Abstract 683: Regression of Plaque Volume in One Arterial Bed is not Necessarily Associated with Similar Changes in Other Vessels
Background: Population-based studies have shown good correlation between severity of atherosclerotic disease in one arterial bed and involvement of other vessels. However, in patients with coronary artery disease (CAD), it remains unclear whether atherosclerotic plaque in an artery might regress or progress in parallel with other vessels. Accordingly, the present study was performed in patients with CAD to compare changes in plaque volume (PV) between the left main (LMT) and right coronary arteries (RCA), thoracic descending aorta (TDA) and common carotid artery (CCA), and to clarify clinical factors and biomarkers which might affect changes in PV in each artery.
Methods: Using 64-multislice computed tomography, PVs in each artery were determined before and after 2.0-year follow-up period in 52 patients with CAD (67.4±9.9yo). Based on our previous study using ultrasound, CCA-PV was determined at windows of 90–240HU and TDA-PV determined manually. Coronary soft plaque was determined at windows of 0–75HU. Plasma levels of hsCRP, matrix metalloproteinase (MMP)-9 and urinary 8-iso-prostaglandin F2α(PGF) were determined at baseline.
Results: At baseline, PVs of TDA were correlated with CCA-PV (r=0.38, p<0.02), but PVs of other arteries did not correlate to each other. Two-year later, PVs of LMT, RCA, TDA, and CCA were reduced in 41, 62, 27, and 39% of patients, respectively. Changes in LMT-PV were weakly related with those of TDA-PV (r=0.37, p=0.02) and RCA-PV (r=0.31, p=0.08), but there were no relation between other arteries. The multivariate analysis revealed that treatment with statin and low LDL-cholesterol (C, <100mg/dl) were independent variables regarding a reduction in DTA-PV, but, in LMT, only low LDL-C was independent variable. However, there were no independent variables in RCA or CCA. The ratio of soft PV to total PV was similar between LMT (45.2±7.1%) and RCA (45.7±4.9%) at baseline and was unchanged in the follow-up study. None of hsCRP, MMP-9 or PGF levels was related with PVs of any arteries at baseline and with changes in PVs.
Conclusions: Regression of PV in one arterial bed dose not necessarily allow us to predict atherosclerotic changes in the other vessels. Major factors which affect changes in PV may not be homogeneous between arteries.