A Cautionary Tale on Atrial Capture Management, Biventricular Pacing, and Recurrent Asystole.

Capture management algorithms in current cardiac implantable electronic devices (CIEDs) can enhance device performance and battery longevity. Although generally safe, these algorithms have on rare occasions been implicated in the onset of significant complications, especially in pacemaker-dependent patients. CIEDs implanted in patients with postoperative congenital heart disease (CHD) often require epicardial pacing leads rather than transvenous leads; unfortunately, epicardial leads can experience higher rates of malfunction. We herein report on a young adult with a status of postoperative CHD and complete atrioventricular block following implantation of a epicardial dual-chamber cardiac resynchronization therapy pacemaker (CRT-P; Consulta®; Medtronic, Minneapolis, MN, USA) who developed frequent periods of asystole after malfunction of one of the ventricular leads. The underlying cause of asystole was found to be due to the atrial capture management (ACM) algorithm of the CRT-P device, temporarily converting biventricular to right ventricular-only pacing as part of the algorithm. This case highlights implications of the ACM algorithm in devices with a similar platform for pacemaker-dependent patients.

Long-term atrial and ventricular epicardial pacemaker lead survival after cardiac operations in pediatric patients with congenital heart disease.

BACKGROUND: Multiple cardiac operations and resultant myocardial scarring have been implicated in the overall reduced performance of epicardial pacing systems in patients with congenital heart disease (CHD). OBJECTIVE: The aim of the study is to evaluate long-term permanent epicardial pacing lead survival in patients with CHD who had epicardial lead placement in association with surgical repair or palliation. METHODS: A retrospective review of patients who had implantation of epicardial pacing systems between January 1984 and June 2010 was conducted. Inclusion criteria were as follows: (1) presence of CHD and (2) cardiac operation(s) concomitant with or before initial permanent epicardial lead implantation. Patients were divided into 2 anatomical groups: single ventricle (SV) and biventricle (Bi-V). RESULTS: Epicardial leads were implanted in 663 patients during the study period. One hundred fifty-five patients (76 SV [49%] and 79 Bi-V [51%]) were included, resulting in 259 leads and 946 lead-years of follow-up. There were 2 deaths and 8 infections attributable to pacemaker placement. Overall atrial lead survival at 1, 2, 5, and 10 years (99%, 93%, 83%, and 72%) was comparable with ventricular lead survival (97%, 90%, 74%, and 60%) (P = .540) and was also similar between SV and Bi-V patients. Cox regression analysis demonstrated that SV palliation and an earlier era of lead implantation (1984-1999) was significantly associated with ventricular, but not atrial, lead malfunction. CONCLUSION: Epicardial leads had acceptable longevity despite cardiac operations for complex CHD, suggesting the long-term reliability of this pacing method.

Utility of electrocardiogram in the assessment and monitoring of pulmonary hypertension (idiopathic or secondary to pulmonary developmental abnormalities) in patients≤18 years of age.

Electrocardiograms have utility in disease stratification and monitoring in adult pulmonary arterial hypertension (PAH). We examined the electrocardiographic findings that are common in pediatric PAH and assessed for correlation with disease severity and progression. We retrospectively identified patients aged≤18 years followed at a single institution from January 2001 to June 2012 with catheterization-confirmed diagnosis of idiopathic PAH and PAH secondary to pulmonary developmental abnormalities. Patients with an electrocardiography performed within 60 days of catheterization were included. Primary and secondary outcomes are the prevalence of abnormal electrocardiographic findings at the time of catheterization and the association between electrocardiographic and hemodynamic findings and electrocardiographic changes with disease progression on follow-up catheterization, respectively. Of the 100 electrocardiography-catheterization pairs derived from the 46 patients identified, 93% had an electrocardiographic abnormality: 78% had right ventricular hypertrophy (RVH) and 52% had right axis deviation (RAD) for age. In patients with idiopathic PAH, the presence of RVH and RAD correlated with pulmonary vascular resistance and transpulmonary gradient. RAD and RVH on baseline electrocardiogram was associated with an increased risk of disease progression on subsequent catheterization (odds ratio 11.0, 95% confidence interval 1.3 to 96.2, p=0.03) after adjusting for PAH subgroup. The sensitivity, specificity, and positive and negative predictive values of RAD and RVH on baseline electrocardiogram for disease progression were 92%, 48%, 33%, and 95%, respectively. In conclusion, electrocardiographic abnormalities are common in pediatric PAH. RAD and RVH on electrocardiogram were associated with worse hemodynamics, whereas their absence is suggestive of a lack of disease progression.

Role for platelet-endothelial cell adhesion molecule-1 in macrophage Fcgamma receptor function.

Platelet-endothelial cell adhesion molecule-1 (PECAM-1) (CD31), a 130-kD transmembrane glycoprotein that functions in adhesion and signaling, is thought to play a role in some forms of leukocyte transmigration. In the lung, PECAM-1 is highly expressed, yet there have been few studies examining its role in pulmonary pathology. We therefore examined the inflammatory response (measured by bronchoalveolar lavage cell counts and protein content) after several types of lung injury in wild-type and PECAM-1 knockout mice. Consistent with studies in other organs, instillation of an endothelial stimulant (interleukin-1) was PECAM-1-dependent. In contrast, we noted that three other forms of acute lung injury (acid aspiration, adenoviral instillation, and tumor necrosis factor instillation) were completely PECAM-1-independent. Interestingly, in situ immune complex deposition injury, another complex lung disease, was also PECAM-1-dependent. This surprising finding was investigated in more detail and found to be due to a defect in macrophage activation, and not to a blockade of leukocyte transmigration. Experiments in bone marrow chimeric mice as well as ex vivo data demonstrated that Fcgamma receptor-dependent phagocytosis and tumor necrosis factor release were significantly reduced in macrophages derived from PECAM-1 knockout mice. Although PECAM-1 may not be required for transmigration of leukocytes into the alveolar space in many forms of complex lung inflammation, it is important in the function of Fcgamma receptors on alveolar macrophages.