Clinical study | Therapeutic intervention | Number | Outcome | Potential mechanisms underlying cardioprotection |
---|---|---|---|---|
Kitakaze et al61 J-WIND | 72 h intravenous carperitide (atrial natriuretic peptide analogue) infusion started prior to PPCI | 569 | 15% reduction in 72 h AUC total CK 2.0% absolute increase in LVEF | Atrial natriuretic peptide targets prosurvival kinase pathways such as the cGMP and RISK pathways |
Piot et al62 | Intravenous ciclosporin-A (2.5 mg/kg) bolus 10 min prior to PPCI | 58 | 44% reduction in MI size (72 h AUC total CK) 20% reduction in MI size (CMR subset) 28% reduction in MI size and smaller LVESV on CMR at 6 months88 | Ciclosporin-A inhibits the opening of the mitochondrial permeability transition pore, a critical determinant of lethal myocardial reperfusion injury |
Lonborg et al63 | Intravenous infusion of exenatide started 15 min prior to PPCI and continued for 6 h | 107 | Increase in myocardial salvage index (0.62 to 0.71) 23% reduction in MI size at 3 months on CMR Patients presenting with short ischaemic times (≤132 min) had greater myocardial salvage89 | Exenatide, a GLP-1 analogue, targets prosurvival kinase pathways such as the RISK pathway |
Ibanez et al64 | Intravenous metoprolol (3×5 mg) in ambulance prior to PPCI | 270 | Reduction in MI size by CMR at 1 week. Increased LVEF at 6 months Improvement in clinical outcome at 2 years Reduced: incidence of severely depressed LVEF (<35%) at 6 months by 60%; less need for ICD by 65% at 6 months and reduced HF at 2 years90 | The mechanism of cardioprotection is not currently clear |
AUC, area under curve; cGMP, cyclic guanosine monophosphate; CK, creatine kinase; CMR, cardiovascular MRI; GLP-1, glucagon-like peptide-1; ICD, implantable cardioverter defibrillator; HF, heart failure; LVESV, LV end-systolic volume; MI, myocardial infarct; PPCI, primary percutaneous intervention; RISK, reperfusion injury salvage kinase; STEMI, ST segment elevation myocardial infarction.