Table 2.
Novel interventional adjuncts to primary percutaneous coronary intervention with clinical potential
| Study | Patients | Mechanism of cardioprotection | Therapeutic strategy | Outcome measures |
|---|---|---|---|---|
| Therapeutic hypothermia | ||||
| Dixon et al. (2002)65 | 42 patients | Experimental data suggests that lowering myocardial temperature during ischaemia but not reperfusion can limit MI size by reducing metabolic demand | Cooling using the Radiant SetPoint Endovascular Temperature Management System to lower body core temperature to 34°C (mean temperature at reperfusion of 34.7±0.9°C) | Major adverse cardiac events occurred in (0% vs. 10% control, p>0.05) |
| Ant/Inf STEMI | Median MI size at 30 d by SPECT (2% vs. 8% control of LV, p>0.05) | |||
| <6 h | Endovascular cooling safe | |||
| All TIMI flow | ||||
| Collaterals included | ||||
| O’Neill et al. (2003)66 (COOL-MI) | 325 patients | Cooling using the Radiant SetPoint Endovascular Temperature Management System to lower body core temperature to 34°C (mean temperature at reperfusion of 34.7±0.9°C) | No difference in MI size at 30 d by SPECT (13.8% control vs. 14.1%, p>0.05) | |
| Ant/Inf STEMI | Longer door-PCI time in treated group (92±47 min vs. 110±41 min, p=0.0003) | |||
| <6 h | Ant MI patients in whom temperature lowered to 35°C MI size was significantly reduced | |||
| All TIMI flow | Plan to organize COOL-MI II trial | |||
| Collaterals included | ||||
| Grines et al. (2004)67 (ICE-IT-1) | 224 patients | Cooling using the Philips Innercool Celsius Control System to lower body core temperature | No difference in MI size at 30 d by SPECT (10.2% control vs. 13.2%, p=0.14) | |
| Ant/Inf STEMI | Only one-third of patients achieved 35°C by reperfusion | |||
| <6 h | Plan to organize ICE-IT-2 trial | |||
| All TIMI flow | ||||
| Collaterals included | ||||
| Dixon et al. (2007) (COOL-MI; IINCT00248196) | 225 patients | Cooling using the Radiant Reprieve Endovascular Temperature Therapy System to lower body core temperature for 30 min prior to PPCI | Primary endpoint has been MI size by SPECT | |
| Ant/Inf STEMI | Study aborted 2008 | |||
| <6 h | ||||
| All TIMI flow | ||||
| Collaterals included | ||||
| Gotberg et al. (2010)41 (RAPID-MI-ICE) | 20 patients | Cooling by infusion of cold saline endovascular cooling achieved 35°C without significant delay in door-PCI time | Cooling by IV infusion of 1–2 litres of cold saline and central venous catheter cooling with Philips InnerCool RTx Endovascular System prior to PPCI achieved core body temperature of 35°C without delaying door-PPCI time | Significant reduction in MI size as % of AAR on CMR at 4 d (29.8±12.6% vs. 48.0±21.6%, p=0.041) |
| Ant/Inf STEMI | Significant reduction (43%) in peak and cumulative tropinin T release | |||
| <6 h | Plan to organise CHILL-MI trial | |||
| All TIMI flow | ||||
| Collaterals included | ||||
| Erlinge et al. (CHILL-MI; NCT01379261) | 120 patients | Cooling by IV infusion of 1–2 litres of cold saline and central venous catheter cooling with Philips InnerCool RTx Endovascular System prior to PPCI and continued for 1 h after | Ongoing multicentre study will investigate whether cooling prior to PPCI reduces MI size (as a % of AAR) by CMR at 4 days | |
| Ant/Inf STEMI | Scheduled to complete recruitment by May 2012 | |||
| <6 h | ||||
| All TIMI flow | ||||
| Collaterals included | ||||
| Therapeutic hyperoxaemia | ||||
| Dixon et al. (2002)68 | 29 patients | Experimental data suggests that hyperbaric oxygen reduces MI size by decreasing tissue oedema, reducing formation of lipid peroxide radicals, altering NOS expression and inhibition of leukocyte adherence, and plugging in the microcirculation | IC hyperbaric hyperoxaemic reperfusion started after PPCI and continued for 60–90 min | No adverse events |
| Ant/Inf STEMI | Improved WMSI at 24 h | |||
| <24 h | Trend to increased LVEF | |||
| All TIMI flow | Therapeutic hyperoxaemia safe | |||
| Collaterals included | Plan for AMIHOT trial | |||
| O’Neill et al. (2007)69 (AMIHOT I) | 269 patients | IC hyperbaric hyperoxaemic reperfusion started after PPCI and continued for 90 min | No difference in primary endpoints (14 d MI size | |
| Ant/Inf STEMI | No difference in 30 d major adverse cardiac events (5.2% vs. 6.7%, p=0.62) | |||
| <24 h | Ant STEMI patients <6 h had greater improvement in WMSI, smaller MI size and improved STR | |||
| All TIMI flow | Plan for AMIHOT-II trial | |||
| Collaterals included | ||||
| Stone et al. (2009)70 (AMIHOT II) | 281 patients | IC hyperbaric hyperoxaemic reperfusion started after PPCI and continued for 90 min | No adverse events | |
| Ant STEMI | No difference in MI size by SPECT at 14 d or peak CK-MB or tropinin | |||
| <6 h | No difference LVEF | |||
| All TIMI flow | Pooled analysis of AMIHOT I and II trials suggested beneficial effects on MI size and major adverse cardiovascular events | |||
| Collaterals included | ||||
AAR, area at risk; CMR, cardiac MRI; LV, left ventricular; MI: myocardial infarct; PPCI: primary percutaneous coronary intervention; SPECT, single photon emission CT; STEMI: ST-segment elevation MI; STR: ST-segment resolution; TIMI, thrombolysis in myocardial infarction; WMSI, wall motion score index.