What is the clinical evidence from this study?

Study design: Other. Population: Myocardial infarction. Intervention: Lentivirus-mediated overexpression of Ang-(1-7) vs. Control (MI without intervention). Primary outcome: Cardiac function (fractional shortening, dP/dt, left ventricular end-diastolic pressure, ventricular hypertrophy).

What question did this study set out to answer?

The study aims to evaluate whether lentivirus-mediated overexpression of angiotensin-(1-7) can protect the myocardium from ischaemic injury and improve cardiac function post-myocardial infarction.

June 18, 2011Experimental Physiology

Lentivirus-mediated overexpression of angiotensin-(1-7) attenuated ischaemia-induced cardiac pathophysiology

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Key result

Lentivirus-mediated cardiac overexpression of Ang-(1-7) prevented MI-induced impairments in cardiac function and attenuated left ventricular remodelling in rats.

Population

5-day-old male Sprague-Dawley rats subjected to myocardial infarction by left anterior descending coronary…

Comparison

Single bolus of 3.5 × 10^8 transducing units of… vs Rats with induced myocardial infarction without…

Design

Preclinical

Follow-up

4 weeks post-MI

Authors

YQYanfei QiThe University of Sydney VSVinayak ShenoyPenn State Milton S. Hershey Medical Center FWFong WongUF Health Shands Hospital

Discussion

Member takes

Implication

Hypothesis-generating for Ang-(1-7) overexpression post-MI in rats; human translation requires prospective trials.

Key Points

The study aims to evaluate whether lentivirus-mediated overexpression of angiotensin-(1-7) can protect the myocardium from ischaemic injury and improve cardiac function post-myocardial infarction.
Lentivirus carrying Ang-(1-7) injected into the left ventricle of neonatal rats.
Myocardial infarction induced by ligation of the left anterior descending coronary artery at 6 weeks of age.
Cardiac function assessed using echocardiography and haemodynamic parameters four weeks post-MI.
Post-MI, fractional shortening and dP/dt decreased significantly, while left ventricular end-diastolic pressure increased.
Overexpression of Ang-(1-7) prevented myocardial wall thinning and improved ACE2 and BKR2 gene expression.
In vitro results showed Ang-(1-7) reduced hypoxia-induced cell death and lowered inflammatory cytokine levels.

Structured PICO

Population

Male Sprague-Dawley rats subjected to myocardial infarction at 6 weeks of age, following lentivirus-mediated overexpression of Ang-(1-7) at 5 days of age.

Intervention

Single bolus of 3.5 × 10^8 transducing units of lenti-Ang-(1-7) injected into the left ventricle

Comparator

Rats with induced myocardial infarction without lenti-Ang-(1-7) treatment

Outcome

Cardiac function (fractional shortening, dP/dt, left ventricular end-diastolic pressure) and ventricular hypertrophy assessed 4 weeks post-MIsurrogate

Lentivirus-mediated overexpression of Ang-(1-7) attenuates left ventricular remodeling and improves cardiac function post-myocardial infarction in a rat model.

Cite This Study

Qi et al. (2011) studied Myocardial infarction. Lentivirus-mediated overexpression of Ang-(1-7) vs. Control (MI without intervention) was evaluated on Cardiac function (fractional shortening, dP/dt, left ventricular end-diastolic pressure, ventricular hypertrophy). Lentivirus-mediated cardiac overexpression of Ang-(1-7) prevented MI-induced impairments in cardiac function and attenuated left ventricular remodelling in rats.

synapsesocial.com/papers/6a2017dea05ff06c2ba1a3f2 https://doi.org/10.1113/expphysiol.2011.056994

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Lentivirus-mediated overexpression of angiotensin-(1-7) attenuated ischaemia-induced cardiac pathophysiology

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Lentivirus-mediated overexpression of angiotensin-(1-7) attenuated ischaemia-induced cardiac pathophysiology

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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