OBJECTIVEThis coronary artery spasm review aimed to explore the most possible pathogenic trigger mechanism of vulnerable plaque rupture.

DATA SOURCESData used in this coronary artery spasm review were mainly from Medline and Pubmed in English.

STUDY SELECTIONThese reports from major review on coronary artery spasm. and these research included coronary artery conception, pathogenesis of spasm, mechanisms of plaque rupture, epidemiological evidence, clinical manifestation and the relationship between coronary artery spasm and vulnerable plaque rupture.

RESULTSCoronary artery spasm is somehow related to the presence of atherosclerotic intima disease in the coronary artery. However, chronic low-grade inflammation causes coronary vessel smooth muscle cell hypersensitivity, which can directely cause coronary artery spasm. Myocardial infarction and sudden cardiac death may be initiated by a sudden intense localized contraction of coronary artery smooth muscle.

CONCLUSIONCoronary artery spasm may be one trigger that can initiate and exacerbate vulnerable plaque rupture.

Coronary Vasospasm ; complications ; pathology ; physiopathology ; Humans ; Plaque, Atherosclerotic ; pathology

Humans ; Microvessels ; Neovascularization, Pathologic ; Neovascularization, Physiologic ; Plaque, Atherosclerotic ; pathology

Primary prevention and early detection of cardiovascular disease is important, as it is the leading cause of death throughout world. Risk stratification algorithms, such as Framingham Risk Score and European Systematic Coronary Risk Evaluation, that utilize a combination of various traditional risk factors have been developed to improve primary prevention. However, the accuracy of these algorithms for screening high risk patients is moderate at best. Accordingly, the use of biomarkers or imaging studies may improve risk stratification. Carotid ultrasound, which measures both carotid intima-media thichkness (cIMT) and carotid plaque, is useful in detecting the degree of subclinical carotid atherosclerosis, and has the advantage of being noninvasive and safe. Several large epidemiologic studies have indicated that cIMT and carotid plaque are closely related with other cardiovascular risk factors and may be useful for risk reclassification in subjects deemed to be at intermediate risk by traditional risk scores. Moreover, recent clinical guidelines for management of hypertension or dyslipidemia highlight the usefulness of cIMT in high risk patients. In this article, we review evidence for the usefulness of measurement of cIMT and carotid plaque for cardiovascular risk stratification.
Cardiovascular Diseases/*pathology/*ultrasonography ; *Carotid Intima-Media Thickness ; Humans ; Plaque, Atherosclerotic/*pathology/*ultrasonography ; Risk Factors

BACKGROUNDWith features of high tissue contrast, MRI can be used for the qualitative and quantitative evaluation of atherosclerosis plaques. In this study we investigated the development of atherosclerosis plaque with high resolution 3T MRI in a rabbit model and compared the findings with the histopathological results.

METHODTwenty male New Zealand white rabbits were randomly allocated into an experimental group (n = 16) and a control group (n = 4). Atherosclerotic lesions were induced in the abdominal aorta by balloon injury and cholesterol feeding. Multiple sequences MRI examination (ToF, T1WI, T2WI, and CE T1WI) were performed at the 2nd, 3rd, and 4th months after aortic denudation. Vessel wall thickness, total vessel area, lumen area, and vessel wall area were recorded. Plaque components were analyzed using histological results as a standard reference.

RESULTSSeventeen rabbits (14 in the experimental group and 3 in the control group) received all three MR examinations. Gradually, from 2 months to 4 months, vessel wall thickness and area in the experimental group increased significantly compared with the control group (P < 0.01). In the lumen area progressive stenosis was not found, even a slight dilation had developed in the experimental group. Lipid, fibrotic and calcified plaques can be differentiated by MR image. According to histological results, MRI had good performance in detection of lipid plaque.

CONCLUSIONMRI can be used to monitor progression of atherosclerosis and differentiate plaque components.

Animals ; Aorta, Abdominal ; pathology ; Magnetic Resonance Imaging ; methods ; Male ; Plaque, Atherosclerotic ; pathology ; Rabbits ; Random Allocation

OBJECTIVETo assess the reproducibility of 3.0 T high-resolution magnetic resonance imaging (HR MRI) for evaluation of atherosclerotic stenosis in the middle cerebral artery (MCA).

METHODSFrom February, 2011 to December, 2013, 66 consecutive patients with MCA-M1 atherosclerotic stenosis (50%-99%) confirmed by digital subtractive angiography (DSA) received examinations with 3.0 T HR MRI for measurement of the vessel area (VA) and lumen area (LA) at the maximum narrow site (VA(narrow) and LA(narrow)) and the reference site (VA(reference) and LA(reference)) as well as the plaque distribution (ventral, dorsal, superior, and inferior). Two independent readers reviewed all the images and one reader reevaluated these images 4 weeks later. The inter- and intra-observer reproducibility was evaluated using the intraclass correlation coefficient (ICC).

RESULTSThe measurements of VA(narrow), VA(reference), and LA(reference) using HR MRI showed excellent inter- (ICC=0.801, 0.843, and 0.808, respectively) and intra-observer reproducibility (ICC=0.811, 0.916, and 0.958, respectively), but the measurement of LA(narrow) had only moderate inter- and intra-observer reproducibility (ICC=0.584 and 0.625, respectively). For plaque distribution analysis (ventral, dorsal, superior, and inferior plaques), HR MRI also showed excellent inter- (ICC=0.856, 0.836, 0.791, and 0.905, respectively) and intra-observer reproducibility (ICC=0.876, 0.827, 0.825, and 0.950, respectively).

CONCLUSIONHR MRI shows good inter- and intra-observer reproducibility in identifying MCA-M1 atherosclerotic plaque distribution and vessel and lumen measurements, but its reliability for lumen area measurement at the maximum narrowing site needs to be improved.

Constriction, Pathologic ; Humans ; Magnetic Resonance Imaging ; Middle Cerebral Artery ; pathology ; Plaque, Atherosclerotic ; diagnosis ; Reproducibility of Results

CD36 is a membrane glycoprotein that is present on various types of cells, including monocytes, macrophages, microvascular endothelial cells, adipocytes and platelets. Macrophage CD36 participates in atherosclerotic arterial lesion formation through its interaction with oxidized low-density lipoprotein (oxLDL), which triggers signaling cascades for inflammatory responses. CD36 functions in oxLDL uptake and foam cell formation, which is the initial critical stage of atherosclerosis. In addition, oxLDL via CD36 inhibits macrophage migration, which may be a macrophage-trapping mechanism in atherosclerotic lesions. The role of CD36 was examined in in vitro studies and in vivo experiments, which investigated various functions of CD36 in atherosclerosis and revealed that CD36 deficiency reduces atherosclerotic lesion formation. Platelet CD36 also promotes atherosclerotic inflammatory processes and is involved in thrombus formation after atherosclerotic plaque rupture. Because CD36 is an essential component of atherosclerosis, defining the function of CD36 and its corresponding signaling pathway may lead to a new treatment strategy for atherosclerosis.
Animals ; Antigens, CD36/chemistry/genetics/*metabolism ; Atherosclerosis/*metabolism/pathology ; Humans ; Macrophages/metabolism/pathology ; Plaque, Atherosclerotic/*metabolism/pathology

In the background of the high incidence and high mortality of cardiovascular diseases,atherosclerosis is the main pathological feature of cardiovascular diseases and the core pathological basis for disease progression. In the evolution of atherosclerotic plaques,the rupture of unstable plaques,plaque shedding and formation of thrombosis are the most dangerous parts. In this process,the formation of plaque fibrosis is the core mechanism regulating plaque stability. Additionally,fibrosis reflects dynamic changes in the inflammatory processes and pathological changes. In view of the inflammation regulation and fibrosis regulation,this paper clarified the process of atherosclerotic plaque,explained the roles of relevant inflammatory cells and cytokines in plaque stability,and summed up drug researches related with stable plaque in recent years. In the future,improving the fibrosis will be a new idea for stabilizing plaque in atherosclerosis drug development.
Atherosclerosis ; drug therapy ; pathology ; Cytokines ; Fibrosis ; Humans ; Inflammation ; Plaque, Atherosclerotic ; drug therapy ; pathology ; Thrombosis ; drug therapy ; pathology

BACKGROUNDNoninvasive detection of vulnerable plaque has a significant implication for prevention and treatment of atherosclerotic diseases. The aim of this study is to investigate the difference between vulnerable plaques and stable plaques in magnetic resonance (MR) images.

METHODSAtherosclerosis was induced in twenty male New Zealand white rabbits by high cholesterol diet and balloon injury of the abdominal aorta. After baseline (pre-triggering) MR imaging (MRI) scan, the rabbits underwent pharmaceutical triggering with Russell's viper venom and histamine to induce atherothrombosis, followed by another MRI scan 48 hours later (post-triggering). Rabbits were euthanized to obtain pathological and histological data. The results of MRI were compared with those of pathology and histology.

RESULTSMRI showed that abdominal aorta of the rabbits had pathological change of atherosclerosis in different degrees. Seventy-five plaques were analysed, among which 14 had vulnerable thrombi and 61 stable. Thrombosis was identified in 7 of 11 rabbits by post-triggering MRI, the sensitivity and K value of MR in detection of vulnerable plaque was 71% and 0.803 (P < 0.05). MRI data significantly correlated with the histopathological data in fibrous cap thickness (r = 0.749) plaque area (r = 0.853), lipid core area (r = 0.900). Compared with stable plaques, vulnerable plaques had a significantly thinner fibrous cap ((0.58 ± 0.27) mm vs. (0.95 ± 0.22) mm), larger lipid core area ((7.56 ± 2.78) mm(2) vs. (3.29 ± 1.75) mm(2)), and a higher ratio of lipid core area/plaque area ((55 ± 16)% vs. (27 ± 17)%), but plaque area was comparable in two groups on MRI. The ratio of lipid core area/plaque area was a strong predictor of vulnerable plaques.

CONCLUSIONMRI could distinguish vulnerable plaques from stable plaques in a rabbit model of atherothrombosis and may thus be useful as a noninvasive modality for detection of vulnerable plaques in humans.

Animals ; Aorta, Abdominal ; pathology ; Disease Models, Animal ; Magnetic Resonance Imaging ; methods ; Male ; Plaque, Atherosclerotic ; pathology ; Rabbits ; Thrombosis ; diagnosis

OBJECTIVEAtherosclerosis is an inflammatory process that results in complex lesions or plaques that protrude into the arterial lumen. Carotid atherosclerotic plaque rupture, with distal atheromatous debris embolization, causes cerebrovascular events. This review aimed to explore research progress on the risk factors and outcomes of human carotid atherosclerotic plaques, and the molecular and cellular mechanisms of human carotid atherosclerotic plaque vulnerability for therapeutic intervention.

DATA SOURCESWe searched the PubMed database for recently published research articles up to June 2016, with the key words of "risk factors", "outcomes", "blood components", "molecular mechanisms", "cellular mechanisms", and "human carotid atherosclerotic plaques".

STUDY SELECTIONThe articles, regarding the latest developments related to the risk factors and outcomes, atherosclerotic plaque composition, blood components, and consequences of human carotid atherosclerotic plaques, and the molecular and cellular mechanisms of human carotid atherosclerotic plaque vulnerability for therapeutic intervention, were selected.

RESULTSThis review described the latest researches regarding the interactive effects of both traditional and novel risk factors for human carotid atherosclerotic plaques, novel insights into human carotid atherosclerotic plaque composition and blood components, and consequences of human carotid atherosclerotic plaque.

CONCLUSIONCarotid plaque biology and serologic biomarkers of vulnerability can be used to predict the risk of cerebrovascular events. Furthermore, plaque composition, rather than lesion burden, seems to most predict rupture and subsequent thrombosis.

Biomarkers ; blood ; Carotid Stenosis ; blood ; epidemiology ; metabolism ; pathology ; Humans ; Plaque, Atherosclerotic ; blood ; complications ; metabolism ; pathology ; Risk Factors

OBJECTIVETo observe pathohistological features of vulnerable plaques in coronary arteries.

METHODSAutopsy coronary samples from 67 patients died of acute coronary syndrome (ACS) and 60 patients of non-cardiac death from 1992 to 2006 in Beijing Hospital were examined. Morphological features of vulnerable plaques of ACS cases were evaluated in terms of thrombus, ratio of lipid core, the minimal thickness of fibrous cap and the density of inflammatory infiltration.

RESULTS(1) There are 305 plaques in ACS group and the incidence of big lipid core is 153 (50.16%), thin fibrous cap is 187(61.31%), inflammatory infiltration is 263 (86.23%), neovasculature conformation is 217 (71.15%), severe stenosis is 26 (8.52%), calcification is 238 (78.03%), superficial calcified nodule is 26 (8.52%), fissured plaque is 12 (3.93%), endothelial denudation is 3 (0.98%) and intraplaque hemorrhage is 54 (17.70%), which are significantly higher than control samples except endothelial denudation (P < 0.01). (2) The incidence of vulnerable plaques in ACS group is significantly higher than in the control group (89.51% vs. 21.98%, P < 0.01). There are 4.07 sections of vulnerable plaques with high density of inflammatory infiltration out of 4.55 sections reviewed in ACS patients, while there are 0.85 sections of vulnerable plaques with mild inflammatory infiltration out of 3.87 sections reviewed in the control cases.

CONCLUSIONSFormation of vulnerable plaque was an important pathological factor for the development of ACS. The major morphological characteristics of vulnerable plaque are big lipid core, thin fibrous cap, inflammatory infiltration, neovascularization, severe stenosis, plaque rupture, and endothelial denudation suggesting inflammation performed an important role in the formation of vulnerable plaque.

Acute Coronary Syndrome ; pathology ; Aged ; Aged, 80 and over ; Case-Control Studies ; Female ; Humans ; Inflammation ; Male ; Middle Aged ; Plaque, Atherosclerotic ; pathology