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on September 3, 2002

Circulation. 2002
Published online before print September 3, 2002, doi: 10.1161/01.CIR.0000030189.27175.4E
A more recent version of this article appeared on September 24, 2002
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Submitted on May 5, 2002
Revised on June 28, 2002
Accepted on June 28, 2002

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

Jun-ichi Kotani MD, Shinsuke Nanto MD*, Gary S. Mintz MD, Masafumi Kitakaze MD, PhD, Tomoki Ohara MD, Takakazu Morozumi MD, Seiki Nagata MD, and Masatsugu Hori MD, PhD

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.

* To whom correspondence should be addressed. E-mail: AC6S-NNT{at}asahi-net.or.jp.

Background—No-reflow associated with direct angioplasty (PCI) of patients with acute coronary syndromes (ACS) is associated with unfavorable results.

Methods and Results—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 (P<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.

Conclusions—No-reflow after angioplasty may be caused by gruel that formed from an atheroma attributable to mechanical plaque disruption during intervention.


Key words: angioplasty • embolism • thrombus • plaque




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