Graham Nichol (Department of Medicine, University of Washington-Harborview Center for Prehospital Emergency Care, Seattle, USA) and others—with Gregg W Stone (Columbia University Medical Center, The Cardiovascular Research Foundation, New York, USA) as the lead investigator—report in Circulation: Cardiovascular Interventions that peritoneal lavage is a feasible method of inducing rapid cooling (ie. hypothermia) in patients with ST-segment elevation myocardial infarction (STEMI), but add that it does not reduce infarct size and is associated with a significantly increased rate of adverse events. Furthermore, it is associated with a trend towards an increased rate of stent thrombosis.
The authors note that inducing mild hypothermia in STEMI patients prior to percutaneous coronary intervention (PCI) is associated with reduced infarct size, but add that current techniques (eg. endovascular catheter-based cooling) of inducing hypothermia are not quick enough—ie. the time taken to achieve the adequate temperature (≤35 degrees) may cause an excessive delay in the door-to-balloon time. They state: “A small observational study reported that peritoneal hypothermia in patients with STEMI and cardiac arrest is feasible and results in rapid cooling. We, therefore, performed a multicentre, randomised trial to assess the feasibility, safety, and efficacy of peritoneal hypothermia to reduce infarct size in patients with acute STEMI.”
In the study, 54 STEMI patients were randomised to receive peritoneal hypothermia prior to primary PCI (28 initially but 27 after one patient was subsequently found to have aortic dissection rather than STEMI) or to primary PCI alone (26; control group). Nichol et al write that in the peritoneal hypothermia group, “hypothermia to
Hypothermia was initiated (after successful peritoneal access) in 96.3% of the patients in the peritoneal hypothermia group, with goal temperature (≤34.9 degrees) being achieved in 88.9% of patients at median time of 17 minutes after cooling onset. This led to a significant but moderate increase in door-to-balloon time: 62 minutes vs. 47 minutes for the control group (p=0.007).
While peritoneal hypothermia was found to be a feasible method for inducing rapid cooling, it was not associated with a significant reduction in infarct size compared with the control group (17.2% median infarct size vs. 16.1%, respectively; p=0.54). Furthermore, the rate of the primary safety endpoint (a composite of outcomes including death, reinfarction, ischaemia-driven target vessel revascularisation, and major bleeding) at 30 days was significantly higher in the peritoneal hypothermia group—21.4% vs. 0% for the control group (p=0.01).
Nichol et al also observed a trend towards an increased rate of stent thrombosis with peritoneal hypothermia (11% vs. 0%, respectively; p=0.09). They explain hypothermia increased platelet activation, which “directly contributes to thrombosis” and may also attenuate the efficacy of antiplatelet drugs. “Hypothermia may also induce cholesterol crystallisation, which could trigger plaque rupture. It is also possible that hypothermia may delay gastric absorption and reduce the bioavailability of oral antiplatelet agents,” the authors comment.
Concluding, Nichol et al state: “Adequately powered randomised trials (likely limited to patients with anterior myocardial infarction) are needed to assess the effect of rapidly induced hypothermia on myocardial salvage and clinical outcomes after primary PCI.” They add that future studies also need “carefully examine” the risk of stent thrombosis with hypothermia “although large prospective studies may be required to determine whether hypothermia is causally related to this event.”
