Case Presentation:
A 67‐year‐old African American male presented to another hospital with COPD exacerbation. His medical history included chronic obstructive pulmonary disease (COPD), hypertension, and hypercholesterolemia. He was treated with albuterol, ipratropium nebulizer, and intravenous steroids. On the second day of admission, he had sharp retrosternal chest pain. ECG done during the episode showed T‐wave inversions in leads II, III, and V2 through V6. Cardiac enzymes were elevated. The patient was diagnosed as having a non‐ST elevation myocardial infarction and was transferred to our hospital for cardiac catheterization. Physical exam was within normal limits. Aspirin, ACE inhibitor, statin, and heparin drip were started. He had a syncopal episode, followed by severe chest pain and respiratory distress. ECG showed acute ST elevations in leads V2 through V6, consistent with anterolateral myocardial infarction (STEMI). Emergent cardiac catheterization revealed normal coronary arteries. Left ventriculogram showed severe anterolateral and apical hypokinesia with apical ballooning consistent with Takotsubo cardiomyopathy. He responded well with standard ischemic and heart failure therapy. Beta‐blockers were avoided because of COPD. Repeat echocardiography on day 6 showed significant improvement in left ventricular systolic function with only mild apical and lateral wall hypokinesis. The patient was discharged to home in stable condition on the seventh day of admission.
Discussion:
Takotsubo cardiomyopathy (TC), also known as stress‐induced cardiomyopathy or transient left ventricular apical ballooning syndrome, is named after the prominent ventricular ballooning that looks similar to the Japanese octopus trap. Two thirds of patients have a preceding emotional or physical stressful event, and 90% cases have been reported in women. The exact etiology of TC remains unclear, but it is hypothesized to be secondary to excessive catecholamine production, with stunning of the myocardium and subsequent myocarditis. Significantly higher levels of plasma catecholamine levels are reported in patients with TC compared to patients with myocardial infarction. These patients have an acute onset of chest pain, ECG changes, and elevation of cardiac enzymes resembling an acute myocardial infarction. There is no angiographic evidence of coronary artery stenosis Initial management is similar to the treatment of myocardial ischemia and heart failure The systolic dysfunction and regional wall molion abnormalities are often transient and resolve completely within days to weeks. Patients with COPD may have significant sympathetic nervous impairment of the LV myocardium as a result of generalized sympathetic overactivity. We hypothesize that these patients may be at an increased risk of developing TC during acute COPD exacerbation.
Conclusions:
We conclude that the marked sympathetic activation in patients with COPD may lead to left ventricular impairment contributing to a Takotsubo cardiomyopathy.
Author Disclosure:
M. Trivedi, none; K. Heintz, none.