Understanding How Cardiac Arrest Complicates the Analysis of Clinical Trials of Cardiogenic Shock

Cardiogenic shock (CS) and cardiac arrest (CA) are among the most lethal manifestations of acute cardiovascular disease, with in-hospital mortality rates exceeding 30% to 40% despite contemporary supportive care.[1][2][3][4] CS and CA are highly prevalent conditions that cause a substantial number of cardiovascular deaths.5 Although CA and CS frequently occur together due to shared underlying myocardial substrates, their pathophysiological etiologies (ie, electrical instability versus pump failure) and sequelae (ie, anoxic encephalopathy versus multisystem organ failure) often differ.1,3,[6][7][8] The potential for CA to cause anoxic brain injury (ABI), which is unlikely to improve with cardiovascular therapies, suggests that patients with concomitant CA and CS should be analyzed separately from patients with CS without CA in clinical trials. EPIDEMIOLOGY AND OUTCOMES OF CARDIOGENIC SHOCK AND CARDIAC ARRESTCS may complicate up to 5% to 10% of the estimated 800 000 acute myocardial infarctions (AMIs) that occur yearly in the United States, plus a substantial number of non-AMI patients.1,5 More than 350 000 people suffer out-of-hospital CA in the United States each year, plus 200 000 yearly in-hospital CA events.5 Approximately half of patients with CS from AMI experience a CA, whereas two-thirds of patients with CA have shock requiring vasopressors.[1][2][3][4]6 Patients with both CA and CS are a uniquely high-risk group, with a mortality risk that substantially exceeds that of patients with CS alone.6,9 Among 4511 patients with ST-segment-elevation AMI, patients with either CS or CA accounted for >75% of hospital deaths, and the subgroup with concomitant CS and CA (4% of the population) accounted for one-third of all hospital deaths.9 Hospital mortality risk among patients with CS can be predicted using the Society for Cardiovascular Angiography and Intervention CS classification, and the presence of CA substantially increases the risk of death at any level of shock severity.6 CA has not been consistently associated with an increased risk of subsequent mortality in patients who survive hospitalization, whereas CS confers a persistent mortality hazard after hospital discharge.1 The simple dichotomization based on the presence or absence of CA alone used in prior studies belies the spectrum of acuity, differences in end-organ complications, pathophysiologic responses, and unique risk factors for mortality among CA patients. CAUSES OF DEATH IN CARDIOGENIC SHOCK AND CARDIAC ARRESTThe causes and predictors of death differ between CS and CA: ABI is the primary cause of death in patients with CA, whereas CS patients typically die via refractory shock, organ failure, and arrhythmias.[1][2][3]7,8 Although physiological param-

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