Nine percent of cardiac arrest survivors with myoclonus after cardiac arrest had good functional outcomes, usually in patients without associated epileptiform activity and after prolonged hospitalization. Deaths occurred early and primarily after withdrawal of life support. It is uncertain whether prolonged care would yield a higher percentage of good outcomes, but myoclonus of itself should not be considered a sign of futility.
The CREST model stratified patients immediately after resuscitation according to risk of a circulatory-etiology death. The tool may allow for estimation of circulatory risk and improve the triage of survivors of cardiac arrest without ST-segment-elevation myocardial infarction at the point of care.
The Arctic Sun Temperature Management System was an effective means of performing therapeutic hypothermia after cardiac arrest. Infrequent skin injuries were associated with vasopressor use and low ejection fraction.
Background
Patients resuscitated from cardiac arrest (
CA
) have highly variable neurological, circulatory, and systemic ischemia‐reperfusion injuries. After the initial hypoxic‐ischemic insult, a cascade of immune and inflammatory responses develops and is often fatal. The role of the immune response in pathophysiological characteristics and recovery is not well understood. We studied immune cell activity and its association with outcomes in a cohort of CA survivors.
Methods and Results
After informed consent, we collected blood samples at intervals over a week after resuscitation from
CA
. We examined the expression of
CD
39 and
CD
73 (alias 5′‐nucleotidase), production of tumor necrosis factor‐α, generation of reactive oxygen species, and secretion of vascular endothelial growth factor by circulating myeloid and lymphoid cells, in comparison to cells obtained from control subjects before coronary artery bypass grafting surgery. The number of circulating total and
CD
73‐expressing lymphocytes correlated with survival after
CA
. Incubation of immune cells, obtained from post‐
CA
subjects, with
AMP
, a substrate for
CD
73, resulted in inhibition of tumor necrosis factor‐α production and generation of reactive oxygen species. This effect was blocked by adenosine 5′‐(α, β‐methylene) diphosphate, a specific inhibitor of
CD
73 and
ZM
241385, an A2 adenosine receptor antagonist. We also found that
AMP
‐dependent activation of
CD
73 induces production of vascular endothelial growth factor.
Conclusions
CD
73‐expressing lymphocytes mediate cellular protection from inflammation after
CA
through inhibition of proinflammatory activation of myeloid cells and promotion of vascular endothelial growth factor secretion. The contribution of
CD
73 lymphocytes in the regulation of acute inflammation and tissue injury after
CA
warrants further study.
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