminate who will die after CRT and who will not. NYHA Class IV strongly influences the clinical outcome, suggesting that, in future studies planned on mortality and rehospitalization as major endpoints, baseline NYHA Class IV should be separately taken into account.