Pacing-induced Ventricular Dysfunction Research Articles

Long-term outcome of permanent epicardial pacemaker implantation in neonates: Experience from an Indian center.

Permanent pacemaker implantation (PPI) in neonates is challenging with respect to indications, device selection, implantation technique, and long-term outcomes. Complex anatomy, the need for long-term pacing with high rates, and a problematic postoperative period are the major problems. We prospectively followed up 22 newborns who underwent PPI below 28 days of life at our institute. The median age at implantation was 2 days (interquartile range 1-9 days), and 9% were born preterm. The average heart rate before implantation was 46.4 ± 7.2 bpm. Maternal lupus antibodies were positive in 8 (36.4%) neonates, whereas 11 (50.0%) had associated congenital heart disease. Nineteen neonates underwent single chamber (VVI) and three underwent dual chamber (DDD) pacemaker implantation. Over a median follow-up of 46 months (range 2-123 months), the average ventricular pacing percentage was 87.5 ± 24.9%, with a stable pacing threshold. Seven children underwent pulse generator replacement due to battery depletion at a median age of 47 months. Pacing-induced ventricular dysfunction was seen in five children at a median age of 23.6 months, and two underwent upgradation to cardiac resynchronization therapy. Overall mortality was 13.6%, all due to tissue hypoperfusion and lactic acidosis in the postimplantation period. PPI in neonates has a favorable outcome with excellent lead survival. Overall mortality is 13.6%, which is predominantly in the postimplantation period and related to myocardial dysfunction.

Zero or near-zero x-ray pacemaker implantation in paediatric patients. dream or reality?

Abstract Funding Acknowledgements Type of funding sources: None. Background/Introduction Transvenous implantation of pacemaker is performed with fluoroscopy for leads’ insertion and implantation in the heart. This implies radiation exposure for patients and operators. Fluoroscopy allows a two-dimensional view of lead movements, and sometimes it is difficult to implant lead in the complex heart anatomy, or in alternative right ventricular (RV) pacing sites, that often requires higher radiation doses. These alternative pacing sites may prevent pacing-induced ventricular dysfunction. They are his bundle pacing area (HBP), ventricular septum close to the conduction system area (VS), RV outflow tract (RVOT). The use of three-dimensional-electroanatomic mapping system (3D-EAM) may reduce fluoroscopy and guide lead implantation. Published median fluoroscopy data for similar procedure are: 6 mGy (1), 13 mGy and 231 microGy/m2 (2). Purpose of this study is to seek out if a 3D-EAM-guided transvenous implantation into RV alternative sites pacing in paediatric patients can be accomplished with zero or near-zero X-rays. Methods Retrospective analysis of children and adolescents with congenital or acquired (idiopathic) complete atrioventricular block (CAVB) without other congenital heart defects who underwent 3D-EAM-guided pacing in alternative RV sites. The implant procedure was divided in 4 steps: 1-contrast venography; 2- 3D mapping: with a steerable catheter (femoral vein), the 3D-EAM acquired geometric reconstruction of the right heart and a pacing map identified RV sites with narrower paced QRS; 3-axillary vein puncture; 4-lead and pacemaker implantation: 3D-EAM guided stylet-directed screw-in lead implantation toward desired RV sites. Data are reported as median (25th-75th centiles). Results 54 CAVB patients (42 females), underwent 3D EAM-guided pacing (27 VVIR, 27 DDD) at age 11.5 (7.7-14) years, weight 42 (26-54) kg. Pacing sites were: 10 HBP, 4 RVOT, 40 VS (Figure 1). Procedure time was 170 (143-193) min, total fluoroscopy exposure and that of the 4 steps are reported in Table 1. The lowest exposures were: 0.2 mGy, 8 microGy/m2 (VVIR) and 0.6 mGy, 15 microGy/m2 (DDD). Paced QRS was 115 (100-120) ms. Conclusions 3D-EAM-guided alternative RV pacing sites was accomplished with very low fluoroscopic exposure, close to zero in some cases. Therefore, with 3D-EAM we can significantly reduce radiological doses also in difficult pacing procedures in paediatric patients, thus reducing radiological risks and preserving ventricular function. The dream is becoming reality.

Implantation techniques and outcomes after cardiac resynchronization therapy for congenitally corrected transposition of the great arteries

Patients with congenitally corrected transposition of the great arteries (CCTGA) are at risk of congestive heart failure (CHF). There are limited data on cardiac resynchronization therapy (CRT) techniques and long-term outcomes in this population. The purpose of this study was to determine implantation techniques and efficacy of CRT for CCTGA. A 15-year retrospective review of patients with CCTGA undergoing CRT was performed. Twenty patients were identified (mean age 40.1 ± 15.3 years; baseline New York Heart Association class 2.0 [interquartile range 1.5-3.5]). Indication was pacing-induced ventricular dysfunction in 12 (60%), atrioventricular block with anticipation for >40% ventricular pacing in 5 (25%), and intact atrioventricular conduction with CHF and QRS prolongation in 3 (15%). A transvenous approach was successful in 18 of 19 patients (95%) in whom it was attempted, with cannulation of a posteroseptal ostium in 14 (78%), vein of Marshall in 2 (11%), and superior ectopic ostium in 2 (11%). Of patients with baseline CHF, 8 (67%) were acute responders, with loss of response in 2 patients (median 1.1 and 1.5 years, respectively). Of 4 patients referred for heart transplantation, 3 (75%) could be de-listed following CRT. Only lead location inthe right ventricular outflow tract predicted poor CRT response (P= .026). Post-procedure, the QRS duration increased by 4.3 ms/y (P< .001) despite stable pacing characteristics. CRT revision was required in 4 patients for infection (n = 2) or phrenic nerve capture (n = 2) and was associated with loss of CRT response in 1 patient. A transvenous approach to CRT involving distinct coronary venous patterns is feasible for most patients with CCTGA anatomy. Long-term outcome is favorable, but is characterized by return of right ventricular dysfunction in some patients.

The development of pacing induced ventricular dysfunction is influenced by the underlying structural heart defect in children with congenital heart disease

BackgroundRight ventricular pacing can cause pacing-induced ventricular dysfunction (PIVD) correctable with biventricular pacing (BiVP). Factors associated with PIVD are poorly understood. MethodsWe reviewed children receiving epicardial dual-chamber pacemakers for complete heart block (CHB) after congenital heart disease (CHD) surgery. PIVD was defined as% fractional shortening <15% improving after BiVP. ResultsBetween 2005 and 2014, 47 children <2years developed CHB after CHD surgery. All had biventricular hearts and underwent epicardial dual chamber pacemaker implantation. Nine of the 47 (19%) developed PIVD. PIVD occurred in 0/10 with ventricular septal defect (VSD), 0/6 with tetralogy of Fallot, 2/6 with double outlet right ventricle, 2/6 with transposition and VSD, 3/9 with atrioventricular canal defect, 1/2 with mitral valve replacement; 1/3 with congenitally corrected TGA repair; and 0/3 with atrioventricular canal plus tetralogy of Fallot and 0/1 with subaortic membrane. QRS duration (QRSD) was 84–170 (median 135ms) in the non PIVD group and 100–168 (median 124) ms in the PIVD group. Percentage fractional shortening (%FS) while paced was 16–46, median 30% in the non-PIVD group and 6–15 (median 11%) in the PIVD group.%FS post upgrade to BiVP (with an epicardial LV lead) in the 9 patients with PIVD was 23–33 (median 29%). ConclusionsPIVD occurred in certain CHD but not others. Prolonged QRSD was not associated with PIVD. The predilection for RV pacing to result in PIVD in certain types of CHD needs further study.

Pacing therapy in children.

The importance of ventricular pacing site in pediatric pacemaker therapy has gradually become recognized. We reviewed our experience with a left ventricular (LV)-prioritized pacing strategy. METHODS AND RESULTS: Between 2000 and 2012, 60 patients underwent 76 permanent pacemaker implantations. Eight of the 29 reoperations involved ventricular lead repositioning for pacing-induced ventricular dysfunction. Freedom from ventricular lead failure was 96.3%, 86.8%, and 81.0% at 1, 3, and 5 years, respectively. The independent predictors of ventricular lead failure were age (P=0.026) and peak minimal energy threshold within 6 months (P=0.035). At the measured points, redo bipolar, steroid-eluting leads had significantly better pacing properties than did redo non-steroid-eluting, screw-in leads (P=0.0009-0.03). Ventricular lead repositioning was effective in the 5 patients with systemic LV pacing, whereas its efficacy was inconsistent in patients with single-ventricle or systemic right ventricular (RV) pacing. At a median follow-up of 59 months, the 28 patients with LV pacing had preserved ventricular function (LV fraction shortening, 0.34±0.09). The outcome of this LV-prioritized pacing strategy in pediatric patients was excellent, demonstrating preserved ventricular function. Bipolar, steroid-eluting, epicardial pacing leads achieved good pacing properties, even in reoperation patients. In children with systemic LV and RV pacing-induced ventricular dysfunction, a conversion to LV apex pacing was an attractive alternative to cardiac resynchronization therapy.

Pacing-induced cardiomyopathy: pathophysiological insights through matrix metalloproteinases

Pacing-induced ventricular dysfunction and pacing-induced cardiomyopathy (PiCMP) are recognized complications of chronic right ventricular pacing. Alterations in myocardial perfusion and sympathetic innervation contribute to the development of pacing-induced heart disease. However, it is unlikely that these are the only processes involved. Matrix metalloproteinases (MMPs) are proteolytic enzymes that degrade the collagenous extracellular matrix and play a central role in left ventricular remodelling during the development of heart failure. While the pathophysiological mechanisms and altered MMP expression that occur in chronic pressure overload, ischaemic and non-ischaemic dilated cardiomyopathy have been defined, those that occur in the clinicalsetting of pacing-induced ventricular dysfunction and PiCMP have not been reported. Here we review the clinical epidemiology of pacing-induced ventricular dysfunction and discuss how data derived from animal models provide insight into how changes in MMP expression and function contribute to the development of PiCMP. The review concludes by exploring pacing strategies that may be used to prevent pacing-induced ventricular dysfunction.

Effects of low-dose dobutamine on coronary hemodynamics, myocardial metabolism, and anginal threshold in patients with coronary artery disease.

Fourteen patients with coronary artery disease and normal or near-normal left ventricular function were studied at rest and during atrial pacing until the occurrence of angina (12 patients) before and during infusion of dobutamine (3.80 +/- 0.45 micrograms/kg/min). At rest, during the infusion, three patients developed chest pain, mean ST segment depression increased from 0.02 to 0.08 mV (p less than .001), and myocardial lactate extraction fell from +17.5% to -1.4% (p less than .05). These ischemic changes were associated with significant increases in arterial systolic pressure (134 to 149 mm Hg), heart rate (79 to 91 beats/min), coronary sinus flow (89 to 113 ml/min), and myocardial oxygen consumption (10.8 to 13.5 cc/min). In contrast, during atrial pacing, dobutamine did not reduce the pacing threshold or further increase myocardial oxygen consumption or ST segment changes; however, arterial mean and diastolic pressures were significantly lower with pacing during dobutamine infusion compared with control pacing. In the absence of heart failure, dobutamine in low doses can cause myocardial ischemia in patients with coronary artery disease. The absence of increased ischemia from dobutamine during pacing may reflect reversal of pacing-induced ventricular dysfunction.