Rapp Joseph H, Pan Xian Mang, Yu Bo, Swanson Raymond A, Higashida Randall T, Simpson Paul, Saloner David
Surgical Service (112G), San Francisco DVA Medical Center, 4150 Clement St, San Francisco, Calif 94121, USA.
Stroke. 2003 Aug;34(8):1976-80. doi: 10.1161/01.STR.0000083400.80296.38. Epub 2003 Jul 10.
To determine the importance of emboli not trapped by carotid angioplasty filtration devices, we examined fragments <100 microm released with ex vivo angioplasty and asked if fragment composition and size correlated with brain injury.
Human carotid plaques (21) were excised en bloc, and ex vivo carotid angioplasty was performed. Eight plaques were selected as either highly calcified (4) or highly fibrotic (4) by high-resolution MRI (200 microm3). Fragments were counted by a Coulter counter. Before injection into male Sprague-Dawley rats, fragments from calcified and fibrotic plaques were sized with 60-, 100-, and 200-microm filters. Brain ischemia and infarction were assessed by MRI scans (7-T small-bore magnet) and by immunohistologic staining for HSP70 and NueN.
All 5 animals injected with 100- to 200-microm calcified fragments had infarctions. One was lethal. After injection of 60- to 100-microm calcified fragments, 7 of 12 animals had cerebral infarctions, whereas only 1 of 11 had infarctions with fibrous fragments (P<0.02). HSP70 staining showed that ischemia was more common and more extensive than infarction. Ischemia was found in 10 of 12 animals after injection of calcified fragments and in 9 of 11 after injection of fibrous fragments. The mean number of 60- to 100-microm fragments released was 375+/-510; the mean number of 20- to 60-microm fragments was 34 196 (range, 2230 to 186 927).
Hundreds of thousands of microemboli can be shed during carotid angioplasty. Fragments from calcified plaques cause greater levels of infarction than fragments from fibrous plaques, although ischemia is common with both fragment types.
