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Published on: August 1, 2016
Coupling interval variability of premature ventricular contractions in patients with different underlying pathology:
Lennart J de Vries1, Mihran Martirosyan1, Ron T van Domburg2
1Department of Cardiology, Electrophysiology, Erasmus Medical Center, Rotterdam, The Netherlands.
Insights
Premature ventricular contraction (PVC) coupling interval variability differs across myocardial diseases. High variability in PLN/LMNA patients suggests distinct arrhythmia mechanisms compared to idiopathic or non-ischemic dilated cardiomyopathy.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Arrhythmias
Background:
- Coupling interval (CI) variability in premature ventricular contractions (PVCs) is a key indicator of underlying arrhythmia mechanisms.
- Understanding these mechanisms is crucial for diagnosing and managing various cardiac conditions.
Purpose of the Study:
- To compare CI variability of PVCs across different myocardial disease entities.
- To gain insights into the specific arrhythmia mechanisms associated with each condition.
Main Methods:
- Sixty-four patients with idiopathic, non-ischemic dilated cardiomyopathy (NIDCM), familial cardiomyopathy (PLN/LMNA), and post-myocardial infarction (post-MI) PVCs were studied.
- Coupling intervals of the dominant PVC morphology were measured from Holter registrations.
- Median ΔCI and mean standard deviation of CI/√R-R were calculated to assess CI variability.
Main Results:
- The PLN/LMNA group exhibited the largest ΔCI (220 ms), significantly greater than the post-MI group (130 ms).
- Mean SD of CI/√R-R was also significantly higher in the PLN/LMNA group compared to the post-MI group.
- Idiopathic PVCs showed the lowest ΔCI (120 ms).
Conclusions:
- Low CI variability in idiopathic and NIDCM PVCs suggests re-entry or triggered activity as likely mechanisms.
- High CI variability in PLN/LMNA patients indicates that re-entry and triggered activity are less probable mechanisms.
- Abnormal automaticity or modulated parasystole are unlikely mechanisms for idiopathic and NIDCM PVCs.
Purpose:
Coupling interval (CI) variability of premature ventricular contractions (PVCs) is influenced by the underlying arrhythmia mechanism. The aim of this study was to compare CI variability of PVCs in different myocardial disease entities, in order to gain insight into their arrhythmia mechanism.
Methods:
Sixty-four patients with four underlying pathologies were included: idiopathic (n = 16), non-ischemic dilated cardiomyopathy (NIDCM) (n = 16), familial cardiomyopathy (PLN/LMNA) (n = 16), and post-MI (n = 16)-associated PVCs. The post-MI group was included as a reference, on account of its known re-entry mechanism. On Holter registrations, the first 20 CIs of the dominant PVC morphology were measured manually after which median ΔCI and mean SD of CI/√R-R (= CI of PVC corrected for underlying heart rate) were obtained. Two observers independently measured PVC CIs on pre-selected Holter registrations in order to determine inter- and intra-observer reliability.
Results:
The largest ΔCI was seen in the PLN/LMNA group (220 ms (120-295)), the lowest in the idiopathic group (120 ms (100-190)). The ΔCI in the PLN/LMNA group was significantly larger than the post-MI group (220 ms (120-295) vs 130 ms (105-155), p = 0.023). Mean SD of CI/√R-R in the PLN/LMNA group was also significantly higher than in the post-MI group (p = 0.044). Inter- and intra-observer reliability was good (ICC = 0.91 vs 0.86 and 0.96 vs 0.77, respectively).
Conclusions:
Low ΔCI and SD of CI/√R-R of idiopathic and NIDCM PVCs suggest that the underlying arrhythmia mechanisms might be re-entry or triggered activity. Abnormal automaticity or modulated parasystole are unlikely mechanisms. High CI variability in PLN/LMNA patients suggests that the re-entry and triggered activity are less likely mechanisms in this group.
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