What question did this study set out to answer?

To determine whether chronic inhibition of the Na+/H+ exchanger isoform 1 with cariporide attenuates cardiac hypertrophy and preserves left ventricular function under pressure overload.

February 1, 2004British Journal of PharmacologyOpen Access

Na⁺/H⁺ exchange inhibition attenuates left ventricular remodeling and preserves systolic function in pressure‐overloaded hearts

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Why the study?

Does cariporide attenuate left ventricular remodeling and preserve systolic function in mice with pressure-overloaded hearts?

Population

Male CD-1 mice with cardiac pressure overload induced by thoracic aortic banding

Comparison

Cariporide supplemented in diet at 6000 p.p.m… vs Control diet in banded mice, and sham-operated…

Design

Preclinical, Mice were randomized to receive either a control diet or an…

Follow-up

5 weeks

Authors

GMGiuseppe MaranoUniversità Cattolica del Sacro Cuore AVAlessandro VergariAgostino Gemelli University Polyclinic LCLiviana CatalanoNational Institute of Health

Discussion

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Implication

Hypothesis-generating for NHE-1 inhibition in pressure-overload remodeling; requires validation before clinical consideration.

Key Points

To determine whether chronic inhibition of the Na+/H+ exchanger isoform 1 with cariporide attenuates cardiac hypertrophy and preserves left ventricular function under pressure overload.
Male CD-1 mice were randomized to receive a standard diet or a diet containing 6,000 p.p.m. cariporide before undergoing thoracic aortic banding to induce chronic pressure overload.
Left ventricular geometry and systolic/diastolic performance were evaluated via echocardiography and cardiac catheterization at 2 and 5 weeks post-surgery, followed by histological analysis.
At 2 weeks, vehicle-banded mice exhibited an approximate 50% increase in normalized left ventricular weight, whereas cariporide treatment markedly attenuated hypertrophy while preserving contractility.
At 5 weeks, vehicle-banded mice showed chamber enlargement and dysfunction (+16% left ventricular end-diastolic diameter, -36% contractility, -26% fractional shortening), whereas cariporide maintained normal chamber size and systolic function.
Histological assessment revealed cariporide prevented cardiomyocyte hypertrophy but did not alter the extent of pressure overload-induced myocardial fibrosis.

Structured PICO

Does cariporide attenuate left ventricular remodeling and preserve systolic function in mice with pressure-overloaded hearts?

Population

Male CD-1 mice with cardiac pressure overload induced by thoracic aortic banding

Intervention

Cariporide (selective NHE-1 inhibitor) supplemented in diet at 6000 p.p.m. for 2 and 5 weeks

Comparator

Control diet (vehicle) in banded mice, and sham-operated mice

Outcome

Left ventricular (LV) dimension, systolic and diastolic function, and LV mass/hypertrophy assessed by echocardiography, cardiac catheterization, and histologysurrogate

NHE-1 inhibition with cariporide attenuates cardiomyocyte hypertrophy and prevents the deterioration of left ventricular performance induced by pressure overload in a mouse model.

Cite This Study

Marano et al. (2004) studied this question.

synapsesocial.com/papers/6a833726f2457b8164eff403 https://doi.org/10.1038/sj.bjp.0705631

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Na⁺/H⁺ exchange inhibition attenuates left ventricular remodeling and preserves systolic function in pressure‐overloaded hearts

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Na⁺/H⁺ exchange inhibition attenuates left ventricular remodeling and preserves systolic function in pressure‐overloaded hearts

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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