Key result
In a mouse model, 12 weeks of doxorubicin treatment reduced fractional shortening (20.3% vs 32.4%, P=0.011) and increased myocardial 18F-CP18 uptake, indicating apoptosis.
Why the study?
Does 18F-CP18 imaging detect myocardial apoptosis in a mouse model of anthracycline-induced cardiotoxicity?
Population
Mouse model of anthracycline cardiotoxicity
Comparison
Doxorubicin 3 mg/kg/week for 12 weeks and… vs Vehicle (control)
Design
Preclinical
Follow-up
12 weeks
Authors
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Supports apoptosis imaging development for cardiotoxicity; leaves open clinical translation beyond this mouse model.
Does 18F-CP18 imaging detect myocardial apoptosis in a mouse model of anthracycline-induced cardiotoxicity?
Absolute Event Rate: 20.3% vs 32.4%
p-value: p=0.011
18F-CP18 imaging can detect anthracycline-induced myocardial apoptosis in a preclinical model, potentially offering a noninvasive method to monitor cardiotoxicity.
Su et al. (2015) studied Anthracycline-induced cardiotoxicity. Doxorubicin vs. Vehicle (control) was evaluated on Left ventricular fractional shortening at 12 weeks (p=0.011). In a mouse model, 12 weeks of doxorubicin treatment reduced fractional shortening (20.3% vs 32.4%, P=0.011) and increased myocardial 18F-CP18 uptake, indicating apoptosis.