TY - JOUR
T1 - Significance of automated stenosis detection during quantitative angiography
T2 - Insights gained from intracoronary ultrasound imaging
AU - Escaned, Javier
AU - Baptista, Jose
AU - Di Mario, Carlo
AU - Haase, Jürgen
AU - Ozaki, Yukio
AU - Linker, David T.
AU - De Feyter, Pim J.
AU - Roelandt, Jos R.T.C.
AU - Serruys, Patrick W.
PY - 1996
Y1 - 1996
N2 - Background: Automated stenosis analysis is a common feature of commercially available quantitative coronary angiography (QCA) systems, allowing automatic detection of the boundaries of the stenosis, interpolation of the expected dimensions of the coronary vessel at the point of obstruction, and angiographically derived estimation of atheromatous plaque size. However, the ultimate meaning of this type of analysis in terms of the degree of underlying atherosclerotic disease remains unclear. We investigated the relationship between stenosis analysis performed with QCA and the underlying degree of atherosclerotic disease judged by intracoronary ultrasound (ICUS) imaging. Methods and Results: In 40 coronary stenoses, automated identification of the sites of maximal luminal obstruction and the start of the stenosis was performed with QCA by use of curvature analysis of the obtained diameter function. Plaque size at these locations also was estimated with ICUS, with an additional ICUS measurement immediately proximal to the start of the stenosis. Crescentlike distribution of plaque, indicating an atheroma-free are of the arterial wall, was recorded. At the site of the obstruction, total vessel area measured with ICUS was 16.65±4.04 mm2, whereas an equivalent measurement obtained from QCA-interpolated reference dimensions was 7.48±3.30 mm2 (P=.0001). Plaque area derived from QCA data was significantly less than that calculated from ICUS (6.32±3.21 and 13.29±4.22 mm2, respectively, mean difference, 6.92±4.43 mm2; P=.0001). At the start of the stenosis identified by automated analysis, ICUS plaque area was 9.38±3.17 mm2 and total vessel area was 18.77±5.19 mm2 (50±11% total vessel area stenosis). The arterial wall presented a disease-free segment in 28 proximal locations (70%) but in only 5 sites (12% corresponding to the start of the stenosis and none at the obstruction (P=.0001). At the site of obstruction, all vessels showed a complete absence of a disease-free segment, and the atheroma present a cufflike or all-around distribution with a variable degree of eccentricity. Conclusions: At the site of maximal obstruction, QCA underestimated plaque size as measured with ICUS. Atherosclerotic disease was consistently present at the start of the stenosis and was used as a reference site by automated stenosis analysis. At the start of the stenosis, ICUS demonstrated a mean 50±11% total vessel area stenosis, with a characteristic loss of disease-free arcs of arterial wall present in proximal locations. Thus, the side identified by automated stenosis analysis as the start of the stenosis does not represent a disease-free site but rather the place where compensatory vessel enlargement fails to preserved luminal dimensions, a phenomenon that seems related to the observed loss of a remnant are of normal arterial wall.
AB - Background: Automated stenosis analysis is a common feature of commercially available quantitative coronary angiography (QCA) systems, allowing automatic detection of the boundaries of the stenosis, interpolation of the expected dimensions of the coronary vessel at the point of obstruction, and angiographically derived estimation of atheromatous plaque size. However, the ultimate meaning of this type of analysis in terms of the degree of underlying atherosclerotic disease remains unclear. We investigated the relationship between stenosis analysis performed with QCA and the underlying degree of atherosclerotic disease judged by intracoronary ultrasound (ICUS) imaging. Methods and Results: In 40 coronary stenoses, automated identification of the sites of maximal luminal obstruction and the start of the stenosis was performed with QCA by use of curvature analysis of the obtained diameter function. Plaque size at these locations also was estimated with ICUS, with an additional ICUS measurement immediately proximal to the start of the stenosis. Crescentlike distribution of plaque, indicating an atheroma-free are of the arterial wall, was recorded. At the site of the obstruction, total vessel area measured with ICUS was 16.65±4.04 mm2, whereas an equivalent measurement obtained from QCA-interpolated reference dimensions was 7.48±3.30 mm2 (P=.0001). Plaque area derived from QCA data was significantly less than that calculated from ICUS (6.32±3.21 and 13.29±4.22 mm2, respectively, mean difference, 6.92±4.43 mm2; P=.0001). At the start of the stenosis identified by automated analysis, ICUS plaque area was 9.38±3.17 mm2 and total vessel area was 18.77±5.19 mm2 (50±11% total vessel area stenosis). The arterial wall presented a disease-free segment in 28 proximal locations (70%) but in only 5 sites (12% corresponding to the start of the stenosis and none at the obstruction (P=.0001). At the site of obstruction, all vessels showed a complete absence of a disease-free segment, and the atheroma present a cufflike or all-around distribution with a variable degree of eccentricity. Conclusions: At the site of maximal obstruction, QCA underestimated plaque size as measured with ICUS. Atherosclerotic disease was consistently present at the start of the stenosis and was used as a reference site by automated stenosis analysis. At the start of the stenosis, ICUS demonstrated a mean 50±11% total vessel area stenosis, with a characteristic loss of disease-free arcs of arterial wall present in proximal locations. Thus, the side identified by automated stenosis analysis as the start of the stenosis does not represent a disease-free site but rather the place where compensatory vessel enlargement fails to preserved luminal dimensions, a phenomenon that seems related to the observed loss of a remnant are of normal arterial wall.
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U2 - 10.1161/01.CIR.94.5.966
DO - 10.1161/01.CIR.94.5.966
M3 - Article
C2 - 8790033
AN - SCOPUS:0029812128
SN - 0009-7322
VL - 94
SP - 966
EP - 972
JO - Circulation
JF - Circulation
IS - 5
ER -