Author: Irfan Asif, MD
Co Author #1: Jonathan A. Drezner, MD
Co Author #2: Kimberly G. Harmon, MD
Co Author #3: David Owens, MD, Jordan Prutkin, MD, Jack Salerno MD, and Karen Stout MD
Editor: Daniel Parker, MD, MPH
An 18 year-old African American male Division I basketball player was found to have a markedly abnormal ECG as an incoming freshman. Initial ECG showed left ventricular hypertrophy (LVH) with strain pattern and prominent T wave inversion in the inferior and lateral leads. He denied any cardiovascular symptoms, and there was no family history of cardiac disease or sudden death.
An initial echocardiogram (9/2008) showed concentric LVH without asymmetry or outflow obstruction: LV end-diastolic diameter (LVEDD) 4.9 cm, Intraventricular septum (IVS) thickness (diastole) 1.5 cm, Posterior wall thickness (diastole) 1.6 cm, Ejection fraction 77%, and normal LV function.
A cardiac MRI (9/2008) was requested for further evaluation: Ventricle wall measurements (end diastole): base 0.9-1.2 cm, mid-cavity: 0.9-1.2 cm, apex 0.3-0.9 cm, thickest segment noted in the mid-septum measuring 1.3 cm
Cardiopulmonary exercise testing (9/2008) showed a VO2 max of 36.6 ml/Kg/min and evidence of a hypertensive response to exercise.
Based on this work-up, his abnormal ECG and mild concentric LVH were thought to be physiologic or perhaps related to hypertension with exercise. The cardiac MRI measurements were thought to be a more accurate assessment than the echocardiogram, and a maximum wall thickness of 1.3 cm with normal diastolic function was not consistent with a pathologic diagnosis. He was cleared to participate, and serial cardiac evaluation was recommended.
Several months later, his ECG (4/2009) was unchanged with LVH strain pattern and persistent T wave inversions in the infero-lateral leads.
An echocardiogram (4/2009): LVEDD 5.5 cm, IVS thickness 1.0 cm, Posterior wall 0.9 cm, EF 76%, and normal LV function.
One year later, his ECG (3/2010) demonstrated LVH with strain pattern again noted with more prominent T wave inversion in anterior and infero-lateral leads.
His echocardiogram (5/2010) showed: LVEDD 5.3 cm, IVS thickness 1.2 cm, Posterior wall 1.2 cm, EF 64%, and normal LV function.
Prior to his 2010-2011 season, he presented for follow-up. He denied any cardiovascular symptoms such as shortness of breath, chest pain, dyspnea on exertion, lightheadedness, syncope, etc.
On physical exam, his vitals were: BP: 107/56, HR 73 bpm, Ht 6’7”, Wt 260 lbs He had no murmurs with standing, lying supine, or with Valsalva. There were symmetric radial and femoral pulses. The rest of his exam was otherwise normal. ECG (9/2010) showed deepening of lateral T wave inversion measuring a maximum of 15-16 mm compared to his initial ECG (maximum depth 6 mm).
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