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Acute Myocardial Infarction in Rats
Published on: February 16, 2011
Stress Induced Cardiomyopathy Triggered by Acute Myocardial Infarction: A Case Series Challenging the Mayo Clinic
Georgios Christodoulidis1, Vishwa Kundoor2, Edo Kaluski1
1Department of Cardiology, The Guthrie Clinic/Robert Packer Hospital, Sayre, PA, USA.
Insights
Acute myocardial infarction can trigger stress induced cardiomyopathy, a novel finding in cardiac research. This condition presents with extensive, reversible heart muscle dysfunction beyond the infarct zone.
Area of Science:
- Cardiology
- Internal Medicine
Background:
- Stress induced cardiomyopathy (SIC) is typically triggered by emotional or physical stressors.
- Acute myocardial infarction (AMI) has not been previously recognized as a trigger for SIC.
Observation:
- Four patients presented with AMI, exhibiting echocardiographic wall motion abnormalities extending beyond the infarct artery's distribution.
- Patients had a mean age of 59, with three women and two with prior psychiatric history.
- ECG showed ST elevation in anterior leads (3/4), prolonged QTc (4/4), and moderately elevated troponin levels.
Findings:
- All patients had a single culprit lesion in the left anterior descending artery.
- Initial echocardiography showed reduced ejection fraction with basal segment sparing.
- Repeat echocardiography demonstrated significant improvement in left ventricular function.
Implications:
- This case series is the first to report AMI as a trigger for SIC.
- Extensive reversible wall motion abnormalities, modest troponin elevation, and QTc prolongation suggest superimposed SIC.
- Recognizing SIC in AMI patients is crucial for accurate diagnosis and management.
Abstract:
BACKGROUND Various physical and emotional factors have been previously described as triggers for stress induced cardiomyopathy. However, acute myocardial infarction as a trigger has never been reported. CASE REPORT We describe four patients who presented with an acute myocardial infarction, in whom the initial echocardiography revealed wall motion abnormalities extending beyond the coronary distribution of the infarct artery. Of the four patients identified, the mean age was 59 years; three patients were women and two patients had underlying psychiatric history. Electrocardiogram revealed ST elevation in the anterior leads in three patients; QTc was prolonged in all cases. All patients had ≤ moderately elevated troponin. Single culprit lesion was found uniformly in the proximal or mid left anterior descending artery. Initial echocardiography revealed severely reduced ejection fraction with relative sparing of the basal segments, whereas early repeat echocardiography revealed significant improvement in the left ventricular function in all patients. CONCLUSIONS This is the first case series demonstrating that acute myocardial infarction can trigger stress induced cardiomyopathy. Extensive reversible wall motion abnormalities, beyond the ones expected from angiography, accompanied by modest elevation in troponin and marked QTc prolongation, suggest superimposed stress induced cardiomyopathy.
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