Diaphragmatic pacemaker induced ventricular tachycardia leading to cardiac arrest: A case report

Background Diaphragmatic pacemakers are used to assist respiration in ventilator-dependent patients. Electromagnetic interference with intrinsic cardiac electrical activity is a theoretical risk but has never been reported in the literature. This case highlights a serious complication of cardiac arrest as a result of diaphragmatic pacing. Case Summary We report a quadriplegic patient with recent diaphragmatic pacemaker implantation who presented with ventricular tachycardia leading to cardiac arrest. Extensive workup was negative for other etiologies for ventricular arrythmias. Reduction of the left-sided diaphragmatic pacemaker voltage resulted in cessation of ventricular ectopy. Discussion Diaphragmatic pacing at high voltages can cause unwanted transmission of impulses to the cardiac myocytes as a rare complication. This should be noted as a possible complication of intramuscular diaphragmatic pacing, and efforts should be taken to circumvent this risk in the future.

Magnetic Resonance Detects Structural Heart Disease in Patients with Frequent Ventricular Ectopy and Normal Echocardiographic Findings

The prognosis of patients with ventricular ectopy and a normal heart, as evaluated by echocardiography, is virtually unknown. Cardiac magnetic resonance (CMR) can detect focal ventricular anomalies that could act as a possible site of origin for premature ventricular contractions (PVCs). The aim of this study was to investigate the presence of cardiac anomalies in patients with normal findings at echocardiogram. Methods: Fifty-one consecutive patients (23 women, 28 men, mean age 59 years) with very high PVC burden (>10,000 PVC/day) and normal findings at standard echocardiography and exercise test were examined with CMR. The outcome was pathologic findings, defined as impaired ejection fraction, regional wall motion abnormalities, abnormal ventricular volume, myocardial edema and fibrosis. Results: Sixteen out of 51 patients (32%) had structural ventricular abnormalities at CMR. In five patients CMR showed impairment of the left ventricular and/or right ventricular systolic function, and six patients had a dilated left and/or right ventricle. Regional wall motion abnormalities were seen in six patients and fibrosis in four. No patient had CMR signs of edema or met CMR criteria for arrhythmogenic right ventricular cardiomyopathy. Five patients had extra-ventricular findings (enlarged atria in three cases, enlarged thoracic aorta in one case and pericardial effusion in one case). Conclusions: In this study 16 out of 51 patients with a high PVC burden and normal findings at echocardiography showed signs of pathology in the ventricles with CMR. These findings indicate that CMR should be considered in evaluating patients with a high PVC burden and a normal standard investigation.