TY - JOUR
T1 - Angioscopic and virtual histology intravascular ultrasound characteristics of culprit lesion morphology underlying coronary artery thrombosis
AU - Sanidas, Elias A.
AU - Maehara, Akiko
AU - Mintz, Gary S.
AU - Kashiyama, Toshikazu
AU - Guo, Jun
AU - Pu, Jun
AU - Shang, Yunpeng
AU - Claessen, Bimmer
AU - Dangas, George D.
AU - Leon, Martin B.
AU - Moses, Jeffrey W.
AU - Stone, Gregg W.
AU - Ueda, Yasunori
N1 - Funding Information:
Dr. Guo, Dr. Pu and Dr. Yunpeng Shang received a grant from Boston Scientific Corporation , Beijing, China. Dr. Maehara and Dr. Mintz received research/grant support from Volcano Corporation (Rancho Cordova, California) and Boston Scientific Corporation (Boston, Massachusetts). Dr. Stone received research grants from InfraReDx (Boston, Massachusetts) and Volcano Corporation .
PY - 2011/5/1
Y1 - 2011/5/1
N2 - Although rupture of vulnerable plaque with subsequent thrombosis is the most common mechanism of acute coronary syndromes, a significant percentage of patients with acute coronary syndrome may not have plaque rupture. We used angioscopy and virtual histology intravascular ultrasound (VH-IVUS) to investigate the underlying morphology of coronary thrombosis. We correlated the angioscopic diagnosis of coronary thrombosis in 42 lesions (37 patients) with gray-scale and VH-IVUS findings of the underlying plaque. By angioscopy plaque rupture was present in 19 thrombotic lesions (45.2%), whereas 23 (54.8%) had no rupture. VH-IVUS findings comparing thrombotic lesions with to those without angioscopic plaque rupture were remarkably similar except that angioscopic nonruptures tended to have more necrotic core (NC) at the minimum lumen area site (22.2 ± 12.5% vs 16.3 ± 9.3%, p = 0.09) and at the maximum NC site (32.7 ± 12.8% vs 25.0 ± 12.1%, p = 0.053) compared to angioscopic ruptures. Furthermore, among 19 lesions with angioscopic plaque rupture, there were 11 VH thin-cap fibroatheromas (TCFAs; 57.9%); among 23 lesions without angioscopic rupture, there were 17 VH-TCFAs (73.9%, p = 0.22). In conclusion, the similarity of VH-IVUS plaque composition (percentage of NC and percentage of VH-TCFA) in lesions with or without angioscopic plaque rupture suggest a spectrum of underlying morphologies to explain thrombosis in the absence of a ruptured plaque including classic erosions, small (and undetectable) plaque ruptures, and potentially unruptured TCFAs with superimposed thrombosis.
AB - Although rupture of vulnerable plaque with subsequent thrombosis is the most common mechanism of acute coronary syndromes, a significant percentage of patients with acute coronary syndrome may not have plaque rupture. We used angioscopy and virtual histology intravascular ultrasound (VH-IVUS) to investigate the underlying morphology of coronary thrombosis. We correlated the angioscopic diagnosis of coronary thrombosis in 42 lesions (37 patients) with gray-scale and VH-IVUS findings of the underlying plaque. By angioscopy plaque rupture was present in 19 thrombotic lesions (45.2%), whereas 23 (54.8%) had no rupture. VH-IVUS findings comparing thrombotic lesions with to those without angioscopic plaque rupture were remarkably similar except that angioscopic nonruptures tended to have more necrotic core (NC) at the minimum lumen area site (22.2 ± 12.5% vs 16.3 ± 9.3%, p = 0.09) and at the maximum NC site (32.7 ± 12.8% vs 25.0 ± 12.1%, p = 0.053) compared to angioscopic ruptures. Furthermore, among 19 lesions with angioscopic plaque rupture, there were 11 VH thin-cap fibroatheromas (TCFAs; 57.9%); among 23 lesions without angioscopic rupture, there were 17 VH-TCFAs (73.9%, p = 0.22). In conclusion, the similarity of VH-IVUS plaque composition (percentage of NC and percentage of VH-TCFA) in lesions with or without angioscopic plaque rupture suggest a spectrum of underlying morphologies to explain thrombosis in the absence of a ruptured plaque including classic erosions, small (and undetectable) plaque ruptures, and potentially unruptured TCFAs with superimposed thrombosis.
UR - https://www.scopus.com/pages/publications/79954589530
U2 - 10.1016/j.amjcard.2010.12.037
DO - 10.1016/j.amjcard.2010.12.037
M3 - Article
C2 - 21414594
AN - SCOPUS:79954589530
SN - 0002-9149
VL - 107
SP - 1285
EP - 1290
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 9
ER -