Why the study?
Does chronic aspirin therapy prevent cardiac hypertrophy and oxidative stress in cardiomyopathic hamsters?
Does chronic aspirin therapy prevent cardiac hypertrophy and oxidative stress in cardiomyopathic hamsters?
Chronic aspirin therapy prevents oxidative stress and slows the development of cardiac hypertrophy and fibrosis in a hamster model of cardiomyopathy.
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Hypothesis-generating for aspirin in cardiomyopathy; should not yet change clinical practice pending human trials.
OBJECTIVE: To evaluate the capacity of chronic ASA therapy to prevent cardiac alterations and increased oxidative stress in cardiomyopathic hamsters. METHODS AND RESULTS: Male Syrian cardiomyopathic and age-matched inbred control hamsters received ASA orally from the age of 60 days. Animals were sacrificed at the age of 150, 250, and 350 days to evaluate the time course of cardiac hypertrophy and cardiovascular tissue superoxide anion (O(2)(-)) production. At the age of 150 days, the ventricular weight over body weight ratio, resting heart rate, and cardiovascular O(2)(-) production were much higher in cardiomyopathic hamsters than those in control. At the age of 250 days, in addition to the continual deterioration of these parameters with age, the blood pressure started to fall and the signs of heart failure appeared. In these cardiomyopathic hamsters, chronic ASA treatment (a) completely prevented elevated O(2)(-) production and the NAD(P)H oxidase activity, (b) significantly slowed down the development of the cardiac hypertrophy and fibrosis. CONCLUSIONS: Chronic ASA treatment significantly prevents the deterioration of cardiac function and structure as well as the increased oxidative stress in the cardiomyopathic hamster. Our findings suggest that ASA presents a therapeutic potential to prevent cardiac dysfunction.
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Wu et al. (2012) studied this question.
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