Intravascular ultrasound evidence of angiographically silent allograft vasculopathy inversely correlates with circulating level of hepatocyte growth factor.

BACKGROUND

Cardiac allograft vasculopathy (CAV) is the major determinant of long-term survival after heart transplantation. The characteristic diffuse concentric intimal thickening of CAV detected by intravascular ultrasound (IVUS) imaging may not be perceivable on coronary angiogram. Previous studies of hepatocyte growth factor (HGF) in murine models suggested the protective effects on vascular endothelium and allograft survival. However, the possible role of circulating HGF that contributes to the development of CAV in human is unclear.

METHODS

IVUS was used to assess the left anterior descending coronary arteries of 47 patients who had survived cardiac transplantation for more than 1 year and had no angiographically detectable CAV. The IVUS measurements for the extent of intimal hyperplasia, including volume index (calculated as [total plaque volume/total vessel volume] x 100) and maximum area stenosis, were compared with plasma levels of HGF by linear regression analyses.

RESULTS

The volume index significantly correlated with maximum area stenosis in the IVUS measurements (r = 0.90, p < 0.0001). Both volume index and maximum area stenosis inversely correlated with plasma HGF levels (r = -0.39, p = 0.007 and r = -0.42, p = 0.003, respectively).

CONCLUSIONS

In angiographically silent CAV, circulating HGF may have a protective effect on vascular endothelium and thus attenuate the severity of intimal hyperplasia.