Simvastatin‐sodium delays cell death of anoxic cardiomyocytes by inhibition of the Na+/Ca2+ exchanger
Why the study?
Does simvastatin-sodium delay cell necrosis in cultured neonatal cardiomyocytes under anoxic conditions?
Population
Cultured neonatal cardiomyocytes subjected to anoxic conditions
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Should not change ischemic heart disease management; leaves open translation of simvastatin's anti-necrotic effects from neonatal cardiomyocytes.
Structured PICO
Does simvastatin-sodium delay cell necrosis in cultured neonatal cardiomyocytes under anoxic conditions?
P
Population
Cultured neonatal cardiomyocytes subjected to anoxic conditions
I
Intervention
Simvastatin-sodium (20 and 50 microM)
O
Outcome
Cell necrosis and intracellular Ca2+ concentration ([Ca2+]i)surrogate
Simvastatin-sodium demonstrates a cardioprotective effect against anoxia-induced necrosis in cardiomyocytes, likely mediated by the inhibition of the sarcolemmal Na+/Ca2+ exchanger rather than its cholesterol-lowering properties.
Cite This Study
Bastiaanse et al. (1994) studied this question.