title: Changes in coronary anatomy and physiology after heart transplantation.
abstract: Cardiac allograft vasculopathy (CAV) is a progressive process involving the epicardial and microvascular coronary systems. The timing of the development of abnormalities in these 2 compartments and the correlation between changes in physiology and anatomy are undefined. The invasive evaluation of coronary artery anatomy and physiology with intravascular ultrasound, fractional flow reserve, coronary flow reserve, and the index of microcirculatory resistance (IMR) was performed in the left anterior descending coronary artery during 151 angiographic evaluations of asymptomatic heart transplant recipients from 0 to >5 years after heart transplantation (HT). There was no angiographic evidence of significant CAV, but during the first year after HT, fractional flow reserve decreased significantly (0.89 +/- 0.06 vs 0.85 +/- 0.07, p = 0.001), and percentage plaque volume derived by intravascular ultrasound increased significantly (15.6 +/- 7.7% to 22.5 +/- 12.3%, p = 0.0002), resulting in a significant inverse correlation between epicardial physiology and anatomy (r = -0.58, p <0.0001). The IMR was lower in these patients compared with those > or =2 years after HT (24.1 +/- 14.3 vs 29.4 +/- 18.8 units, p = 0.05), suggesting later spread of CAV to the microvasculature. As the IMR increased, fractional flow reserve increased (0.86 +/- 0.06 to 0.90 +/- 0.06, p = 0.0035 comparing recipients with IMRs < or =20 to those with IMRs > or =40), despite no difference in percentage plaque volume (21.0 +/- 11.2% vs 20.5 +/- 10.5%, p = NS). In conclusion, early after HT, anatomic and physiologic evidence of epicardial CAV was found. Later after HT, the physiologic effect of epicardial CAV may be less, because of increased microvascular dysfunction.
authors.affiliation: Center for Research in Cardiovascular Interventions, Division of Cardiovascular Medicine, Stanford University Medical Center, Stanford, California, USA.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Hirohata
authors.forename: Mamoo
authors.initials: M
authors.lastname: Nakamura
authors.forename: Katsuhisa
authors.initials: K
authors.lastname: Waseda
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Honda
authors.forename: David P
authors.initials: DP
authors.lastname: Lee
authors.forename: Randall H
authors.initials: RH
authors.lastname: Vagelos
authors.forename: Sharon A
authors.initials: SA
authors.lastname: Hunt
authors.forename: Hannah A
authors.initials: HA
authors.lastname: Valantine
authors.forename: Paul G
authors.initials: PG
authors.lastname: Yock
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Fitzgerald
authors.forename: Alan C
authors.initials: AC
authors.lastname: Yeung
authors.forename: William F
authors.initials: WF
authors.lastname: Fearon
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001783:Blood Flow Velocity; D017023:Coronary Angiography; D003326:Coronary Circulation; D023921:Coronary Stenosis / Q000000981:diagnostic imaging / Q000503:physiopathology; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology*; D005260:Female; D016027:Heart Transplantation; D006801:Humans; D016014:Linear Models; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D011184:Postoperative Period; D012107:Research Design; D014184:Transplantation, Homologous; D018084:Ultrasonography, Interventional; D014655:Vascular Resistance