Patients with conventional SC-ICD indication were randomized to DC-ICD, SC-ICD, or a DC-ICD programmed as an SC-ICD (SC-simulated) and followed for 16 months. Patients in the DC and SC-simulated groups crossed over after 8 months. The primary endpoint was a composite of CSAE: all-cause mortality; invasive intervention; hospitalization (>24 h) for cardiovascular causes; inappropriate shocks (two or more episodes); and sustained symptomatic AT lasting >48 h. The outcome variable was a pre-specified score that corrected for clinical severity and follow-up duration. Three hundred and thirty-four patients were analysed (DC-ICD, n = 112; SC-ICD, n = 111; SC-simulated, n = 111). The mean left ventricular ejection fraction was 0.36 ± 0.13, 69% were in functional class ≥II. CSAE occurred in 65 DC-ICD, 82 SC-ICD, and 84 SC-simulated patients. The outcome variable was 33% lower in the DC-ICD group (OR 0.31; 95% CI 0.14–0.67; P = 0.0028). Mortality was 4% in DC, 9% in SC, and 10% in SC-simulated.

In patients with a standard SC-ICD indication, DC-ICD was associated with less CSAE when compared with SC-ICD.

Thirty-one patients experiencing device recalls answered questions regarding their knowledge about the recall and their decision whether to replace the device. Fifty patients whose devices were not recalled reported demographic data. In both groups, psychological factors were assessed. No significant differences were found for psychological factors. Most patients reported being informed of their recall by their physician. Most estimated the risk of device failure to be low or very low, but they overestimated the fail rate. Thirty-six per cent of patients reported feeling anxious about the recall.

No significant differences existed in psychological factors and QOL between patients whose ICDs were recalled compared with those whose devices were not. The majority of patients whose ICDs are the subject of an FDA advisory/recall have a realistic understanding of the risks of device failure. Prompt information, support, and reassurance provided by healthcare professionals may allay patient distress.

Surviving patients (n = 610) who received an ICD in our institution since 1989 completed the Short Form Health Survey (SF-36) and the Hospital Anxiety and Depression Scale. Mean age was 62.4 years with 18% females. In a multivariate logistic regression analysis, symptomatic heart failure was the most important correlate of impaired QOL (SF-36) across all eight subscales [odds ratios (ORs) ranging from 5.21 to 22.53)], whereas psychotropic medication, age, comorbidity, amiodarone, and ICD shocks all correlated to a lesser extent. Symptomatic heart failure was also the most dominant correlate of anxiety [OR 5.15 (3.08–8.63), P < 0.001] and depression [OR 6.82 (3.77–12.39), P < 0.001]. Implantable cardioverter-defibrillator shocks correlated less yet significantly with anxiety [OR 2.21 (1.32–3.72) P < 0.01] and depression [OR 2.00 (1.06–3.80), P < 0.05].

Symptomatic heart failure was the single most important clinical correlate of impaired QOL, anxiety, and depression, with ICD shocks playing only a secondary role. This suggests that comorbidity rather than ICD therapy per se influences patients' device acceptance, supporting the increasing use of prophylactic ICD implantation.

We examined consecutive patients in whom CRT was implanted disregarding the atrial rhythm. Atrial fibrillation was defined as either current or earlier AF, response to CRT was defined as a decrease in the left ventricular end-systolic volume of ≥10% after 6 months. Total atrial conduction time (TACT), a measure to predict the risk of developing AF, was determined by echocardiography. We included 114 patients, of whom 56 (49%) were known with AF (23 current AF and 33 earlier AF). The other 58 patients had no history of AF. After 6 months, response in current and earlier AF and that in SR patients was comparable (56, 58 and 55%, respectively). In AF patients, multivariate analysis revealed a shorter TACT at baseline [odds ratio (OR) 16.7 (1.5–185.3), P = 0.02] and an interventricular mechanical delay (IVMD) >40 ms [OR 10.4 (1.0–110.9), P = 0.05] as predictors for response. Non-responders more frequently suffered from new-onset AF (P = 0.02).

Failure to CRT is associated with new-onset AF. Total atrial activation time may be a parameter to predict response in AF patients.

A total of 200 consecutive HF patients (158 males, mean age 56 ± 13.5 years) with standard indications for cardiac resynchronization therapy (CRT) were evaluated prospectively. The prevalence of an interventricular mechanical delay ≥40 ms was lower in patients with pure right bundle branch block (RBBB) than that in those with RBBB plus left fascicular hemiblock (RBBB-LFH) and those with left bundle branch block (LBBB) (33 vs. 50 vs. 54%, P = 0.05). A maximal difference in peak myocardial systolic velocity among all 12 segments (Ts)>100 ms was found in 63% of the patients with LBBB, whereas it was present in 31% of the patients with pure RBBB and in 42% of those with RBBB-LFH (P < 0.001). A standard deviation of Ts (Ts-SD)>34 ms was present in 58% of the LBBB subjects, but in only 29% and 42% of the patients with pure RBBB and RBBB-LFH, respectively (P < 0.001). Intraventricular dyssynchrony, however, was not different in patients with pure RBBB and in those with RBBB-LFH in terms of maximal difference in Ts (P = 0.25) and Ts-SD (P = 0.17).

Although LBBB was more often associated with intraventricular dyssynchrony, ECG sign of additional left ventricular (LV) conduction delay is not a helpful tool for the identification of intra-LV mechanical dyssynchrony in HF patients with RBBB who would benefit from CRT.

We randomized 98 patients with atrioventricular block (AV-block) undergoing pacemaker implantation to positioning the ventricular lead in the high or mid septum (n = 53) or in the apex (n = 45) of the right ventricle. N-terminal pro-brain natriuetic peptide (BNP) levels, left ventricular ejection fraction (LVEF), and exercise capacity were analysed 3 days, 3 months, and 18 months after the implantation. The primary endpoints were the changes of these parameters from baseline to 18 months.

Changes of BNP levels, LVEF, and exercise capacity from baseline to 18 months were statistically not different between septal and apical stimulation. The clinical occurrence or deterioration of overt heart failure was similar in both treatment arms.

With regard to different parameters of congestive heart failure, a septal stimulation site is not superior to conventional apical pacing in unselected patients undergoing pacemaker implantation for AV-block.

Twelve consecutive patients with standard pacemaker indication (9 male, 74 ± 9 years) entered the study. Pacing leads were implanted in the right ventricular apex and directly in the His bundle, and were connected to different ports of the pacemaker. All patients first underwent 3 months of DHBP, followed by 3 months of RVAP. At the end of each 3-month period, myocardial perfusion was measured at rest using scintigraphy with Tc99m-SestaMIBI. The average values of perfusion were evaluated on a 20-segment basis. All patients also underwent clinical evaluation, echocardiography, and tissue Doppler imaging (TDI), to measure dyssynchrony, and a blood sample was taken for brain natriuretic peptide (BNP) assay. The perfusion score during DHBP pacing was significantly better than during RVAP (0.44 ± 0.5 vs. 0.71 ± 0.53, respectively; P = 0.011). None of the patients showed lower perfusion during DHBP than during RVAP. We found no significant difference in NYHA class, ventricular volumes, ejection fraction, or plasmatic BNP between DHBP and RVAP. However, mitral regurgitation (0.26 ± 0.21 vs. 0.37 ± 0.25; P < 0.001) and dyssynchrony (13.75 ± 4.28 vs. 22.02 ± 8.44; P = 0.008) were significantly less during DHBP than during RVAP.

Direct His bundle pacing is superior to RVAP in preserving the physiologic distribution of myocardial blood flow and reducing mitral regurgitation and left ventricular dyssynchrony.

A total number of 70 patients with paroxysmal AF and episodes ≤24 h were scanned on a 1.5-T-CMRI before and 6 months after PVI during sinus rhythm. End-diastolic volume, end-systolic volume, and LVEF were determined by epicardial and endocardial measurements. Patients were categorized into two groups regarding cardiac function as assessed by CMRI: group 1 patients (n = 18) with an LVEF < 50% and patients with an LVEF > 50% (group 2, n = 52). Group 1 patients demonstrated a significant lower success rate than patients of group 2 after a follow-up of 152 ± 40 days (50 vs. 73%, P < 0.05). Cardiac magnetic resonance imaging in group 1 patients demonstrated a significant improvement in cardiac function after AF ablation (41 ± 6 vs. 51 ± 12%, P = 0.004), whereas group 2 patients did not show significant differences (60 ± 6 vs. 59 ± 9%, P = 0.22) after a 6 months follow-up.

Pulmonary vein isolation improves cardiac function in patients with paroxysmal AF and impaired LVEF. These data suggest that an impaired LV function can be partially attributed to AF with short-lasting paroxysms.

A total of 106 cases (58 males, average age 66.0 ± 8.8 years) with paroxysmal AF were included for ablation. They were allocated randomly to two groups: CPVI group (n = 54) and CPVI + SVCI group (n = 52). All cases underwent the procedure successfully. Pulmonary vein isolation was achieved in all cases. The procedural time and fluoroscopic time were comparable between the two groups. The mean ablation time for SVC was 7.8 ± 2.7 min. Superior vena cava isolation was obtained in 50/52 cases. In the remaining two cases, SVCI was not achieved because of obviating diaphragmatic nerve injury. During a mean follow-up of 4 ± 2 months, 12 (22.2%) cases in the CPVI group and 10 (19.2%) cases in the CPVI + SVCI group had atrial tachyarrhythmias (ATa) recurrence (P = 0.70). Nine of 12 cases in the CPVI group and 8/10 cases in the CPVI + SVCI group underwent reablation (P = 0.86), and PV reconnection occurred in 7/9 cases in the CPVI group and in 8/8 cases in the CPVI + SVCI group. All PV reconnection was reisolated by gaps ablation. There was no SVC reconnection in the CPVI + SVCI group. In two cases without PV reconnection from the CPVI group, SVC-originated short run of atrial tachycardia was identified and eliminated by the SVCI. At the end of 12 months of follow-up, 50 cases (92.6%) in the CPVI group and 49 (94.2%) in the CPVI + SVC group were free of ATa recurrence (P = 0.73).

In our series of paroxysmal AF patients, empirically adding SVCI to CPVI did not significantly reduce the AF recurrence after ablation. Superior vena cava isolation may be useful, however, in selected patients in whom the SVC is identified as a trigger for AF. However, because of the preliminary property of the study and its relatively small sample size, the impact of SVCI on clinical results should be evaluated in a large series of patients.

Thirty-nine patients with ECG documented atrial fibrillation (AF) scheduled for coronary artery bypass grafting (CABG) with or without concomitant valve surgery were consecutively elected for epicardial RF ablation. Thirty-nine age- and gender-matched patients scheduled for CABG with or without concomitant valve surgery only and with documented AF served as controls. The follow-up after ablation was 32 ± 11 months. The percentage of patients in sinus rhythm (SR) at long-term follow-up was 62 vs. 33% (P = 0.03) after ablation and no ablation, respectively. SR at 3 months was highly predictive of that at 32 months (sensitivity 95%, positive predictive value 86%). Long-term SR was associated with better QoL, fewer symptoms, higher ejection fraction, and smaller left and right atria than AF.

SR at 3 months was highly predictive of long-term SR that was associated with clinical improvement when compared with patients still in AF. AF at 3 months did not preclude a later stabilization to SR.

A retrospective cohort study was designed. A group of marathon runners (n = 252) and a population-based sample of sedentary men (n = 305) recruited in 1990–92 and 1994–96, respectively, were contacted in 2002–03 and invited to attend an outpatient clinic to identify suggestive symptoms of having experienced an arrhythmia requiring medical attention. In those with suggestive symptoms of atrial fibrillation, medical records were reviewed. Finally, LAF was diagnosed on the basis of the presence of atrial fibrillation in an electrocardiographic recording. In the group of marathon runners, an echocardiogram was performed at inclusion and at the end of the study. The annual incidence rate of LAF among marathon runners and sedentary men was 0.43/100 and 0.11/100, respectively. Endurance sport practice was associated with a higher risk of incident LAF in the multivariate age- and blood pressure-adjusted Cox regression models (hazard ratio = 8.80; 95% confidence interval: 1.26–61.29). In the group of marathon runners, left atrial inferosuperior diameter and left atrial volume were both associated with a higher risk of incident LAF.

Long-term endurance sport practice is associated with a higher risk of symptomatic LAF in men. This risk is associated with a larger left atrial inferosuperior diameter and volume in physically active subjects.

We included 470 patients who underwent an electrophysiological study for paroxysmal, regular, and narrow-QRS complex tachycardia without pre-excitation in sinus rhythm. The ECG recordings were reviewed for the presence of the following: (i) pseudo r' deflection (V1) and/or pseudo s-wave (inferior leads), (ii) identifiable P-wave after the QRS complex, (iii) QRS alternans, and (iv) repolarization abnormalities during tachycardia. We performed a cross-validation method using the first 300 patients to develop a logistic model to predict the tachycardia diagnosis. The model was validated through the remaining 170 patients. The invasive study demonstrated AVNRT in 314 patients and AVRT in 156 patients. The presence of pseudo r' deflection and/or pseudo s-wave, a visible P-wave after the QRS complex, and QRS alternans were selected by a stepwise multiple logistic regression analysis as predictors for the diagnosis of AVNRT. The application of the model in the validation group showed a shrinkage prediction factor of 3%. Diagnostic probabilities for both tachycardia mechanisms depending on every combination of selected ECG criteria were >75% in 70% of the patients.

The presence of pseudo r' deflection and/or pseudo s-wave, an identifiable P-wave after the QRS, and QRS alternans during tachycardia permit us to derive a reliable logistic model to predict the mechanism of paroxysmal AVRT in patients without pre-excitation. Precise probabilities for a correct diagnosis associated with every combination of those classical ECG criteria are presented.

A six step regimen of oral therapy was used in 55 infants with SVT: (i) propafenone (P); (ii) flecainide (F); (iii) flecainide plus propranolol (FP); (iv) amiodarone (A); (v) amiodarone plus propranolol (AP); (vi) amiodarone plus flecainide plus propranolol (AFP). If one step was not successful, the patient was passed on to the next treatment step and so on. Transesophageal atrial pacing (TAP) was used to evaluate treatment efficacy and the evolution of SVT at the end of the first, second, and third year. Propafenone was successful in 32.7% of the patients, F in 14.5%, FP in 23.6%, A alone in 5.4%, and AP in 18.1%; only 7.2% reached step 6. At month 12, after therapy wash out, SVT recurred spontaneously in 2 patients (3.6%) and remained inducible in 25 (45.5%). Inducibility was significantly higher in patients treated with A. At 24 months, SVT was inducible or spontaneous in 86% of the cases and at 36 months in 87%. There were no recurrences using the treatment confirmed by TAP. No further predictor of SVT inducibility was identified.

Supraventricular tachycardia disappeared in ~50% of the patients during the first year of life and in another 20% thereafter. The necessity for A treatment is the only predictor of persistence of the re-entry circuit during the first year of life. Transesophageal atrial pacing is useful in guiding the medical treatment.