Author + information
- Received March 19, 2012
- Revision received May 25, 2012
- Accepted July 4, 2012
- Published online October 1, 2012.
- David V. Daniels, MD⁎,
- Marcel van't Veer, MSc, PhD†,‡,
- Nico H.J. Pijls, MD, PhD†,‡,
- Arjen van der Horst, MSc‡,
- Andy S. Yong, MBBS, PhD⁎,
- Bernard De Bruyne, MD, PhD§ and
- William F. Fearon, MD⁎,⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. William F. Fearon, Stanford University Medical Center, 300 Pasteur Drive, H2103, Stanford, California 94305
Objectives The aim of this study was to assess the validity of measuring fractional flow reserve (FFR) of the left main (LM) coronary artery in the setting of concomitant left anterior descending (LAD) or left circumflex (LCX) stenoses.
Background The theoretical impact of a stenosis in the LAD on the FFR assessment of intermediate LM disease with the pressure wire in an unobstructed LCX is currently unknown.
Methods A previously validated in vitro model of the coronary circulation was used to create a fixed intermediate stenosis of the LM and a variable downstream LAD or LCX stenosis. The true LM FFR (FFRLM true), with no concomitant downstream disease, was compared to the apparent LM FFR (FFRLM apparent), with concomitant downstream disease measured with different degrees of LAD or LCX disease. Additionally, an equation based on a resistors model was derived to predict the effect of downstream stenosis on LM FFR (FFRLM predicted).
Results In the setting of isolated moderate LM disease (FFR 0.72 ± 0.08), mild to moderate proximal LAD or LCX lesions did not significantly affect LM FFR. Lesions with a composite FFR (LM + downstream disease) ≥0.65 resulted in an FFRLM apparent that was not significantly different from FFRLM true (0.76 ± 0.06 vs. 0.76 ± 0.05, p = 0.124). Our equation for FFRLM predicted accurately modeled the effects of concomitant disease (r = 0.95, p < 0.001).
Conclusions These data suggest that in the presence of proximal mild to moderate LAD or LCX disease, LM FFR can be reliably measured with the pressure wire placed in the uninvolved epicardial artery.
Drs. Pijls, De Bruyne, and Fearon have received research support from St. Jude Medical.
All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Daniels and van't Veer contributed equally to this work.
- Received March 19, 2012.
- Revision received May 25, 2012.
- Accepted July 4, 2012.
- American College of Cardiology Foundation