Coronary Artery Anomaly in Takotsubo Cardiomyopathy: Cause or Innocent Bystander?
Insights
Coronary artery anomalies may not always explain takotsubo cardiomyopathy. This case highlights a patient with both conditions, where the anomaly was likely incidental, and symptoms resolved with medical therapy.
Area of Science:
- Cardiology
- Cardiovascular Medicine
- Medical Case Reports
Background:
- Coronary artery anomalies are known triggers for vasospasm and endothelial dysfunction, potentially leading to takotsubo cardiomyopathy.
- Takotsubo cardiomyopathy typically affects apical myocardial regions, not aligning with specific coronary artery territories.
Observation:
- A 74-year-old woman presented with acute respiratory failure and suspected myocardial infarction.
- The patient had a left coronary artery anomaly, dominant right coronary artery supply, takotsubo cardiomyopathy, and reduced left ventricular ejection fraction without atherosclerotic disease.
Findings:
- The anomalous left coronary artery, with dominant right coronary supply, did not appear to cause the observed apical wall-motion abnormalities.
- The patient's ejection fraction normalized after six weeks of medical treatment, and she remained asymptomatic one year later.
Implications:
- This case suggests that coronary artery anomalies may coexist with takotsubo cardiomyopathy without being the primary cause.
- It underscores the importance of considering other etiologies for takotsubo cardiomyopathy, even in the presence of coronary anomalies.
- This is the first reported instance of coexisting takotsubo cardiomyopathy and anomalous coronary artery presenting with acute dyspnea.
Abstract:
Coronary artery anomalies can provoke intermittent vasospasm and endothelial dysfunction, which can cause takotsubo cardiomyopathy. However, in takotsubo cardiomyopathy, apical myocardial regions are typically affected, and these do not correlate with a specific epicardial coronary distribution territory. We report the case of a 74-year-old woman who presented with acute respiratory failure and suspected myocardial infarction. She had a left coronary artery anomaly, dominant right coronary artery supply, takotsubo cardiomyopathy, depressed left ventricular ejection fraction, and no atherosclerotic disease. In the absence of exercise ischemia, we considered the anomalous artery to be an incidental finding. After 6 weeks of medical therapy, the patient's ejection fraction was normal; one year later, she remained asymptomatic. The anomalous left coronary artery in the presence of dominant right coronary supply did not explain the diffuse apical regional wall-motion abnormalities in our patient. To our knowledge, this is the first report of coexisting takotsubo cardiomyopathy and anomalous coronary artery in a patient presenting with acute dyspnea.
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