Jérémie Joffre1, Olivier Varenne2, Wulfran Bougouin1, Julien Rosencher2, Jean-Paul Mira3, Alain Cariou4. 1. Medical Intensive Care Unit, Cochin Hospital, Hôpitaux Universitaires Paris Centre, Assistance Publique des Hôpitaux de Paris, 27 rue du Faubourg Saint-Jacques, 75014 Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Faculté de médecine, 15 rue de l'Ecole de Médecine, 75006 Paris, France; INSERM U970, Paris Cardiovascular Research Center (PARCC), European Georges Pompidou Hospital, 56 rue Leblanc, 75015 Paris, France. 2. Cardiology Department, Cochin Hospital, Hôpitaux Universitaires Paris Centre, Assistance Publique des Hôpitaux de Paris, 27 rue du Faubourg Saint-Jacques, 75014 Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Faculté de médecine, 15 rue de l'Ecole de Médecine, 75006 Paris, France. 3. Medical Intensive Care Unit, Cochin Hospital, Hôpitaux Universitaires Paris Centre, Assistance Publique des Hôpitaux de Paris, 27 rue du Faubourg Saint-Jacques, 75014 Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Faculté de médecine, 15 rue de l'Ecole de Médecine, 75006 Paris, France. 4. Medical Intensive Care Unit, Cochin Hospital, Hôpitaux Universitaires Paris Centre, Assistance Publique des Hôpitaux de Paris, 27 rue du Faubourg Saint-Jacques, 75014 Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Faculté de médecine, 15 rue de l'Ecole de Médecine, 75006 Paris, France; INSERM U970, Paris Cardiovascular Research Center (PARCC), European Georges Pompidou Hospital, 56 rue Leblanc, 75015 Paris, France. Electronic address: alain.cariou@cch.aphp.fr.
Abstract
BACKGROUND: The leading cause of sudden cardiac death is myocardial ischemia. As for uncomplicated acute myocardial infarction (AMI), international guidelines plead for early coronary angiography with, in case of culprit lesion, angioplasty and stent implantation. However after cardiac arrest (CA), shock, hypothermia and changes in antiplatelet pharmacokinetic may promote stent thrombosis (ST). Incidence of ST in this situation has never been studied. OBJECTIVE: The aim of this study was to investigate incidence and determinants of ST after ischemic CA successfully revascularized. METHODS: We analyzed 208 consecutive patients admitted in our institution for AMI and who underwent PCI with stent implantation. Among these patients, 55 presented a resuscitated CA and were compared to 153 without CA (control group). All patients in the CA group received hypothermia (33 °C for 24 h) following resuscitation and PCI. RESULTS: There was no difference between the 2 groups for age, gender, cardiovascular risk factors, coronary lesions and type of stent. In the CA group, patients were less frequently pre-treated with heparin (50.9% vs 98.7%, p<0.001) and aspirin (52.7% vs 99%, p<0.001). In the CA group, we observed a significantly higher incidence of confirmed acute or subacute ST than in the control group: 10.9% vs 2.0% (p=0.01). None of CA patients had received a dual antiplatelets therapy (0% vs 99%). LVEF at admission was lower in the CA group (40.3% vs 48%; p<0.001), and shock was more frequent (83.6% vs 8.5%; p<0.001). Survival at 28 days was 50.1% in CA group vs 98.0% (p<0.001). In multivariate analysis, CA before stenting appears to be an independent risk factor for confirmed ST (OR=12.9; 95%CI 1.3-124.6; p=0.027). CONCLUSION: In CA patients treated with cooling, stenting for AMI is associated with a high risk of ST. Shock, insufficient antithrombotic treatment, pharmacokinetic changes related to hypothermia may contribute to this higher risk. A strategy aiming to reduce this complication may probably improve prognosis of patients who underwent coronary sudden death.
BACKGROUND: The leading cause of sudden cardiac death is myocardial ischemia. As for uncomplicated acute myocardial infarction (AMI), international guidelines plead for early coronary angiography with, in case of culprit lesion, angioplasty and stent implantation. However after cardiac arrest (CA), shock, hypothermia and changes in antiplatelet pharmacokinetic may promote stent thrombosis (ST). Incidence of ST in this situation has never been studied. OBJECTIVE: The aim of this study was to investigate incidence and determinants of ST after ischemic CA successfully revascularized. METHODS: We analyzed 208 consecutive patients admitted in our institution for AMI and who underwent PCI with stent implantation. Among these patients, 55 presented a resuscitated CA and were compared to 153 without CA (control group). All patients in the CA group received hypothermia (33 °C for 24 h) following resuscitation and PCI. RESULTS: There was no difference between the 2 groups for age, gender, cardiovascular risk factors, coronary lesions and type of stent. In the CA group, patients were less frequently pre-treated with heparin (50.9% vs 98.7%, p<0.001) and aspirin (52.7% vs 99%, p<0.001). In the CA group, we observed a significantly higher incidence of confirmed acute or subacute ST than in the control group: 10.9% vs 2.0% (p=0.01). None of CA patients had received a dual antiplatelets therapy (0% vs 99%). LVEF at admission was lower in the CA group (40.3% vs 48%; p<0.001), and shock was more frequent (83.6% vs 8.5%; p<0.001). Survival at 28 days was 50.1% in CA group vs 98.0% (p<0.001). In multivariate analysis, CA before stenting appears to be an independent risk factor for confirmed ST (OR=12.9; 95%CI 1.3-124.6; p=0.027). CONCLUSION: In CA patients treated with cooling, stenting for AMI is associated with a high risk of ST. Shock, insufficient antithrombotic treatment, pharmacokinetic changes related to hypothermia may contribute to this higher risk. A strategy aiming to reduce this complication may probably improve prognosis of patients who underwent coronary sudden death.
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