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

Objectives We 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. Background There are no serial IVUS studies of disease progression or luminal compromise in SVGs. Methods We 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. Results Overall, from baseline to follow-up, plaque area increased (Delta = + 0.58 +/- 1.25 mm(2), p = 0.003), and SVG and minimum lumen area (MLA) decreased (Delta = -0.50 +/- 1.14 mm(2), p = 0.002, and Delta = -1.08 +/- 1.28 mm(2), p < 0.001, respectively). The MLA decreased in 34 lesions (Delta = -1.67 +/- 1.08 mm(2)), and MLA increased in 16 lesions (Delta = +0.19 +/- 0.47 mm(2)). 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 mm(2) vs. 11.55 +/- 2.30 mm(2), p < 0.001; 7.97 +/- 3.77 mm(2) vs. 4.27 +/- 1.92 mm(2), 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 (Delta = -0.96 +/- 1.05 mm(2) vs. +0.48 +/- 0.58 mm(2), p < 0.001) and greater increase in plaque area (Delta = +0.71 +/- 1.47 mm(2) vs. +0.29 +/- 0.45 mm(2), p < 0.001). The Delta MLA correlated with both Delta plaque area (r = -0.589, p < 0.001) and Delta SVG area (r = 0.470, p = 0.001), and Delta plaque area correlated with Delta SVG area (r = 0.436, p = 0.002). There were linear relations between both the Delta plaque area (r = 0.519, p < 0.001) and Delta lumen 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. Conclusions Lumen 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. (J Am Coll Cardiol 2009; 53: 1257-64) (c) 2009 by the American College of Cardiology Foundation