What does this research mean for the field?

Repetitive monomorphic ventricular tachycardia (RMVT) is driven by a mechanism of cAMP-mediated triggered activity, as demonstrated by its consistent termination by adenosine and verapamil. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This research aims to elucidate the cellular mechanisms underlying repetitive monomorphic ventricular tachycardia (RMVT).

August 1, 1995Circulation

Mechanism of Repetitive Monomorphic Ventricular Tachycardia

Q: What is the clinical evidence from this study?

Study design: Observational. Population: Repetitive Monomorphic Ventricular Tachycardia (RMVT) (n=12). Intervention: Electropharmacological probes and electrophysiological study. Primary outcome: Termination of VT in response to interventions lowering intracellular cAMP or calcium current.

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Key result

Electrophysiological testing in 12 patients showed RMVT termination by adenosine (12 of 12) and verapamil (10 of 12), indicating a mechanism of cAMP-mediated triggered activity.

Population

12 patients with repetitive monomorphic ventricular tachycardia (RMVT)

Design

Case_series

Authors

BLBruce B. LermanElectrophysiology KSKenneth M. SteínElectrophysiology EEErica D. EngelsteinRush University Medical Center

Discussion

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Implication

Supports cAMP-mediated mechanism in RMVT; hypothesis-generating and should not yet change practice.

Key Points

This research aims to elucidate the cellular mechanisms underlying repetitive monomorphic ventricular tachycardia (RMVT).
Twelve patients with RMVT underwent electrophysiological study.
Heart rate variability was monitored over 24 hours for 7 patients.
Genomic DNA was extracted from myocardial biopsy samples and analyzed for G alpha s mutations.
Sustained VT was induced and facilitated by rapid pacing in 11 patients.
Termination of VT occurred with cAMP-lowering interventions in 8 of 9 and was consistent with increased sympathetic tone before nonsustained VT.
DNA analysis showed no activating mutations in G alpha s in sampled myocardial tissue.

Study Design

Type

Observational (n=12)

Structured PICO

Population

12 patients with repetitive monomorphic ventricular tachycardia (RMVT)

Intervention

Electrophysiological study with electropharmacological probes (isoproterenol, adenosine, edrophonium, beta-blockade, verapamil), 24-hour ambulatory monitoring, and myocardial biopsy for genetic analysis

Outcome

Mechanism of RMVT at the cellular level, potential autonomic triggers, and presence of somatic activating mutations in G alpha ssurrogate

The mechanism of repetitive monomorphic ventricular tachycardia (RMVT) is consistent with cAMP-mediated triggered activity, similar to paroxysmal exercise-induced VT.

Cite This Study

Lerman et al. (1995) conducted an observational in Repetitive Monomorphic Ventricular Tachycardia (RMVT) (n=12). Electropharmacological probes and electrophysiological study was evaluated on Termination of VT in response to interventions lowering intracellular cAMP or calcium current. Electrophysiological testing in 12 patients showed RMVT termination by adenosine (12 of 12) and verapamil (10 of 12), indicating a mechanism of cAMP-mediated triggered activity.

synapsesocial.com/papers/6a163f0cf508cb2fcbc1f022 https://doi.org/10.1161/01.cir.92.3.421

Topics

Ventricular arrhythmias

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Mechanism of Repetitive Monomorphic Ventricular Tachycardia

Discussion

Member takes

Implication

Key Points

Study Design

Structured PICO

Cite This Study

Topics

Mechanism of Repetitive Monomorphic Ventricular Tachycardia

Discussion

Member takes

Implication

Key Points

Study Design

Structured PICO

Cite This Study

Also Consider

Topics

Also Consider