Cha, Yong‐Mei

Endovascular Stimulation for Treatment of HypotensionBackgroundWe have previously shown that sympathetic ganglia stimulation via the renal vein rapidly increases blood pressure. This study further investigated the optimal target sites and effective energy levels for stimulation of the renal vasculatures and nearby sympathetic ganglia for rapid increase in blood pressure.MethodsThe pre‐study protocol for endovascular stimulations included 2 minutes of stimulation (1–150 V and 10 pulses per second) and at least 2 minutes of rest during poststimulation. If blood pressure and/or heart rate were changed during the stimulation, time to return to baseline was allowed prior to the next stimulation.ResultsIn 11 acute canine studies, we performed 85 renal artery, 30 renal vein, and 8 hepatic vasculature stimulations. The mean arterial pressure (MAP) rapidly increased during stimulation of renal artery (95 ± 18 mmHg vs. 103 ± 15 mmHg; P < 0.0001), renal vein (90 ± 16 mmHg vs. 102 ± 20 mmHg; P = 0.001), and hepatic vasculatures (74 ± 8 mmHg vs. 82 ± 11 mmHg; P = 0.04). Predictors of a significant increase in MAP were energy >10 V focused on the left renal artery, bilateral renal arteries, and bilateral renal veins (especially the mid segment). Overall, heart rate was unchanged, but muscle fasciculation was observed in 22.0% with an output >10 V (range 15–150 V). Analysis after excluding the stimulations that resulted in fasciculation yielded similar results to the main findings.ConclusionsStimulation of intra‐abdominal vasculatures promptly increased the MAP and thus may be a potential treatment option for hypotension in autonomic disorders. Predictors of optimal stimulation include energy delivery and the site of stimulation (for the renal vasculatures), which informs the design of subsequent research.

Background— Transvenous lead removal (TLR) has made significant progress with respect to innovation, efficacy, and safety. However, limited data exist regarding trends in use and adverse outcomes outside the centers of considerable experience for TLR. The aim of our study was to examine use patterns, frequency of adverse events, and influence of hospital volume on complications. Methods and Results— Using the Nationwide Inpatient Sample, we identified 91 890 TLR procedures. We investigated common complications including pericardial complications (hemopericardium, cardiac tamponade, or pericardiocentesis), pneumothorax, stroke, vascular complications (consisting of hemorrhage/hematoma, incidents requiring surgical repair, and accidental arterial puncture), and in-hospital deaths described with TLR, defining them by the validated International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis code. We specifically assessed in-hospital death (2.2%), hemorrhage requiring transfusion (2.6%), vascular complications (2.0%), pericardial complications (1.4%), open heart surgery (0.2%), and postoperative respiratory failure (2.4%). Independent predictors of complications were female sex and device infections. Hospital volume was not independently associated with higher complications. There was a significant rise in overall complication rates over the study period. Conclusions— The overall complication rate in patients undergoing TLR was higher than previously reported. Female sex and device infections are associated with higher complications. Hospital volume was not associated with higher complication rates. The number of adverse events in the literature likely underestimates the actual number of complications associated with TLR.

BackgroundLeft ventricular (LV) pacing in cardiac resynchronization therapy (CRT) can be achieved via a transvenous or epicardial route. A surgically implanted epicardial LV (eLV) lead is used after a standard transvenous LV (tLV) lead implantation has failed. However, studies of clinical outcomes in patients with eLV leads and comparisons of outcome between tLV and eLV‐CRT are sparse. Therefore, the purpose of this study is to compare clinical response between tLV‐CRT and eLV‐CRT, as well as to understand the differences within the eLV‐CRT population.MethodsForty‐four patients received eLV‐CRT following unsuccessful attempts of tLV‐CRT implantation between 2002 and 2013 at the University of California, San Diego (UCSD) and Mayo Clinics. These patients were matched for age, gender, and etiology of cardiomyopathy in a 1:2 ratio with a cohort of patients who received tLV‐CRT during the same time period.ResultsDuring a mean follow‐up of 57 months, similar clinical outcomes and survival rate were noted between tLV and eLV‐CRT patients (all P > 0.05). Within the eLV‐CRT group, dilated cardiomyopathy patients had significant improvement in New York Heart Association class and ejection fraction (both P < 0.05), while ischemic cardiomyopathy patients did not (both P > 0.05). eLV‐CRT patients with nonanterior lead location had significantly improved survival (P < 0.001). There was also a trend for improved survival in those with nonapical lead location (P = 0.09).ConclusionIn this case‐matched two‐centered study, comparable improvements were noted in patients with tLV‐CRT and eLV‐CRT. Operators should target nonanterior and nonapical locations during eLV‐CRT implantation. Use of eLV‐CRT should be considered a viable alternative for CRT candidates.

The failing ventricular myocardium is characterized by reduction of high-energy phosphates and reduced activity of the phosphotransfer enzymes creatine kinase (CK) and adenylate kinase (AK), which are responsible for transfer of high-energy phosphoryls from sites of production to sites of utilization, thereby compromising excitation-contraction coupling. In humans with chronic atrial fibrillation (AF) unassociated with congestive heart failure (CHF), impairment of atrial myofibrillar energetics linked to oxidative modification of myofibrillar CK has been observed. However, the bioenergetic status of the failing atrial myocardium and its potential contribution to atrial electrical instability in CHF have not been determined. Dogs with ( n = 6) and without ( n = 6) rapid pacing-induced CHF underwent echocardiography (conscious) and electrophysiological (under anesthesia) studies. CHF dogs had more pronounced mitral regurgitation, higher atrial pressure, larger atrial area, and increased atrial fibrosis. An enhanced propensity to sustain AF was observed in CHF, despite significant increases in atrial effective refractory period and wavelength. Profound deficits in atrial bioenergetics were present with reduced activities of the phosphotransfer enzymes CK and AK, depletion of high-energy phosphates (ATP and creatine phosphate), and reduction of cellular energetic potential (ATP-to-ADP and creatine phosphate-to-Cr ratios). AF duration correlated with left atrial area ( r = 0.73, P = 0.01) and inversely with atrial ATP concentration ( r = −0.75, P = 0.005), CK activity ( r = −0.57, P = 0.054), and AK activity ( r = −0.64, P = 0.02). Atrial levels of malondialdehyde, a marker of oxidative stress, were significantly increased in CHF. Myocardial bioenergetic deficits are a conserved feature of dysfunctional atrial and ventricular myocardium in CHF and may constitute a component of the substrate for AF in CHF.

Arrhythmogenic Substrate of Ventricular Arrhythmias at the AMCIntroductionCatheter ablation of ventricular arrhythmia (VA) at the fibrous aortic mitral continuity (AMC) has been described, yet the nature of the arrhythmogenic substrate remains unknown.MethodsProcedural records of 528 consecutive patients undergoing ablation of VA at Mayo Clinic, Rochester, MN, were reviewed. The electrocardiographic and electrophysiologic characteristics of patients with successful ablation at the AMC were analyzed to characterize the underlying arrhythmogenic substrate.ResultsOf the 21 patients (mean age 53.2 ± 13.4 years, 47.6% male) who underwent ablation of VA at the AMC with acute success, prepotentials (PPs) were found at the ablation sites preceding the ventricular electrogram (VEGM) during arrhythmias in 13 (61.9%) patients and during sinus rhythm in 7 (53.8%) patients. VAs with PPs were associated with a significantly higher burden of premature ventricular complexes (PVCs; 26.1 ± 10.9% vs. 14.9 ± 10.1%, P = 0.03), shorter VEGM to QRS intervals (9.0 ± 28.5 milliseconds vs. 33.1 ± 8.8 milliseconds, P = 0.03), lower pace map scores (8.7 ± 1.6 vs. 11.4 ± 0.8, P = 0.001), and a trend toward shorter V‐H intervals during VA (32.1 ± 38.6 milliseconds vs. 76.3 ± 11.1 milliseconds, P = 0.06) as compared to those without PP. A strong and positive correlation was found between V‐H interval and QRS duration during arrhythmia in those with PPs (B = 2.11, R2 = 0.97, t = 13.7, P < 0.001) but not in those without PPs.ConclusionLocal EGM characteristics and relative activation time of the His bundle suggest the possibility of conduction tissue as the origin for VA arising from the fibrous AMC. Specific identification and targeting of PPs when ablating VAs at this location may improve procedural success.

BackgroundWe aimed to determine the long‐term outcomes of percutaneous lead extraction and stent placement in patients with pacemaker‐induced superior vena cava (SVC) syndrome.MethodsThe study retrospectively screened patients who underwent lead extraction followed by central vein stent implantation at Mayo Clinic (Rochester, MN, USA), from January 2005 to December 2012, to identify the patients with pacemaker‐induced SVC syndrome. Demographic, clinical, and follow‐up characteristics of those patients were collected from electronic medical records.ResultsSix cases were identified. The mean (standard deviation) age was 56 (15) years (male, 67%). All patients had permanent dual‐chamber pacemakers, with a mean 11‐year history of pacemaker placement. The entire device system was explanted in five patients; one patient had a 21‐year‐old pacemaker lead that could not be removed. Eight stents were implanted in six patients: five patients had one stent, one patient had three. A new pacemaker system was reimplanted through the stented vein in five patients. Technical success was achieved in all patients, without any complication. Symptoms rapidly resolved in all patients after stent deployment. The mean follow‐up duration was 48 months (range, 10–100 months). Three patients remained symptom free. Reintervention with percutaneous balloon venoplasty was successful in three patients with symptom recurrence.ConclusionPercutaneous stent implantation after lead removal followed by reimplantation of leads is a feasible alternative therapy for pacemaker‐induced SVC syndrome, although some cases may require repeat intervention.

Percutaneous Lead Revision for Cardiac PerforationIntroductionCardiac perforation is an infrequent but potentially life‐threatening complication associated with placement of a cardiac implantable electronic device (CIED). The objective of this study was to determine the outcomes of percutaneous lead revision in patients who had lead perforation of the myocardium after CIED placement.Methods and ResultsWe reviewed records of 1,458 patients who underwent CIED lead extraction or repositioning. Of these, 31 (2.1%) had the procedure performed for lead perforation as a complication of CIED placement. Demographic, clinical, and follow‐up characteristics of the patients were analyzed. Mean (SD) patient age was 65 (23) years. Cardiac perforation was detected within 24 hours after implantation in 9 patients, within 1 month in 17, and greater than 1 month in 5. Pericardiocentesis was performed with a pigtail drainage catheter in place before the lead revision in 17 patients (55%) who had pericardial effusion, with or without hemodynamic compromise. All culprit leads were successfully managed with percutaneous lead removal (n = 3 [10%]), new lead placement (n = 12 [38%]), or lead repositioning (n = 16 [52%]). Of the 17 patients with pericardiocentesis before the reoperation, none had tamponade develop; in contrast, 3 of the remaining 14 patients had tamponade develop and required urgent pericardiocentesis. All patients survived without requiring open chest surgery.ConclusionPercutaneous removal or repositioning of the perforating lead is feasible and appears effective. Placement of a prophylactic pericardial drain catheter may reduce the incidence of urgent pericardiocentesis during or after a procedure.

IntroductionAbandoned cardiovascular implantable electronic device (CIED) leads remain a contraindication to magnetic resonance imaging (MRI) studies, largely due to in vitro data showing endocardial heating secondary to the radiofrequency field. We tested the hypothesis that abandoned CIED leads do not pose an increased risk of clinical harm for patients undergoing MRI.MethodsThis single‐center retrospective study examined the outcomes of patients who had device generators removed before MRI, rendering the device leads abandoned. Information was gathered through chart review. Data collected included lead model, pacing threshold before MRI, anatomic region examined, threshold data after generator reimplantation, and clinical patient outcome.ResultsPatients (n = 19, 11 men and eight women) ranged in age from 19 to 85 at the time of MRI. There was a mean of 1.63 abandoned leads at the time of imaging; none of the leads were MRI conditional. Of the three implantable cardioverter defibrillator (ICD) leads, two of three were dual coil. Most (31/35) of the scans performed were of the central nervous system, including head and spinal imaging. There were no adverse events associated with MRI in any of these patients with abandoned leads within 7 days of the scan. No lead malfunctions or clinically significant change in pacing thresholds were noted with generator reimplantation.ConclusionThe use of MRI in patients with abandoned cardiac device leads appears feasible when performed under careful monitoring, with no adverse events, although the experience is small. MRI did not affect the function of leads that were subsequently reconnected to a cardiac device.

Mitral Valve Injury with Catheter AblationIntroductionAn increasing number of catheter ablations involve the mitral annular region and valve apparatus, increasing the risk of catheter interaction with the mitral valve (MV) complex. We review our experience with catheter ablation‐related MV injury resulting in severe mitral regurgitation (MR) to delineate mechanisms of injury and outcomes.MethodsWe searched the Mayo Clinic MV surgical database over a 19‐year period (1993–2012) and the electrophysiologic procedures database over a 23‐year period (1990–2013) and identified 9 patients with catheter ablation related MV injury requiring clinical intervention.ResultsIndications for ablation included atrial fibrillation (AF) [n = 4], ventricular tachycardia (VT) [n = 3], and left‐sided accessory pathways [n = 2]. In all 4 AF patients, a circular mapping catheter entrapped in the MV apparatus was responsible for severe MR. In all 3 VT patients, radiofrequency energy delivery led to direct injury to the MV apparatus. In the 2 patients with accessory pathways, both mechanisms were involved (1 per patient). Six patients required surgical intervention (5 MV repair, 1 catheter removal). One patient developed severe functional MR upon successful endovascular catheter disentanglement that improved spontaneously. Two VT patients with persistent severe postablation MR were managed nonsurgically, 1 of whom died 3 months postprocedure.ConclusionCircular mapping catheter entrapment and ablation at the mitral annulus are the most common etiologies of MV injury during catheter ablation. Close surveillance of the MV is needed during such procedures and early surgical repair is important for successful salvage if significant injury occurs.