Mechanism and extent of myocardial injury associated with out-of-hospital cardiac arrest.

We investigated the mechanism and extent of myocardial injury associated with out-of-hospital cardiac arrest (OHCA). 159 consecutive patients undergoing immediate coronary angiography after OHCA were included and divided into groups with acute culprit lesion (A), stable obstructive coronary disease (B) and non-obstructive or absent coronary disease (C). Post-resuscitation electrocardiogram (ECG) and serial measurements of high sensitivity cardiac troponin I (cTnI) were compared. ST-elevation myocardial infarction (STEMI) was documented in 65% in group A, 26% in group B, and 11% in group C (p < 0.001). cTnI, which was 0.88 ng/mL, 0.44 ng/mL and 0.19 ng/mL in groups A, B and C on admission (p < 0.001), increased to a maximum of 63.96 ng/mL, 10.00 ng/mL and 2.35 ng/mL, respectively (p < 0.001). Within the group A, cTnI was significantly larger in patients with acute occlusion than in patients with spontaneous reperfusion at initial angiography. Within groups B and C, peak cTnI correlated with duration of resuscitation, number of defibrillations and cumulative adrenaline (epinephrine) dose. If admission cTnI exceeded 0.46 ng/mL and STEMI was present in ECG, sensitivity for detection of acute culprit lesion was 88% and specificity 54%. Significant myocardial injury associated with OHCA occurs in the presence of acute culprit lesion while extent of myocardial injury in stable or absent coronary disease is significantly smaller and correlates with the duration and intensity of cardiac resuscitation. Admission cTnI, although combined with post-resuscitation ECG, have insufficient accuracy to securely predict presence of acute culprit lesion.

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