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Letter to the Editor| Volume 180, P60-62, February 01, 2015

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Dynamic left ventricular outflow tract obstruction causing myocardial ischemia

  • Julie He
    Affiliations
    Yale University, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, United States
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  • Brian Malm
    Correspondence
    Corresponding author at: Department of Cardiology, VA Connecticut Healthcare System, 950, Campbell Avenue, West Haven, CT 06516, United States.
    Affiliations
    Yale University, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, United States

    Department of Cardiology, VA Connecticut Healthcare System, West Haven, CT, United States
    Search for articles by this author
Published:November 26, 2014DOI:https://doi.org/10.1016/j.ijcard.2014.11.136
      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.
      Figure thumbnail gr1
      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.
      Figure thumbnail gr2
      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).
      Figure thumbnail gr3
      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).

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