Cardiac abnormalities are frequently reported in acute subarachnoid hemorrhage (SAH) patients. However, frank ST-elevation and myocardial dysfunction mimicking acute coronary syndrome is a rare occurrence. Systemic and local catecholamine release mediate myocardial injury and may explain raised troponin levels, concordant regional wall motion abnormalities and systolic dysfunction. These findings can pose a significant problem in the acute setting where “time-is-muscle” paradigm can rush clinicians towards a “rule – in” diagnosis of acute myocardial infarction. We present the case of a 60-year-old male who presented to a regional emergency department with loss of consciousness, chest pain and headache. His ECG showed ST-elevation in precordial leads with corresponding region wall motion abnormalities and dynamically elevated troponin levels which supported a diagnosis of acute myocardial infarction. Percutaneous coronary intervention was attempted but found no hemodynamically significant lesions and the patient was managed conservatively with antithrombotic treatment. Further work-up for his headache led to the diagnosis of aneurysmal SAH and subsequent endovascular coiling. The patient was discharged with a good clinical outcome. We discuss the potential catastrophic consequences of interpreting neurologic myocardial stunning as STEMI. Use of potent antithrombotic therapies, like bridging thrombolysis, in this setting can lead to dismal consequences. Clinical history should still be carefully obtained in the acute setting in this era of sensitive biomarkers.

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PubMed