Brief PVC Episodes May Trigger Acute Left Atrial Appendage Dysfunction: Study

Embolic stroke continues to be a major health issue, affecting roughly 26 million individuals globally each year. While not traditionally considered a standard risk factor, frequent PVCs have been independently linked to embolic stroke. LAA dysfunction is well-documented as a stroke risk factor in atrial fibrillation, but its significance during sinus rhythm, particularly when PVCs cause atrioventricular dyssynchrony, has remained uncertain. The present in-vivo study was explicitly designed to investigate whether acute LAA dysfunction acts as the crucial bridging link between frequent ventricular ectopy and the elevated risk of thromboembolic events.

The crossover study was conducted on patients undergoing an elective electrophysiology study and radiofrequency ablation for paroxysmal supraventricular tachycardia (PSVT). The analysis included ten adult participants with structurally normal hearts, normal left ventricular ejection fraction (LVEF), and normal baseline LAA function. Under local anaesthesia, a transoesophageal echocardiogram was utilized to acquire LAA flow doppler velocities. To replicate the effects of PVCs in a bigeminal rhythm, researchers delivered single paced beats from the right ventricle for a duration of five minutes. Doppler recordings were meticulously analyzed at three stages: baseline, immediately after five minutes of pacing, and five minutes following the cessation of pacing.

The Key findings from the study include:

• Among the ten patients analyzed, the average LDEV decreased significantly after just five minutes of PVCs (55.68 ± 16.33 cm/s, p = 0.01) compared to a healthy baseline of 68.01 ± 10.34 cm/s.

• Notably, the LDEV almost fully returned to baseline (63.13 ± 16.16 cm/s, p = 0.277) after a brief five-minute resting period, demonstrating the acute and reversible nature of the dysfunction.

• The left atrial appendage filling velocity (LAAFV) displayed a statistically non-significant trend toward reduction following the five minutes of pacing, decreasing from a baseline of 51.31 ± 14.11 cm/s to 45.70 ± 10.85 cm/s.

For practicing cardiologists and physicians, the study highlights that even short bursts of PVCs can trigger acute LAA dysfunction. The rapid decline in LDEV likely predisposes patients to blood stasis and subsequent thrombus formation. Identifying transient atrioventricular dyssynchrony as a primary driver of reduced appendage contractility reinforces the potential need for proactive monitoring of stroke risk in patients with frequent ventricular ectopy . Although further expansive research is required, addressing heavy PVC burdens may become an essential strategy for optimizing cardiovascular outcomes and preventing cardioembolic strokes.

Reference

Sukumaran SK, Bhargav A, Balaguru S, Anantharaj A, Satheesh S, Selvaraj RJ. Acute changes in left atrial appendage function with premature ventricular complexes. Indian Heart Journal. 2025 May 2.