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February 18, 2012AJP Heart and Circulatory PhysiologyOpen Access

Sympathetic stimulation increases dispersion of repolarization in humans with myocardial infarction

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Key result

Direct sympathetic stimulation with isoproterenol and reflex stimulation with nitroprusside significantly increased regional differences and dispersion of repolarization in patients with postinfarct cardiomyopathy compared to structurally normal hearts.

Why the study?

Does sympathetic stimulation (direct and reflex) increase regional dispersion of repolarization in patients with postinfarct cardiomyopathy compared to structurally normal hearts?

Population

10 patients total: 5 with postinfarct cardiomyopathy and recurrent ventricular arrhythmias referred for…

Comparison

Direct sympathetic stimulation with… vs Baseline measurements and patients with…

Design

Other

Authors

MVMarmar VaseghiElectrophysiologyRLRobert L. LuxRonald Reagan UCLA Medical Center
Aman Mahajan
Aman MahajanUniversity of Southern California

Discussion

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Member takes

Overview

Suggests heightened arrhythmic vulnerability during sympathetic stress post-MI; leaves open whether modulation alters clinical events.

Structured PICO

Does sympathetic stimulation (direct and reflex) increase regional dispersion of repolarization in patients with postinfarct cardiomyopathy compared to structurally normal hearts?

P
Population
10 patients, including 5 with postinfarct cardiomyopathy and 5 with structurally normal hearts, undergoing electrophysiological study to assess the effects of sympathetic stimulation on ventricular repolarization.
I
Intervention
Direct sympathetic stimulation with isoproterenol infusion (to increase heart rate by ≥20 beats/min) and reflex sympathetic stimulation with nitroprusside infusion (to decrease systolic blood pressure by ≥20 mmHg).
C
Comparator
Baseline measurements (intra-patient control) and patients with structurally normal hearts (inter-patient control).
O
Outcome
Activation recovery interval (ARI) and ARI dispersion (a surrogate for action potential duration) measured from unipolar intracardiac electrograms in normal, scar, and border zone regions.surrogate

Main Result

p-value: p=0.015

Direct and reflex sympathetic stimulation significantly increases regional repolarization heterogeneity in postinfarct cardiomyopathy, providing a mechanistic basis for ventricular arrhythmogenesis in these patients.

Limitations

  • Small number of patients enrolled in the study
  • Many patients with ischemic cardiomyopathy were on amiodarone and beta-blockers, which have sympatholytic effects
  • Repolarization measurements in scar can be difficult to obtain due to low T waves
  • Nitroprusside can reduce wall strain, potentially complicating the effect of the reflex sympathetic nervous system
  • Potential underestimation of responses due to heterogeneity of perfusion
  • Mapping was limited to electrodes feasible under the approved protocol
  • Heterogeneity in remodeling of adrenergic signaling pathways could not be controlled for

Cite This Study

Vaseghi et al. (2012) studied Postinfarct cardiomyopathy (n=10). Isoproterenol and nitroprusside infusion vs. Baseline (within-patient) and structurally normal hearts was evaluated on Change in activation recovery interval (ARI) and ARI dispersion (p=0.015). Direct sympathetic stimulation with isoproterenol and reflex stimulation with nitroprusside significantly increased regional differences and dispersion of repolarization in patients with postinfarct cardiomyopathy compared to structurally normal hearts.

synapsesocial.com/papers/6a79b35a14b028facf0def4dhttps://doi.org/10.1152/ajpheart.01106.2011
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Correlation between refractory periods and activation-recovery intervals from electrograms: effects of rate and adrenergic interventions.1985 · 251 citations
  2. 2Influences of anisotropic tissue structure on reentrant circuits in the epicardial border zone of subacute canine infarcts.1988 · 522 citations
  3. 3Correlation between in vivo transmembrane action potential durations and activation-recovery intervals from electrograms. Effects of interventions that alter repolarization time.1990 · 401 citations
  4. 4Prevention of Sudden Cardiac Death After a First Myocardial Infarction by Pharmacologic or Surgical Antiadrenergic Interventions1992 · 175 citations
  5. 5Failure of Beta-Adrenergic Receptor Blockade to Prevent Arrhythmias Induced by Sympathetic Nerve Stimulation1974 · 23 citations