We experienced a case of takotsubo cardiomyopathy with cardiogenic shock in which
norepinephrine, often an effective vasopressor for shock, caused an adverse effect.
A 75-year-old woman with hypertension was referred to our hospital with syncope and
bilateral shoulder pain. Her blood pressure was 109/73 mmHg. Electrocardiography revealed
ST segment depression on I, II, aVL, V4-6. Troponin I was elevated. Echocardiography
showed severe MR and SAM. CAG showed normal coronary artery and LVG showed dyskinesia
in mid-septal portion of left ventricle. During procedure, the systolic pressure went
down to below 70 mmHg and norepinephrine was administered. It caused abrupt elevation
of left ventricular systolic pressure to 220 mmHg and decrease in SpO2. Pull-back pressure tracking showed LVOT gradient of 60 mmHg. Instead, phenylephrine
and landiolol were administered intravenously. Her clinical state improved and both
medication could be decreased gradually. Repeated echocardiography revealed improvement
in LV function and resolution of the LVOT gradient. Takotsubo disease with mid-ventricle
dyskinesia results in LVOT obstruction and cardiogenic shock. Norepinephrine acts
on α1 adrenergic receptors and used as first line vasopressor, but it also acts on
β1 adrenergic receptors and therefore worsens the degree of LVOT obstruction and results
in the exacerbation of heart failure in such cases. The recognition of this pathophysiology
is crucial for rapid selection of vasopressors and consequent hemodynamic stabilization.
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