Delayed cardiac perforation by defibrillator lead placed in the right ventricular outflow tract resulting in massive pericardial effusion.

A 76-year-old man received a dual-chamber implantable cardioverter defibrillator (ICD), with the defibrillator lead positioned within the right ventricular outflow tract. The lead parameters at the time of implantation were satisfactory and the post-procedure chest X-ray showed the leads were in place. The patient was cardioverted from atrial fibrillation during defibrillation threshold testing and commenced on anticoagulation immediately. One month post implantation, he experienced multiple ventricular tachycardia episodes all successfully treated with antitachycardia pacing and shocks by his ICD, but he fell and hit his chest against a hard surface during one of these attacks. He developed a massive pericardial effusion and computed tomography confirmed cardiac perforation by the defibrillator lead. Pericardiocentesis was performed and the defibrillator lead replaced with a different model positioned at the right ventricular apex. The patient made an uneventful recovery. The management and avoidance of delayed cardiac perforation by transvenous leads were discussed.

ST segment elevation in lead aVR during exercise testing is associated with LAD stenosis.

PURPOSE: To evaluate, in patients with chest pain, the diagnostic value of ST elevation (STE) in lead aVR during stress testing prior to (99m) Tc-sestamibi scanning correlating ischaemic territory with angiographic findings. METHODS: Consecutive patients attending for (99m) Tc-sestamibi myocardial perfusion imaging (MPI) completed a treadmill protocol. Peak exercise ECGs were coded. STE >or=0.05 mV in lead aVR was considered significant. Gated perfusion images and findings at angiography were assessed. RESULTS: STE in lead aVR occurred in 25% (138/557) of the patients. More patients with STE in aVR had a reversible defect on imaging compared with those who had no STE in aVR (41%, 56/138 vs 27%, 114/419, p=0.003). Defects indicating a left anterior descending artery (LAD) culprit lesion were more common in the STE in aVR group (20%, 27/138 vs 9%, 39/419, p=0.001). There was a trend towards coronary artery stenosis (>70%) in a double vessel distribution involving the LAD in those patients who had STE in aVR compared with those who did not (22%, 8/37 vs 5%, 4/77, p=0.06). Logistic regression analysis demonstrated that STE in aVR (OR 1.36, p=0.233) is not an independent predictor of inducible abnormality when adjusted for STD >0.1 mV (OR 1.69, p=0.026). However, using anterior wall defect as an end-point, STE in aVR (OR 2.77, p=0.008) was a predictor even after adjustment for STD (OR 1.43, p=0.281). CONCLUSION: STE in lead aVR during exercise does not diagnose more inducible abnormalities than STD alone. However, unlike STD, which is not predictive of a territory of ischaemia, STE in aVR may indicate an anterior wall defect.