What question did this study set out to answer?

To assess mitochondrial respiratory capacity under normoxic and hypoxic conditions, measure reactive oxygen species generation, and evaluate antioxidant expression in chronically ischemic human myocardium.

March 30, 2013AJP Heart and Circulatory Physiology

Impaired mitochondrial function in chronically ischemic human heart

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Why the study?

Does chronic ischemia impair mitochondrial function and increase ROS production in human myocardium?

Population

9 human subjects with chronic ischemic heart disease

Comparison

Biopsies from ischemic regions of the left… vs Biopsies from nonischemic regions of the left…

Design

Cross-sectional

Authors

NSNis StrideGentofte Hospital SLSteen LarsenUniversity of Copenhagen MHMartin Hey‐MogensenUniversity of Copenhagen

Discussion

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Implication

Associated with mitochondrial impairment in ischemic human myocardium; hypothesis-generating for ROS-targeted therapies.

Key Points

To assess mitochondrial respiratory capacity under normoxic and hypoxic conditions, measure reactive oxygen species generation, and evaluate antioxidant expression in chronically ischemic human myocardium.
Obtained paired left ventricular myocardial biopsies from ischemic and nonischemic regions within the same heart in 9 human subjects (N=9).
Assessed maximal oxidative phosphorylation capacity, respiratory control ratio during hyperoxia and ex vivo hypoxia, reactive oxygen species (ROS) production, and antioxidant protein levels.
Maximal oxidative phosphorylation capacity in fresh muscle fibers was significantly lower in ischemic compared with nonischemic myocardium (P < 0.05), whereas the respiratory control ratio did not differ significantly (P > 0.05).
Ex vivo hypoxia revealed no protective chronic ischemic preconditioning effect in ischemic myocardial regions (P > 0.05).
ROS production was significantly increased in ischemic myocardium (P < 0.05), accompanied by reduced levels of antioxidant protein expression.

Structured PICO

Does chronic ischemia impair mitochondrial function and increase ROS production in human myocardium?

Population

9 human subjects with chronic ischemic heart disease

Intervention

Biopsies from ischemic regions of the left ventricle

Comparator

Biopsies from nonischemic regions of the left ventricle of the same heart

Outcome

Mitochondrial respiratory capacity during hyperoxia and hypoxia, ROS production, and myocardial antioxidant levelssurrogate

Chronic ischemia in human hearts is associated with diminished mitochondrial respiration capacity and excessive ROS production, with no evidence of chronic ischemic preconditioning.

Cite This Study

Stride et al. (2013) studied this question.

synapsesocial.com/papers/6a908f2fc7b7d4543f89f985 https://doi.org/10.1152/ajpheart.00991.2012

Topics

Women and heart disease

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Impaired mitochondrial function in chronically ischemic human heart

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Impaired mitochondrial function in chronically ischemic human heart

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Topics

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