BACKGROUND: Previous long-term (>1 year) studies have suggested that saphenous vein bypass grafts (SVGs) undergo vascular remodeling similar to native coronary arteries. However, early morphologic stages of SVG remodeling have not been characterized in vivo. METHODS: Thirty SVGs were studied 12 months after implantation using an intravascular ultrasound automated pullback system. Intravascular ultrasound images were analyzed between 10 and 60 mm from the tip of the guide. Lumen area (LA), intima area (IA), and vessel area (VA, defined as the area within the outer border of a hypoechoic intimal layer) were computed at 3 cross sections: the minimum LA (MLA) site and the proximal and distal reference sites. Area changes (Delta) were calculated as the MLA site minus the average of the reference sites. RESULTS: In this cohort, 70% of the MLA sites had a smaller VA than the average references. On average, MLA sites had significantly smaller VA (9.7 +/- 2.9 vs 10.7 +/- 3.2 mm2, P < .01) and larger IA (2.5 +/- 2.1 vs 1.2 +/- 1.3 mm2, P < .01) than at the reference sites. The relative contribution of DeltaVA (-1.0 +/- 1.4 mm2) and DeltaIA (1.3 +/- 1.3 mm2) to lumen compromise (-2.3 +/- 1.4 mm2) were 43% and 57%, respectively. On the other hand, simple linear regression analysis revealed a significant positive correlation between DeltaIA and DeltaVA (y = -1.7 + 0.52x, r = 0.50, P < .01). CONCLUSIONS: Within the first year, the mechanism of lumen compromise in SVG is a combination of negative remodeling and intimal hyperplasia. Positive remodeling is seen in a minority of cases. However, the direction and extent of remodeling correlated with change in intimal thickness.
BACKGROUND: Previous long-term (>1 year) studies have suggested that saphenous vein bypass grafts (SVGs) undergo vascular remodeling similar to native coronary arteries. However, early morphologic stages of SVG remodeling have not been characterized in vivo. METHODS: Thirty SVGs were studied 12 months after implantation using an intravascular ultrasound automated pullback system. Intravascular ultrasound images were analyzed between 10 and 60 mm from the tip of the guide. Lumen area (LA), intima area (IA), and vessel area (VA, defined as the area within the outer border of a hypoechoic intimal layer) were computed at 3 cross sections: the minimum LA (MLA) site and the proximal and distal reference sites. Area changes (Delta) were calculated as the MLA site minus the average of the reference sites. RESULTS: In this cohort, 70% of the MLA sites had a smaller VA than the average references. On average, MLA sites had significantly smaller VA (9.7 +/- 2.9 vs 10.7 +/- 3.2 mm2, P < .01) and larger IA (2.5 +/- 2.1 vs 1.2 +/- 1.3 mm2, P < .01) than at the reference sites. The relative contribution of DeltaVA (-1.0 +/- 1.4 mm2) and DeltaIA (1.3 +/- 1.3 mm2) to lumen compromise (-2.3 +/- 1.4 mm2) were 43% and 57%, respectively. On the other hand, simple linear regression analysis revealed a significant positive correlation between DeltaIA and DeltaVA (y = -1.7 + 0.52x, r = 0.50, P < .01). CONCLUSIONS: Within the first year, the mechanism of lumen compromise in SVG is a combination of negative remodeling and intimal hyperplasia. Positive remodeling is seen in a minority of cases. However, the direction and extent of remodeling correlated with change in intimal thickness.
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