Combination Therapy to Target Reperfusion Injury After ST-Segment–Elevation Myocardial Infarction
A More Effective Approach to Cardioprotection
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Article, see p 894
Timely reperfusion therapy by primary percutaneous coronary intervention (PPCI) combined with effective secondary preventive therapy has contributed to a decline in mortality rates after ST-segment–elevation myocardial infarction (STEMI) over the last few years. However, the incidence and severity of heart failure after STEMI are rising. Therefore, novel cardioprotective therapies are required to reduce myocardial infarct (MI) size and preserve left ventricular (LV) systolic function to prevent heart failure and improve clinical outcomes after PPCI.1,2
Over recent years, a large number of cardioprotective therapies, which have been demonstrated to be effective at reducing MI size in the laboratory setting, have been unable either to reduce MI size or to improve clinical outcomes after STEMI. The reasons for this are manifold and have been discussed extensively in the recent literature.1–3 In summary, the failure to translate cardioprotection for patient benefit has been attributed to several key factors: the inadequacy of the animal models used for testing novel cardioprotective therapies in the laboratory setting, a failure to demonstrate consistent and robust cardioprotection in experimental studies before proceeding to clinical studies, and poorly designed clinical cardioprotection studies.1–3
Another major reason for the failure to translate cardioprotection may have been the adoption of a single-targeted monotherapy approach, a strategy that may be inadequate to address the multifaceted components of myocardial reperfusion injury, including endothelial dysfunction, microvascular obstruction, oxidative stress, calcium overload, mitochondrial dysfunction, and inflammation.2,4 To address this issue, an emerging concept in the cardioprotection field has been to adopt …