JACC Letter: Hypothermia Therapy May Increase Stent Thrombosis Risk


A group of Spanish clinicians reports a “disturbingly high number” of stent thrombosis cases in patients with acute coronary syndromes (ACS) who had been treated with hypothermia therapy for cardiac arrest, according to a research letter published online December 19, 2012, ahead of print in the Journal of the American College of Cardiology.

Diego Penela, MD, of the University of Barcelona (Barcelona, Spain), and colleagues looked at 28 comatose patients (mean age 55 ± 18 years) admitted to their hospital for out-of-hospital cardiac arrest and treated with hypothermia therapy between January 2010 and March 2012. Although not widely used in the United States, hypothermia therapy is strongly recommended by the European Resuscitation Council in such patients. Randomized trials have shown the clinical applicability of this therapy in comatose patients who were survivors of an out-of-hospital cardiac arrest secondary to shockable rhythms.

Stent Thrombosis Much Higher Than in Primary PCI Population

Angiography was performed in 65% of patients (n = 18), most of whom had a final diagnosis of ACS (66% STEMI). Of these, 11 underwent PCI, receiving a total of 16 stents (13 BMS, 3 DES). The mean door-to-balloon time was 78 ± 39 min.

Five cases of definite stent thrombosis (31.2%) occurred during follow up. Of these, 4 were in cases where BMS were used and all 5 were STEMI patients. In all cases, stent thrombosis led to MI. The mean time from primary PCI to thrombotic event was 174 ± 146 hours (range, 8-376 hours). During the same time period, the same hospital performed 2,737 PCIs with a 0.44% (0.7% in the 42% of patients undergoing primary PCI) rate of definite stent thrombosis.

The findings are of concern, the researchers write, since they add to accumulating evidence of an association between hypothermia therapy and stent thrombosis, including a recent study showing a stent thrombosis rate of 14.8% in 27 patients treated with hypothermia therapy and PCI (Ibrahim K. Eur Heart J. 2011;32[suppl 1]:252). The vasodilator stimulated phosphoprotein index was higher in patients treated with hypothermia therapy than those in a control group. “There are recent experimental data that correlate [hypothermia therapy] with an increase in platelet activation, with platelet adenosine diphosphate receptor P2Y12 playing a central role,” Dr. Penela and colleagues write.

Dual Antiplatelet Therapy May Be ‘Inefficient’

All patients in the current study received dual antiplatelet therapy that included aspirin (100 mg/day), clopidogrel (75 mg/day) plus intravenous heparin, and glycoprotein IIb/IIIa inhibitors if a large thrombus was seen in the catheterization laboratory.

“Because platelet adenosine diphosphate receptor P2Y12 is a pivotal target for antiplatelet treatment in ACS, particularly in patients with an implanted stent, we hypothesize that the dual antiplatelet therapy used may be inefficient in hypothermic conditions,” the researchers write. “Moreover, metabolic conversion of clopidogrel in the liver may be reduced in hypothermia conditions.” They also point out that patients with hypothermia therapy are mechanically ventilated and require nasogastric tubes for dual antiplatelet therapy and may need correction for cardiovascular instability.

“Under these conditions, absorption of antiplatelet drugs may be reduced, and prothrombotic status resulting from a critical state after cardiac arrest cannot be ruled out,” they conclude.

Hypothermia therapy was started in the emergency department by the administration of 4-degree Celsius saline, 30 ml/kg (maximum: 2 l) infused over 30 minutes. Infusion was stopped if body temperature was less than 33.5 degrees Celsius (91.4 degrees Fahrenheit). Hypothermia therapy continued via an extracorporeal system (Medivance Arctic Sun System, Louisville, CO) to control temperature. The goal was to reduce the core temperature to 33 degrees Celsius within 8 hours and maintain that level for 24 hours, gradually rewarming patients from 24 to 30 hours until core temperature returned to normal.

 


Source:
Penela D, Magaldi M, Fontanals J, et al. Hypothermia in Acute Coronary Syndrome: Brain Salvage Versus Stent Thrombosis? J Am Coll Cardiol. 2013;Epub ahead of print.

 

 

Related Stories:

Disclosures
  • The research letter contains no information regarding conflicts of interest.

Comments