Prevalence of newly diagnosed sarcoidosis in patients with ventricular arrhythmias: a cardiac magnetic resonance and 18F-FDG cardiac PET study.

Cardiac sarcoidosis (CS) is known to be associated with ventricular tachycardia (VT); however, most investigations to date have focused on patients with known extra-cardiac sarcoidosis. The presence of CS is typically evaluated using 18F-fluorodeoxyglucose (18F-FDG) uptake on cardiac positron emission tomography (PET) or late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR). In this study, we sought to determine the prevalence of primary CS and the relationship between myocardial 18F-FDG uptake and LGE in patients with VT without known sarcoidosis. We retrospectively identified 67 patients without known sarcoidosis or active ischemic heart disease (i.e. significant ischemic disease that had not been previously revascularized) referred for both CMR and PET for evaluation of VT. Standard cine- and LGE- CMR and cardiac PET protocols were used. Myocardial LGE was defined as signal intensity > 5 SDs above the mean signal intensity of normal myocardium. Cardiac PET images were considered positive if there was focal myocardial 18F-FDG uptake having greater activity than the left ventricular blood pool. 45 patients (67%) had LGE, while only 4 (6%) had myocardial FDG uptake. Nine percent of patients with LGE had FDG-uptake while none without LGE did, and 10% of the cohort had indeterminate FDG uptake presumably from poor dietary preparation. Of those with both FDG uptake and LGE, 3/4 ultimately received a clinical diagnosis of CS. 4.5% of patients without previously known sarcoidosis or active ischemic heart disease presenting with VT have newly diagnosed CS. Detection of CS can be increased using a CMR first approach followed by cardiac PET for patients with non-ischemic LGE.

Increased Rate of Pump Thrombosis and Cardioembolic Events Following Ventricular Tachycardia Ablation in Patients Supported With Left Ventricular Assist Devices.

Ventricular arrhythmias are common following left ventricular assist device implantation (LVAD), and the effects of ventricular tachycardia (VT) ablation on thrombosis and embolic events are unknown. We aimed to assess LVAD thrombosis, stroke, and embolic event rates after VT ablation. Left ventricular assist device implantation patients from two academic centers who underwent endocardial VT ablation between 2009 and 2016 were compared to a control group with VT who were not ablated and followed for one year. The primary composite outcome was confirmed or suspected LVAD thrombosis, stroke, or other embolic event. Survival analysis was conducted with Kaplan-Meier curves, log-rank tests, and Cox regression. Forty-three LVAD patients underwent VT ablation, and 73 LVAD patients had VT but were not ablated. Patients who were ablated were more likely have VT prior to LVAD (p = 0.04), monomorphic VT (p < 0.01), and to be on antiarrhythmics (p < 0.01). Fifty-eight percent of the patients in the ablation group experienced the primary composite outcome (11% had confirmed device thrombosis [DT], 41% suspected DT, 39% had a stroke or embolic event) compared to 30% in the control group (12% with confirmed DT, 11% with suspected DT, 14% with stroke or embolic event) (p = 0.002). In multivariable regression, ablation was an independent predictor of the primary composite outcome (hazard ratios, 2.24; 95% confidence interval, 1.09-4.61; p = 0.03). Patients with LVADs referred for endocardial VT ablation had elevated rates of DT and embolic events.

Estimation of Central Venous Pressure by Pacemaker Lead Impedances in Left Ventricular Assist Device Patients.

Volume status assessment in left ventricular assist device (LVAD) patients remains challenging. Cardiac resynchronization therapy (CRT) devices are common in LVAD patients, and the impedance across the CRT leads may be associated with hemodynamics and serve as a tool for noninvasive estimation of volume status. Ninety-one sets of measurements including cardiac filling pressures and lead impedances were prospectively obtained during ramp tests from 11 LVAD patients (65.5 ± 9.7 years old; nine male) with CRT devices. Right atrial (RA), right ventricular (RV), and left ventricular (LV) lead impedances were all significantly associated with central venous pressure (CVP) (p < 0.05). We derived the following equation: estimated CVP = 47.90-(0.086 × RA lead impedance) + (0.013 × RV lead impedance)-(0.020 × LV lead impedance). The estimated CVP had a significant correlation (r = 0.795) and good agreement with the measured CVP (mean difference -0.14 ± 1.77 mmHg). Applying the above equation on the validation cohort of twenty-one patients also maintained a strong association with measured CVP (r = 0.705). In conclusion, we have derived a novel equation to estimate CVP using lead impedance measurements. This finding may allow noninvasive monitoring of volume status in LVAD patients.

Feasibility and utility of intraoperative epicardial scar characterization during left ventricular assist device implantation.

INTRODUCTION: Ventricular arrhythmias (VA) after left ventricular assist device (LVAD) placement are associated with increased morbidity and mortality. We sought to assess epicardial voltage characteristics at the time of LVAD implantation and investigate relationships between scar burden and postimplant VA. METHODS AND RESULTS: Consecutive patients underwent open chest epicardial electroanatomic mapping immediately before LVAD implantation. Areas of low voltage and sites with local abnormal potentials were identified. Patients were followed prospectively for postimplant VA and clinical outcomes. Between 2015 and 2017, 36 patients underwent high-density intraoperative epicardial voltage mapping; 15 had complete maps suitable for analysis. Mapping required a median of 11.8 (interquartile range [IQR], 8.5-12.7) minutes, with a median of 2650 (IQR, 2139-3191) points sampled per patient. Over a median follow-up of 311 (IQR, 168-469) postoperative days, four patients (27%) experienced sustained VA. Patients with postimplant VA were more likely to have had preimplant implantable cardioverter defibrillator shocks (100% vs 27%; P = 0.03), ventricular tachycardia storm (75% vs 9%; P = 0.03), and lower ejection fraction (13.5 vs 19.0%, P = 0.05). Patients with postimplant VA also had a significantly higher burden of epicardial low bipolar voltage points: 55.4% vs 24.9% of points were less than 0.5 mV (P = 0.01), and 88.9% vs 63.7% of points less than 1.5 mV (P = 0.004). CONCLUSIONS: Intraoperative high-density epicardial mapping during LVAD implantation is safe and efficient, facilitating characterization of a potentially arrhythmogenic substrate. An increased burden of the epicardial scar may be associated with a higher incidence of postimplant VA. The role of empiric intraoperative epicardial ablation to mitigate risk of postimplant VA requires further study.

Characterization of Ventricular Tachycardia After Left Ventricular Assist Device Implantation as Destination Therapy: A Single-Center Ablation Experience.

OBJECTIVES: This study sought to report mechanisms of ventricular tachycardia (VT) and outcomes of VT ablation in patients with a left ventricular assist device (LVAD) as destination therapy. BACKGROUND: Continuous flow LVAD implantation plays a growing role in the management of end-stage heart failure, and VT is common. There are limited reports of VT ablation in patients with a destination LVAD. METHODS: Patients with a continuous-flow LVAD referred for VT ablation from 2010 to 2016 were analyzed retrospectively. Baseline patient characteristics, procedural data, and clinical follow-up were evaluated. Arrhythmia-free survival was assessed. RESULTS: Twenty-one patients (90% male, 62 ± 10 years) underwent catheter ablation of VT at a median of 191 days (interquartile range: 55 to 403 days) after LVAD implantation (15 HeartMate II, 6 HeartWare HVAD). Five patients (24%) had termination (n = 4) or slowing (n = 1) of VT with ablation near the apical inflow cannula, and 3 (14%) had bundle-branch re-entry. Freedom from recurrent VT among surviving patients was 64% at 1 year, with overall survival 67% at 1 year for patients without arrhythmia recurrence and 29% for patients with recurrence (p = 0.049). One patient had suspected pump thrombosis within 30 days of the ablation procedure, with no other major acute complications. CONCLUSIONS: In this relatively large, single-center experience of VT ablation in destination LVAD, freedom from recurrent VT and implantable cardioverter-defibrillator shocks was associated with improved 1-year survival. Bundle branch re-entry was more prevalent than anticipated, and cannula-adjacent VT was less common. This challenging population remains at risk for late pump thrombosis and mortality.