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 DeltaMLA correlated with both Deltaplaque area (r = -0.589, p < 0.001) and DeltaSVG area (r = 0.470, p = 0.001), and Deltaplaque area correlated with DeltaSVG area (r = 0.436, p = 0.002). There were linear relations between both the Deltaplaque area (r = 0.519, p < 0.001) and Deltalumen 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.
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 DeltaMLA correlated with both Deltaplaque area (r = -0.589, p < 0.001) and DeltaSVG area (r = 0.470, p = 0.001), and Deltaplaque area correlated with DeltaSVG area (r = 0.436, p = 0.002). There were linear relations between both the Deltaplaque area (r = 0.519, p < 0.001) and Deltalumen 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.
Authors: Margreet R de Vries; Karin H Simons; J Wouter Jukema; Jerry Braun; Paul H A Quax Journal: Nat Rev Cardiol Date: 2016-05-19 Impact factor: 32.419