Asirvatham, Samuel J

AbstractBackgroundCardiovascular implantable electronic devices (CIEDs) can be life‐saving. However, complications from CIED infection can be life‐threatening, often requiring device removal. Despite publication of CIED infection management guidelines, there remains marked variation in clinical practice.ObjectiveTo better understand and quantify these differences, we conducted a multinational survey of practitioners of CIED management.MethodsAn electronic survey was sent to Heart Rhythm Society members, spanning 70 countries across six continents. All responses were collected anonymously.Results227 out of 3,600 (6.3%) responded to the survey. The majority of surveys were completed by practitioners from the United States (168; 68.3%) and 53.8% of these practiced in academic medical centers. The large majority (92.7%) of sites had protocols to ensure appropriate timing of prophylactic antibiotics. Superficial (incisional) site infections were treated with antibiotics alone 52.5% of the time (consistent with guidelines); in contrast, deep pocket infections were treated with antibiotics (with device removal) in accordance to guidelines only 37.4% of the time. Almost all providers (98.7%) were inclined to perform complete hardware removal in cases of CIED‐related endocarditis. In contrast, 82.2% of survey participants suggested complete CIED system removal in patients with an occult Gram‐positive bacteremia, 65.5% with occult Gram‐negative bacteremia, and 59.3% with prolonged bacteremia due to a source other than CIED.ConclusionsThese data suggest wide variability in clinical practice in managing CIED infection with significant deviations from published guidelines. There is critical need to increase awareness and develop institutional protocols to ensure adherence with evidence‐based guidelines to optimize outcomes.

AbstractIntroductionCardiac pacing from the right ventricular apex is associated with detrimental long‐term effects and nonapical pacing locations may be associated with improved outcomes. There is little data regarding complications with nonapical lead positions. The aim of this study was to assess long‐term outcomes and lead‐related complications associated with differing ventricular lead tip position.Methods and resultsAll adult patients who underwent dual‐chamber pacemaker implantation from 2004 to 2014 were included if they had postprocedure chest radiographs amenable to lead position determination. Long‐term outcomes and lead‐related complication rates were recorded. These were compared at 5 years between: (1) apical and septal leads, (2) apical and nonseptal nonapical (NSNA), and (3) apical and septal with >40% ventricular pacing. We retrospectively evaluated 3,450 patients, which included 238 with a septal position and 733 with NSNA lead positions. Septal lead position was associated with a lower mortality compared to apical leads (24% vs. 31%, P = 0.02). In patients with greater than 40% pacing, septal leads were associated with significantly higher rates of incident atrial fibrillation compared to apical leads (49% vs. 34%, P = 0.04). NSNA positions were associated with a significantly higher rate of lead dislodgement (4% vs. 2%, P = 0.005) and need for revision (8% vs. 5%, P = 0.005).ConclusionsSeptal pacemaker lead position is associated with a lower mortality compared to apically placed leads, but a higher incidence of atrial fibrillation with higher percentage ventricular pacing. NSNA lead locations are associated with more complications and should be avoided.

BackgroundProlongation of the QT on the surface electrocardiogram can be due to either genetic or acquired causes. Distinguishing congenital long QT syndrome (LQTS) from acquired QT prolongation has important prognostic and management implications. We aimed to investigate if quantitative T‐wave analysis could provide a tool for the physician to differentiate between congenital and acquired QT prolongation.MethodsPatients were identified through an institution‐wide computer‐based QT screening system which alerts the physician if the QTc ≥ 500 ms. ECGs were retrospectively analyzed with an automated T‐wave analysis program. Congenital LQTS was compared in a 1:3 ratio to those with an identified acquired etiology for QT prolongation (electrolyte abnormality and/or prescription of known QT prolongation medications). Linear discriminant analysis was performed using 10‐fold cross‐validation to statistically test the selected features.ResultsThe 12‐lead ECG of 38 patients with congenital LQTS and 114 patients with drug‐induced and/or electrolyte‐mediated QT prolongation were analyzed. In lead V5, patients with acquired QT prolongation had a shallower T wave right slope (−2,322 vs. −3,593 mV/s), greater T‐peak‐Tend interval (109 vs. 92 ms), and smaller T wave center of gravity on the x axis (290 ms vs. 310 ms; p < .001). These features could distinguish congenital from acquired causes in 77% of cases (sensitivity 90%, specificity 58%).ConclusionT‐wave morphological analysis on lead V5 of the surface ECG could successfully differentiate congenital from acquired causes of QT prolongation.

Background— This study sought to investigate external photon beam radiation for catheter-free ablation of the atrioventricular junction in intact pigs. Methods and Results— Ten pigs were randomized to either sham irradiation or irradiation of the atrioventricular junction (55, 50, 40, and 25 Gy). Animals underwent baseline electrophysiological evaluation, cardiac gated multi-row computed tomographic imaging for beam delivery planning, and intensity-modulated radiation therapy. Doses to the coronary arteries were optimized. Invasive follow-up was conducted ≤4 months after the irradiation. A mean volume of 2.5±0.5 mL was irradiated with target dose. The mean follow-up length after irradiation was 124.8±30.8 days. Out of 7 irradiated animals, complete atrioventricular block was achieved in 6 animals of all 4 dose groups (86%). Using the same targeting margins, ablation lesion size notably increased with the delivered dose because of volumetric effects of isodose lines around the target volume. The mean macroscopically calculated atrial lesion volume for all 4 dose groups was 3.8±1.1 mL, lesions extended anteriorly into the interventricular septum. No short-term side effects were observed. No damage was observed in the tissues of the esophagus, phrenic nerves, or trachea. However, histology revealed in-field beam effects outside of the target volume. Conclusions— Single-fraction doses as low as 25 Gy caused a lesion with interruption of cardiac impulse propagation using this respective target volume. With doses of ≤55 Gy, maximal point-doses to coronary arteries could be kept <7Gy, but target conformity of lesions was not fully achieved using this approach.

Background— People with heart failure and preserved ejection fraction develop increases in left ventricular (LV) end-diastolic pressures during exercise that contribute to dyspnea. In normal open-chest animal preparations, the pericardium restrains LV filling when central blood volume increases. We hypothesized that resection of the pericardium using a minimally invasive epicardial approach would mitigate the increase in LV end-diastolic pressure that develops during volume loading in normal and diseased hearts with the chest intact. Methods and Results— Invasive hemodynamic assessment was performed at baseline and after saline load before and after pericardial resection in normal canines with open (n=3) and closed chest (n=5) and in a pig model with features of human heart failure and preserved ejection fraction with sternum intact (n=4). In closed-chest animals, pericardiotomy was performed using a novel subxiphoid procedure. In both experimental preparations of normal dogs, pericardiotomy blunted the increase in LV end-diastolic pressure with saline infusion, while enhancing the saline-mediated increase in LV end-diastolic volume. With chest intact in the pig model, percutaneous pericardial resection again blunted the increase in LV end-diastolic pressure secondary to volume expansion (+4±3 versus +13±5 mm Hg; P =0.014), while enhancing the saline-mediated increase in LV end-diastolic volume (+17±1 versus +10±2 mL; P =0.016). Conclusions— This proof of concept study demonstrates that pericardial resection through a minimally invasive percutaneous approach mitigates the elevation in LV filling pressures with volume loading in both normal animals and a pig model with diastolic dysfunction. Further study is warranted to determine whether this method is safe and produces similar acute and chronic hemodynamic benefits in people with heart failure and preserved ejection fraction.

AbstractAimsPlatelets retain cytoplasmic messenger RNA and are capable of protein biosynthesis. Several diseases are known to impact the platelet transcriptome but the effect of non‐valvular atrial fibrillation (NVAF) on platelet RNA transcript is essentially unknown. The aim of this study was to evaluate the impact of NVAF on platelet RNA transcript by measuring platelet genes expression in consecutive NVAF patients before and 3‐4 months after pulmonary vein isolation (PVI) and compared to normal sinus rhythm controls (NSR).Methods and ResultsRNA from isolated platelets were reverse transcribed, assayed against 15 genes using real‐time qPCR, and expressed as mean cycle threshold (ΔCt) using beta‐2‐microglobulin as endogenous control. Expression of all evaluated genes, except cathepsin A gene, was significantly lower (higher ΔCt) in 103 NVAF patients compared to 55 NSR controls. Insulin‐like growth factor binding protein acid labile subunit gene (IGFALS) had expression more than 16 fold‐lower (17.0±2.8 vs 12.5±3.8, P<.001), follow by genes encoding for prostacyclin receptor, and for von Willebrand factor which had fourfold lower expression compared to NSR controls. Gender, type of atrial fibrillation, heart failure, hypertension, prior stroke, diabetes mellitus, and atherosclerosis were associated with different gene expression. Following PVI, expression of four genes significantly increased, particularly IGFALS gene (increased 256‐fold) and ADAMT gene increased 16‐fold); expression of three genes significantly decreased, and expression of eight genes has not changed.ConclusionsPlatelets are capable to respond to the circulatory environment of NVAF by altering transcript and changing prothrombotic status. This shows platelet potential for molecular “reprogramming” possibly induced by flow disturbances of NVAF.

Background— Ventricular tachycardia and premature ventricular complexes (PVCs) most frequently occur in the context of structural heart disease. However, the burden of idiopathic ventricular arrhythmias (IVA) in the general population is unknown. Methods and Results— We identified incident cases of IVA between 2005 and 2013 from Olmsted County, Minnesota, using the Rochester Epidemiology Project database. For PVC cohorts, we included those with frequent (defined as ≥100 PVC/24 hours) symptomatic PVCs. We defined IVA-associated cardiomyopathy as a drop in ejection fraction of ≥10% from baseline. Between 2005 and 2013, we identified 614 individuals with incident IVA (229 [37.3%] were male; average age was 52.1±17.2 years). Of these, 177 (28.8%) had idiopathic ventricular tachycardia, 408 (66.5%) had symptomatic PVCs, and 29 (4.7%) had IVA-associated cardiomyopathy. The age- and sex-adjusted incidence rates in 2005 to 2007, 2008 to 2010, and 2011 to 2013 were 44.9 per 100 000 (95% confidence interval [CI], 38.0–51.8), 47.6 per 100 000 (95% CI, 40.8–54.5), and 62.0 per 100 000 (95% CI, 54.4–69.6), respectively. In idiopathic ventricular tachycardia, there was an increase in incidence rate with ages ( P <0.001) but not between sexes ( P =0.12). The age-adjusted incidence of symptomatic PVC was higher in females than in males (46.2 per 100 000 [95% CI, 40.9–51.6] versus 20.5 per 100 000 [95% CI, 16.8–24.3]; P <0.001). The small number of individuals with IVA-associated cardiomyopathy precluded any formal testing. Conclusions— The incidence of IVA is increasing. Furthermore, overall incidence increases with age. Although the rate of idiopathic ventricular tachycardia is similar across sexes, women have a higher incidence of symptomatic PVC.