Key result
Patients with subarachnoid hemorrhage and stunned myocardium had significantly lower peak cardiac troponin values compared to historical MI controls (0.22 vs 2.8 ng/ml, p < 0.001).
Why the study?
Can peak cardiac troponin values and echocardiography differentiate reversible neurogenic left ventricular dysfunction from myocardial infarction in patients with subarachnoid hemorrhage?
Observational (n=10)
Can peak cardiac troponin values and echocardiography differentiate reversible neurogenic left ventricular dysfunction from myocardial infarction in patients with subarachnoid hemorrhage?
Absolute Event Rate: 0.22% vs 2.8%
p-value: p=< 0.001
Supports neurogenic stunned myocardium as distinct from ischemic injury; hypothesis-generating and should not yet change troponin interpretation.
OBJECT: Differentiating myocardial infarction (MI) from reversible neurogenic left ventricular dysfunction (stunned myocardium [SM]) associated with aneurysmal subarachnoid hemorrhage (SAH) is critical for early surgical intervention. The authors hypothesized that the cardiac troponin (cTn) trend and/or echocardiogram could be used to differentiate between the two entities. METHODS: A retrospective study was conducted for the period between 1995 and 2000. All patients included in the study met the following criteria: 1) no history of cardiac problems; 2) new onset of abnormal cardiac function (ejection fraction [EF] < 40% on echocardiograms); 3) serial cardiac markers (cTn and creatine kinase MB isoform [CK-MB]); 4) surgical intervention for their aneurysm; and 5) cardiac output monitoring either by repeated echocardiograms or invasive hemodynamic monitoring during the first 4 days post-SAH when the patients were euvolemic. Of the 350 patients with SAH, 10 (2.9%) had severe cardiac dysfunction. Of those 10, six were women and four were men. The patients' mean age was 53.5 years (range 29-75 years) and their SAH was classified as Hunt and Hess Grade III or IV. Aneurysm distribution was as follows: basilar artery tip (four); anterior communicating artery (two); middle cerebral artery (one); posterior communicating artery (two); and posterior inferior cerebellar artery (one). The mean EFonset was 33%. The changes on echocardiograms in these patients did not match the findings on electrocardiograms (EKGs). Within 4.5 days, dramatic improvement was seen in cardiac output (from 4.93 +/- 1.16 L/minute to 7.74 +/- 0.88 L/minute). Compared with historical controls in whom there were similar levels of left ventricular dysfunction after MI, there was no difference in peak CK-MB. A 10-fold difference, however, was noted in cTn values (0.22 +/- 0.25 ng/ml; control 2.8 ng/ml; p < 0.001). CONCLUSIONS: The authors determined the following: 1) that the CK-MB trend does not allow differentiation between SM and MI; 2) that echocardiograms revealing significant inconsistencies with EKGs are indicative of SM; and 3) that cTn values less than 2.8 ng/ml in patients with EFs less than 40% are consistent with SM.
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Bulsara et al. (2003) conducted an observational in Aneurysmal subarachnoid hemorrhage with severe cardiac dysfunction (n=10). Aneurysmal subarachnoid hemorrhage with stunned myocardium vs. Historical controls with myocardial infarction was evaluated on Peak cardiac troponin (cTn) values (p=< 0.001). Patients with subarachnoid hemorrhage and stunned myocardium had significantly lower peak cardiac troponin values compared to historical MI controls (0.22 vs 2.8 ng/ml, p < 0.001).
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