胸主动脉粥样斑块的经食管超声研究

本文应用多平面经食管超声技术检测了２４０例受试者的胸主动脉，旨在探讨胸主动脉粥样斑块的超声特征、好发部位及临床意义。结果显示，检出斑块７３例，其中单纯型占５８．９０％，复合型占４２．４６％。复合型斑块的发生率在心脑血管病变组明显高于高血压组（５２．９０％ＶＳ１９．０５％，Ｐ＜０．０１）。胸主动脉粥样斑块的好发部位为同时发生于主动脉弓和降主动脉（５８．９１％），其次为降主动脉（２１．９５）和主动脉弓部（１９．２５％），Ｐ均＜０．００１。结果表明，复合型斑块与心脑血管病变密切相关，经食管超声技术是检测活体胸主动脉粥样硬化病变的重要方法     

经胸超声心动图诊断升主动脉瘤

目的探讨应用TTE对升主动脉瘤的诊断价值.方法对16例经CT、MRI及手术证实为升主动脉瘤的声像图及CDFI进行了分析,并结合文献总结了其CDFI的诊断与鉴别诊断.结果升主动脉瘤分为真性动脉瘤、假性动脉瘤及夹层动脉瘤三种类型.真性10例,假性1例,夹层主动脉瘤5例.真性主动脉瘤管腔局部扩张,当升主动脉扩张＞50mm时可诊断为动脉瘤.夹层主动脉瘤病变动脉内可见撕裂的动脉内膜.假性动脉瘤是由动脉壁部分破裂,血液溢出血管外形成的包裹性血肿,而非真性动脉扩张.结论TTE可对绝大多数的升主动脉瘤做出明确诊断.可作为随访观察升主动脉扩张及筛检升主动脉瘤的首选方法.     

Plaque and structural characteristics of the descending thoracic aorta using transesophageal echocardiography

The in vivo acoustic and structural characteristics of atherosclerosis in the descending thoracic aorta have not been well delineated. We prospectively evaluated the descending thoracic aorta of 147 patients (35 women and 112 men; age, 61 +/- 14 years) who underwent clinically indicated transesophageal echocardiography. Patients with suspected disease of the aorta were excluded. Thirty-eight patients (26%) had protruding plaques (men, 25%; women, 29%). Six patients had mobile intimal densities with the mobile area ranging up to 1 cm2. As expected, aortic lumen area was decreased (plaque-free, 3.53 cm2; plaque, 3.19 cm2; p less than 0.05) and wall area was increased (plaque-free, 1.51 cm2; plaque, 1.92 cm2; p less than 0.05) in the regions of the plaque. However, total arterial area was not increased (plaque-free, 5.04 cm2; plaque, 5.09 cm2; difference not significant) in a compensatory manner as observed in other arterial beds. Plaque gray scale was less than the gray scale of plaque-free wall (plaque-free, 141.2; plaque, 122.7; p less than 0.05) when compared at the same level of the descending thoracic aorta or with a second aortic plaque-free level (plaque-free, 150.4; plaque, 122.7; p less than 0.05). Standard deviation of gray scale level was similar between plaque and normal regions. Unsuspected protruding plaques in the descending thoracic aorta occurred in one quarter of the patients referred for routine transesophageal examination. Plaques tended to have lower echogenicity and were differentiated from plaque-free walls within patients. Plaque formation did not result in increased total arterial area. These data suggest that the degree or character of compensatory atherosclerotic remodeling in the highly elastic descending thoracic aorta may differ from other arterial beds.     

经食管超声对冠心病患者胸主动脉粥样硬化的研究

目的　探讨胸主动脉粥样硬化与冠状动脉粥样硬化的关系。方法　用多平面经食管超声技术, 检测了４１例正常人和４９例冠心病患者胸主动脉。对胸主动脉内径、内膜－中层厚度（ＩＭＴ）、僵硬度（β）和粥样斑块进行了评价。结果　与对照组比较, 冠心病组胸主动脉内径扩大, ＩＭＴ增厚, β值增大（Ｐ＜ ０．０５～０．００１）; 胸主动脉粥样斑块对冠心病诊断的敏感性为６３．２７％ , 特异性为９７．５６％ 。阳性预测值为９６．８８％ , 阴性预测值为６８．９７％ 。结论　冠心病人胸主动脉的解剖和功能发生了明显的变化; 胸主动脉粥样斑块是预测冠心病的较为敏感而特异的指标。     

Aortic plaque imaging and monitoring atherosclerotic plaque interventions

The atherosclerotic process that results in coronary artery disease (CAD) is recognized to be a generalized process that may involve the entire vasculature. The association between CAD and atherosclerotic plaques in the thoracic aorta has often been reported using transesophageal echocardiography. An autopsy study showed plaques in the abdominal aorta, but not in the thoracic aorta, to be severe in patients with cardiac events. However, studies evaluating an association between abdominal aortic plaques and CAD are scarce. Recently, magnetic resonance imaging (MRI) has become a useful tool for the noninvasive evaluation of atherosclerotic plaques in both the thoracic and abdominal aortas. Plaques in the thoracic and abdominal aortas were found to be characteristically associated with hypercholesterolemia and smoking, respectively, suggesting different susceptibilities to risk factors. Because patients have various risk factors, it seems to be preferable to evaluate atherosclerosis in multiple vascular beds than in just 1 bed. Magnetic resonance imaging can evaluate atherosclerosis in multiple vascular beds in the same examination session. Complex aortic plaques, especially in the abdominal aorta, were found to be associated with myocardial infarction and complex coronary lesions, suggesting a link between aortic and coronary plaque instability. Aortic MRI may thus be useful for identifying vulnerable patients. Moreover, MRI is a powerful tool to serially evaluate plaque progression and regression. Intensive lipid-lowering therapy can regress aortic plaques, but the susceptibility to lipid lowering and the process of plaque regression may differ between the thoracic and abdominal aortic plaques.     

Possibilities of transesophageal MRI for assessment of aortic disease: a review

The thoracic aortic wall is a common site of atherosclerotic plaque in humans. Tools for serial, non-invasive assessment of these plaques are of value for addressing gaps in our basic understanding of the biology of plaque rupture and its relationship to atherosclerotic disease progression as well as for monitoring response to anti-atherosclerotic interventions in therapeutic clinical trials. Common approaches to assessment of the wall of the thoracic aorta in vivo are limited. Here we discuss some of the challenges and limitations encountered by conventional techniques and review a novel approach, transesophageal MRI (TEMRI). Initial experiences in applying the TEMRI approach to assessment of aortic morphology and pathology are discussed.     

Vessel wall apoptosis and atherosclerotic plaque instability

Atherosclerotic cardiovascular disease remains the leading cause of death in the industrialized world. Most cardiovascular deaths result from acute coronary syndromes, including unstable angina pectoris and acute myocardial infarction. Coronary syndromes often arise from acute coronary thrombosis, itself commonly a result of disruption or rupture of the fibrous cap of a lipid-laden atherosclerotic plaque. Despite this huge clinical burden of atherosclerotic plaque instability, our understanding of the molecular mechanisms mediating atherosclerotic plaque disruption and rupture, at a cellular level, remains limited. Placed in a clinical context, this review discusses our current understanding of the molecular basis for atherosclerotic plaque instability, with particular emphasis on the process of apoptosis-or programmed cell death-seen increasingly as playing a key role in a number of cell types within the vessel wall.     

High phosphate diet reduces atherosclerosis formation in apolipoprotein E-deficient mice

Although higher serum phosphate level is a risk factor for cardiovascular diseases in general population as well as chronic kidney disease patients, it has not been clarified whether higher phosphate can affect atherosclerotic plaque formation. In this study, we investigated the effect of prolonged-intake of different concentrations of phosphate on atherosclerosis formation using apolipoprotein E-deficient mice. Apolipoprotein E-deficient mice were fed with high fat diet including 0.6%, 1.2% or 1.8% phosphate. After 20-week treatment, atherosclerotic plaque formation in aorta in 1.8% phosphate diet group was unexpectedly less than that in the other groups. To elucidate mechanisms of suppression of plaque formation by high phosphate diet, we hypothesized that high phosphate diet may modify a profile of monocytes/macrophages suppressing plaque formation. We confirmed that elevated peripheral monocytes (CD11b+, F4/80+ cell numbers) in apolipoprotein E-deficient mice were decreased by feeding with 1.8% P diet. In addition, ex vivo study indicated that high dose of phosphate induced macrophage apoptosis. These observations suggest that excess phosphate intake decreased atherosclerosis formation, at least in part, by changing the profile of peripheral monocytes or inducing apoptosis of macrophages in apolipoprotein E-deficient mice.     

Noninvasive imaging of atherosclerotic vessels by MRI for clinical assessment of the effectiveness of therapy

Atherosclerosis and its thrombotic complications are the major cause of morbidity and mortality in the industrialized countries. Despite advances in our understanding of the mechanisms of pathogenesis and new treatment modalities, the absence of an adequate noninvasive method for early detection limits prevention or treatment of patients with various degrees and localizations of atherothrombotic disease. The ideal clinical imaging modality for atherosclerosis should be safe, inexpensive, noninvasive or minimally invasive, accurate, and reproducible, thus allowing longitudinal studies in the same patients. Additionally, the results should correlate with the extent of atherosclerotic disease and have high predictive values for clinical events. In vivo, high-resolution magnetic resonance imaging (MRI) has recently emerged as one of the most promising techniques for the noninvasive study of atherothrombotic disease in several vascular beds such as the aorta, the carotid arteries, and the coronary arteries. Most importantly MRI can be used to characterize plaque composition as it allows the discrimination of lipid core, fibrosis, calcification, and intra-plaque hemorrhage deposits. MRI findings have been extensively validated against pathology in ex vivo studies of carotid, aortic, and coronary artery specimens obtained at autopsy and using experimental models of atherosclerosis. In vivo MRI of carotid arteries of patients referred for endarterectomy has shown a high correlation with pathology and with previous ex vivo results. A recent study in patients with plaques in the thoracic aorta showed that compared with transesophageal echocardiography plaque composition and size are more accurately characterized and measured using in vivo MRI. The composition of the plaque rather than the degree of stenosis determines the patient outcome. Therefore, a reliable noninvasive imaging tool able to detect early atherosclerotic disease in the various regions and identify the plaque composition is clinically desirable. MRI has potential in the detection arterial thrombi and in the definition of thrombus age. MRI has been used to monitor plaque progression and regression in several animal model of atherosclerosis and more recently in human. Advances in diagnosis prosper when they march hand-in-hand with advances in treatment. We stand at the threshold of accurate noninvasive assessment of atherosclerosis. Thus, MRI opens new strategies ranging from screening of high-risk patients for early detection and treatment as well as monitoring the target areas for pharmacological intervention.     

Gene transfer of manganese superoxide dismutase reverses vascular dysfunction in the absence but not in the presence of atherosclerotic plaque

Impaired endothelium-dependent vasorelaxation (EDVR) is observed in hypercholesterolemia both in the presence and absence of morphological abnormalities and may be due to superoxide anions. Our aim was to assess the effect of gene transfer of manganese superoxide dismutase (MnSOD) to blood vessels from hypercholesterolemic animals with and without atherosclerotic plaque and to compare the effects of endothelial nitric oxide synthase (eNOS) and MnSOD over-expression on vascular dysfunction in the setting of atherosclerosis. Rabbits received a high-cholesterol diet for 10 weeks, resulting in abnormal EDVR in the absence of plaque in the carotids and the presence of plaque in the aorta. In Group 1, adenoviral vectors encoding MnSOD (AdMnSOD) or beta-galactosidase (Ad(beta)gal) were delivered to the carotid arteries in vivo. Four days later, transgene expression and vascular reactivity were assessed. In Group 2, segments of the aorta were transduced ex vivo with AdMnSOD, AdeNOS or both. Transgene expression and vascular reactivity were assessed 24 hr later. In Group 1, MnSOD expression was detected in AdMnSOD-ransduced vessels and impaired EDVR was reversed in the absence of atherosclerotic plaque. In Group 2 (with atherosclerotic plaque present), MnSOD and eNOS expression were detected by western analysis, and eNOS, but not MnSOD over-expression, improved EDVR whereas simultaneous over-expression of eNOS and MnSOD was no better than eNOS alone. Adenovirus-mediated gene transfer of MnSOD to nonatherosclerotic carotid arteries, but not atherosclerotic aorta, normalizes EDVR. eNOS gene transfer improves EDVR, even in the presence of plaque.     

Comparison of fatty acid profiles of aorta and internal mammary arteries in patients with coronary artery disease

BACKGROUND: Atherosclerosis represents the principal cause of death in the many societies. Since few data have been published about the composition of fatty acids in atherosclerotic arteries such as the aorta comparing to the non affected internal mammary artery which is used for aortocoronary bypass grafting, we compared the fatty acid profiles of atherosclerotic aorta and internal mammary arteries in human individuals. METHODS: Twenty-one angiographically documented coronary artery disease (CAD) patients who were admitted to the open heart surgery division enrolled in this study. They were operated electively for coronary artery bypass grafting surgery (CABG). Small segments of ascending aorta and internal mammary arteries were sampled during open heart surgery. The samples were subjected to lipid extraction and fatty acid analysis by high performance liquid chromatography. RESULTS: The results showed that different fatty acid profiles were seen in the aorta and internal mammary arteries. The atherosclerotic aorta contained lower amounts of unsaturated fatty acids (including trans isomer of oleic acid) and higher proportions of saturated fats comparing to the internal mammary. In the aorta also, the amounts of omega6 series of fatty acids were more and levels of omega3 fats were less than the internal mammary. CONCLUSION: This study suggests that modification of fatty acids may play a role during atherogenesis.     

Penetrating aortic atherosclerotic ulcer complicated by periesophageal hematoma.

Penetrating aortic atherosclerotic ulcers have been recently recognized as an entity among the acute aortic syndromes with a potentially fatal outcome. We describe the case of a patient presenting with severe chest pain who died as a result of a thoracic-aorta penetrating atherosclerotic ulcer complicated by a intramural hematoma of the esophagus and stomach, leading to exsanguination. To our knowledge this is the first case reported in the literature of such a complication from penetrating aortic atherosclerotic ulcers.     

Epicardial adipose tissue thickness predicts descending thoracic aorta atherosclerosis shown by multidetector computed tomography

Human epicardial adipose tissue (EAT) is a type of visceral adipose tissue functioning as an endocrine organ by secreting hormones and adipocytokines which have an important role in the atherosclerotic process. In this study, we aimed to assess the relationship between EAT measured by dual source multidetector computed tomography (MDCT) and descending thoracic aorta (DTA) atherosclerosis. A total of 148 patients who underwent MDCT for the evaluation of coronary artery disease were enrolled in this study. Thickness of the EAT was measured on contrast enhanced multiplanar reformat images with parasternal short axis view at basal, mid-ventricular and apical levels and horizontal long axis view. The atherosclerotic plaque was scored from 0 to 4 points by the percentage of the luminal surface at the cross sectional area of proximal, mid and distal segments of descending aorta. Among the study population, 84 (56.8%) were male and age was (mean ± standart deviation) 56.9 ± 11.7 years. In patients with critical coronary atherosclerosis, DTA atherosclerosis had a significant relationship with EAT (P = 0.012). Multivariate linear regression analysis revealed that in addition to critical coronary stenosis, age and total epicardial fat thickness were associated with aortic atherosclerosis (β value, 0.058 and 0.035; t value, 4.74 and 2.28, respectively; P < 0.05) after adjustment for traditional cardiovascular risk factors. In this study we demonstrated that atherosclerotic plaque burden of DTA was associated with the amount of EAT thickness among patients with suspected CAD shown by MDCT. Further large scale prospective studies are needed to address the interaction of EAT as well as the mediators of inflammation and adipocytokines with the development of atherosclerotic plaques in aorta and effects on cardiovascular outcomes.     

Multidetector CT of the thoracic aorta

Recent advancement of MDCT provides high-resolution axial images with optimal contrast enhancement and 3D reformatted images of the thoracic aorta. MDCT is now playing a dominant and critical role in the evaluation of thoracic aortic disease. This article will focus on procedural considerations of MDCT: acquisition parameters, contrast injection and post-processing techniques and imaging findings of thoracic aortic diseases including, aortic dissection, intramural hematoma, penetrating atherosclerotic ulcer, aneurysm, and traumatic injury.     

Adeno-associated virus vector-mediated interleukin-10 gene transfer inhibits atherosclerosis in apolipoprotein E-deficient mice

Inflammation is a major contributor to atherosclerosis by its effects on arterial wall biology and lipoprotein metabolism. Interleukin-10 (IL-10) is an anti-inflammatory cytokine that may modulate the atherosclerotic disease process. We investigated the effects of adeno-associated virus (AAV) vector-mediated gene transfer of IL-10 on atherogenesis in apolipoprotein E (ApoE)-deficient mice. A murine myoblast cell line, C2C12, transduced with AAV encoding murine IL-10 (AAV2-mIL10) secreted substantial amounts of IL-10 into conditioned medium. The production of monocyte chemoattractant protein-1 (MCP-1) by the murine macrophage cell line, J774, was significantly inhibited by conditioned medium from AAV2-mIL10-transduced C2C12 cells. ApoE-deficient mice were injected with AAV5-mIL10 into their anterior tibial muscle at 8 weeks of age. The expression of MCP-1 in the vascular wall of the ascending aorta and serum MCP-1 concentration were decreased in AAV5-mIL10-transduced mice compared with AAV5-LacZ-transduced mice. Oil red-O staining of the ascending aorta revealed that IL-10 gene transfer resulted in a 31% reduction in plaque surface area. Serum cholesterol concentrations were also significantly reduced in AAV5-mIL10-transduced mice. To understand the cholesterol-lowering mechanism of IL-10, we measured the cellular cholesterol level in HepG2 cells, resulting in its significant decrease by the addition of IL-10 in a dose-dependent manner. Furthermore, IL-10 suppressed HMG-CoA reductase expression in the HepG2 cells. These observations suggest that intramuscular injection of AAV5-mIL10 into ApoE-deficient mice inhibits atherogenesis through anti-inflammatory and cholesterol-lowering effects.     

Spontaneous retrograde dissection of ascending aorta from descending thoracic aorta--a case review

A 56-year-old man with sudden onset chest pain, absent right lower limb pulses and ECG changes suggestive of inferior ST elevation MI underwent coronary angiogram through the right radial artery with a view to primary percutaneous coronary intervention (PCI). The left coronary angiogram demonstrated severe proximal stenotic disease in the left anterior descending and circumflex coronary arteries, but the right coronary artery could not be selectively cannulated. An ascending aortogram to visualise the right coronary artery not only failed to demonstrate it, but revealed, instead, a dissection flap in the ascending aorta, arch and descending thoracic aorta, with moderately severe aortic regurgitation. At operation, the patient was found to have an acute dissection of the ascending aorta, arch and descending aorta with an entry tear in the descending aorta below the left subclavian artery origin. Triple coronary artery bypass grafting with re-suspension of the aortic valve, supracoronary replacement of the ascending aorta and hemiarch and transaortic repair of the descending aortic tear was performed. The patient made an uncomplicated recovery, with the re-appearance of right limb pulses. A postoperative magnetic resonance (MR) scan revealed complete thrombosis of the false channel in the residual arch and a considerably shrunken false channel in the descending aorta and no aortic regurgitation. Retrograde dissection of the ascending aorta from the descending aorta has been reported infrequently in the past. We believe the scale of the problem has been underestimated because of the failure to adopt open distal anastomosis routinely in the past and, hence, failure to inspect the arch and the descending aorta routinely, particularly when the intimal tear was not identified in the ascending aorta. Retrograde dissection of the ascending aorta from an intimal tear in the descending aorta, when identified as such, has been managed, either on the principle of exclusion of the tear in the descending aorta by various elephant trunk procedures and their variants or, alternatively, on the principle of excision of the tear by extended one-stage aortic replacement, usually combined with an elephant trunk procedure. Neither of these procedures is widely adopted, owing to procedural, institutional and outcome considerations. We describe a transaortic repair of the intimal tear in the descending aorta with supracoronary interposition graft replacement of the ascending aorta and hemiarch with excellent clinical and radiological result. We also review the diagnostic and therapeutic approaches to this incompletely understood lethal disease.     

Multimodal cardiovascular magnetic resonance quantifies regional variation in vascular structure and function in patients with coronary artery disease: Relationships with coronary disease severity

Background

Cardiovascular magnetic resonance (CMR) of the vessel wall is highly reproducible and can evaluate both changes in plaque burden and composition. It can also measure aortic compliance and endothelial function in a single integrated examination. Previous studies have focused on patients with pre-identified carotid atheroma. We define these vascular parameters in patients presenting with coronary artery disease and test their relations to its extent and severity.

Methods and Results

100 patients with CAD [single-vessel (16%); two-vessel (39%); and three-vessel (42%) non-obstructed coronary arteries (3%)] were studied. CAD severity and extent was expressed as modified Gensini score (mean modified score 12.38 ± 5.3). A majority of carotid plaque was located in the carotid bulb (CB). Atherosclerosis in this most diseased segment correlated modestly with the severity and extent of CAD, as expressed by the modified Gensini score (R = 0.251, P < 0.05). Using the AHA plaque classification, atheroma class also associated with CAD severity (rho = 0.26, P < 0.05). The distal descending aorta contained the greatest plaque, which correlated with the degree of CAD (R = 0.222; P < 0.05), but with no correlation with the proximal descending aorta, which was relatively spared (R = 0.106; P = n. s.). Aortic distensibility varied along its length with the ascending aorta the least distensible segment. Brachial artery FMD was inversely correlated with modified Gensini score (R = -0.278; P < 0.05). In multivariate analysis, distal descending aorta atheroma burden, distensibility of the ascending aorta, carotid atheroma class and FMD were independent predictors of modified Gensini score.

Conclusions

Multimodal vascular CMR shows regional abnormalities of vascular structure and function that correlate modestly with the degree and extent of CAD.     

A focus on inflammation as a major risk factor for atherosclerotic cardiovascular diseases

Atherosclerosis is a dynamic, pathogenic process in the artery wall, with potential adverse outcome for the host. Acute events such as myocardial infarction and ischemic stroke often result from rupture of unstable atherosclerotic lesions. Understanding the underlying pathology of such lesions and why and when they rupture, is therefore of great interest for the development of new diagnostics and treatment. Inflammation is one of the key drivers of atherosclerotic plaque development and the interplay between inflammation and lipids constitutes the hallmark of atherosclerotic disease. This review summarizes the role of inflammation in atherosclerosis and presents some of the latest discoveries as well as unmet needs regarding the role of inflammation as major risk factor in atherosclerotic disease.     

Plaque progression and regression in atherothrombosis

Summary.  Atherosclerotic disease is a pathological process characterized by the deposition of lipid and other blood-borne material within the arterial wall. The deposition of these materials and the subsequent thickening of the wall may significantly compromise the vessel lumen. Atherosclerosis is a diffuse disease with focal clinical manifestations that are the consequence of thrombotic complications on disrupted atherosclerotic lesions. Until recently, atherosclerosis development was envisaged as an incessant progressing process; however, new evidence has shown that atherosclerotic plaque homeostasis is not necessarily a constantly progressing process. There are many data showing that atherosclerotic plaque formation can be slowed, stopped or even reversed. Comprehension of the underlying mechanisms involved in the homeostasis of atherosclerotic plaque (progression/regression) should allow the development of interventions enhancing the regression pathway. Novel imaging technology has allowed the accurate evaluation of plaque progression, vital in the assessment of the efficacy of interventions. In this review we discuss the processes involved in the formation and progression of atherosclerotic lesions, the triggers for plaque disruption, as well as new therapies. We also deal with the potential pathways of plaque regression, as well as tools for accurate serial atherosclerotic quantification.     

Simultaneous measurement of vibrations on arterial wall upstream and downstream of arteriostenosis lesion and their analysis

Acute myocardial infarction and cerebral infarction are generally known to be caused primarily by the rupture of atherosclerotic plaques. It is thus necessary for clinical treatment to predict the rupture of these plaques. Blood-flow velocity around atherosclerotic plaques increases as the arteriostenosis lesion progresses, resulting in turbulence downstream of the lesion. The resulting change in blood pressure produces shear stress, and change in this stress affects the rupture of the atherosclerotic plaques. Cerebral ischemic paroxysm and cerebral infarction have been reported to occur in a high percentage of cases in which inner vessel diameter has decreased to less than 70% of its original diameter as a result of stenosis. This explains the use of standard ultrasonic diagnostic equipment to measure blood flow in the screening of the carotid arteries. On the other hand, the noise signal radiated from an aneurysm as a result of blood flow has been measured using the bruit sensor used to diagnose cerebrovascular diseases. Many unsolved problems with regard to the relationship between noise and turbulence in blood flow remain, however. Here, small vibrations on the arterial wall were measured transcutaneously and analyzed both upstream and downstream of the atherosclerotic plaque of a human carotid artery. Characteristics of the resultant vibrations upstream of the stenosis clearly differed from those downstream of it. These results should prove useful in predicting the rupture of atherosclerotic plaques.