What is the clinical evidence from this study?

Population: Congestive heart failure post-myocardial infarction. Intervention: FK506, isoproterenol, and metoprolol vs. Sham and MI without CHF. Primary outcome: Root mean square of sarcomere length (RMSSL) fluctuations and RyRS2808 phosphorylation (p=<0.05).

What does this research mean for the field?

Acute phosphorylation of the cardiac ryanodine receptor at serine-2808 (RyRS2808) alone does not cause spontaneous contractile waves due to RyR2 destabilization in failing rat hearts. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To evaluate the role of ryanodine receptor phosphorylation at serine-2808 in driving spontaneous diastolic sarcomere length fluctuations and impaired contractility in heart failure.

August 23, 2005Cardiovascular Research

Spontaneous diastolic contractions and phosphorylation of the cardiac ryanodine receptor at serine-2808 in congestive heart failure in rat

Q: What are the key findings of this study?

Acute RyRS2808 phosphorylation by itself does not cause spontaneous contractile waves owing to RyR2 destabilization in failing rat hearts.

Q: What does this research mean for the field?

Acute phosphorylation of the cardiac ryanodine receptor at serine-2808 (RyRS2808) alone does not cause spontaneous contractile waves due to RyR2 destabilization in failing rat hearts. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To evaluate the role of ryanodine receptor phosphorylation at serine-2808 in driving spontaneous diastolic sarcomere length fluctuations and impaired contractility in heart failure.

View Full Paper

Ask AI

Bookmark

Key result

Acute RyRS2808 phosphorylation by itself does not cause spontaneous contractile waves owing to RyR2 destabilization in failing rat hearts.

Population

Male Lewis Brown-Norway rats 3 months after myocardial infarction

Comparison

FK506, isoproterenol, and chronic metoprolol… vs Sham, MI without CHF, and untreated MI with CHF

Design

Preclinical

Follow-up

3 months

Authors

MOMasakazu ObayashiKyushu University BXBo XiaoQueen's University Belfast BSBruno D. StuyversMemorial University of Newfoundland

Discussion

Member takes

Implication

Questions RyRS2808 phosphorylation as sole driver of waves in failing hearts; leaves open multifactorial RyR2 mechanisms for further study.

Key Points

To evaluate the role of ryanodine receptor phosphorylation at serine-2808 in driving spontaneous diastolic sarcomere length fluctuations and impaired contractility in heart failure.
Studied five groups of male Lewis Brown-Norway rats 3 months post-myocardial infarction: sham, MI with congestive heart failure, MI without heart failure, and metoprolol-treated MI (with and without heart failure).
Measured root mean square of sarcomere length fluctuations (RMSSL) and twitch force in right ventricular trabeculae following electrical stimulation and exposure to FK506 or isoproterenol.
RyRS2808 phosphorylation increased significantly in the left ventricle (approximately 58%, P<0.05) but not in the right ventricle (not significant) in rats with post-MI congestive heart failure.
Isoproterenol stimulation modestly increased RMSSL in nonfailing trabeculae alongside an approximate 60% increase in right ventricular RyRS2808 phosphorylation (P<0.05), but induced fluctuations in failing trabeculae without increasing phosphorylation.
Chronic metoprolol beta-blockade reduced stimulation-induced RMSSL, while right ventricular RyRS2808 phosphorylation levels remained indistinguishable from untreated failing hearts.

Structured PICO

Population

Male Lewis Brown-Norway rats 3 months after myocardial infarction (MI) (groups: Sham, MI with CHF, MI without CHF, metoprolol-treated MI with and without CHF)

Intervention

FK506, isoproterenol, and chronic metoprolol treatment

Comparator

Sham, MI without CHF, and untreated MI with CHF

Outcome

Twitch force (Ftw), root mean square of sarcomere length (RMSSL) fluctuations in right ventricular trabeculae, and RyRS2808 phosphorylationsurrogate

Main Result

p-value: p=<0.05

Spontaneous contractile waves in congestive heart failure are not caused by RyRS2808 phosphorylation alone, suggesting other factors affect RyR function.

Cite This Study

Obayashi et al. (2005) studied Congestive heart failure post-myocardial infarction. FK506, isoproterenol, and metoprolol vs. Sham and MI without CHF was evaluated on Root mean square of sarcomere length (RMSSL) fluctuations and RyRS2808 phosphorylation (p=<0.05). Acute RyRS2808 phosphorylation by itself does not cause spontaneous contractile waves owing to RyR2 destabilization in failing rat hearts.

synapsesocial.com/papers/6a14f5f69ff8b2b0e129e01b https://doi.org/10.1016/j.cardiores.2005.07.010

Topics

Heart failure HFrEF treatment Echocardiography

View Full Paper

Ask AI

Bookmark

Implication

Questions RyRS2808 phosphorylation as sole driver of waves in failing hearts; leaves open multifactorial RyR2 mechanisms for further study.