Although sudden cardiac death has been broadly studied, little is known on cerebrovascular events revealed by out-of-hospital cardiac arrest. We aimed to describe clinical features and prognosis of these patients and identify characteristics that could suggest a cerebrovascular etiology of the out-of-hospital cardiac arrest.
Retrospective review (1999–2012) of databases of three regional referral ICU centers for out-of-hospital cardiac arrest.
Patients admitted to ICU for management of successfully resuscitated out-of-hospital cardiac arrest.
Patients were included when subarachnoid hemorrhage, intracranial hemorrhage, ischemic stroke, sub/epidural hematoma, or cerebral thrombophlebitis was identified as the primary cause of out-of-hospital cardiac arrest. Traumatic or infectious causes were excluded. Patients were compared with a group of out-of-hospital cardiac arrest of nonneurological origin.
All medical records of the three prospective ICU databases, registered according to the Utstein style, were reviewed.
Among 3,710 patients admitted for out-of-hospital cardiac arrest, 86 were included (mainly subarachnoid hemorrhage, n = 73). Prodromes were mostly neurological but falsely evoked a cardiac origin in six patients. Electrocardiogram displayed abnormalities in 64% of patients, with 23% of pseudoischemic pattern (ST-segment elevation or left bundle branch block). Mortality rate was 100%, with brain death as the leading cause. In comparison with the nonneurological out-of-hospital cardiac arrest group, female gender, onset of neurological prodromes, lack of other prodromes, initial nonshockable rhythm, and unspecific electrocardiogram repolarization abnormalities were independent predictive factors of a primary cerebrovascular etiology. When present, the combination of these elements displayed an area under the receiver operating characteristic curve of 0.86 (95% CI, 0.81–0.91).
Presentation of cerebrovascular event complicated with out-of-hospital cardiac arrest may mimic coronary etiology, but several clinical elements may help to identify brain causes. Even if survival is null, the high proportion of brain deaths provides opportunity for organ donation.
1Medical Intensive Care Unit, Cochin Hospital, Hôpitaux Universitaires Paris Centre, Assistance Publique des Hôpitaux de Paris, Paris, France.
2Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, Paris, France.
3INSERM U955, Equipe 3, “Physiopathologie et Pharmacologie des Insuffisances Coronaires et Cardiaques,” Créteil, Paris, France.
4Medical and Toxicological Intensive Care Unit, Lariboisière Hospital, Université Paris Sorbonne Cité, Paris Diderot, Assistance Publique des Hôpitaux de Paris, Paris, France.
5Intensive Care Unit, Versailles Hospital Center, Le Chesnay, France.
6Emergency Department, Cochin Hospital, Hôpitaux Universitaires Paris Centre, Assistance Publique des Hôpitaux de Paris, Paris, France.
7INSERM U970, Paris Cardiovascular Research Centre (PARCC), European Georges Pompidou Hospital, Paris, France.
* See also p. 508.
Drs. Arnaout and Mongardon contributed equally to this work and considered as first authors.
Dr. Pène lectured for Merck Sharp and Dohme (MSD) and Laboratoire français du fractionnement et des biotechnologies (LFB). His institution received grant support from European Society of Intensive Care Medicine and Société de Réanimation de Lagnue Française. Dr. Chiche served as a board member for GE Healthcare and Nestlé, consulted for AstraZeneca and Orion Pharma, and lectured for GE Healthcare and Pfizer. Dr. Mira served as a board member for MSD, Astellas, and Gilead; consulted for LFB, Astellas, and Thermofischer; and lectured for Astellas. The remaining authors have disclosed that they do not have any potential conflicts of interest.
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