Michael Benser

Attenuation of Left Ventricular Adverse Remodeling With Epicardial Patching After Myocardial Infarction

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.

Atrial activation time and pattern of linear triple-site vs. single-site atrial pacing after cardioversion in patients with atrial fibrillation.

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.

Blood pressure response to transition from supine to standing posture using an orthostatic response algorithm.

Upon standing from a supine position, the normal response is an increase in heart rate to maintain blood pressure (BP). In patients with chronotropic incompetence, heart rate may not increase upon standing, and they may experience orthostatic hypotension (OH). We evaluated a new orthostatic response (OSR) pacing algorithm that uses an accelerometer signal to detect sudden activity following prolonged rest to trigger a 2 minutes increase in pacing rate to 94 bpm. Ten recipients of DDDR pacemakers which contain the OSR compensation algorithm (mean age = 77 ± 9 years, 8 women) with sick sinus syndrome (n = 6) or atrioventricular block (n = 4) were studied. In all patients BP was measured before and 0.5, 1, 1.5, 2, and 3 minutes after standing at their programmed base rate. A 20 mmHg fall in systolic BP upon standing was observed in five patients (OH patients), while the other five were considered non‐OH patients. The measurements were repeated with the OSR algorithm turned on. Mean BP was defined as 1/3 systolic BP + 2/3 diastolic BP. Baseline heart rate was significantly slower in OH patients (62 ± 2 bpm) than non‐OH patients (71 ± 7 bpm, P < 0.05). In OH patients mean BP increased significantly upon standing (P < 0.05 for all comparisons) with the algorithm ON instead of decreasing with the algorithm OFF, at 1 minute (+3.4 vs −10.3 mmHg), 1.5 minutes (+7.0 vs −4.9 mmHg), 2 minutes (+1.6 vs −6.7 mmHg), and 3 minutes (+2.5 vs −8.5 mmHg). These preliminary results suggest that the OSR algorithm maintains BP upon standing in patients with OH.

Transient Overdrive Pacing Upon Standing Prevents Orthostatic Hypotension in Elderly Pacemaker Patients with Chronotropic Incompetence

Background: Elderly pacemaker patients with chronotropic incompetence (CI) may experience orthostatic hypotension (OH) upon standing. The objective of this study was to determine whether a transient increase in heart rate (HR) by overdrive pacing upon standing prevents OH in elderly pacemaker patients.

Time Course of Subsequent Shocks After Initial Implantable Cardioverter-Defibrillator Discharge and Implications for Driving Restrictions

IMPORTANCE Although guidelines recommend driving restrictions for 3 to 6 months after appropriate implantable cardioverter-defibrillator (ICD) shocks, contemporary data to support these recommendations are lacking. OBJECTIVE To define the time course of subsequent shocks after an initial ICD discharge. DESIGN, SETTING, AND PARTICIPANTS Retrospective analysis of a nationwide cohort of 14 230 ICD recipients enrolled in a remote monitoring program. Participants underwent ICD implantation from October 1, 2008, to December 31, 2013, and experienced at least 1 shock. The risk of driving after an ICD shock was estimated using the risk for harm (RH) formula, and an annual RH of less than 5 events per 100 000 ICD recipients was deemed safe. The likelihood of loss of consciousness associated with an ICD shock was estimated using a cautious value of 32% and an estimate of 14% based on contemporary data. Data were extracted and analyzed from December 17, 2014, to October 31, 2015. MAIN OUTCOMES AND MEASURES Time course of subsequent shocks after an initial ICD discharge. RESULTS Of 73 503 ICD recipients who underwent remote monitoring, 14 230 (19.4%) experienced at least 1 ICD shock and were included in this analysis (10 870 men [76.4%]; 3360 women [23.6%]; median age at device implantation, 68 years; interquartile range [IQR], 60-76 years). The cumulative incidence of receiving a second shock was 14.5% (IQR, 13.9%-15.1%) at 1 month and 28.7% (IQR, 27.9%-29.5%) at 6 months. The time from implantation to initial shock had an inverse association with the likelihood of receiving a second shock (lowest quartile of time at 6 months, 31.6% [95% CI, 30.2%-33.2]; highest quartile of time at 6 months, 25.3% [95% CI, 23.8%-26.9%]). The number of ICD therapy zones was also significantly associated with the incidence of a second shock (1 therapy zone, 20.8% [95% CI, 19.4%-22.3%] at 3 months to 51.5% [95% CI, 48.5%-53.7%] at 3 years; 3 therapy zones, 26.9% [95% CI, 24.8%-29.0%] at 3 months to 57.3% [95% CI, 54.1%-60.5%] at 3 years). When a likelihood of loss of consciousness of 32% associated with an ICD shock was used, the RH while driving fell below the accepted threshold at 4 to 6 months after an initial shock. However, when a contemporary estimate for loss of consciousness associated with an ICD shock of 14% was used, the RH fell below the threshold at 1 month after an initial shock. CONCLUSIONS AND RELEVANCE In this large cohort of ICD recipients, the incidence of a second shock after an initial ICD discharge was lower than previously reported and depended on several programmed ICD variables. These data, with future research to derive contemporary estimates of the likelihood of fatality resulting from an ICD shock while driving, should support the development of evidence-based guidelines for driving restrictions in ICD recipients.

Acute and Chronic Performance Evaluation of a Novel Epicardial Pacing Lead Placed by Percutaneous Subxiphoid Approach in a Canine Model

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 &OHgr; at implant to 1066±207 &OHgr; 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.

Dynamic ventricular overdrive stimulation in atrial fibrillation: effects on ventricular rate irregularity, ventricular pacing, and fusion beats.

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.