September 16, 2013PLoS ONEOpen Access

Iron Deposition following Chronic Myocardial Infarction as a Substrate for Cardiac Electrical Anomalies: Initial Findings in a Canine Model

Q: What is the clinical evidence from this study?

Study design: Other. Population: Chronic Myocardial Infarction (n=22). Intervention: Chronic myocardial iron deposition (>1.5% volume) vs. Minimal/no iron deposition (<1.5% volume). Primary outcome: 24-hour QTc interval (ms) (p=<0.001).

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Key result

In a canine model of chronic myocardial infarction, myocardial iron deposition greater than 1.5% was associated with significantly prolonged 24-hour QTc intervals compared to minimal iron deposition.

Why the study?

Does iron deposition within chronic myocardial infarction lead to electrical anomalies in a canine model?

Population

22 mongrel dogs subjected to myocardial infarction by permanently ligating the left anterior descending…

Comparison

Myocardial regions with iron deposition… vs Myocardial regions without iron deposition or…

Design

Preclinical, An operator blinded to the MR details of the infarct…

Follow-up

16 weeks

Authors

ICIvan CokicCedars-Sinai Medical Center AKAvinash KaliAstana Medical University XWXunzhang WangCedars-Sinai Medical Center

Discussion

Member takes

Implication

Should not yet inform post-MI care; hypothesis-generating for iron deposition as arrhythmogenic substrate.

Structured PICO

Does iron deposition within chronic myocardial infarction lead to electrical anomalies in a canine model?

Population

22 mongrel dogs (20-25 kg) subjected to myocardial infarction by permanently ligating the left anterior descending (LAD) artery, studied at 16 weeks post-MI. Divided into ex-vivo (n=12) and in-vivo (n=10) groups.

Intervention

Myocardial regions with iron deposition (IRON+) following chronic myocardial infarction

Comparator

Myocardial regions without iron deposition (IRON-) or remote non-infarcted myocardium

Outcome

Electrical permittivity and conductivity (ex-vivo), ECG parameters including QT, QTc, and QTcd, and spatial locations of isolated late potentials (ILPs) (in-vivo)surrogate

Main Result

Absolute Event Rate: 312% vs 298.9%

p-value: p=<0.001

Iron deposition within infarcted zones alters electrical behavior and may serve as an arrhythmogenic substrate post-myocardial infarction.

Limitations

Measurements of electrical permittivity and conductivity were made from ex-vivo sections, which only account for extracellular characteristics
Did not explore mechanistic insight into how iron deposition mediates electrical anomalies
Surface ECG recordings were limited to a 24-hour period
Small sample size limited statistical significance for some metrics
Findings in the canine model remain to be investigated in humans following myocardial infarction

Cite This Study

Cokic et al. (2013) studied Chronic Myocardial Infarction (n=22). Chronic myocardial iron deposition (>1.5% volume) vs. Minimal/no iron deposition (<1.5% volume) was evaluated on 24-hour QTc interval (ms) (p=<0.001). In a canine model of chronic myocardial infarction, myocardial iron deposition greater than 1.5% was associated with significantly prolonged 24-hour QTc intervals compared to minimal iron deposition.

synapsesocial.com/papers/6a0ec2ef218372ada647b495 https://doi.org/10.1371/journal.pone.0073193

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Iron Deposition following Chronic Myocardial Infarction as a Substrate for Cardiac Electrical Anomalies: Initial Findings in a Canine Model

Discussion

Member takes

Implication

Structured PICO

Main Result

Limitations

Cite This Study

Iron Deposition following Chronic Myocardial Infarction as a Substrate for Cardiac Electrical Anomalies: Initial Findings in a Canine Model

Discussion

Member takes

Implication

Structured PICO

Main Result

Limitations

Cite This Study

Also Consider

Also Consider