Why the study?
It remains unknown whether intravenous atorvastatin administered during ongoing myocardial infarction provides superior cardioprotection compared to oral preloading therapy.
Does intravenous atorvastatin during ongoing myocardial infarction improve cardioprotection compared to oral preloading therapy in a hypercholesterolaemic pig model?
Does intravenous atorvastatin during ongoing myocardial infarction improve cardioprotection compared to oral preloading therapy in a hypercholesterolaemic pig model?
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This preclinical study aims to determine if intravenous atorvastatin during ongoing myocardial infarction provides superior cardioprotection compared to oral preloading in a hypercholesterolaemic pig model.
Infarct size is associated with all-cause mortality and heart failure hospitalization underscoring the need for effective cardioprotection beyond timely reperfusion.1 Guidelines recommend administering high-potency statins early after ST-elevation myocardial infarction (STEMI) in order to reduce LDL-cholesterol levels as soon as possible.2 However, statins may provide clinical benefits in acute coronary syndrome patients beyond lipid-lowering effects. We have demonstrated in hypercholesterolaemic pigs through cardiac magnetic resonance (CMR) imaging and molecular/histological analyses that intravenous administration of a modified preparation of atorvastatin (i.v.-atorvastatin) during myocardial infarction (MI) limits ischaemia-related cardiac damage3,4 with a legacy effect that attenuates subsequent myocardial injury and preserves cardiac function during reinfarction.5 In addition, we have shown that this i.v.-atorvastatin approach exerts higher cardioprotective effects than those observed when atorvastatin is orally administered early after reperfusion.4 Furthermore, this new cardioprotective strategy is effective in the presence of comorbidities such as diabetic cardiomyopathy.6 However, it remains unknown whether i.v.-atorvastatin during ongoing MI provides superior cardioprotection compared to oral preloading therapy. Here we test this hypothesis in a highly translatable hypercholesterolaemic pig model using CMR.
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Otero et al. (2026) studied this question.
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