What question did this study set out to answer?

To identify molecular mechanisms contributing to chronic regional contractile dysfunction in hibernating myocardium.

October 1, 1999AJP Heart and Circulatory Physiology

Regional alterations in SR Ca2+-ATPase, phospholamban, and HSP-70 expression in chronic hibernating myocardium

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Population

Pigs instrumented with a left anterior descending artery stenosis

Comparison

Left anterior descending artery stenosis for 3… vs Sham-operated pigs / normal myocardium

Design

Preclinical

Follow-up

3 months

Authors

JFJames A. FallavollitaCook County Health and Hospitals System SJSaji JacobRoyal College of Surgeons in Ireland RYRebeccah F. YoungBuffalo State University

Discussion

Member takes

Implication

May indicate early SR dysfunction in reversible ischemia; leaves open whether these changes precede human ischemic cardiomyopathy.

Key Points

To identify molecular mechanisms contributing to chronic regional contractile dysfunction in hibernating myocardium.
Swine models underwent surgical placement of a left anterior descending coronary artery stenosis for 3 months to induce chronic hibernating myocardium.
Regional perfusion, adenosine flow reserve, and anterior wall motion were evaluated using angiography alongside histological analysis to check for tissue necrosis.
Northern and Western blot analyses assessed regional mRNA and protein levels of sarcoplasmic reticulum calcium-handling proteins (SR Ca2+-ATPase, phospholamban, calsequestrin) and heat shock protein-70 (HSP-70).
Stenotic models showed severe anterior hypokinesis (P < 0.001 vs. shams), reduced subendocardial perfusion (0.73 ± 0.05 vs. 1.01 ± 0.06 ml·min⁻¹·g⁻¹; P < 0.001), and impaired adenosine flow (1.0 ± 0.17 vs. 3.84 ± 0.26 ml·min⁻¹·g⁻¹; P < 0.001) without histological necrosis.
Hibernating myocardium exhibited significant regional mRNA downregulation of phospholamban (0.76 ± 0.08 vs. 1.07 ± 0.06; P < 0.02) and SR Ca2+-ATPase (0.83 ± 0.06 vs. 1.02 ± 0.06; P < 0.05), whereas calsequestrin mRNA remained unchanged (1.08 ± 0.06 vs. 0.96 ± 0.05; P = NS).
Regional HSP-70 mRNA was markedly induced (2.4 ± 0.3 vs. 1.0 ± 0.11; P < 0.01), with corresponding protein alterations confirmed by Western blot analysis.

Structured PICO

Population

Pigs instrumented with a left anterior descending artery stenosis

Intervention

Left anterior descending artery stenosis for 3 months

Comparator

Sham-operated pigs / normal myocardium

Outcome

Expression of sarcoplasmic reticulum (SR) proteins (phospholamban, SR Ca2+-ATPase, calsequestrin) and Heat shock protein (HSP)-70 mRNA and proteinsurrogate

Hibernating myocardium exhibits a molecular phenotype similar to end-stage ischemic cardiomyopathy, suggesting that sarcoplasmic reticulum dysfunction from reversible ischemia may be an early defect in the progression of left ventricular dysfunction.

Cite This Study

Fallavollita et al. (1999) studied this question.

synapsesocial.com/papers/6a82b71c57df60cfb510bbc4 https://doi.org/10.1152/ajpheart.1999.277.4.h1418

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Regional alterations in SR Ca2+-ATPase, phospholamban, and HSP-70 expression in chronic hibernating myocardium

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Regional alterations in SR Ca2+-ATPase, phospholamban, and HSP-70 expression in chronic hibernating myocardium

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Also Consider