What question did this study set out to answer?

To evaluate the alterations in Hsp60 levels and mitochondrial function within viable left ventricular myocardium following myocardial infarction, and to determine the cardioprotective effects of long-term trandolapril treatment.

January 1, 2007Biological and Pharmaceutical BulletinOpen Access

Changes in Hsp60 Level of the Failing Heart Following Acute Myocardial Infarction and the Effect of Long-Term Treatment with Trandolapril

Q: What is the clinical evidence from this study?

Study design: Other. Population: Myocardial infarction and chronic heart failure. Intervention: Trandolapril vs. Vehicle (0.25% carboxymethylcellulose sodium). Primary outcome: Left ventricular end-diastolic pressure (LVEDP) at 8 weeks (mmHg) (p=<0.05).

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Key result

Long-term treatment with trandolapril in rats with myocardial infarction significantly attenuated the increase in myocardial Hsp60 content, improved hemodynamics including LVEDP, and preserved mitochondrial function.

Why the study?

Does trandolapril attenuate the increase in Hsp60 and improve mitochondrial function in a rat model of post-myocardial infarction heart failure?

Population

Male Wistar rats weighing 210-240 g with myocardial infarction induced by left coronary artery ligation and…

Comparison

Trandolapril 3 mg/kg/d orally from the 2nd to… vs Vehicle or sham operation.

Design

Preclinical

Follow-up

8 weeks

Authors

WTWakako TogaNovartis (Switzerland)KTKouichi TanonakaHeart Failure / Cardiomyopathy STSatoshi TakeoSapporo Medical University

Discussion

Member takes

Implication

Identifies Hsp60 and mitochondrial pathways as potential post-MI targets; hypothesis-generating in rats and leaves open human translation.

Key Points

To evaluate the alterations in Hsp60 levels and mitochondrial function within viable left ventricular myocardium following myocardial infarction, and to determine the cardioprotective effects of long-term trandolapril treatment.
Induced myocardial infarction in rats via left coronary artery ligation (CAL), alongside sham-operated controls.
Administered oral trandolapril (3 mg/kg/day) or vehicle to CAL and sham rats from week 2 through week 8 post-surgery.
Evaluated hemodynamics, ventricular weights, Hsp60 expression, mitochondrial oxygen consumption rates, and thiobarbituric acid reactive substances in surviving left ventricular muscle at 8 weeks.
At 8 weeks, untreated CAL rats developed chronic heart failure characterized by elevated Hsp60 content, reduced mitochondrial oxygen consumption rates, and increased lipid peroxidation in the viable left ventricle.
Increased myocardial Hsp60 content correlated significantly with depressed mitochondrial respiration and elevated left ventricular end-diastolic pressure.
Trandolapril therapy from weeks 2 to 8 improved hemodynamic profiles, attenuated Hsp60 overexpression, restored mitochondrial oxygen consumption, and suppressed mitochondrial oxidative stress.

Structured PICO

Does trandolapril attenuate the increase in Hsp60 and improve mitochondrial function in a rat model of post-myocardial infarction heart failure?

Population

Male Wistar rats with induced myocardial infarction and chronic heart failure, treated with trandolapril or vehicle for 6 weeks.

Intervention

Trandolapril 3 mg/kg/d orally (suspended in 0.25% carboxymethylcellulose sodium) from the 2nd to 8th week after surgery.

Comparator

Vehicle (0.25% carboxymethylcellulose sodium) or sham operation.

Outcome

Changes in Hsp60 content, mitochondrial oxygen consumption rate (OCR), mitochondrial thiobarbiturate-reacting substance (TRS) of the viable left ventricular muscle, and hemodynamic parameters at 8 weeks.surrogate

Main Result

Absolute Event Rate: 16.9% vs 32.9%

p-value: p=<0.05

Trandolapril attenuates the increase in Hsp60 and improves mitochondrial function in failing hearts after myocardial infarction, suggesting these mechanisms contribute to its beneficial effects in chronic heart failure.

Limitations

The exact function of Hsp60 in failing hearts remains unclear
Cannot determine whether the increase in Hsp60 is beneficial for cardioprotection or not due to lack of evidence
Cannot determine whether the increase in Hsp60 is beneficial for cardioprotection or detrimental in the development of chronic heart failure.

Cite This Study

Toga et al. (2007) studied Myocardial infarction and chronic heart failure. Trandolapril vs. Vehicle (0.25% carboxymethylcellulose sodium) was evaluated on Left ventricular end-diastolic pressure (LVEDP) at 8 weeks (mmHg) (p=<0.05). Long-term treatment with trandolapril in rats with myocardial infarction significantly attenuated the increase in myocardial Hsp60 content, improved hemodynamics including LVEDP, and preserved mitochondrial function.

synapsesocial.com/papers/6a946387a0ae96a16adf34fe https://doi.org/10.1248/bpb.30.105

Topics

Heart failure HFrEF treatment

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Implication

Identifies Hsp60 and mitochondrial pathways as potential post-MI targets; hypothesis-generating in rats and leaves open human translation.

Changes in Hsp60 Level of the Failing Heart Following Acute Myocardial Infarction and the Effect of Long-Term Treatment with Trandolapril

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Limitations

Cite This Study

Topics

Changes in Hsp60 Level of the Failing Heart Following Acute Myocardial Infarction and the Effect of Long-Term Treatment with Trandolapril

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Limitations

Cite This Study

Also Consider

Topics

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