LAUSR

A 70-year-old hypertensive male patient presented with shortness of breath of 1-month duration. On examination, his pulse rate was 40 bpm and blood pressure was 150/90 mm Hg. His clinical examination and blood investigations were within normal limits. He was not on any rate-lowering drugs. His echocardiogram showed concentric left ventricular hypertrophy with a left ventricular ejection fraction of 55%. His coronary angiogram was normal. He underwent a VVI permanent pacemaker implantation. At implantation, the ventricular lead pacing threshold was 0.7 V at a pulse width of 0.4 millisecond, and the lead impedance was 1148 Ω. The pacing rate was kept at 70 ppm. Two months after the initial implantation, he again presented with shortness of breath. On examination, he was found to have a pulse rate of 38 bpm. An ECG showed complete loss of ventricular pacing. The underlying rhythm was atrial fibrillation with complete heart block. We suspected ventricular lead displacement. On fluoroscopy, the lead position appeared the same as it was at the time of initial implantation. Pacemaker interrogation showed a lead impedance of 1240 Ω. We increased the pacing output to look for ventricular capture. He had a complete loss of pacing until the pacing output was increased to 8.0 V at a pulse width of 1.5 milliseconds when there was an intermittent pacing capture. There was a lack of consistent ventricular sensing (Figure 1A). We noticed a particular pattern of ventricular capture (Figure 1B). What is the possible mechanism to explain why some pacing spikes capture and others do not? Please turn the page to read the diagnosis. Nivedita Rohini Calton, MBBS Amit Gulati, MD, DM Rajneesh Kumar Calton, MD, DM