Extracranial Carotid Atherosclerosis Evaluation and Stroke Occurrence: Role of the Echotomographic Analysis

Parnetti, Lucilla; Mercuri, Michele; Susta, A; Lupattelli, Graziana; Ciuffetti, Giovańni; Senin, Umberto

doi:10.1177/000331978803900801

Cited by 8 publications

(3 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In place of angiography for evaluation of carotid atherosclerosis [16,18], several evaluating systems using carotid ultrasonography have been proposed. Echostructural profiles such as soft, mixed, and hard plaque have been discussed in relation to clinical event or progression and regression of plaques [6,[21][22][23][24][25]. Some have used the percent stenosis for quantification of carotid atherosclerosis [7,8], others, the thickness of the intimal-medial complex [19,20].…”

Section: Discussionmentioning

confidence: 99%

Progression of carotid atherosclerosis in Japanese patients with coronary artery disease

Sueyoshi¹,

Tanaka²,

Mandai³

et al. 1994

Int J Angiol

View full text Add to dashboard Cite

Background and Purpose: Along with the recent changes in lifestyle in Japan, the incidence of coronary artery disease has increased while the incidence of stroke appears to be decreasing. We investigated the relation between the progression of carotid atherosclerosis and the severity of coronary artery disease in the Japanese population.Methods: The 2-year change in extracranial carotid atherosclerosis in 50 Japanese patients who underwent coronary angiography was evaluated using carotid echotomography. To quantify the extent of carotid atherosclerosis, the maximal thickness measurements of all plaques were summed for an individual plaque score, except for new plaques found on reexamination. Carotid disease progression was evaluated by the sum of plaque score change and the thickness of the new plaque found on reexamination.Results: The plaque score changed by -3.2 to 10.1 mm (mean±SD, 1.06±2.42 mm). The extent of coronary atherosclerosis (p<0.02) and serum total cholesterol level (p<0.01) were different between the progressing (n=17) and the nonprogressing (n=30) groups of carotid atherosclerosis when the progressing group included the patients with a A plaque score of >1.0 mm. Neither age, serum triglyceride level, serum high-density lipoprotein cholesterol level, pack-years of smoking, percentage of smokers, percentage of hypertensive patients, nor percentage of diabetic patients was different between the two groups. Carotid disease progression was significantly higher in patients with three-vessel coronary disease than in patients without significant coronary artery disease (p<0.005). There was a significant positive linear correlation between carotid disease progression and Gensini's coronary artery disease score (R=0.4ll, p<0.005).Conclusions: Our data showed that severe coronary artery disease and a high serum total cholesterol level were strong predictors for carotid disease progression in Japanese patients with high rates of coronary artery disease. (Stroke 1992;23:946-951) KEY WORDS • cardiovascular diseases • carotid artery diseases • Japan • ultrasonics

show abstract

Section: Discussionmentioning

confidence: 99%

Progression of carotid atherosclerosis in Japanese patients with coronary artery disease

Sueyoshi¹,

Tanaka²,

Mandai³

et al. 1994

Int J Angiol

View full text Add to dashboard Cite

show abstract

“…Since that time, various studies, mainly using angiographic techniques, have suggested that in 20-82% of cases, ischemic cerebral symptoms were associated with carotid stenosis involving a reduction of 50% or more in luminal diameter. 15,16 In this report, we describe 2 patients with plaque fissuring of and hemorrhage into lipid-rich atheromas of the carotid arteries, resulting in fatal massive cerebral infarction. 13,14 Furthermore, studies have undertaken to identify those ultrasonographic features of carotid atheromatous plaque that indicate an increased risk of subsequent neurologic symptoms.…”

Section: Introductionmentioning

confidence: 97%

Massive Cerebral Infarction: A Potential Fatal Complication of Plaque Fissuring of Lipid-Rich Atheromas of the Carotid Artery Case Reports

Chow

Lee

1996

Angiology

View full text Add to dashboard Cite

The authors report 2 patients who died of massive cerebral infarction secondary to plaque fissuring of and hemorrhage into their carotid atheromas, resulting in overlying thrombosis and total occlustion of the internal carotid arteries. In both cases, the atheromas caused more than 75% reduction in luminal size of the carotid artery. In addition, they were rich in lipid content, which accounted for more than 40% of the cross-sectional area of the atheromatous plaques. It is postulated that high-grade stenotic carotid atheromatous plaques with a high lipid content are at an increased risk of giving rise to subsequent neurologic complications, including massive cerebral infarction, as exemplified by the present 2 reported cases.

show abstract

“…It is a major risk factor for stroke that leads to brain damage [3–4]. Carotid stenosis is usually caused by atherosclerosis [5–6], characterized by the atherosclerostic plagues accumulating in the artery wall, thus occluding the blood flow. In the past decade, carotid angioplasty and stenting (CAS) has been developed into a credible alternative treatment to carotid endarterectomy (CEA) for the patients with symptomatic moderate- and high-grade stenosis [7–8].…”

Section: Introductionmentioning

confidence: 99%

Crosstalk between TGF-β/Smad3 and BMP/BMPR2 signaling pathways via miR-17–92 cluster in carotid artery restenosis

et al. 2013

View full text Add to dashboard Cite

In the past decades, carotid angioplasty and stenting (CAS) has been developed into a credible option for the patients with carotid stenosis. However, restenosis remains a severe and unsolved issue after CAS treatment. Restenosis is characterized by neointimal hyperplasia, which is partially caused by vascular smooth muscle cells (VSMC) proliferation. However, the molecular mechanism involved in the restenosis is still unclear. In this study, we demonstrated a functional crosstalk between two TGF-β superfamily signaling pathway members, Smad3 and BMPR2, in VSMC proliferation. Smad3 plays an important role in the TGF-β/Smad3 signaling pathway, and is significantly up-regulated in the carotid artery with restenosis to promote VSMC proliferation. In contrast, BMP receptor II (BMPR2), an inhibitor of VSMC proliferation is down-regulated in carotid restenosis. We further found that BMPR2 down-regulation is mediated by miR-17~92 cluster, which is transcriptionally regulated by Smad3. Thus, Smad3 up-regulation and Smad3/miR-17~92 cluster -dependent BMPR2 down-regulation are likely to promote VSMC proliferation and restenosis. Taken together, our results may provide novel clues for early diagnosis of carotid restenosis and developing new therapeutic strategy.

show abstract

Extracranial Carotid Atherosclerosis Evaluation and Stroke Occurrence: Role of the Echotomographic Analysis

Cited by 8 publications

References 13 publications

Progression of carotid atherosclerosis in Japanese patients with coronary artery disease

Progression of carotid atherosclerosis in Japanese patients with coronary artery disease

Massive Cerebral Infarction: A Potential Fatal Complication of Plaque Fissuring of Lipid-Rich Atheromas of the Carotid Artery Case Reports

Crosstalk between TGF-β/Smad3 and BMP/BMPR2 signaling pathways via miR-17–92 cluster in carotid artery restenosis

Contact Info

Product

Resources

About