Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Continuous concealed ventricular arrhythmias

R R Hope, B J Scherlag, N El-Sherif

    The American Journal of Cardiology
    |November 1, 1977
    PubMed
    Summary
    This summary is machine-generated.

    Related Concept Videos

    You might also read

    Related Articles

    Articles linked to this work by shared authors, journal, and citation graph.

    Sort by
    Same author

    The Role of the Atrial Neural Network In Atrial Fibrillation: The Metastatic Progression Hypothesis.

    Journal of atrial fibrillation·2017
    Same author

    Functional anatomy of AV conduction: changing concepts in the ablation era.

    Journal of electrocardiology·2002
    Same author

    Spatial alterations of Kv channels expression and K(+) currents in post-MI remodeled rat heart.

    Cardiovascular research·2001
    Same author

    Calcineurin inhibition ameliorates structural, contractile, and electrophysiologic consequences of postinfarction remodeling.

    Journal of cardiovascular electrophysiology·2001
    Same author

    Efficacy of azimilide and dofetilide in the dog right atrial enlargement model of atrial flutter.

    Journal of cardiovascular electrophysiology·2001
    Same author

    Cycle length-associated modulation of the regional dispersion of ventricular repolarization in a canine model of long QT syndrome.

    Pacing and clinical electrophysiology : PACE·2001
    Same journal

    Balloon-expandable versus Self-expanding Valves in Patients with Small Aortic Annuli Undergoing Transcatheter Aortic Valve Replacement.

    The American journal of cardiology·2026
    Same journal

    Drug-Coated Balloons versus Drug-Eluting Stents following Coronary Atherectomy in Severely Calcified Lesions: A Systematic Review and Meta-Analysis.

    The American journal of cardiology·2026
    Same journal

    Prehospital Statin Therapy and Outcomes in ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.

    The American journal of cardiology·2026
    Same journal

    Semaglutide for the Silent Phenotype: A Translational Signal in Obesity-Driven HFpEF.

    The American journal of cardiology·2026
    Same journal

    Feasibility and Yield of a Diagnostic Protocol for Myocardial Infarction with Non-Obstructive Coronary Arteries.

    The American journal of cardiology·2026
    Same journal

    Prognostic Utility of the BCIS-CHIP Score in Imaging-Guided Percutaneous Coronary Intervention.

    The American journal of cardiology·2026
    See all related articles

    This study examined how heart attacks in dogs lead to hidden, or concealed, irregular heartbeats. Researchers found that damaged heart tissue creates continuous electrical signals that can trigger dangerous rhythms when the heart is paced. These findings help explain how certain heart conditions persist even when they are not immediately visible on a standard heart monitor.

    Area of Science:

    • Cardiovascular physiology and continuous concealed ventricular arrhythmias research
    • Veterinary cardiology and electrophysiology

    Background:

    The mechanisms underlying persistent cardiac rhythm disturbances following ischemic injury remain poorly understood. Prior research has shown that damaged heart tissue often harbors abnormal electrical pathways. That uncertainty drove investigators to examine how these zones influence heart rhythm stability. It was already known that standard sinus rhythm might mask underlying electrical instability in post-infarction models. This gap motivated a detailed look at how specific pacing protocols reveal hidden triggers. No prior work had resolved how subepicardial damage maintains continuous electrical signals between beats. Previous studies often focused on manifest arrhythmias rather than those hidden from conventional observation. This investigation addresses the specific conditions required to unmask these latent electrical events in canine models.

    Purpose Of The Study:

    The aim of this study was to investigate the mechanisms of concealed ventricular arrhythmias following myocardial infarction. Researchers sought to determine why certain heart rhythm disturbances remain hidden during normal sinus activity. They aimed to evaluate whether specific pacing protocols could successfully induce and reveal these latent electrical patterns. The study addressed the hypothesis that damaged subepicardial tissue maintains continuous electrical signals between heartbeats. Investigators intended to clarify the relationship between fractionated electrical activity and the manifestation of various ventricular rhythms. This effort was motivated by the need to understand how post-infarction damage supports persistent electrical instability. The team sought to document the prevalence of these rhythms across a controlled canine model. Ultimately, the work aimed to provide insight into the electrical behavior of the infarct zone under stress.

    Keywords:
    cardiac electrophysiologyinfarct zonesubepicardial activityheart rhythm stability

    Frequently Asked Questions

    The researchers propose that continuous electrical activity within the infarct zone acts as the primary mechanism. This activity bridges the interval between successive beats, manifesting as ventricular arrhythmia during atrial pacing or emerging as ventricular tachycardia once pacing stops.

    The authors utilized atrial pacing and long-short cycle sequences to induce these rhythms. These techniques were necessary to reveal the latent electrical patterns that remained hidden during standard sinus rhythm.

    A sinus nodal crush procedure or vagal stimulation was required to assess ventricular automaticity. These methods ensured that the baseline automaticity remained within normal ranges, confirming that the induced arrhythmias were not due to inherent nodal dysfunction.

    The study utilized electrical recordings from the subepicardium to identify delayed and fractionated activity. This data type allowed the researchers to map the specific infarct zone signals that bridged the gaps between heartbeats.

    Related Experiment Videos

    Main Methods:

    The review approach involved analyzing twenty canine subjects three to nine days post-injury. Investigators monitored heart activity during sinus rhythm to establish a baseline for comparison. They employed atrial pacing protocols to challenge the electrical stability of the heart. The team also utilized long-short cycle sequences to provoke latent rhythm disturbances. Researchers performed sinus nodal crush or vagal stimulation to evaluate intrinsic automaticity levels. They recorded electrical signals directly from the subepicardial region of the damaged tissue. This design allowed for the identification of delayed and fractionated electrical events. The approach focused on correlating these specific signals with the manifestation of various ventricular patterns.

    Main Results:

    The strongest finding indicates that continuous electrical activity within the infarct zone bridges the interval between successive beats. All twenty animals exhibited induced ventricular arrhythmias when subjected to regular atrial pacing or cycle sequences. Quadrigeminal and pentageminal rhythms appeared in nineteen of the twenty subjects during the observation period. Trigeminal rhythms were documented in seventeen of the twenty animals tested. Bigeminal ventricular patterns occurred in eight of the twenty dogs. These rhythms were consistently linked to delayed and fractionated electrical activity in the subepicardium. The recorded signals either manifested as arrhythmias during pacing or emerged as tachycardia when pacing ceased. These results demonstrate that pacing maneuvers successfully unmask previously concealed electrical events in the damaged heart.

    Conclusions:

    The authors propose that continuous electrical activity within damaged subepicardium serves as a primary driver for these rhythm disturbances. Their synthesis suggests that pacing maneuvers effectively expose hidden triggers that otherwise remain silent during normal sinus activity. These findings imply that the infarct zone acts as a persistent source of abnormal signals. The researchers conclude that the presence of fractionated electrical events correlates strongly with the observed ventricular patterns. This review of evidence indicates that the transition from concealed to manifest tachycardia depends on the cessation of external pacing. The authors argue that these observations clarify the pathophysiology of post-infarction rhythm instability. Their work highlights the importance of considering latent electrical pathways in clinical assessments. These conclusions provide a framework for understanding how damaged tissue supports complex, multi-beat electrical phenomena.

    The researchers observed quadrigeminal, pentageminal, trigeminal, and bigeminal rhythms. These patterns were present in nearly all subjects, with quadrigeminal and pentageminal rhythms appearing in 19 of the 20 dogs studied.

    The authors suggest that these findings clarify how damaged heart tissue maintains hidden electrical instability. They propose that this continuous activity explains why certain arrhythmias persist even when they are not immediately apparent on standard diagnostic monitors.