Faculty Bibliography

Cardiac perforation by a pacemaker lead is a rare complication of pacemaker implantation. Presentation can vary from chest pain and shortness of breath to the patient being completely asymptomatic. Diagnosis is usually made by high-resolution computed tomography (HRCT) scan of the chest. Electrocardiograph (EKG) usually shows the absence of a paced rhythm, but it doesn't provide a definitive diagnosis. We describe a case of late cardiac perforation by an atrial pacemaker lead with no signs or symptoms of pericardial tamponade.

Atrial fibrosis appears to be a key factor in the genesis and/or perpetuation of atrial fibrillation (AF). The pathological distribution of atrial fibrosis is geographically consistent with the attachments between the posterior left atrium and the pericardium along the reflections where wall stiffness is increased and structural changes are found. While there is a wide range of complex etiological factors and electrophysiological mechanisms in AF, there is evidence for a common pathophysiological pathway that could account for deliberate substrate formation and progression of AF. Anatomical stresses along the atrium, mediated by the elastic modulus mismatch between atrial tissue and the pericardium, result in inflammatory and fibrotic changes which create the substrate for atrial fibrillation. This may explain the anatomical predominance of pulmonary vein triggers earlier in the development of atrial fibrillation and the increasing involvement of the atrium as the disease progresses. Ablative treatments that address the progressive nature of atrial fibrillation and fibrosis may yield improved success rates.

Arrhythmias are commonly mapped using a timing reference signal. There are a number of situations where mapping may be difficult or even impossible using conventional reference-based mapping. Wobbling arrhythmias or those who do not maintain a 1:1 relationship with the reference signal are problematic. Local vector mapping may be performed in these situations to map arrhythmias without the use of a reference signal.

OBJECTIVE:To evaluate warfarin prescription, quality of international normalised ratio (INR) monitoring and of INR control in patients with atrial fibrillation (AF) and chronic kidney disease (CKD). METHODS:We performed a retrospective cohort study of patients with newly diagnosed AF in the Veterans Administration (VA) healthcare system. We evaluated anticoagulation prescription, INR monitoring intensity and time in and outside INR therapeutic range (TTR) stratified by CKD. RESULTS:Of 123 188 patients with newly diagnosed AF, use of warfarin decreased with increasing severity of CKD (57.2%-46.4%), although it was higher among patients on dialysis (62.3%). Although INR monitoring intensity was similar across CKD strata, the proportion with TTR≥60% decreased with CKD severity, with only 21% of patients on dialysis achieving TTR≥60%. After multivariate adjustment, the magnitude of TTR reduction increased with CKD severity. Patients on dialysis had the highest time markedly out of range with INR <1.5 or >3.5 (30%); 12% of INR time was >3.5, and low TTR persisted for up to 3 years. CONCLUSIONS:There is a wide variation in anticoagulation prescription based on CKD severity. Patients with moderate-to-severe CKD, including dialysis, have substantially reduced TTR, despite comparable INR monitoring intensity. These findings have implications for more intensive warfarin management strategies in CKD or alternative therapies such as direct oral anticoagulants.