Plaque Gruel of Atheromatous Coronary Lesion May Contribute to the No-Reflow Phenomenon in Patients With Acute Coronary Syndrome

DOI Web Site 被引用文献64件
  • Jun-ichi Kotani
    From the Cardiovascular Division, Kansai Rosai Hospital (J.K., S.N., T.O., T.M., S.N.), Amagasaki, Japan; Cardiovascular Research Foundation (G.S.M.), New York, NY; and the Department of Internal Medicine and Therapeutics (M.H., M.K.), Osaka University Graduate School of Medicine, Osaka, Japan.
  • Shinsuke Nanto
    From the Cardiovascular Division, Kansai Rosai Hospital (J.K., S.N., T.O., T.M., S.N.), Amagasaki, Japan; Cardiovascular Research Foundation (G.S.M.), New York, NY; and the Department of Internal Medicine and Therapeutics (M.H., M.K.), Osaka University Graduate School of Medicine, Osaka, Japan.
  • Gary S. Mintz
    From the Cardiovascular Division, Kansai Rosai Hospital (J.K., S.N., T.O., T.M., S.N.), Amagasaki, Japan; Cardiovascular Research Foundation (G.S.M.), New York, NY; and the Department of Internal Medicine and Therapeutics (M.H., M.K.), Osaka University Graduate School of Medicine, Osaka, Japan.
  • Masafumi Kitakaze
    From the Cardiovascular Division, Kansai Rosai Hospital (J.K., S.N., T.O., T.M., S.N.), Amagasaki, Japan; Cardiovascular Research Foundation (G.S.M.), New York, NY; and the Department of Internal Medicine and Therapeutics (M.H., M.K.), Osaka University Graduate School of Medicine, Osaka, Japan.
  • Tomoki Ohara
    From the Cardiovascular Division, Kansai Rosai Hospital (J.K., S.N., T.O., T.M., S.N.), Amagasaki, Japan; Cardiovascular Research Foundation (G.S.M.), New York, NY; and the Department of Internal Medicine and Therapeutics (M.H., M.K.), Osaka University Graduate School of Medicine, Osaka, Japan.
  • Takakazu Morozumi
    From the Cardiovascular Division, Kansai Rosai Hospital (J.K., S.N., T.O., T.M., S.N.), Amagasaki, Japan; Cardiovascular Research Foundation (G.S.M.), New York, NY; and the Department of Internal Medicine and Therapeutics (M.H., M.K.), Osaka University Graduate School of Medicine, Osaka, Japan.
  • Seiki Nagata
    From the Cardiovascular Division, Kansai Rosai Hospital (J.K., S.N., T.O., T.M., S.N.), Amagasaki, Japan; Cardiovascular Research Foundation (G.S.M.), New York, NY; and the Department of Internal Medicine and Therapeutics (M.H., M.K.), Osaka University Graduate School of Medicine, Osaka, Japan.
  • Masatsugu Hori
    From the Cardiovascular Division, Kansai Rosai Hospital (J.K., S.N., T.O., T.M., S.N.), Amagasaki, Japan; Cardiovascular Research Foundation (G.S.M.), New York, NY; and the Department of Internal Medicine and Therapeutics (M.H., M.K.), Osaka University Graduate School of Medicine, Osaka, Japan.

抄録

<jats:p> <jats:bold> <jats:italic>Background—</jats:italic> </jats:bold> No-reflow associated with direct angioplasty (PCI) of patients with acute coronary syndromes (ACS) is associated with unfavorable results. </jats:p> <jats:p> <jats:bold> <jats:italic>Methods and Results—</jats:italic> </jats:bold> We used a new thrombectomy device to treat 51 lesions in 48 consecutive ACS patients (40 male and 8 female; mean age 63 years) and conducted a microscopic analysis of aspirates and blood samples retrieved from the culprit coronary artery. The first aspirate was collected before PCI and the second was collected separately after percutaneous transluminal coronary angioplasty or stenting, including samples from the no-reflow lumen. Light microscopy showed that the materials obtained from the pre-PCI aspiration consisted of thrombus in 37.5%, thrombus and atheroma in 35.0%, and atheromatous plaque in 27.5%. The materials collected from the post-PCI aspiration were thrombus in 8.3%, thrombus and atheroma in 41.7%, and atheromatous plaque in 50.0%. We then compared the 9 lesions (19.1%) with no-reflow to those without no-reflow. There was no difference in the pre-PCI aspirates. However, after PCI, there was more atheromatous plaque retrieved from patients with no-reflow ( <jats:italic>P</jats:italic> <0.001) as well as significantly more platelet and fibrin complex, macrophages, and cholesterol crystals in the blood aspirated from no-reflow cases. Aspiration of these elements improved the no-reflow in 7 of 9 lesions to TIMI-3 flow. </jats:p> <jats:p> <jats:bold> <jats:italic>Conclusions—</jats:italic> </jats:bold> No-reflow after angioplasty may be caused by gruel that formed from an atheroma attributable to mechanical plaque disruption during intervention. </jats:p>

収録刊行物

  • Circulation

    Circulation 106 (13), 1672-1677, 2002-09-24

    Ovid Technologies (Wolters Kluwer Health)

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