There is considerable controversy over the mechanism of restenosis after percutaneous balloon angioplasty (PTCA). Vessel remodeling and plaque increase are among the possible contributors but angiography is methodolog...There is considerable controversy over the mechanism of restenosis after percutaneous balloon angioplasty (PTCA). Vessel remodeling and plaque increase are among the possible contributors but angiography is methodologically limited since it can not differentiate these different mechanisms. For evaluating the contribution of vessel and plaque changes after PTCA, we analyzed serial intravascular ultrasound (IVUS) studies in 59 lesions. IVUS study (3.5 F, 20 MHz catheter, Boston Scientific Co,; Hewlett Packard console) was performed immediately after PTCA (POST), and at follow up (FU, 6±1 months). At follow up, 40 lesions (Group Ⅰ) did not show restenosis and 19 (32.2%) lesions (Group Ⅱ) developed restenosis (area Department of Cardiology, University of Essen, Essen, Germany (Liu FQ, Ge JB, Baumgart D, Grge G, Haude M and Erbel R) stenosis >50%). Cross sectional vessel area (VA, mm 2), plaque area (PA, mm 2), and percent area stenosis (A%) were measured. [BHDFG1*2,WK3,WK5,WK11,WK11W]GROUP Ⅰ (±s)GROUP Ⅱ (±s) [BHDZ,WK3ZQ,WK5ZQ,WK11,WK11ZQ2W]VAPOST18.1±4.919.1±5.6FU17.7±4.618.9±6.2PAPOST9.9±3.212.0±4.7 *FU10.2±3.415.4±5.0 * A%POST55.6±7.568.4±6.3 *FU58.4±8.781.6±3.4 * * P <0.05, Group I vs Group II. In summary, plaque increase contributed significantly to late restenosis. This may be partly due to “recovery” of the plaque from redistribution (induced by balloon compression) and/or partly due to intimal proliferation. Greater residual plaque burden was also related to higher possibility of rstenosis.展开更多
文摘There is considerable controversy over the mechanism of restenosis after percutaneous balloon angioplasty (PTCA). Vessel remodeling and plaque increase are among the possible contributors but angiography is methodologically limited since it can not differentiate these different mechanisms. For evaluating the contribution of vessel and plaque changes after PTCA, we analyzed serial intravascular ultrasound (IVUS) studies in 59 lesions. IVUS study (3.5 F, 20 MHz catheter, Boston Scientific Co,; Hewlett Packard console) was performed immediately after PTCA (POST), and at follow up (FU, 6±1 months). At follow up, 40 lesions (Group Ⅰ) did not show restenosis and 19 (32.2%) lesions (Group Ⅱ) developed restenosis (area Department of Cardiology, University of Essen, Essen, Germany (Liu FQ, Ge JB, Baumgart D, Grge G, Haude M and Erbel R) stenosis >50%). Cross sectional vessel area (VA, mm 2), plaque area (PA, mm 2), and percent area stenosis (A%) were measured. [BHDFG1*2,WK3,WK5,WK11,WK11W]GROUP Ⅰ (±s)GROUP Ⅱ (±s) [BHDZ,WK3ZQ,WK5ZQ,WK11,WK11ZQ2W]VAPOST18.1±4.919.1±5.6FU17.7±4.618.9±6.2PAPOST9.9±3.212.0±4.7 *FU10.2±3.415.4±5.0 * A%POST55.6±7.568.4±6.3 *FU58.4±8.781.6±3.4 * * P <0.05, Group I vs Group II. In summary, plaque increase contributed significantly to late restenosis. This may be partly due to “recovery” of the plaque from redistribution (induced by balloon compression) and/or partly due to intimal proliferation. Greater residual plaque burden was also related to higher possibility of rstenosis.
