TY - JOUR
T1 - Quantitative assessment with intracoronary ultrasound of the mechanisms of restenosis after percutaneous transluminal coronary angioplasty and directional coronary atherectomy
AU - Di Mario, Carlo
AU - Gil, Robert
AU - Camenzind, Edoardo
AU - Ozaki, Yukio
AU - von Birgelen, Clemens
AU - Umans, Victor
AU - de Jaegere, Peter
AU - de Feyter, Pim J.
AU - Roelandt, Jos R.T.C.
AU - Serruys, Patrick W.
PY - 1995/4/15
Y1 - 1995/4/15
N2 - The mechanisms of immediate and late changes after percutaneous transluminal coronary angioplasty (PTCA) and directional coronary atherectomy (DCA) were assessed by serial ultrasound imaging in 18 patients treated with PTCA and 16 treated with DCA before, immediately after, and 6 months after coronary interventions. A reduction in plaque area was the main operative mechanism of DCA, explaining 66% of lumen enlargement. In the PTCA group, the increase in lumen area was the result of a more balanced combination of plaque reduction (52% of lumen increase) and increase in total lumen area (48%); p < 0.05 versus DCA. In the PTCA group, this last mechanism was prevalent (p < 0.05) in the lesions showing wall fracture or dissection after treatment and in the lesions with a mixed or calcific composition. In the PTCA group, concentric lesions showed a greater plaque compression than eccentric lesions (p < 0.02). Plaque increase was responsible for 92% and 32% of the late lumen loss after DCA and after PTCA, respectively (p < 0.05). In PTCA patients, a chronic reduction in total vessel area was the main operative mechanism of lumen reduction (67%) and was prevalent in lesions with a mixed or calcific composition (p < 0.05).
AB - The mechanisms of immediate and late changes after percutaneous transluminal coronary angioplasty (PTCA) and directional coronary atherectomy (DCA) were assessed by serial ultrasound imaging in 18 patients treated with PTCA and 16 treated with DCA before, immediately after, and 6 months after coronary interventions. A reduction in plaque area was the main operative mechanism of DCA, explaining 66% of lumen enlargement. In the PTCA group, the increase in lumen area was the result of a more balanced combination of plaque reduction (52% of lumen increase) and increase in total lumen area (48%); p < 0.05 versus DCA. In the PTCA group, this last mechanism was prevalent (p < 0.05) in the lesions showing wall fracture or dissection after treatment and in the lesions with a mixed or calcific composition. In the PTCA group, concentric lesions showed a greater plaque compression than eccentric lesions (p < 0.02). Plaque increase was responsible for 92% and 32% of the late lumen loss after DCA and after PTCA, respectively (p < 0.05). In PTCA patients, a chronic reduction in total vessel area was the main operative mechanism of lumen reduction (67%) and was prevalent in lesions with a mixed or calcific composition (p < 0.05).
UR - http://www.scopus.com/inward/record.url?scp=0028946587&partnerID=8YFLogxK
U2 - 10.1016/S0002-9149(99)80409-3
DO - 10.1016/S0002-9149(99)80409-3
M3 - Article
C2 - 7717277
AN - SCOPUS:0028946587
SN - 0002-9149
VL - 75
SP - 772
EP - 777
JO - The American journal of cardiology
JF - The American journal of cardiology
IS - 12
ER -