Abstract 15369: Patients With Coronary Microvascular Dysfunction Have High Plaque Burden and Diffuse Epicardial Atherosclerotic Disease on Intravascular Ultrasound
Background: Coronary microvascular dysfunction (CMD) often coexists with epicardial atherosclerotic coronary artery disease (CAD). Although CMD has been implicated as a marker of early or diffuse CAD, the relationship between CMD and epicardial CAD remains undefined. We hypothesized that CMD will be associated with a greater burden and diffuseness of epicardial CAD.
Methods: Seventy-seven patients (men and women) with non-obstructive CAD (fractional flow reserve [FFR] > 0.75) underwent coronary angiography, intravascular ultrasound (IVUS), and invasive Doppler velocity and pressure measurements of the left coronary artery. At maximal adenosine-induced hyperemia, hyperemic microvascular resistance (HMR), as an index of pure coronary microvascular function, was calculated as ratio of distal pressure to average peak velocity and FFR as ratio of distal to proximal pressure. CMD was defined as HMR ≥2.0 mm Hg/cm/s. Diffuse epicardial CAD was quantified based on the percentage of IVUS frames with plaque burden ≥50% (PB: plaque area/vessel area х 100). Minimum, median, and maximum of PB for each vessel was calculated.
Results: Median age was 57 years, 49% were women, 23% had diabetes and 71% had hypertension. CMD was present in 30 (39%) patients. There were no differences in FFR or minimal lumen area between patients with or without CMD (Table). Compared to patients with normal microvascular function, those with CMD had higher minimum, median, and maximum PB (p<0.05 for all) as well as higher percentage of IVUS frames with PB≥50% (5 [0, 39]% vs. 26 [6, 54]%, p=0.024) suggesting more diffuse CAD. Moreover, Log-HMR correlated with Log-minimum PB (r=0.261, p=0.02) in the entire population.
Conclusions: In patients with non-obstructive CAD, CMD is associated with greater burden of plaque and more diffuse epicardial CAD. These novel findings improve our understanding of mechanisms of development of CMD and related myocardial ischemia.
Author Disclosures: P. Eshtehardi: None. O.Y. Hung: None. Y. Bouchi: None. W. Zeng: None. M.T. Corban: None. R. Gandhi: None. H. Hosseini: None. B.D. Gogas: None. P.K. Mehta: None. L.J. Shaw: None. A.A. Quyyumi: None. H. Samady: None.
- © 2016 by American Heart Association, Inc.