What is the clinical evidence from this study?

Study design: Other. Population: Cardiac hypertrophy. Intervention: Transfection of human ACE vector. Primary outcome: Thickness and areas of cardiac myocytes and collagen content (p=<0.01).

February 1, 2000Arteriosclerosis Thrombosis and Vascular Biology

In Vivo Evidence of the Importance of Cardiac Angiotensin-Converting Enzyme in the Pathogenesis of Cardiac Hypertrophy

Q: What are the key findings of this study?

Local overexpression of cardiac ACE via gene transfer in rat myocardium significantly increased cardiac myocyte thickness, area, and collagen content (P<0.01).

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

This research aims to evaluate the role of cardiac angiotensin-converting enzyme in the development of cardiac hypertrophy.

View Full Paper

Ask AI

Bookmark

Key result

Local overexpression of cardiac ACE via gene transfer in rat myocardium significantly increased cardiac myocyte thickness, area, and collagen content (P<0.01).

Why the study?

Does local overexpression of cardiac ACE cause cardiac hypertrophy independent of systemic factors in a rat model?

Population

Rat myocardium (in vivo model)

Design

Preclinical

Follow-up

2 weeks

Authors

JHJitsuo HigakiGeneral / Preventive / Lipids MAMotokuni AokiTokyo Medical and Dental University RMRyuichi MorishitaVascular / Pulmonary Vascular

Discussion

Member takes

Implication

Local ACE overexpression may drive rat myocyte hypertrophy independently; leaves open translation to human cardiac remodeling.

Key Points

This research aims to evaluate the role of cardiac angiotensin-converting enzyme in the development of cardiac hypertrophy.
Utilized in vivo gene transfer to overexpress cardiac ACE in rat myocardium.
Measured cardiac ACE activity and morphometric changes post-transfection.
Assessed the effects of ACE vector transfection on collagen content and hypertrophy.
Transfection increased cardiac ACE activity significantly (P<0.01).
Morphometry showed increased thickness and areas of cardiac myocytes (P<0.01).
Collagen content increased significantly (P<0.01), but effects were reversible with perindopril.

Structured PICO

Does local overexpression of cardiac ACE cause cardiac hypertrophy independent of systemic factors in a rat model?

Population

Rats undergoing in vivo gene transfer of human ACE vector to the myocardium to assess the effects of increased cardiac angiotensin.

Intervention

Transfection of the human ACE vector into rat myocardium to obtain local overexpression of cardiac ACE

Outcome

Cardiac hypertrophy (thickness and areas of cardiac myocytes) and collagen contentsurrogate

Main Result

p-value: p=<0.01

Local overexpression of cardiac ACE directly causes cardiac hypertrophy independent of systemic blood pressure or circulating renin-angiotensin system effects.

Cite This Study

Higaki et al. (2000) studied Cardiac hypertrophy. Transfection of human ACE vector was evaluated on Thickness and areas of cardiac myocytes and collagen content (p=<0.01). Local overexpression of cardiac ACE via gene transfer in rat myocardium significantly increased cardiac myocyte thickness, area, and collagen content (P<0.01).

synapsesocial.com/papers/6a20bf956aba112f1d337996 https://doi.org/10.1161/01.atv.20.2.428

View Full Paper

Ask AI

Bookmark

In Vivo Evidence of the Importance of Cardiac Angiotensin-Converting Enzyme in the Pathogenesis of Cardiac Hypertrophy

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

In Vivo Evidence of the Importance of Cardiac Angiotensin-Converting Enzyme in the Pathogenesis of Cardiac Hypertrophy

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Also Consider

Also Consider