TY - JOUR
T1 - High platelet reactivity on clopidogrel therapy correlates with increased coronary atherosclerosis and calcification
T2 - A volumetric intravascular ultrasound study
AU - Chirumamilla, Amala P.
AU - Maehara, Akiko
AU - Mintz, Gary S.
AU - Mehran, Roxana
AU - Kanwal, Sunil
AU - Weisz, Giora
AU - Hassanin, Ahmed
AU - Hakim, Diaa
AU - Guo, Ning
AU - Baber, Usman
AU - Pyo, Robert
AU - Moses, Jeffrey W.
AU - Fahy, Martin
AU - Kovacic, Jason C.
AU - Dangas, George D.
N1 - Funding Information:
Dr. Maehara has received a research grant from Boston Scientific and speaker's honoraria from Volcano-Japan. Dr. Mintz is a consultant to and has received grant support from Boston Scientific and Volcano , he has also received honoraria from Boston Scientific. Drs. Mehran and Dangas have received research grants from Sanofi-Aventis , Bristol-Myers Squibb , The Medicines Co. , Eli Lilly , and Daichi Sankyo , and consultant honoraria from AstraZeneca, Bristol-Myers Squibb, and Johnson & Johnson. Dr. Mehran has served on the Advisory Board for Abbott, Ortho McNeil, and Regado. Dr. Moses has consulted for BSC and Abbott. Dr. Kovacic is supported by National Institutes of Health grant 1K08HL111330–01 . Neil J. Weissman, MD, served as Guest Editor for this paper.
PY - 2012/5
Y1 - 2012/5
N2 - Objectives: This study sought to evaluate the relationship between platelet reactivity and atherosclerotic burden in patients undergoing percutaneous coronary intervention (PCI) with pre-intervention volumetric intravascular ultrasound (IVUS) imaging. Background: Atherosclerosis progresses by the pathologic sequence of subclinical plaque rupture, thrombosis, and healing. In this setting, increased platelet reactivity may lead to more extensive arterial thrombosis at the time of plaque rupture, leading to a more rapid progression of the disease. Alternatively, abnormal vessel wall biology with advanced atherosclerosis is known to enhance platelet reactivity. Therefore, it is possible that by either mechanism, increased platelet reactivity may be associated with greater atherosclerotic burden. Methods: This study included patients who underwent PCI with pre-intervention IVUS imaging and platelet reactivity functional assay (P2Y 12 reaction units) performed >16 h after PCI, after the stabilization of clopidogrel therapy (administered before PCI). Platelet reactivity >230 P2Y 12 reaction units defined high on-treatment platelet reactivity (HPR). Results: Among 335 patients (mean age 65.0 years, 71% men), there were 109 patients with HPR (32.5%) and 226 without HPR (67.5%), with HPR being associated with diabetes and chronic renal insufficiency. By IVUS analysis, patients with HPR had significantly greater target lesion calcium lengths, calcium arcs, and calcium indexes. Furthermore, patients with HPR tended to have longer lesions and greater volumetric dimensions, indicating higher plaque volume, larger total vessel volume, and also greater luminal volume, despite similar plaque burden. By multivariate analysis controlling for baseline clinical variables, HPR was the single consistent predictor of all IVUS parameters examined, including plaque volume, calcium length, and calcium arc. Conclusions: Increased platelet reactivity on clopidogrel treatment, defined as >230 P2Y 12 reaction units, is associated with greater coronary artery atherosclerotic disease burden and plaque calcification.
AB - Objectives: This study sought to evaluate the relationship between platelet reactivity and atherosclerotic burden in patients undergoing percutaneous coronary intervention (PCI) with pre-intervention volumetric intravascular ultrasound (IVUS) imaging. Background: Atherosclerosis progresses by the pathologic sequence of subclinical plaque rupture, thrombosis, and healing. In this setting, increased platelet reactivity may lead to more extensive arterial thrombosis at the time of plaque rupture, leading to a more rapid progression of the disease. Alternatively, abnormal vessel wall biology with advanced atherosclerosis is known to enhance platelet reactivity. Therefore, it is possible that by either mechanism, increased platelet reactivity may be associated with greater atherosclerotic burden. Methods: This study included patients who underwent PCI with pre-intervention IVUS imaging and platelet reactivity functional assay (P2Y 12 reaction units) performed >16 h after PCI, after the stabilization of clopidogrel therapy (administered before PCI). Platelet reactivity >230 P2Y 12 reaction units defined high on-treatment platelet reactivity (HPR). Results: Among 335 patients (mean age 65.0 years, 71% men), there were 109 patients with HPR (32.5%) and 226 without HPR (67.5%), with HPR being associated with diabetes and chronic renal insufficiency. By IVUS analysis, patients with HPR had significantly greater target lesion calcium lengths, calcium arcs, and calcium indexes. Furthermore, patients with HPR tended to have longer lesions and greater volumetric dimensions, indicating higher plaque volume, larger total vessel volume, and also greater luminal volume, despite similar plaque burden. By multivariate analysis controlling for baseline clinical variables, HPR was the single consistent predictor of all IVUS parameters examined, including plaque volume, calcium length, and calcium arc. Conclusions: Increased platelet reactivity on clopidogrel treatment, defined as >230 P2Y 12 reaction units, is associated with greater coronary artery atherosclerotic disease burden and plaque calcification.
KW - atherosclerosis
KW - clopidogrel
KW - plaque progression
KW - platelet reactivity
KW - platelets
UR - https://www.scopus.com/pages/publications/84861140209
U2 - 10.1016/j.jcmg.2011.12.019
DO - 10.1016/j.jcmg.2011.12.019
M3 - Article
C2 - 22595163
AN - SCOPUS:84861140209
SN - 1936-878X
VL - 5
SP - 540
EP - 549
JO - JACC: Cardiovascular Imaging
JF - JACC: Cardiovascular Imaging
IS - 5
ER -
