Sonographic Detection of Abnormal Plaque Motion of the Carotid Artery: Its Usefulness in Diagnosing High-Risk Lesions Ranging from Plaque Rupture to Ulcer Formation.

We investigated the feasibility of using sonography of abnormal plaque motion to diagnose high-risk carotid lesions ranging from plaque rupture to ulcer formation. Fifty consecutive carotid arteries of 49 patients (71 ± 7 y, 37 males) who underwent carotid endarterectomy were investigated by carotid sonography to find a plaque concavity (sonographic ulcer [SU]), fine trembling motion inside the plaque (FTMI) and systolic retractive motion of the plaque surface (SRMS). Plaque rupture or ulcer, necrotic core and intra-plaque hemorrhage were determined at carotid endarterectomy. Twenty-two SUs, 41 cases of FTMI and 20 cases of SRMS were detected by carotid sonography. The sensitivity and specificity of SU in diagnosing plaque rupture or ulcer at carotid endarterectomy were 48% and 90%, and those of FTMI were 93% and 60%. Plaques with SRMS more frequently had both a necrotic core and intra-plaque hemorrhage than those without SRMS (80% vs. 30%, p = 0.0005). Abnormal plaque motion detected by carotid sonography is useful in detecting a ruptured or ulcerated plaque with a necrotic core and/or hemorrhage.

Prevalence and clinical importance of spontaneous echo contrast within the carotid artery in patients with ischemic cerebrovascular disease.

OBJECTIVE: Spontaneous echo contrast (SEC) is composed of numerous microechoes swirling in the cardiovascular lumen, usually appearing during blood stasis. This study aimed to clarify the clinical importance of SEC in the carotid artery (CA) in patients with ischemic cerebrovascular disease (ICVD). METHODS: In 264 CAs of 132 consecutive patients with ICVD and in 40 CAs of 20 healthy control subjects, SEC was classified as none, faint, or dense, and CA abnormalities, including plaque, plaque ulcer, mural thrombus, and internal CA stenosis, were assessed with 10-MHz sonography. RESULTS: The overall prevalence of SEC was greater in CAs of patients with ICVD (164/264 [62%]) than in CAs of control subjects (6/40 [15%]; P < .0001). Dense SEC was more specifically detected in CAs of ICVD with the prevalence of 81 (31%) of 264, which was greater than that of controls (1/40 [3%]; P = .0002). Dense SEC was more frequently detected in CAs with plaque (38/98 [39%]) than in those without (43/166 [26%]; P = .0285), in CA plaque with ulcerative lesions (7/10 [70%]) than in those without (31/88 [35%]; P = .0325), in CA plaque with a thrombus (11/12 [92%]) than in those without (27/86 [31%]; P < .0001), and in CAs with severe stenosis (11/13 [85%]) than in those with mild stenosis (25/75 [33%]; P = .0005) and in those without stenosis (45/176 [26%]; P < .0001). CONCLUSIONS: Dense SEC was frequently observed in CAs of patients with ICVD, especially in those with local atheromatous lesions, although the influence of systemic factors could not be excluded. Dense SEC within a CA may be a marker of ICVD.

[Effects of low-dose pergolide therapy on cardiac valves in patients with Parkinson's disease].

BACKGROUND: Pergolide mesilate is widely used to treat Parkinson's disease in both the USA and Japan, but the maintenance dose is distinctly different between the USA (usually more than 1.5 mg/day) and Japan (usually less than 1.5 mg/day). Although several reports from the USA have suggested that mitral, aortic, and tricuspid valvular lesions were caused by pergolide, it is unclear whether low-dose pergolide therapy causes such valvular lesions. OBJECTIVES: The effects of low-dose pergolide therapy on cardiac valves were studied in Japanese patients with Parkinson's disease. METHODS: One hundred and five consecutive patients with Parkinson's disease approved for our protocol were enrolled in this study. Forty patients were treated with low-dose pergolide (0.05-1.5 mg/day for 2-115 months), and were included in the pergolide group (mean age 71 +/- 6 years). The other 44 patients received no ergot-derived dopamine receptor agonists, and 32 patients acted as age-matched controls (mean age 71 +/- 7 years). Both groups of patients underwent echocardiographic examination to detect organic lesions in cardiac valves such as thickening of the leaflet, annular calcification, restriction of valve motion and valvular tenting, and valvular regurgitation greater than 2 + on the 4-point scale. RESULTS: No significant difference was observed in the incidence of aortic, mitral and pulmonic valve lesions between the pergolide group and the control group. Although no organic lesions were detected in the tricuspid valve, the incidence of tricuspid regurgitation was significantly higher in the pergolide group than in the control group (p < 0.05). CONCLUSIONS: Although low-dose pergolide of less than 1.5 mg/day does not cause serious damage in the left-sided valves, it may induce tricuspid regurgitation.