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Introduction: Shoulder pain and disability ipsilateral to the implant site is a common complication of cardiac rhythm device implantation, yet very little has been published about this morbidity. We designed a study to assess the potential benefit of a simple exercise protocol in preventing shoulder pain postoperatively., Methods and Results: Patients undergoing subcutaneous device implantation were randomized to one of two groups. The control group received standard instructions, whereas the exercise group was instructed on specific exercises aimed at strengthening or stretching the shoulder girdle, to be completed 3 days per week. Groups were postoperatively monitored for the development of shoulder discomfort and shoulder impingement by using physical examination and disability questionnaires. At 1 month, seven of 21 control patients reported developing shoulder pain or discomfort compared to one of 23 in the exercise group (P = 0.02). At 6 months, four of 23 control patients still reported worsening shoulder symptoms, compared to none in the exercise group (P = 0.11). In the control group, five of 19 patients developed a positive impingement test at 1 month, versus none in the exercise group (P = 0.01). Scores for the questionnaires designed to assess shoulder pain and dysfunction were worse in the control group. There were no activity-related complications in either group., Conclusion: Shoulder pain and disability occurs often following cardiac rhythm management device implantation. A simple exercise program aimed at strengthening the shoulder girdle is effective at preventing this complication., (©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.)

Introduction: Multiple pharmacological therapies currently in prevalent clinical use for cardiac diseases have antifibrotic properties. Spironolactone, a potent antifibrotic agent, is currently used for advanced heart failure. Therapies such as HMG-CoA reductase inhibitors (statins) and angiotensin-converting enzyme inhibitors (ACEi) also have antifibrotic properties. However, the effect of these medications on the ventricular arrhythmia phenotype is currently unknown. Therefore, we set out to define the ventricular arrhythmia rates in patients actively treated with such therapies., Methods and Results: We retrospectively evaluated the ventricular tachycardia (VT) rates in patients with structural heart disease actively treated with therapies with antifibrotic properties. VT rates were significantly diminished in patients treated with spironolactone (158 ± 26 beats per minute [bpm], n = 21) compared to patients on no medications (205 ± 22 bpm, n = 13) or those who were on similar heart-failure therapies but not on spironolactone (186 ± 32 bpm, n = 82). In addition, we observed that VT rates showed a significant trend toward lower rates in patients receiving either statins or ACEi, compared to patients on no medical therapy. In multivariate analysis, spironolactone therapy was identified as the single most significant variable for reduced VT rate., Conclusion: Use of spironolactone in patients with heart failure is associated with reduced VT rate. Similar but less-significant reductions in VT rates were observed with use of other pharmacological agents with antifibrotic properties, such as statins and ACEi. Our findings, at least in part, could account for reduction in sudden cardiac death rates documented with use of these therapies., (©2010, The Authors. Journal compilation ©2010 Wiley Periodicals, Inc.)

We describe a patient whose presentation of ICD generator failure was excruciating shoulder pain lasting 3 hours. This painful episode prompted evaluation and subsequent generator replacement. Destructive analysis of the explanted device revealed a short circuit of three battery filter capacitors, which resulted in the battery "dumping" its full energy very rapidly, since the impedance across the battery terminal was < 1 ohm. The duration of the painful episode was equal to the estimated ICD battery life under this low impedance condition.

It is apparent that pacing threshold increases following an ICD shock, although the degree of change observed is dependent on the method used to assess pacing and the lead design used. We previously demonstrated a rise in postshock pacing threshold using a lead with integrated bipolar pacing in which the distal shocking coil also serves as the pacing anode. In this study, we sought to investigate whether the postshock pacing threshold increased significantly in an endocardial, steroid-eluting lead with dedicated bipolar pacing electrodes. Twenty patients (16 men, 4 women; median age 73, ejection fraction [EF] 0.17-0.58) were studied during pectoral ICD implantation (Medtronic active can model 7221Cx or 7223Cx with model 6932-65 lead). The diastolic pulse width pacing threshold at 1 or 2 V was determined. Pacing rate was set > or = 100/min at twice diastolic threshold output to assess pacing immediately following the first DFT test shock. For subsequent shocks, the output was adjusted to establish postshock thresholds as 1, 2, 3, or 4 times the diastolic threshold. The postshock threshold was defined as the output yielding 100% capture > or = 2.5 seconds following a shock. In 8 of 20 patients (ratio 0.40 +/- 0.11), a rise in the post-shock threshold was shown by failure of consistent capture when pacing at 2 times diastolic threshold > or = 2.5 seconds after a DFT test shock. Two of these patients failed at 3 times threshold, but none failed at 4 x threshold. Five of 12 patients with successful capture of 2 times threshold failed to capture at threshold. The postshock threshold increased by a mean factor of 2.83 +/- 0.83 in the group of patients with a threshold rise. Following ICD shock in an active can, steroid-eluting lead system with dedicated bipolar pacing, the post-shock threshold increases significantly. Our studies suggest a need for postshock pacing to be set at least 4 x threshold regardless of the lead design.