What is the clinical evidence from this study?

Study design: Other. Population: Failing heart (cardiomyopathy). Intervention: Losartan vs. Control. Primary outcome: Conduction velocity and interstitial fibrosis (p=<0.05).

What question did this study set out to answer?

To investigate the effects of chronic losartan administration on gap junction conductance, conduction velocity, and interstitial fibrosis in the failing heart.

December 1, 2006Journal of the Renin-Angiotensin-Aldosterone SystemOpen Access

Chronic blockade of angiotensin II AT1-receptors increased cell-to-cell communication, reduced fibrosis and improved impulse propagation in the failing heart

Q: What are the key findings of this study?

Chronic administration of losartan in cardiomyopathic hamsters enhanced conduction velocity (49 vs 38 cm/s, p<0.05) and reduced interstitial fibrosis (14% vs 22%, p<0.05).

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

To investigate the effects of chronic losartan administration on gap junction conductance, conduction velocity, and interstitial fibrosis in the failing heart.

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Key result

Chronic administration of losartan in cardiomyopathic hamsters enhanced conduction velocity (49 vs 38 cm/s, p<0.05) and reduced interstitial fibrosis (14% vs 22%, p<0.05).

Why the study?

Does chronic administration of losartan improve gap junction conductance, conduction velocity, and interstitial fibrosis in cardiomyopathic hamsters with failing hearts?

Population

4-month-old cardiomyopathic hamsters (TO-2) with failing hearts

Comparison

Losartan 25 mg/kg/day orally for two months vs Control (untreated cardiomyopathic hamsters)

Design

Preclinical

Follow-up

2 months

Authors

WMWalmor C. De MelloNational Institutes of Health

Discussion

Member takes

Implication

Hypothesis-generating in hamsters; leaves open whether losartan improves conduction or fibrosis in human heart failure.

Key Points

To investigate the effects of chronic losartan administration on gap junction conductance, conduction velocity, and interstitial fibrosis in the failing heart.
4-month-old cardiomyopathic hamsters (TO-2) were treated with losartan (25 mg/kg/day) for two months.
Gap junction conductance and conduction velocity were measured before and after treatment.
Interstitial fibrosis was assessed in the left ventricular wall.
Gap junction conductance increased, with 28 nS pairs significantly reduced in favor of 18-45 nS pairs.
Conduction velocity improved from 38 cm/s to 49 cm/s (p<0.05) after losartan administration.
Interstitial fibrosis area decreased from 22% to 14% (p<0.05) following treatment.

Structured PICO

Does chronic administration of losartan improve gap junction conductance, conduction velocity, and interstitial fibrosis in cardiomyopathic hamsters with failing hearts?

Population

4-month-old cardiomyopathic hamsters (TO-2) with failing hearts treated for two months.

Intervention

Losartan 25 mg/kg/day orally for two months

Comparator

Control (untreated cardiomyopathic hamsters)

Outcome

Gap junction conductance (gj), conduction velocity, and interstitial fibrosissurrogate

Main Result

Absolute Event Rate: 49% vs 38%

p-value: p=<0.05

Chronic AT1-receptor blockade with losartan improves electrical conduction and reduces fibrosis in a hamster model of heart failure.

Cite This Study

Walmor C. De Mello (2006) studied Failing heart (cardiomyopathy). Losartan vs. Control was evaluated on Conduction velocity and interstitial fibrosis (p=<0.05). Chronic administration of losartan in cardiomyopathic hamsters enhanced conduction velocity (49 vs 38 cm/s, p<0.05) and reduced interstitial fibrosis (14% vs 22%, p<0.05).

synapsesocial.com/papers/6a224dfb42d97c116a7fc7a5 https://doi.org/10.3317/jraas.2006.038

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Chronic blockade of angiotensin II AT1-receptors increased cell-to-cell communication, reduced fibrosis and improved impulse propagation in the failing heart

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Chronic blockade of angiotensin II AT1-receptors increased cell-to-cell communication, reduced fibrosis and improved impulse propagation in the failing heart

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Also Consider

Also Consider