Short-Coupled VF and Unexplained Cardiac Arrest

Aug 10, 2021
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Authors:
Steinberg C, Davies B, Mellor G, et al.
Citation:
Short-Coupled Ventricular Fibrillation Represents a Distinct Phenotype Among Latent Causes of Unexplained Cardiac Arrest: A Report From the CASPER Registry. Eur Heart J 2021;42:2827-2838.
Summary By:
Thomas C. Crawford, MD, FACC

Quick Takes

  • Among patients with unexplained cardiac arrest in the CASPER registry, 6.6% (24/364) were found to have short-coupled ventricular fibrillation, defined as one which is initiated by a triggering PVC with a coupling interval of <350 ms, at the time of presentation, and 79% of subjects manifested the termed disorder during follow-up.
  • Recurrent ventricular fibrillation was treated with quinidine in 50% (12/24) of subjects with excellent arrhythmia control.

Study Questions:

What is the phenotype and frequency of a new entity termed short-coupled ventricular fibrillation (SCVF) in a large cohort of unexplained cardiac arrest survivors?

Methods:

The authors queried the CASPER registry, a multicenter study including unexplained cardiac arrest survivors in Canada. The authors defined “short-coupled ventricular fibrillation” as otherwise unexplained VF initiated by a trigger premature ventricular contraction (PVC) with a coupling interval of <350 ms.

Results:

There were 364 unexplained cardiac arrest survivors, and 24/364 (6.6%) met the above diagnostic criteria for SCVF. The diagnosis of SCVF was obtained in 19/24 (79%) individuals by documented VF during follow-up. Ventricular arrhythmia was initiated by PVCs with a mean coupling interval of 274 ms. Recurrent VF was successfully treated with quinidine in 12/24 (50%) patients.

Conclusions:

SCVF is a distinct primary arrhythmia syndrome accounting for at least 6.6% of unexplained cardiac arrests. As documentation of VF onset is necessary for the diagnosis, most cases are diagnosed at the time of recurrent arrhythmia; thus, the true prevalence of SCVF still remains unknown. Quinidine appears to be protective against recurrent VF.

Perspective:

Among survivors of arrhythmic cardiac arrest without morphologically evident heart disease, about one-half are ultimately diagnosed with a specific genetic abnormality; the other half remain idiopathic. The authors of the present study identify a subgroup of patients within the “idiopathic group,” which is characterized by initiation of VF with a PVC with a very short coupling interval (<350 ms). This entity has previously been referred to as “short-coupled torsade de pointes” and its definition necessarily requires the documentation of the rhythm at the time of arrest. Similar to Brugada and early repolarization syndrome, SCVF is triggered by increased vagal tone, and Purkinje fibers appear to be the source of the triggering PVCs. The authors conducted whole exome sequencing, which did not reveal a pathogenic or likely pathogenic variant. Further studies are needed to begin to describe this proband population more fully.

Clinical Topics: Arrhythmias and Clinical EP, Heart Failure and Cardiomyopathies, Prevention, Implantable Devices, EP Basic Science, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Novel Agents, Statins, Acute Heart Failure

Keywords: Arrhythmias, Cardiac, Heart Arrest, Heart Failure, Phenotype, Purkinje Fibers, Quinidine, Secondary Prevention, Torsades de Pointes, Ventricular Fibrillation, Ventricular Premature Complexes


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