Stress cardiomyopathy misinterpreted as ST-segment elevation myocardial infarction in a patient with aneurysmal
Iulian Enache1, Răzvan Alexandru Radu1,2, Elena Oana Terecoasă1,2
1Department of Neurology, University Emergency Hospital Bucharest.
Insights
Acute subarachnoid hemorrhage (SAH) can cause cardiac issues mimicking heart attacks. Differentiating neurologic myocardial stunning from acute myocardial infarction is crucial to avoid harmful treatments.
Area of Science:
- Cardiology
- Neurology
- Emergency Medicine
Background:
- Cardiac abnormalities are common in subarachnoid hemorrhage (SAH) patients.
- Myocardial dysfunction mimicking acute coronary syndrome is a rare but critical presentation.
Observation:
- A 60-year-old male presented with symptoms suggestive of acute myocardial infarction (MI), including ST-elevation on ECG, wall motion abnormalities, and elevated troponin levels.
- Initial cardiac workup and intervention for suspected MI were inconclusive, revealing no significant coronary lesions.
Findings:
- The patient was diagnosed with aneurysmal SAH, with cardiac findings attributed to neurologic myocardial stunning.
- Elevated troponin and ECG changes in SAH can be caused by catecholamine release, not necessarily acute coronary syndrome.
Implications:
- Misinterpreting neurologic myocardial stunning as STEMI can lead to inappropriate and potentially dangerous treatments, such as potent antithrombotics.
- Careful clinical evaluation and consideration of SAH are essential in patients presenting with cardiac symptoms and neurological signs.
- This case highlights the importance of integrating clinical history with biomarker data in acute settings.
Abstract:
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 arrived at 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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