Disease Progression in Nonintervened Saphenous Vein Graft Segments : A Serial Intravascular Ultrasound Analysis

ObjectivesWe used serial intravascular ultrasound (IVUS) to assess disease progression in nonintervened saphenous vein graft (SVG) segments to determine the natural rate of disease progression in SVG.BackgroundThere are no serial IVUS studies of disease progression or luminal compromise in SVGs.MethodsWe assessed serial (baseline and follow-up at 16.2 ± 7.4 months) IVUS findings in 50 nonintervened SVG segments in 44 patients. The SVG age was 13.5 ± 3.6 years.ResultsOverall, from baseline to follow-up, plaque area increased (Δ = +0.58 ± 1.25 mm2, p = 0.003), and SVG and minimum lumen area (MLA) decreased (Δ = −0.50 ± 1.14 mm2, p = 0.002, and Δ = −1.08 ± 1.28 mm2, p < 0.001, respectively). The MLA decreased in 34 lesions (Δ = −1.67 ± 1.08 mm2), and MLA increased in 16 lesions (Δ = +0.19 ± 0.47 mm2). Compared with lesions with an increase in MLA, lesions with a decrease in MLA were associated with: 1) larger baseline SVG and plaque areas and plaque burden (15.57 ± 3.90 mm2vs. 11.55 ± 2.30 mm2, p < 0.001; 7.97 ± 3.77 mm2vs. 4.27 ± 1.92 mm2, p < 0.001; and 48.7 ± 14.2% vs. 36.0 ± 13.4%, p = 0.004, respectively); and 2) a greater decrease in SVG area (Δ = −0.96 ± 1.05 mm2vs. +0.48 ± 0.58 mm2, p < 0.001) and greater increase in plaque area (Δ = +0.71 ± 1.47 mm2vs. +0.29 ± 0.45 mm2, p < 0.001). The ΔMLA correlated with both Δplaque area (r = −0.589, p < 0.001) and ΔSVG area (r = 0.470, p = 0.001), and Δplaque area correlated with ΔSVG area (r = 0.436, p = 0.002). There were linear relations between both the Δplaque area (r = 0.519, p < 0.001) and Δlumen area (r = −0.500, p < 0.001) versus follow-up low-density lipoprotein (LDL) cholesterol; a follow-up LDL cholesterol of 100 mg/dl predicted no plaque increase.ConclusionsLumen loss in nonintervened SVG segments correlated with an increase in plaque area and a decrease in SVG area (plaque growth and negative remodeling) with a linear relationship between plaque growth versus follow-up LDL cholesterol leading to long-term lumen loss.