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Background: Preliminary reports have suggested the role of annular calcium in independently predicting pacemaker implantation after transcatheter aortic valve replacement (TAVR). Data regarding role of calcium in the aortic-valvular complex on pacemaker dependency is lacking. Hypothesis: Calcium volume and score in the aortic annular region predicts RV (right ventricle) pacing burden. Methods: We conducted a retrospective single-center study at our tertiary care center including patients who had new pacemaker implantation after TAVR procedure (n=47). Standard calcium scoring software was used to demarcate and quantify the calcium along the aortic cusps and subvalvular region and dichotomized into septal and non-septal based on proximity to the interventricular septum. Standard statistical tests were used for analysis with two-sided p-value Results: The mean age was 78.6 ± 10.3 years and females were 42.6%. At baseline, 44.7% had narrow QRS complex, with 31.9% had right bundle branch block (RBBB), 8.5% had left bundle branch block (LBBB). Median Pre-TAVR QRS duration was 112 ms. Median septal and non-septal calcium score were 646 and 474 with a volume of 441 mm 3 and 327.2 mm 3 , respectively. Patients with progression to complete heart block (CHB) during index admission had significantly higher non-septal volume (650 mm 3 vs 344 mm 3 ;p=0.01) and score (892 vs 485;p=0.01) when compared to progression after discharge. Similarly, the high burden of RV pacing (>40%) was associated with lower septal calcium score (989 vs 552, p= 0.03) and volume (717 mm 3 vs 385 mm 3 , p=0.03) within 3 months of TAVR. No septal or non-septal parameters were predictive of pacing burden for mid-term (3-12 months) and long-term (>12 months) follow up. Septal calcium parameters were not predictive of RV pacing burden or progression to CHB. Conclusion: Quantitative calcium in the non-septal and septal regions were predictive of early progression to CHB and a higher burden of RV pacing, respectively. Larger scale studies on calcium distribution and the burden should be performed to validate our findings.

Introduction: Subcutaneous ICD (S-ICD) implantation is a viable alternative to transvenous ICD implantation in patients without a pacing indication. The S-ICD lead is placed near the sternum. The safety of S-ICD implantation and risk for inappropriate shocks is uncertain in patients with prior sternotomy. Methods: This single-center retrospective cohort study included patients that had implantation of an S-ICD between February 2014 - May 2020. The 30-day complication rates and long-term risks of inappropriate shocks were compared between patients with and without prior sternotomy. Results: Ninety-eight patients (52 ± 15 years old, 43% men, BMI 29 ± 6, 72% primary prevention, 28% ischemic cardiomyopathy, median LVEF 30% (IQR 25-45%)) underwent S-ICD implantation, among whom 19 (19.4%) had a prior sternotomy. The median time between sternotomy and S-ICD implantation was 96 (IQR 4.1-306) months. The sternal coil was primarily implanted left of the sternum (n=17/19, 89%). A two-incision technique was used in 79% of patients with prior sternotomy vs. 65% without sternotomy (p=0.23). The 30-day complication rate was similar between those with and without prior sternotomy (n=1/19 vs. n=10/79, 5% vs. 13%, p=0.36). The only 30-day complication in patients with prior sternotomy was a hematoma without intervention. The 30-day complications in patients without prior sternotomy included: superficial site infection resolving with brief antibiotics (n=4), inappropriate shock (n=3), lead migration requiring revision (n=2), and a hematoma without intervention (n=1). Over a median follow-up of 17.1 (IQR 3.4-29.1) months, the frequency of inappropriate shocks was similar between patients with and without prior sternotomy (n=1/19 and n=6/79, 5% vs. 8%, p=0.72). The median time to inappropriate shock from S-ICD implantation was 1.1 (IQR 0.1-19.8) months. The mechanisms of inappropriate shocks were T-wave oversensing or other oversensing (n=5/7, 72%), air in the pocket (n=1/7, 14%), and atrial tachycardia (n=1/7, 14%). Conclusions: Implantation of S-ICD in patients with prior sternotomy was not associated with an increased risk of 30-day complications or inappropriate shocks. These outcomes need to be confirmed in larger, multicenter studies.

Introduction: The Emory risk score has been developed to predict new pacemaker implantation in patients undergoing TAVR procedures. There is limited data on assessing risk of early versus late pacemaker implantation in these patients. Hypothesis: The Emory risk score is similar for patients with both early and late pacemaker implantation in TAVR patients. Methods: A single center observational study was performed at our tertiary care center. All patients who underwent pacemaker implantation after TAVR procedures were included. Patients were categorized as early or late if they had pacemaker implantation within the same admission versus implantation post discharge. Standard statistical tests were used for analysis with two-sided p value Results: A total of 97 patients were studied between January 2017 to April 2020. The mean age was 77.5 ± 7 years and females were 41.2%. At baseline patients with early implantation of pacemakers (n=66) had a higher proportion of underlying RBBB (45.2% vs 23.3%, p=0.43), higher valve size as well as a higher incidence of valve oversizing > 146% (43.9 % vs 19.4 %, p =0.23)when compared to patients with late pacemakers(n=31). There was no difference between patient characteristics, baseline comorbidities, pre procedural ECG parameters as well as use of beta blocking agents. Late pacemaker implantations were associated with a overall lower Emory Risk score (1.06±1.41 vs 1.70±1.35, p =0.037). Conclusions: The Emory Risk score is significantly different for early and late pacemaker implantation. Further studies are needed evaluate risk of late pacemaker implantation.

Introduction: Cardiac resynchronization therapy (CRT) upgrade is indicated for improvement of cardiac function in patients with chronic right ventricular (RV) pacing burden >40% and heart failure with reduced ejection fraction. It is uncertain whether the CRT response is different among patients with high (≥90%) versus intermediate ( Hypothesis: To assess the impact of baseline RV pacing percent on ECG and echocardiographic response after CRT upgrade for pacing induced cardiomyopathy. Methods: We conducted a retrospective study of all CRT upgrades for pacing induced cardiomyopathy at our hospital from January 2017 to December 2018. Cohorts were grouped by RV pacing burden ≥90% or Results: We included 82 patients (age 74 ± 12 yr., 71% male) who underwent CRT upgrade for pacing induced cardiomyopathy. The RV pacing burden was ≥90% [median 99% (IQR 98-99%)] in 61 patients, and Conclusions: A higher baseline RV pacing burden predicts a greater improvement in LVEF after CRT upgrade for pacing induced cardiomyopathy.

In PD, orthostatic hypotension reflects sympathetic noradrenergic denervation. The authors assessed sympathetic cholinergic innervation by the quantitative sudomotor axon reflex test (QSART) in 12 patients who had sympathetic neurocirculatory failure, markedly decreased cardiac 6-[ 18 F] fluorodopamine-derived radioactivity, and subnormal plasma norepinephrine increments during standing. All 12 had normal QSART results. The sympathetic nervous system lesion in PD involves loss of postganglionic catecholaminergic but not cholinergic nerves.

Background— In postural tachycardia syndrome (POTS) and repeated neurocardiogenic presyncope (NCS), orthostatic intolerance occurs without persistent sympathetic neurocirculatory failure. Whether these conditions involve abnormal cardiac sympathetic innervation or function has been unclear. Methods and Results— Patients with POTS or NCS underwent measurements of neurochemical indices of cardiac release, reuptake, and synthesis of the sympathetic neurotransmitter norepinephrine based on entry of norepinephrine into the cardiac venous drainage (cardiac norepinephrine spillover), cardiac extraction of circulating 3 H-norepinephrine, and cardiac production of dihydroxyphenylalanine and measurement of left ventricular myocardial innervation density using 6-[ 18 F]fluorodopamine positron emission tomographic scanning. Mean cardiac norepinephrine spillover in POTS (171±30 pmol/min, N=16) was higher and in NCS (62±9 pmol/min, N=20) was lower than in a large group of healthy volunteers (102±9 pmol/min, N=52) and in a subgroup of age-matched healthy women (106±18 pmol/min, N=11). Both patient groups had normal cardiac extraction of 3 H-norepinephrine, normal cardiac production of dihydroxyphenylalanine, and normal myocardial 6-[ 18 F]fluorodopamine-derived radioactivity. Conclusions— POTS and NCS differ in tonic cardiac sympathetic function, with increased cardiac norepinephrine release in the former and decreased release in the latter. Both groups had normal values for indices of function of the cell membrane norepinephrine transporter, norepinephrine synthesis, and density of myocardial sympathetic innervation. Because POTS and NCS both include specific abnormalities of cardiac sympathetic function, both can be considered forms of dysautonomia.

Background: Patients with PD often have signs or symptoms of autonomic failure, including orthostatic hypotension. Cardiac sympathetic denervation occurs frequently in PD, but this has been thought to occur independently of autonomic failure.Methods: Forty-one patients with PD (18 with and 23 without orthostatic hypotension) and 16 age-matched healthy volunteers underwent PET scanning to visualize sympathetic innervation after injection of 6-[18F]fluorodopamine. Beat-to-beat blood pressure responses to the Valsalva maneuver were used to identify sympathetic neurocirculatory failure and plasma norepinephrine to indicate overall sympathetic innervation.Results: All patients with PD and orthostatic hypotension had abnormal blood pressure responses to the Valsalva maneuver and septal and lateral ventricular myocardial concentrations of 6-[18F]fluorodopamine-derived radioactivity >2 SD below the normal mean. In contrast, only 6 of the 23 patients without orthostatic hypotension had abnormal Valsalva responses (p < 0.0001 compared with patients with orthostatic hypotension), and only 11 had diffusely decreased 6-[18F]fluorodopamine-derived radioactivity in the left ventricular myocardium (p = 0.0004). Of the 12 remaining patients without orthostatic hypotension, 7 had locally decreased myocardial radioactivity. Supine plasma norepinephrine was lower in patients with than in those without orthostatic hypotension (1.40 ± 0.15 vs 2.32 ± 0.26 nmol/L, p = 0.005). 6-[18F]fluorodopamine-derived radioactivity was less not only in the myocardium but also in the thyroid and renal cortex of patients with PD than in healthy control subjects.Conclusions: In PD, orthostatic hypotension reflects sympathetic neurocirculatory failure from generalized sympathetic denervation.

Background: Depolarization of myocytes requires less energy when electrical current flows along the longitudinal axis compared to the transverse axis of myocytes. Since ventricular fibrillation (VF) amplitude in ECG leads reflects the functional electrical orientation of the majority of myocytes, we hypothesized that a defibrillation shock would be more effective if the shock vector was oriented along the functional electrical axis of the majority of myocytes, and this axis could be determined in real time from the relative amplitudes of the VF signal measured in three orthogonal ECG leads. Methods: In closed-chest, anesthetized, swine (22.0 ± SE0.8 kg, n=9), a new directional defibrillation device was used to simultaneously measure the VF amplitude through three orthogonal pairs of defibrillation electrodes: anterior-posterior, lateral-lateral, and superior-inferior. VF was electrically induced and persisted for 15 seconds. During defibrillation, the device identified the electrode pair that measured the largest or smallest peak amplitudes (+ or −) within the previous 100msec through which to deliver the shock. Defibrillation success for the electrodes measuring the largest or smallest VF amplitude was evaluated by delivering four 50J shocks for VF through each of these electrode pairs (in random order). The electrode pair measuring the largest VF signal amplitude was considered to be most closely aligned with the functional VF vector. Results: Fifty J shocks (n=37) delivered through the electrode pair measuring the largest VF signal amplitude had higher defibrillation success than 50J shocks (n=37) delivered through the electrodes measuring the smallest VF signal amplitude (62 ± 10% vs.19 ± 8%, p Conclusions: By using a directional defibrillation device which instantaneously measures the peak VF signal amplitude in three pairs of orthogonally oriented defibrillation electrodes, it is feasible to determine which set of electrodes is oriented more favorably to the functional VF vector and to direct the shock through that set of electrodes. Matching the defibrillation vector to the fibrillation vector improves shock success.