peak velocity

What is the significance (if any) of an increase in peak velocity across the left ventriculat outflow tract from 2.1(resting) m/sec to 5.3 m/sec on low dose Dobutamine during stress echo? What is normal peak velocity and what does an increased peak velocity indicate? This is consistent with a resting gradient of 20 increasing to 120-150 with Dobutamine infusion? If there is no or minimal obstruction at rest, only with stress, can anything be done surgically to correct this? I am on max doses of Atenolol, Cardizem, and Norpace, have a DDDpacer/AICD, and am still symptomatic with HOCM. Also, why would an echo done with Amyl Nitrate not show an obstruction while an echo with Dobutamine would? Any advice you can give would be helpful. I have been seen at CCF and there seemed to be nothing left to offer. I am not giving up until I feel better. I am 48 years old. Thanks

[CCF-M.D.-RCJ]

Baseballfan,

Thanks for the post.  Sorry to read of your ordeal.

An increased peak velocity indicates flow acceleration across an orifice, in this case the outflow tract.  An acceleration occurs when narrowing is present, as can happen with HOCM.  The presence of an obstruction often indicates that a mechanical repair, like surgery or alcohol ablation, may help relieve the symptoms caused by obstruction -- these symptoms may include shortness of breath, fatigue, swelling, passing out, and others.  However, in patients with HOCM, these symptoms may be caused by a weakened (albeit thickened) heart muscle.  So while many people may experience symptom relief, there certainly is no guarantee that a mechanical relief will help.

I don't know why the dobutamine would reveal the gradient but not the amyl.  One possibility is that the amyl was not able to induce a hyperdynamic response because of the atenolol, while the dobutamine was able to saturate the beta-receptors, and thus overcome the beta-blockade.

This new information might be useful to your doctors here at the CCF.  Consider coming back.

Good luck.