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Even at very high levels, neither initial nor peak troponin predicted left ventricular dysfunction, ischemic etiology of cardiac arrest, or survival. Guidelines recommend early coronary angiography for survivors of cardiac arrest, but identifying the patients who may benefit most, or not at all, is challenging. Although troponin is frequently measured after cardiac arrest, the utility of an elevated troponin to identify patients with a likely cardiac cause of arrest is unknown. These researchers retrospectively reviewed records for 145 survivors of in-hospital or out-of-hospital cardiac arrest who underwent serial troponin measurements and transthoracic echocardiography at a single academic medical center. Cases were adjudicated by experts to determine cardiac etiology. None of four troponin cutoff levels analyzed — ranging from 1 to 1000 times the upper limit of normal — had adequate sensitivity or specificity for identifying patients with an ischemic etiology of cardiac arrest, left ventricular dysfunction, or survival to hospital discharge. |
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Recently, studies have shown that immediate (versus routine) percutaneous coronary intervention does not improve survival in patients without ST-segment elevation on postresuscitation electrocardiography (NEJM JW Cardiol May 2019 and N Engl J Med 2019; 380:1397) and that troponin elevations are common in hospitalized patients even when coronary ischemia is not suspected (NEJM JW Emerg Med May 2019 and BMJ 2019; 364:729). A high troponin level does not equal a cardiac cause of cardiac arrest, and we must not let any ancillary study lead to anchoring, premature closure, or other cognitive biases when assessing our most critically ill patients.