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April 13, 2017Circulation ResearchOpen Access

Myeloperoxidase deficiency decreased vulnerability for ventricular tachycardia in mice; in 2,622 patients, baseline myeloperoxidase plasma levels were independently associated with a history of ventricular arrhythmias, sudden cardiac death, or ICD implantation.

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Why the study?

Does myeloperoxidase mediate postischemic arrhythmogenic ventricular remodeling and correlate with ventricular arrhythmias?

Population

Murine models of myocardial ischemia, isolated wild-type cardiomyocytes, induced pluripotent stem…

Comparison

Myeloperoxidase deficiency or intravenous… vs Wild-type mice; untreated cells; humans with…

Design

Preclinical

Authors

MMMartin MollenhauerKFKai FriedrichsMLMax Lange

Discussion

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Member takes

Overview

Identifies myeloperoxidase as a potential therapeutic target for secondary arrhythmia prevention; leaves open whether pharmacological inhibition.

Structured PICO

Does myeloperoxidase mediate postischemic arrhythmogenic ventricular remodeling and correlate with ventricular arrhythmias?

P
Population
Murine models of myocardial ischemia (wild-type, Mpo-/-, CD11b-/- mice), isolated wild-type cardiomyocytes, induced pluripotent stem cell-derived cardiomyocytes, and a human cohort of 2,622 stable patients with ejection fraction >35% undergoing elective diagnostic cardiac evaluation.
I
Intervention
Myeloperoxidase deficiency (Mpo-/-) or intravenous myeloperoxidase infusion in mice; myeloperoxidase/H2O2 incubation in cells; baseline myeloperoxidase plasma levels in humans.
C
Comparator
Wild-type mice; untreated cells; humans with varying myeloperoxidase levels.
O
Outcome
Vulnerability for ventricular tachycardia, electric conduction heterogeneity, Cx43 expression, and ventricular postischemic fibrosis in mice/cells; history of ventricular arrhythmias, sudden cardiac death, or implantable cardioverter-defibrillator implantation in humans.surrogate

Myeloperoxidase is a crucial mediator of postischemic myocardial remodeling and its levels are associated with ventricular arrhythmias, suggesting it as a potential pharmacological target for secondary prevention.

Cite This Study

Mollenhauer et al. (2017) studied this question.

synapsesocial.com/papers/6a7ff5cdcf96de1eb9c858b6https://doi.org/10.1161/circresaha.117.310870
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Also Consider

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

  1. 1Protective Effects of Therapeutic Neutrophil Depletion and Myeloperoxidase Inhibition on Left Ventricular Function and Remodeling in Myocardial Infarction2022 · 17 citations
  2. 2Myeloperoxidase induces arrhythmogenic structural and electrophysiological remodeling: implications for atrial fibrillation2026
  3. 3Myeloperoxidase and Plasminogen Activator Inhibitor 1 Play a Central Role in Ventricular Remodeling after Myocardial Infarction2003 · 253 citations
  4. 4Myeloperoxidase-Generated Oxidants Modulate Left Ventricular Remodeling but Not Infarct Size After Myocardial Infarction2005 · 179 citations
  5. 5Myeloperoxidase as a Promising Therapeutic Target after Myocardial Infarction2024 · 15 citations