Hypothermia Does Not Increase Stent Thrombosis Risk in Primary PCI Patients

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In patients who experience out-of-hospital cardiac arrest before primary percutaneous coronary intervention (PCI), therapeutic hypothermia does not increase the risk of stent thrombosis, according to a research letter published online October 16, 2013, ahead of print in the Journal of the American College of Cardiology. Some research suggests that such cooling, administered to improve neurological outcomes, activates platelets and reduces clopidogrel metabolism. 

Investigators led by Sandra O. Rosillo, MD, of Hospital Universitario La Paz (Madrid, Spain), reviewed data from 1,334 STEMI patients who underwent primary PCI with stenting at their institution between January 2008 and December 2012. Of this cohort, 75 patients who had been in a comatose state after cardiac arrest received therapeutic hypothermia prior to the procedure.

No Difference in Stent Thrombosis

The overall rate of stent thrombosis was 2.3% (n = 32). Thirty events (17 acute and 13 subacute) occurred in the primary PCI-only group, while only 2 events (1 definite acute and 1 probable subacute) were observed in the hypothermia group, yielding equivalent rates within each arm (0.02%). Rates of major bleeding, according to GRACE criteria, were higher in the hypothermia group (8.0% vs. 1.3%; P < 0.001).

At 30 days, all-cause mortality was higher in the hypothermia group (44.0% vs. 4.9%; P < 0.001). Of the 33 hypothermia patients who died, 31 had a reliably-documented cause of death. Eleven who presented with cardiogenic shock and did not improve despite successful revascularization died due to multiple organ failure, while 17 died due to withdrawal of life-sustaining treatment secondary to severe post-anoxic encephalopathy. Only 2 deaths were classified as due to stent thrombosis.

The authors reference prior research suggesting that stent thrombosis risk is increased in hypothermia patients due to multiple organ failure and reduced metabolism of drugs that inhibit ADP P2Y12 receptors and thromboxane A2 synthesis. In fact, stent thrombosis was observed in 31.2% of ACS patients who received therapeutic hypothermia after suffering cardiac arrest, two-thirds of whom subsequently underwent stenting, in a small clinical series (Penela D, et al. J Am Coll Cardiol. 2013;61:686-687).

Any Prothrombotic Effect of Hypothermia ‘Not Clinically Relevant’

But in the current study, even in the setting of more hemodynamic support and a higher frequency of hemorrhagic complications in the hypothermia-treated patients, the incidence of stent thrombosis was similar to that of patients who did not undergo hypothermia, the investigators point out. Thus, the proposed prothrombotic effects of therapeutic hypothermia “are not clinically relevant in patients treated according to general recommendations,” they say.

In an e-mail communication with TCTMD, Michael R. Mooney, MD, of the Minneapolis Heart Institute Foundation (Minneapolis, MN), wrote, “The authors’ viewpoint is supported by our data on over 200 PCI patients treated with hypothermia for out-of-hospital cardiac arrest.”

Dr. Rosillo and colleagues conclude, “We believe that adequate antithrombotic management could be achieved in [the therapeutic hypothermia] population with both the progressive introduction of third-generation P2Y12 inhibitors and consideration that the route (intravenous aspirin and crushed nasogastric P2Y12) and time (prior to [primary] PCI) of administration may influence the final result.”

All patients in the study received a P2Y12 inhibitor. Clopidogrel (600 mg loading dose) was more commonly used in the primary PCI-only group (77.1% vs. 54.7%; P < 0.0001), while prasugrel, though less often prescribed overall, was preferred in the hypothermia group (49.3% vs. 28.1%; P = 0.0002). In addition, the vast majority of patients received aspirin. Glycoprotein IIb/IIIa inhibitors were more commonly used in the primary PCI-only group.

Study Details

Among patients who received hypothermia, cooling was initiated as soon as possible before PCI with IV cold saline followed by use of an automated cooling device. The target temperature (32-34 degrees) was selected by the treating physician and maintained for 24 hours. Afterward, a controlled rewarming was set to reach 37 degrees in 12 to 24 hours.

A mean 2 ± 1.2 stents were implanted in both groups.

 


Source:
Rosillo SO, Lopez-de-Sa E, Iniesta AM, et al. Is therapeutic hypothermia a risk factor for stent thrombosis? J Am Coll Cardiol. 2013;Epub ahead of print.

 

 

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Hypothermia Does Not Increase Stent Thrombosis Risk in Primary PCI Patients

In patients who experience out-of-hospital cardiac arrest before primary percutaneous coronary intervention (PCI), therapeutic hypothermia does not increase the risk of stent thrombosis, according to a research letter published online
Disclosures
  • Drs. Rosillo and Mooney report no relevant conflicts of interest.

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