We studied 15 patients in New York Heart Association classes II–IV and with a QRS duration >130 ms, who had undergone implantation of a biventricular (BiV) pulse generator connected to a right ventricular (RV) PEA sensor. At a mean of 39 ± 15 days after implantation of the CRT system, the patients underwent cardiac catheterization. During single-chamber LV or during BiV stimulation, with initial RV or LV stimulation, and at settings of interventricular intervals between 0 and 40 ms, the AVD was scanned between 60 and 220 ms, while LV dP/dt_max and PEA were measured. The area of PEA curve (PEA_area method) was estimated as the average of PEA values measured during AVD scanning. A ≥10% increase in LV dP/dt_max was observed in 12 of 15 patients (80%), who were classified as responders to CRT. In nine of 12 responders (75%), the optimal pacing configuration identified by the PEA_area method was associated with the greatest LV dP/dt_max.

The concordance of the PEA_area method with measurements of LV dP/dt_max suggests that this new, operator-independent algorithm is a reliable means of CRT optimization.

We conducted a retrospective analysis of 131 consecutive heart failure (HF) patients who underwent CRT implantation. Three groups were considered: SR (n = 78), AF with AVJ ablation (n = 26), and AF without AVJ ablation (n = 27). Patients were evaluated for the occurrence of cardiac death, hospitalization for HF, and responsiveness to CRT (survival with improvement of ≥1 New York Heart Association class at 6 months). The three groups showed a significant improvement in functional class. However, the proportion of responders was significantly lower in AF patients without AVJ ablation (52 vs. 79% in SR and 85% in AF with AVJ ablation, P < 0.008). Atrial fibrillation without AVJ ablation was also independently associated with mortality (HR 5.22, 95% CI: 1.60–17.01, P = 0.006) and hospitalization for HF during the first 12 months (HR 6.23, 95% CI: 2.09–18.54, P = 0.001). The outcomes of AF with AVJ ablation patients were similar to the outcomes of patients in SR.

Sinus rhythm and AF patients display similar survival and clinical improvement after CRT implantation, provided that AVJ ablation is performed in the latter.

At first evaluation, one female had an aborted sudden cardiac death and eight patients suffered from recurrent syncopes. Intrathoracic cardioverter defibrillator (ICD) implantation was done in the patient with aborted sudden cardiac death and in six patients with recurrent syncopes. One of these six patients had intermittant 2–3° AV block. Another patient had inducible ventricular tachycardia (VT) at electrophysiological study. Follow-up over more than 3 years in all but one patient was characterized by documented monomorphic VT in the patient with inducible VT and ICD implantation (6%). The patient with aborted sudden cardiac death had only non-sustained VT’s shortly after ICD implantation. From the eight patients without syncopes two more patients developed AV block and SA block 3° (18%). Lead-associated complications appeared in three of eight patients with ICDs (38%). Repeated ajmaline challenge was positive in four of eight cases (50%). One patient had a new mutation encoding for SCN5A gene.

Ajmaline challenge in typical ARVC characterizes a subgroup of elderly, predominantly female patients with the risk of developing conduction disease. Tachycardia-related events are rare. The indication of ICD implantation in recurrent syncopes is critical as the rate of lead-associated complications in a more than 3 years follow-up is high.

Patients diagnosed with Brugada ECG pattern were enrolled in the study. Four standard cardiac autonomic function tests were performed. The presence of ≥2 abnormal test results were considered definite evidence for the presence of CAN. Types 1, 2, and 3 Brugada ECG pattern were found in 28, 56, and 31 patients, respectively. CAN was detected in 13 (46%) patients with type 1 Brugada ECG pattern. In contrast, none of the type 2 or 3 Brugada patients had CAN. Of 13 patients with CAN, 11 had previous history of cardiac events (84%), whereas only 2 of 15 patients without CAN had history of previous cardiac events (13%; P = 0.01). The most noteworthy finding was that all of the type 1 Brugada patients with CAN were male (CAN was not detected in females).

It was concluded that CAN is an important risk indicator in BS. CAN is more common in men. Male gender, per se, is not an independent risk factor for development of ventricular arrhythmia but also CAN, which is an important risk factor in BS, is more common in men; therefore men are susceptible to the development of cardiac events.

A nation-wide population-based cohort of 8777 patients with AAI- or DDD-mode pacemakers was followed during 12 years. The cohort was linked to national healthcare and census registers. Patients with DDD pacing and without any pre-implant admission for atrial fibrillation or flutter had an increased risk of post-implant fibrillation or flutter, in relation to corresponding AAA patients [hazard ratio (HR) = 1.30; 95% confidence interval (CI) 1.10–1.52]. A slight increase in the risk of any cardiovascular disease (HR = 1.07; CI, 1.00–1.15), and all-cause mortality (HR = 1.12; CI, 1.00–1.25), was seen among DDD patients, in relation to AAI patients, but there was no significant difference in the risk of ischaemic or unspecified stroke (HR = 1.14; CI, 0.94–1.37). Among DDD patients, the all-cause mortality did not differ from the general population [standardized mortality ratio (SMR) = 1.04; CI, 0.98–1.11]. Patients with AAI, however, had a decreased all-cause mortality risk (SMR = 0.89; CI, 0.82–0.97).

Our results support AAI as the preferred mode of pacing in patients with sinus node disease, and a normal AV node function.

The multicentre FOLLOWPACE study prospectively collected data during implantation and follow-up of 1526 patients who received a PM for the first time. A total of 4914 follow-up visits were studied. Mean follow-up was 394 days with a mean of 3.2 visits per patient. At all follow-up visits, the battery condition was tested in >93%, the stimulation threshold in >91%, and sensing in >87%. The pacemaker parameters as stimulation and sensing thresholds, lead impedances, and percentages of pacing remained stable over time, but these values did depend on the lead location, lead fixation, and pulse duration. The majority of PM (re-)programming was performed during implantation and/or shortly before hospital discharge (50%). PM re-programming during follow-up was most frequently performed by the PM technician alone (95%).

Crucial PM parameters are regularly checked. Re-programming of PM parameters declined during the first year after PM implantation. The majority of PM checks were carried out by the PM technician, indicating the major influence of the allied professional on the quality and safety of the pacing therapy.

Data of children with AC (group AC, n = 49) and conventionally programmed devices (group Conv, n = 41) were analysed. A total of 1106 outpatient visits and 147 Holter recordings were screened for device reprogramming and invasive re-intervention. At 2 and 5 years, freedom from reprogramming differed significantly between groups (AC: 63/35% vs. Conv: 13/4%; P < 0.0001), whereas freedom from re-intervention was not different (AC: 95/90% vs. Conv: 95/85%; P = 0.26). Mean yearly rate of reprogramming was lower in group AC (AC: 0.67 ± 0.55 vs. Conv: 1.13 ± 0.82; P = 0.005). Follow-up duration correlated with a decreasing number of reprogramming per year in group Conv ( = –0.73, P < 0.001). No ventricular output reprogramming was required in group AC. Holter recordings required 0.07 ± 0.13 reprogramming per year in group Conv, none in group AC (P < 0.001). Holter-detected lead dysfunction prompted re-intervention in one patient of each group.

Estimated freedom from as well as total yearly rate of device reprogramming was favourable for AC-programmed devices. No difference was seen for the incidence of invasive re-interventions. AC ventricular output control was effective. Structured device follow-up and Holter recordings in specific patient groups remain mandatory for all devices in paediatric patients.

The follow-up results of 264 leads from 184 patients were evaluated using pacemaker follow-up data. Underlying conditions, implant data, and lead features were evaluated for the analysis of lead fracture. During a mean follow-up of 72.8 ± 39.7 months (range 3.2–160.6, median 70), lead fracture developed in 19 leads (7.2%) from 18 patients. The mean duration between implantation and lead fracture was 57.3 ± 35 months (range 6.8–130, median 51). All fractures occurred in the leads implanted by the infraclavicular subclavian approach. Cumulative survival at the end of 5 years was 92.7% in terms of lead fracture. None of the patient-related risk factors correlated with lead fracture. Multivariate analyses of lead-related risk factors revealed a significant correlation only between lead fracture and fixation mechanism (P < 0.05).

Our results indicated that none of the patient-related risk factors was correlated with lead fracture. Among lead-related risk factors, only the fixation mechanism was found to be correlated with lead fracture; thus, it seems that passive fixation mechanism is safer in terms of lead fracture. Although all fractures occurred in the leads implanted by the intrathoracic subclavian approach, statistical analysis revealed no significance for this parameter. The effect of the extrathoracic approach should be investigated in a large group of patients.

The study group consisted of 29 patients referred for radiofrequency catheter ablation: 10 patients with paroxysmal AF, 8 patients with permanent AF, and 10 control patients with Wolf-Parkinson-White (WPW) syndrome and no evidence of AF (mean age 54 ± 11 vs. 57 ± 13 vs. 43 ± 16). No patient had structural heart diseases or inflammatory conditions. High-sensitive C-reactive protein, interleukin-6 (IL-6), and interleukin-8 (IL-8) were assessed in blood samples from the femoral vein, right atrium, coronary sinus, and the left and right upper pulmonary veins. All samples were collected before ablation. Compared with controls and patients with paroxysmal AF, patients with permanent AF had higher plasma levels of IL-8 in the samples from the femoral vein, right atrium, and coronary sinus, but not in the samples from the pulmonary veins (median values in the femoral vein: 2.58 vs. 2.97 vs. 4.66 pg/mL, P = 0.003; right atrium: 2.30 vs. 3.06 vs. 3.93 pg/mL, P = 0.013; coronary sinus: 2.85 vs. 3.15 vs. 4.07, P = 0.016). A high-degree correlation existed between the IL-8 levels in these samples (correlation coefficient between 0.929 and 0.976, P < 0.05). No differences in the C-reactive protein and IL-6 levels were noted between the three groups of patients.

The normal levels of C-reactive protein and IL-6, along with the elevated levels of IL-8 in patients with permanent AF but not in those with paroxysmal AF, suggest a link between a low-grade inflammatory reaction and long-lasting AF. The elevated IL-8 levels in the peripheral blood, right atrium, and coronary sinus but not in the pulmonary veins suggest a possible source of inflammation in the systemic circulation.

We prospectively followed 1445 consecutive patients receiving an ICD for the primary (n = 833) or secondary (n = 612) prevention from December 1997 through January 2007. Outcome measures include incidence of AF/AFL that initiated ICD therapy or was detected during ICD interrogation. Cox hazard regression analyses were conducted to determine the predictors of AF/AFL with and without inappropriate shock delivery and did not include inappropriate shocks resulting from lead dysfunction or other exogenous factors. Patients in this study (n = 1445) were followed over a mean follow-up period of (mean ± SD) 874 ± 805 days. There were 563 episodes of AF/AFL detected, with 200 episodes resulting in inappropriate shock therapy. Overall, 745 patients received statin therapy and 700 did not. The use of statin therapy was associated with an adjusted hazard ratio of 0.472 [95% confidence interval (CI), 0.349–0.638, P < 0.001] for the development of AF/AFL with shock therapy and 0.613 (95% CI, 0.496–0.758, P < 0.001) without shock therapy when compared with the group without statin use.

Among a cohort with ICDs at high risk for cardiac arrhythmias, statin therapy was associated with a reduction in AF/AFL tachyarrhythmia detection and inappropriate shock therapy.

Nine subjects with high RAS activity and nine subjects with low RAS activity were subjected to single-blinded placebo-controlled hypoglycaemia (nadir plasma glucose 2.4 mmol/L). QTc/QTcF and QT dynamics were registered by Holter monitoring. QTc prolonged during [8 (±2.3) ms, P < 0.01] and after [11 (±3) ms, P < 0.001] hypoglycaemia. Dynamic QT parameters reacted ambiguously. Low RAS activity was associated with a slightly more pronounced QT prolongation [6 (±3) ms, P = 0.04]. Adrenaline tended to increase more in the low-RAS group (P = 0.08) and was correlated to QTc (r = 0.67, P < 0.01) and QTcF (r = 0.58, P < 0.05) during hypoglycaemia.

Low basal RAS activity may be associated with a slightly more pronounced QT prolongation during hypoglycaemia, when compared with high RAS activity. The impact, however, is modest and the clinical consequence is unclear.

In isolated rabbit hearts, under pacing condition, QT interval was measured under Ab-β perfusion. Beta-adrenergic activity was also tested in guinea pig ventricular M cells. Furthermore, the immunoglobulin fraction (IgG-β) of the Ab-β was tested on Ito, ICa, and Iks currents in rat, rabbit, and guinea pig myocytes, respectively. Beta-adrenergic activity shortened the QT interval. This effect was abolished in the presence of propranolol. In addition, sera from CChP without beta-adrenergic activity (Ab-β) did not modulate QT interval. The M cell action potential duration (APD) was reversibly shortened by Ab-β. Atenolol inhibited this effect of Ab-β, and Ab- did not modulate the AP of M cells. Ito was not modulated by isoproterenol nor by IgG-β. However, IgG-β increased ICa and IKs.

The shortening of the QT interval and APD in M cells and the increase of IKs and ICa induced by IgG-β contribute to repolarization changes that may trigger malignant ventricular arrhythmias observed in patients with chronic chagasic or idiopathic cardiomyopathy.