Background— Endovascularly implanted leads risk vascular injury and endocarditis, and can be difficult to locate in desired positions for LV pacing. We evaluated the acute and long-term stability, electric performance and histopathology of a percutaneously placed intrapericardial lead (IPL). Methods and Results— Twelve adult mongrel dogs underwent defibrillator implants incorporating IPLs. Successful uncomplicated percutaneous implantation of an IPL was achieved in all. Early fluoroscopic shift noted with 3 of 6 of the initial version IPL-1 was not seen with the modified IPL-2. Mean±95% confidence interval bipolar capture threshold at 0.5-ms pulse width for the IPL increased from 0.69±0.14 V at implant to 1.50±0.34 V ( P =0.003) at 12 weeks. The 12-week thresholds were higher for IPL compared with right ventricular endocardial leads (0.75±0.33 V; P =0.001) but not different compared with coronary sinus leads (1.33±0.58 V; P =0.994). IPL impedance increased from 742±46 Ω at implant to 1066±207 Ω at 12 weeks ( P =0.007). R-wave amplitude at 12 weeks was 8.37±1.52 mV. There was no important phrenic nerve stimulation from IPL pacing. Histopathology in 8 animals showed adequate adhesion of the electrodes or mesh to the epicardium without damage to underlying vasculature. There was no evidence for late pericardial inflammation or effusion. Conclusions— The IPL demonstrated adequate stability of position and acceptable electric parameters without chronic pericardial inflammation in this canine model and offers a potential alternative to endocardial pacing leads.

Background We hypothesized that left atrial pressure (LAP) obtained by a permanent implantable sensor is sensitive to changes in cardiac resynchronization therapy (CRT) settings and could guide CRT optimization to improve the response rate. We investigated the effect of CRT optimization on LAP and its waveform parameters in ambulant heart failure (HF) patients. Methods CRT optimization was performed in eight ambulant HF patients, using echocardiography as reference. LAP waveform was acquired at each of eight atrioventricular (AV) intervals and five inter‐ventricular (VV) intervals. Selected waveform parameters were also evaluated for their sensitivity to CRT changes and agreement with echocardiography‐guided optimal settings. Results Optimal AV and VV intervals varied considerably between patients. All patients exhibited significant changes in waveform morphology with AV optimization. Optimal AV delay determined from echocardiography ranged between 140 ms and 225 ms. Mean LAP tended to be lower at optimal setting 14 ± 3 mmHg compared to shorter (<100 ms) or longer (>160 ms) AV settings (P = 0.16). There were clear trends to smaller peak a‐wave (P = 0.11) and gentler positive a‐slope (P = 0.15) and positive v‐slope (P = 0.09) with longer AV delays. Mean LAP and negative v‐wave slope correlated well with echo‐guided optimal setting, r = 0.91 (P = 0.001) and 0.79 (P = 0.03), respectively. No significant effects on LAP or waveform were seen during VV optimization. Conclusions LAP and its waveform changes considerably with AV optimization. There is good agreement between echo‐guided optimal setting and LAP. LAP could provide an objective guide to CRT optimization. (Clinical Trial Registry information: URL: http://www.clinicaltrials.gov . Unique Identifier: NCT00632372)

Aims In pacemaker patients with preserved atrio-ventricular (AV) conduction, atrial fibrillation (AF) can lead to symptomatic ventricular rate irregularity and loss of ventricular stimulation. We tested if dynamic ventricular overdrive (DVO) as a potentially pacemaker-integrated algorithm could improve both aspects.Methods and results Different settings of DVO and ventricular-ventricular-inhibited-pacing (VVI) with different base rates were tested in two consecutive phases during electrophysiological studies for standard indications. Mean heart rate (HR), HR irregularity and percentage of ventricular pacing were evaluated. A fusion index (FI) indicative of the proportion of fusion beats was calculated for each stimulation protocol. Dynamic ventricular overdrive from the right ventricular apex was acutely applied in 38 patients (11 females, mean age 62.1 +/- 11.5 years) with sustained AF and preserved AV conduction. Dynamic ventricular overdrive at LOW/MEDIUM setting increased the amount of ventricular pacing compared with VVI pacing at 60, 70, and 80 beats per minute (bpm; to 81/85% from 11, 25, and 47%, respectively; P < 0.05). It also resulted in a maximum decrease in interval differences (to 48 +/- 18 ms from 149 +/- 28, 117 +/- 38, and 95 +/- 46 ms, respectively; P < 0.05) and fusion (to 0.13 from 0.41, 0.42, and 0.36, respectively; P < 0.05) compared with VVI pacing at 60, 70, and 80 bpm. However, the application of DVO resulted in a significant increase in HR compared with intrinsic rhythm and VVI pacing at 80 bpm (to 97 bpm from 89 and 94 bpm, respectively; P < 0.05).Conclusion Dynamic ventricular overdrive decreases HR irregularity and increases ventricular pacing rate compared with VVI pacing at fixed elevated base rates and spontaneous rhythm. Fusion index might help to refine information on pacing percentages provided by device counters.

BACKGROUND:Previous studies suggested that epicardial patch applied to the infarcted site after acute myocardial infarction (MI) can alleviate left ventricular (LV) remodeling and improve cardiac performance; however, the effects of regional epicardial patch on chronic phase of LV remodeling remain unclear. METHODS AND RESULTS:We studied 20 pigs with MI induced by distal embolization and impaired LV ejection fraction (LVEF < 45%) as detected by gadolinium-enhanced cardiac magnetic resonance imaging (MRI). Eight weeks post-MI, all animal underwent open chest procedure for sham surgery (control, n = 12) or patch implantation over the infarcted lateral LV wall (patch group, n = 12). In the patch group, +dP/dt increased and LV end-diastolic pressure decreased at 20 weeks compared with immediately post-MI and at 8 weeks (P < .05), but not in the control group (P > .05). As determined by cardiac MRI, LV end-diastolic and end-systolic volumes increased at 20 weeks compared with 8 weeks in both groups (P < .05). However, the increase in LV end-diastolic volume (+14.1 +/- 1.8% vs. +6.6 +/- 2.1%, P = .015) and LV end-systolic volume (+12.1 +/- 2.4% vs. -4.7 +/- 3.7%, P = .0015) were significantly greater in the control group compared with the patch group. Furthermore, the percentage increase in LVEF (+17.3 +/- 4.9% vs. +4.1 +/- 3.9%, P = .048) from 8 to 20 weeks was significantly greater in the patch group compared with the control group. Histological examination showed that LV wall thickness at the infarct region and adjacent peri-infarct regions were significantly greater in the patch group compared with the control group (P < .05). CONCLUSION:Regional application of a simple, passive synthetic epicardial patch increased LV wall thickness at the infarct region, attenuated LV dilation, and improved LVEF and +dP/dt in a large animal model of MI.

AIMS Multisite atrial pacing has been suggested to be effective in suppressing atrial fibrillation (AF), however, the effect of linear triple-site atrial pacing (LTSP) in humans has not been evaluated. We compared the effects of LTSP to single-site atrial pacing (SSP) on the atrial activation and wavefront propagation pattern in patients with persistent AF. METHODS AND RESULTS In 10 patients with persistent AF, the effects of LTSP and SSP were evaluated by left atrial (LA) endocardial non-contact multielectrode array mapping and multipolar catheters. LTSP and SSP were delivered from the high right atrium (HRA), the distal coronary sinus (CS), and within the LA at the site showing maximal overlay of low-voltage zones during sinus rhythm and pacing at HRA and CS. Atrial activation time and pattern, P wave duration, and the prevention of AF induced by burst pacing were assessed with these pacing interventions. Compared with SSP, LTSP at the HRA, CS, and LA shortened atrial activation times (183 +/- 24 vs. 174 +/- 24 ms, 186 +/- 29 vs. 166 +/- 28 ms, and 171 +/- 40 vs. 163 +/- 39 ms; P < 0.05, respectively). P wave duration was shorter with LTSP than SSP at all three sites (141.7 +/- 35.1 vs. 146.9 +/- 38.5 ms, 138.1 +/- 34.6 vs. 145.7 +/- 33.7 ms, and 142.7 +/- 33.4 vs. 151.3 +/- 35.1 ms; P < 0.05, respectively). LTSP initially depolarized a larger area than SSP, and produced more uniform and planar wavefront propagation. LTSP prevented the burst-induction of AF during LA pacing in 3 of 10 patients, while SSP was never successful. CONCLUSION In patients with persistent AF, LTSP provided more rapid and uniform activation of the atria compared with SSP, which was associated with prevention of burst-induction of AF in some patients. Further study is required to determine whether LTSP can modify the substrate of chronic AF, leading to frank AF suppression.