Risk of malignant ventricular arrhythmias in patients with mildly to moderately reduced ejection fraction after permanent pacemaker implantation.

BACKGROUND: Many patients with mildly to moderately reduced left ventricular ejection fraction (LVEF) who require permanent pacemaker (PPM) implantation do not have a concurrent indication for implantable cardioverter-defibrillator (ICD) therapy. However, the risk of ventricular tachycardia/ventricular fibrillation (VT/VF) in this population is unknown. OBJECTIVE: The aim of this study was to describe the risk of VT/VF after PPM implantation in patients with mildly to moderately reduced LVEF. METHODS: Retrospective analysis was performed of 243 patients with LVEF between 35% and 49% who underwent PPM placement and did not meet indications for an ICD. The primary end point was occurrence of sustained VT/VF. Competing risks regression was performed to calculate subhazard ratios for the primary end point. RESULTS: Median follow-up was 27 months; 73% of patients were male, average age was 79 ± 10 years, average LVEF was 42% ± 4%, and 70% were New York Heart Association class II or above. Most PPMs were implanted for sick sinus syndrome (34%) or atrioventricular block (50%). Of 243 total patients, 11 (4.5%) met the primary end point of VT/VF. Multivessel coronary artery disease (CAD) was associated with significantly higher rates of VT/VF, with a subhazard ratio of 5.4 (95% CI, 1.5-20.1; P = .01). Of patients with multivessel CAD, 8 of 82 (9.8%) patients met the primary end point for an annualized risk of 4.3% per year. CONCLUSION: Patients with mildly to moderately reduced LVEF and multivessel CAD undergoing PPM implantation are at increased risk for the development of malignant ventricular arrhythmias. Patients in this population may benefit from additional risk stratification for VT/VF and consideration for upfront ICD implantation.

Diagnostic yield of extensive infectious panel testing in acute pericarditis.

OBJECTIVE: In an attempt to reconsider our local strategy, we evaluated patients with viral/idiopathic pericarditis in order to assess the diagnostic yield of our standard infectious panel, the characteristics of myocardial involvement, the utility of investigating myocardial involvement and the incidence of coronary evaluation tests. METHODS: Seventy-six consecutive cases of idiopathic/viral acute pericarditis treated between March 2005 and March 2008 were retrospectively enrolled. Telephonic questionnaires were answered by all. RESULTS: Myopericarditis was recorded in 45/71 (63.4%) consecutive patients. Sore throat on presentation (38 vs. 12%; p = 0.027) was the only symptom independently associated with myopericarditis. The following clinical features were significantly correlated with pericarditis rather than myopericarditis: age (42 ± 16 vs. 32 ± 12; p = 0.008), C-reactive protein (131 ± 75 vs. 78 ± 58; p = 0.009) and lower CPK and troponin levels (mean 96 vs. mean 489; p < 0.001 and mean 0 vs. mean 10; p < 0.001, respectively). The infectious panel revealed 6 positive results. After an average 3 years' fol- low-up, recurrence was documented in 5 patients (7%). No patient initially regarded idiopathic developed systemic disease during follow-up. CONCLUSIONS: Among patients presenting with presumed idiopathic/viral pericarditis, myopericarditis is relatively common and has a benign evolution. Extensive serological investigation with a broad infectious panel proved to be diagnostically and therapeutically futile in our area.

Synaptic release of zinc from brain slices: factors governing release, imaging, and accurate calculation of concentration.

Cerebrocortical neurons that store and release zinc synaptically are widely recognized as critical in maintenance of cortical excitability and in certain forms of brain injury and disease. Through the last 20 years, this synaptic release has been observed directly or indirectly and reported in more than a score of publications from over a dozen laboratories in eight countries. However, the concentration of zinc released synaptically has not been established with final certainty. In the present work we have considered six aspects of the methods for studying release that can affect the magnitude of zinc release, the imaging of the release, and the calculated concentration of released zinc. We present original data on four of the issues and review published data on two others. We show that common errors can cause up to a 3000-fold underestimation of the concentration of released zinc. The results should help bring consistency to the study of synaptic release of zinc.