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A man in his 70s presented to the emergency department with left-sided hemiparesis, dysarthria, gaze deviation in his right eye, and left-sided hemineglect. His medical history was significant for permanent atrial fibrillation and complete heart block for which he had a pacemaker implanted in the late 1990s that was subsequently upgraded to a biventricular system. His blood pressure was 147/75 mm Hg, heart rate was 84 beats per minute, respiratory rate was 16 breaths per minute, and oxygen saturation was 99% on room air. Computed tomography angiography was consistent with a large middle cerebral artery territory embolic stroke. Embolectomy was advised. An electrocardiogram (Figure 1) was obtained.
Questions: What is the cause of the alternating QRS complex morphology in this patient? What action, if any, should be taken with regard to these findings prior to embolectomy?
The electrocardiogram shows a ventricular-paced rhythm with ventricular bigeminy at an overall mean rate of 84 beats per minute. Two pacing stimuli are visible, best seen in lead II (Figure 2A). The first of each bigeminal complex is initiated by a pacemaker stimulus that results in ventricular depolarization. Each paced QRS complex is followed by a premature ventricular complex (PVC), in which a second pacemaker stimulus occurs about 60 msec after onset of the PVC. The positive R wave deflection in the paced QRS seen in lead V1, in association with a negative paced QRS deflection in lead aVF and an isoelectric paced QRS complex in V6 suggests biventricular pacing with left ventricular depolarization originating from the inferolateral aspect of the base of the heart (Figure 2B). This is not the depolarization pattern expected with a single- or dual-chamber device (ie, RV pacing), which would result in a left bundle branch block pattern consisting of a dominant S wave in V1 and a broad monophasic R wave in leads V5 through V6. In light of biventricular pacing, the second pacemaker stimulus that occurs within the native PVC represents attempted salvage resynchronization and is consistent with normal pacemaker function.
A, Pacing stimuli is emphasized in the electrocardiogram (ECG). The first stimulus of each couplet (black triangle) results in ventricular depolarization. The second stimulus (white triangle) occurs after the beginning of ventricular depolarization and is an attempt to salvage resynchronization. B, Simplified anatomic representation of depolarization originating from the inferobasal aspect of the heart depicted in the sagittal (left), frontal (middle), and transverse (right) planes.
No intervention was performed with respect to the pacemaker. The patient underwent uncomplicated urgent embolectomy with good neurologic recovery. Further history taking revealed that he had been confused about his anticoagulant regimen and had not been taking his prescribed apixaban for several months prior to presentation.
Cardiac resynchronization therapy (CRT), in which biventricular pacing is accomplished by coordinated stimuli delivered to the right and left ventricles, improves outcomes in patients with heart failure with reduced ejection fraction when poor systolic function and ventricular dyssynchrony are present.1-3 It is also indicated in patients with heart failure and an ejection fraction of less than 50% who require a high percentage of right ventricular pacing owing to atrioventricular block.4 This patient falls into the latter category. Long-term right ventricular pacing is known to be deleterious in patients with structural heart disease,5 an effect that is mediated by ventricular dyssynchrony similar to that observed in left bundle branch block.6 Cardiac resynchronization therapy is most effective when biventricular capture is achieved more than 98% of the time; failure to reach this threshold should prompt a search for potential explanations, which range from PVCs to tachyarrhythmias, which do not trigger biventricular pacing, to issues with lead malpositioning or device programming, such as atrial undersensing.7 Regular interrogation is necessary to ensure optimal CRT.
Premature ventricular complexes interfere with resynchronization by causing slow, uncoordinated myocyte-to-myocyte depolarization, resulting in poor clinical outcomes in many patients.8 In patients with poor response to CRT and a PVC burden of more than 10 000 per 24 hours, radiofrequency ablation of ventricular ectopic foci has been shown to improve resynchronization, reduce symptomatic burden, and reverse ventricular remodeling.9 The pacing stimuli seen within the PVCs in this case represent an attempt to limit the adverse effects of dyssynchronous depolarization by partially resynchronizing the left and right ventricles. The device is programmed to monitor for PVCs and respond by delivering ventricular pacing stimuli, decreasing the time necessary to depolarize the ventricles and improving ventricular coordination. The proprietary variations of this concept are referred to differently by each manufacturer. For example, in this patient, who had a Valitude U125 biventricular pacemaker (Boston Scientific), the function is called biventricular trigger, whereas devices produced by Medtronic term the feature ventricular sense response, and the same programming is referred to as ventricular triggered pacing in St Jude devices.
Optimization of CRT is by no means an emergency. In this hemodynamically stable patient presenting with an acute stroke, neurologic interventions take precedence. The device should be interrogated and ablation of the bigeminal ectopic focus considered in the outpatient setting if proven to be significantly burdensome.
The pattern seen in this case, pacemaker stimuli delivered during PVCs, represents normal CRT function.
In addition to those with heart failure with reduced ejection fraction with ventricular dyssynchrony, CRT improves outcomes in patients with heart failure with ejection fractions between 35% and 50% who require frequent pacing.
Ablation of ectopic foci should be considered in patients with poor CRT response and significant PVC burden.
Corresponding Author: Jacob J. Mayfield, MD, Department of Medicine, University of California, San Francisco, 505 Parnassus Ave, PO Box 0119, M1479, San Francisco, CA 94143 (firstname.lastname@example.org).
Published Online: March 23, 2020. doi:10.1001/jamainternmed.2020.0463
Conflict of Interest Disclosures: None reported.
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Mayfield JJ, Goldschlager N. Alternating QRS Complex Morphology in a Man Presenting With Stroke. JAMA Intern Med. Published online March 23, 2020. doi:10.1001/jamainternmed.2020.0463
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