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Yale University, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, United StatesDepartment of Cardiology, VA Connecticut Healthcare System, West Haven, CT, United States
A 71 year old male with hypertension, hyperlipidemia, and diabetes presented to an outside
hospital with exertional chest pain. He underwent an exercise myocardial perfusion
study during which he developed chest pain and ischemic ECG changes (Fig. 1A–B ). His myocardial perfusion imaging was normal. A transthoracic echocardiogram was
obtained and interpreted as showing significant aortic stenosis. He was subsequently
transferred to our medical center for further management. In the interim, he developed
atrial fibrillation with rapid ventricular response. A repeat transthoracic echocardiogram
(Fig. 2 A–B ) revealed severe left ventricular outflow tract (LVOT) obstruction with a peak resting
gradient of 64 mm Hg, mild concentric left ventricular hypertrophy with proximal septal thickening and
preserved ejection fraction. A mobile echodensity was noted in the LVOT suggestive
of systolic anterior motion of the mitral valve versus a sub-aortic membrane. The
aortic valve was tri-leaflet and opened normally. The patient underwent a transesophageal
echocardiogram (Fig. 2 C–D) which revealed a myxomatous anterior mitral valve leaflet with mild mitral regurgitation
and systolic anterior motion leading to LVOT obstruction. There was no sub-aortic
membrane. He was in sinus rhythm during this exam with a peak LVOT gradient of 27 mm Hg. Coronary angiography was normal (Fig. 3A–B ). He subsequently underwent a treadmill stress echocardiogram which was terminated
for chest pain and ischemic ECG changes. Continuous-wave Doppler imaging measured
an LVOT gradient of 17 mm Hg at rest which increased to 84 mm Hg immediately following exercise (Fig. 3C–D). The patient was managed with beta-blockers and referred for mitral valve surgery.
Fig. 112-Lead ECG at rest (A) and during exercise (B) demonstrating ST depressions in leads
II, III, aVF, V5, and V6 consistent with ischemia.
Fig. 2Transthoracic echocardiogram showing an echodensity in the left ventricular outflow
tract (A, arrow) and a continuous wave Doppler peak velocity of 4 m/s (B). Transesophageal echocardiogram showing systolic anterior motion of the mitral
valve (C, arrow) and color Doppler evidence of turbulent flow in the left ventricular
outflow tract (D).
Fig. 3Coronary angiography demonstrating normal left (A) and right (B) coronary arteries.
Continuous-wave Doppler measuring an LVOT gradient of 17 mm Hg at rest (C) and 84 mm Hg following exercise (D).