Contribution of inadequate compensatory enlargement to development of human coronary artery stenosis: An in vivo intravascular ultrasound study

Objectives. This intravascular ultrasound study sought to examine to what extent native coronary artery stenosis is accompanied by vessel wall thickening or inadequate compensatory enlargement (relative vessel constriction), or both.

Background. In human femoral arteries, inadequate compensatory enlargement is reported to be a paradoxic mechanism for the development of severe arterial lumen narrowing. However, it is unclear in human coronary arteries whether inadequate compensatory enlargement contributes to the development of critical arterial stenosis.

Methods. Thirty-five primary coronary artery lesions from 30 patients (19 men, 11 women; mean [±SD] age 65 ± 13 years) were imaged by intravascular ultrasound. The vessel cross-sectional area and lumen area were measured, and the wall area (vessel cross-sectional area minus lumen area) was calculated at the lesion site and at the proximal and distal reference sites. We defined compensatory enlargement to be present when the vessel cross-sectional area at the lesion site was larger than that at the proximal reference site, inadequate compensatory enlargement when the vessel cross-sectional area at the lession site was smaller than that at the distal reference site and intermediate remodelling when the vessel cross-sectional area at the lesion site was intermediate between the two reference sites.

Results. Compensatory enlargement was observed in 19 (54%) of 35 lesions, inadequate compensatory enlargement in 9 (25%) of 35 and intermediate remodeling in 7 (20%) of 35. In the inadequate compensatory enlargement group, reduction of the vessel cross-sectional area contributed to 39% of lumen reduction.

Conclusions. Compensatory enlargement commonly (54%) occurs at stenotic coronary lesions. However, inadequate compensatory enlargement results in a substantial amount (39%) of the lumen area reduction in 26% of primary coronary artery lesions.     

Compensatory enlargement of human coronary arteries during progression of atherosclerosis is unrelated to atheroma burden: serial intravascular ultrasound observations from the REVERSAL trial.

AIMS: On the basis of the evidence from autopsy studies, it is accepted that compensatory enlargement (remodelling) of coronary arteries during progression of atherosclerosis diminishes once atheroma burden (cross-sectional area stenosis) reaches approximately 40%. Our aim was to evaluate whether atheroma burden is a limiting factor for coronary arterial remodelling using in vivo serial intravascular ultrasound (IVUS). METHODS AND RESULTS: From the cohort of the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, we identified 210 focal coronary lesions at baseline IVUS. Of these, 128 lesions that had an increase in atheroma area at the 18-month follow-up IVUS were included in the analysis. Lesions were matched at baseline and follow-up. The increase in external elastic membrane (EEM) area for each mm(2) increase in atheroma area was not significantly different in lesions with <40 and >or=40% atheroma burden at baseline (1.62 vs. 1.28 mm(2), P=0.30). There were no correlations between atheroma burden at baseline and change in EEM (r=0.02, P=0.86) or change in lumen (r=0.04, P=0.64) areas. CONCLUSION: Assessment of coronary arterial remodelling by serial IVUS revealed that compensatory remodelling is not limited by atheroma burden. Atheroma burden is not a determinant of arterial enlargement during the progression of atherosclerosis.     

Shrinkage of human coronary arteries is an important determinant of de novo atherosclerotic luminal stenosis: an in vivo intravascular ultrasound study

Objective—To assess the occurrence of arterial remodelling types and its relation with the severity of luminal stenosis in atherosclerotic coronary arteries.
Patients and methods—Twenty one de novo coronary lesions of 20 patients, who were scheduled for percutaneous transluminal coronary angioplasty (PTCA), were investigated with intravascular ultrasound before PTCA. Local arterial remodelling at the lesion site was studied by measuring the cross sectional area circumscribed by the external elastic lamina (EEL) relative to the reference site: (EEL area lesion/reference EEL area) × 100%. Three groups were defined. Group A: relative EEL area of less than 95% (shrinkage), group B: relative EEL area between 95% and 105% (no remodelling), group C: relative increase in EEL area of more than 105% (compensatory enlargement).
Results—All three types of remodelling were observed at the lesion site: group A (shrinkage) n = 8, group B (no remodelling) n = 5, group C (compensatory enlargement) n = 8. The mean (SD) relative EEL area at the lesion site in group A and C was 83(9)% and 132(30)%, respectively. In group A, 33% of the luminal area stenosis at the lesion site was caused by shrinkage of the artery. In contrast, group C showed that 87% of the plaque area did not contribute to luminal area stenosis because of compensatory arterial enlargement.
Conclusions—These results show that both compensatory enlargement and paradoxical shrinkage occurs in the atherosclerotic coronary artery. Next to plaque accumulation, the type of atherosclerotic remodelling is an important determinant of luminal narrowing.

Keywords: coronary arteries; atherosclerosis; remodelling; intravascular ultrasound     

Plaque distribution and vascular remodeling of ruptured and nonruptured coronary plaques in the same vessel: an intravascular ultrasound study in vivo

OBJECTIVES: This study was designed to identify potential differences between the intravascular ultrasound (IVUS) characteristics of spontaneously ruptured and nonruptured coronary plaques. BACKGROUND: The identification of vulnerable plaques in vivo may allow targeted prevention of acute coronary events and more effective evaluation of novel therapeutic approaches. METHODS: Intravascular ultrasound was used to identify 29 ruptured plaques in arteries containing another nonruptured plaque in an adjacent segment. Intravascular ultrasound characteristics of these plaques were compared with plaques of computer-matched controls without evidence of plaque rupture. Plaque distribution was assessed by measuring the eccentricity of lumen location (inside the total vessel). Lumen cross-sectional area narrowing was calculated as [1 - (target/reference lumen area)] x 100%. A remodeling index was calculated as lesion/reference arterial area (>1.05 = compensatory enlargement, <0.95 = shrinkage). RESULTS: Among the three groups of plaques, there was no significant difference in quantitative angiographic parameters, IVUS reference dimensions and IVUS lumen cross-sectional area narrowing. There was a difference in plaque distribution; lumen location by IVUS was significantly more eccentric in ruptured than in nonruptured (p = 0.002) and control plaques (p < 0.0001). The arc of disease-free vessel wall was larger in ruptured than in control plaques (p < 0.0001). The remodeling pattern of ruptured and nonruptured plaques differed significantly from that of the control plaques (p = 0.0001 and 0.003); compensatory enlargement was found in 66%, 48%, and 17%, whereas shrinkage was found in 7%, 10% and 48%, respectively. CONCLUSIONS: Intravascular ultrasound assessment of plaque distribution and vascular remodeling may help to classify plaques with the highest probability of spontaneous rupture.     

Attenuation of the media of coronary arteries in advanced atherosclerosis

Human coronary artery wall architecture was analyzed in detail in 127 histologic sections with varying degrees of narrowing due to atherosclerotic plaque. A planimetry-microscope system was used to morphometrically determine percent luminal cross-sectional area narrowing due to atherosclerotic plaque, absolute area of the coronary artery media and total cross-sectional area of the coronary artery section. In 65 sections in which the native coronary artery lumen was narrowed less than 75%, the area of the coronary artery media corrected for total coronary cross-sectional area (Mc) was 0.244 +/- 0.055 mm2. In contrast, among 62 sections in which the coronary artery lumen was narrowed more than 75% in cross-sectional area, Mc measured 0.180 +/- 0.078 (p less than 0.001). Thus, in coronary artery segments with advanced atherosclerosis, there is substantial attenuation of the media, normally the principal component of the coronary artery wall.     

Impaired compensatory coronary artery enlargement in atherosclerosis contributes to the development of coronary artery stenosis in diabetic patients: An in vivo intravascular ultrasound study

AIMS: Coronary arteries affected by atherosclerosis undergo focalcompensatory enlargement, which can be detected by intracoronaryultrasound but not by angiography. Diabetic patients when comparedwith non-diabetics have a more accelerated progression of coronaryartery disease and a more diffuse narrowing of the coronaryarteries. Intracoronary ultrasound can clarify if this is dueto less compensatory coronary artery enlargement as a responseto atherosclerosis. METHODS AND RESULTS: Ten non-diabetic and 15 diabetic patients with coronary arterydisease, with angiographically determined one- or two-vesseldisease, underwent intracoronary ultrasound examination of thenon-stenotic coronary artery. Forty-five sites with luminalstenosis, detected by intracoronary ultrasound, were analysed(15 in non-diabetics, 30 in diabetics). Vessel and lumen area,atherosclerotic plaque area and plaque composition were evaluated.Vessel area was also measured proximal and distal to the healthysegment. In the diabetic patients, there was less vessel areaincrease from the proximal healthy segment into the atheroscleroticsegment than in the non-diabetic patients (99% separate-varianceconfidence intervals for differences between diabetics' andnon-diabetics' means=0·29 mm², 2·71 mm²). Theproximal plaque free vessel area, the atherosclerotic plaquearea and plaque composition were similar between the two groups. CONCLUSION: Diabetics with atherosclerosis have less compensatory coronaryartery enlargement than non-diabetics. This may explain thediffuse and accelerated course of coronary artery disease inthese patients.     

Arterial remodeling in the left coronary system: the role of high-density lipoprotein cholesterol.

OBJECTIVES: We sought to evaluate the plaque and patient variables related to arterial remodeling responses of early, de novo atherosclerotic lesions involving the left coronary artery. BACKGROUND: Coronary artery remodeling is a lesion-specific process involving either enlargement or shrinkage of atherosclerotic coronary arteries. There are little histologic data available correlating plaque morphologic and patient clinical characteristics with the degree and type of arterial remodeling in early atherosclerosis. METHODS: We studied 736 serial arterial sections from the left coronary system of 97 autopsy cases (mean age 33 +/- 11 years) by correlating the arterial remodeling response to plaque with demographic, serologic and histologic variables. Using the most proximal section as a reference, and considering the expected degree of internal elastic lamina tapering, remodeling was classified as positive (including neutral remodeling or compensatory enlargement) or negative. RESULTS: Remodeling was classified as positive in 84.3% (compensatory in 30.6%) and negative in 15.7% of sections with an overall mean luminal stenosis of 10.4 +/- 9.9%. In the lesions with the greatest arterial cross-sectional narrowing from each case, compensatory enlargement was associated with higher high-density lipoprotein (HDL) cholesterol (59.4 +/- 27.2 mg/dl) compared with either neutral (49.3 +/- 15.5 mg/dl) or negative remodeling (30.4 +/- 5.2 mg/dl; p = 0.019). In subjects with advanced atherosclerosis (maximum American Heart Association histologic grade 5 atherosclerosis), there was a modest linear relationship between higher HDL cholesterol and the propensity for positive remodeling (r2 = 0.37; p = 0.025). On multivariate analysis, only HDL cholesterol was related to the arterial remodeling response. CONCLUSIONS: Negative arterial remodeling occurs in early atherosclerosis. Higher HDL cholesterol may favor positive remodeling.     

Imaging of atherosclerosis. Remodelling of coronary arteries

Next to plaque formation, arterial geometric remodelling is an important determinant of luminal narrowing in atherosclerotic disease. Expansive remodelling retards, whereas constrictive remodelling accelerates lumen loss by plaque formation. Expansive arterial remodelling is a double edged sword, however. While luminal area is preserved, the plaque beneath the surface of the lumen often reveals large atheroma with heavy inflammation in expansive remodelling. These characteristics have been associated with plaque rupture and subsequent myocardial infarction. Thus, in the long term expansive remodelling may lead to thrombosis of angiographically silent lesions while constrictive remodelling is often associated with stable coronary syndromes. The mechanisms of arterial remodelling are poorly understood. This is mainly due to lack of good in vitro and animal models which makes mechanistic studies difficult.     

Invasion of atheromatous plaques into tunica media causes coronary outward remodeling in WHHLMI rabbits

To clarify the mechanism of coronary outward remodeling, we examined atherosclerotic coronary arteries morphologically using WHHLMI rabbits that develop coronary atherosclerosis spontaneously. Perfusion-fixed coronary segments of WHHLMI rabbits were prepared at 500microm intervals. After immunohistochemical staining and histopathological staining, the areas and lengths of the arterial wall and the lesions were measured. Obvious outward remodeling was observed in coronary sections with greater than 40% cross-sectional narrowing. In coronary sections with greater than 40% cross-sectional narrowing, the tunica media was thick at the shoulder of atheromatous plaque and was thin beneath the atheromatous plaques. Macrophages infiltrated those attenuated tunica media expressed matrix metalloproteinases and oxidized LDL was accumulated in those areas. In those areas, collagen fibers and the internal elastic lamina had disappeared partly and apoptotic smooth muscle cells were observed. Proliferation of smooth muscle cells was observed at the attenuated tunica media and adjacent adventitia. The present results suggest that invasion of atheromatous plaques into the tunica media causes coronary outward remodeling.     

Failure of angiography to accurately depict the extent of coronary artery narrowing in three fatal cases of percutaneous transluminal coronary angioplasty.

The angiographic and pathologic findings are described in three patients who died less than 24 h after failed percutaneous transluminal coronary angioplasty. In two of the three patients, coronary angiography performed before angioplasty disclosed apparently focal lesions in the left anterior descending and right coronary arteries. In these two patients quantitative angiographic analysis disclosed a minimal lumen cross-sectional area of 1.82 and 0.47 mm2, respectively, at the sites of apparently focal stenoses before angioplasty; corresponding percent lumen area narrowing measured 84% and 91%, respectively, by quantitative angiography at these two sites. In the third patient, coronary angioplasty was undertaken when the patient developed spontaneous occlusion of the right coronary artery several hours after diagnostic angiography. Retrospective quantitative angiographic analysis of the right coronary artery revealed a minimal lumen cross-sectional area of 1.14 mm2, with 85% lumen area narrowing at the site of subsequent total occlusion and angioplasty. In each of these three patients, necropsy examination disclosed that the distribution of coronary narrowing in the artery treated by angioplasty was in fact not focal; rather, in each of these three patients, the artery treated by angioplasty, as well as the extramural coronary arteries not treated by angioplasty, were severely narrowed by diffusely distributed atherosclerotic plaque. The angiographic and necropsy findings in these three patients document that coronary narrowing that remains occult by virtue of diffuse distribution may complicate evaluation of patients being considered for coronary angioplasty.     

Amounts of coronary arterial narrowing by atherosclerotic plaque at necropsy in patients with lower extremity amputation.

In 26 patients (mean age at death 68 +/- 9 years) who had undergone amputation (at mean age 63 +/- 12 years) of 1 or both lower extremities due to severe peripheral arterial atherosclerosis, the amounts of narrowing at necropsy in the 4 major (left main, left anterior descending, left circumflex, and right) epicardial coronary arteries were determined. During life, 15 of the 26 patients (58%) had symptoms of myocardial ischemia: angina pectoris alone in 1, acute myocardial infarction alone in 5, and angina and/or infarction plus congestive heart failure or sudden coronary death in 9. Twelve of the 26 patients (42%) died from consequences of myocardial ischemia: acute myocardial infarction in 5, sudden coronary death in 3, chronic congestive heart failure in 3, and shortly after coronary bypass surgery in 1. Grossly visible left ventricular necrosis or fibrosis, or both, was present in 21 patients (81%). Of the 26 patients, 24 (92%) had narrowing 76 to 100% in cross-sectional area of 1 or more major coronary arteries by atherosclerotic plaque. The mean number of coronary arteries per patient severely (> 75%) narrowed was 2.3 +/- 1.0/4.0. Of the 104 major coronary arteries in the 26 patients, 60 (58%) were narrowed > 75% in cross-sectional area by plaque. The 4 major coronary arteries in the 26 patients were divided into 5-mm segments and a histologic section, stained by the Movat method, was prepared from each segment.(ABSTRACT TRUNCATED AT 250 WORDS)     

The natural course of atherosclerosis. Part II: vascular remodeling. Bruneck Study Group.

Arterial remodelling is a potentially important component in atherogenesis aimed at delaying the development of significant lumen compromise. Current knowledge on this phenomenon is mainly restricted to experimental evaluations and a few postmortem studies. We used high-resolution duplex ultrasound to study 5-year changes (1990 to 1995) in vessel geometry in a large random sample of the general population (Bruneck Study). Carotid arteries free of atherosclerosis and wall thickening preserved a normal size to high ages. In contrast, common and internal carotid arteries with elevated intima-media thickness (>/=50th percentile) experienced marked age-dependent dilation that started already in the 5th decade and continuously accelerated thereafter (structural ageing). Vessel diameters were subject to complex regulation involving morphometric characteristics, sex, wall thickness, hypertension, LDL cholesterol levels, and alcohol consumption. Vascular remodelling secondary to incident or slowly progressive (mural) atherosclerosis included local compensation and a generalised dilation response of vascular segments not primarily affected. Adaptive enlargement at the site of active atherogenesis effectively preserved a near-normal lumen in most instances. The current study identified a second main type of plaque growth, characterized by episodic marked increase in lesion volume probably on the basis of plaque thrombosis. In this setting, we did not observe maximum but insufficient compensation but instead usually observed no compensation at all. Failure of vascular remodelling and marked expansion in plaque size acted synergistically in producing significant lumen compromise. The current prospective survey describes fundamental principles and various facets of arterial remodelling and vascular biology in the general population (in vivo). Vessel geometry was subject to marked temporal changes and showed a correspondingly complex (multifactorial) and dynamic regulation. Vascular remodelling emerged as an important compensatory process in human atherogenesis, which crucially contributed to the determination of lumen obstruction. Efficacy and failure of compensation primarily depended on the type and pathomechanisms of underlying atherogenesis and only in second instance on plaque size and location.     

What have we learned about coronary artery disease from high-frequency epicardial echocardiography?

We have used a high frequency epicardial echocardiographic technique to visualize and measure coronary artery lumens and walls in patients undergoing cardiac surgery. A 12 MHz probe (Surgiscan, Biosound Corp.) is sterilized and placed on the exposed epicardial coronary arteries. Transverse cross-sectional views are obtained from the arteries on the anterior surface of the heart: the right coronary artery to the cardiac margin and the left anterior descending coronary artery to the cardiac apex.Numerous echocardiographic-angiographic-pathological correlations have been obtained from this work. We have validated the echocardiographic lumen and wall measurements by comparing the echo measurements to histological material from pressure-distended coronary arterial segments (from animals and fresh human autopsy specimens). We have shown by comparison with angiography that coronary arteries which appear normal or only minimally diseased by angiograms are often diffusely and severely atherosclerotic. We have also evaluated the shape of atherosclerotic lesions and demonstrated a wide range of lumen shapes (oval, circular, complex) and location within the residual coronary lumen (eccentric vs. concentric). Highly eccentric lesions are characterized by relative preservation of portions of the arterial wall, and this may preserve vasoreactivity of the atherosclerotic vessel. We have also demonstrated remodeling of atherosclerotic lesions: enlargement of the total arterial area (wall plus lumen) as a compensatory mechanism to preserve the arterial lumen in the face of encroaching atherosclerosis.High frequency epicardial echocardiography offers an accurate, real-time, in-vivo method for the anatomic and functional evaluation of coronary atherosclerosis. This dynamic, in-vivo technique supports and extends information previously obtainable only from pathologic studies. It contributes to our understanding of the pathologic anatomy of coronary artery disease.     

Intravascular ultrasound assessment of ambiguous coronary lesions

Accurate assessment of coronary lesions is essential for clinical decision-making. While angiography has long been accepted as the gold standard investigation, this technique provides only a planar 2-D silhouette of the arterial lumen and therefore has limited accuracy in the setting of vessel tortuosity or overlap, bifurcational and eccentric lesions, and diffusely diseased arteries. By providing high-resolution cross-sectional imaging through the arterial wall, intravascular ultrasound (IVUS) can overcome many of these limitations and accurately quantify angiographically indeterminate lesions. Angiographic evaluation of the left main coronary artery presents particular challenges that are ideally resolved with IVUS examination. The role of IVUS in the assessment of coronary stenoses of angiographically intermediate severity (50-70%) continues to evolve. Recent data correlating IVUS with intracoronary flow and pressure measurements suggest that epicardial coronary artery lesions with minimum lumen area of less than 3-4 mm2 may be haemodynamically significant. In addition to accurately quantifying minimum lumen diameter and area at the lesion site, IVUS can characterise coronary artery plaque morphology, and it may have the potential to predict plaque complications.     

Vascular remodelling after cardiac transplantation: a 3-year serial intravascular ultrasound study.

AIMS: To assess the time-course of intimal hyperplasia and vascular remodelling, and their relative contributions on luminal narrowing in transplant coronary artery disease (TCAD) by a 3-year serial intravascular ultrasound (IVUS) study. METHODS AND RESULTS: Serial IVUS examinations were performed in 90 cardiac transplant recipients at 1.4+/-0.6 months after transplantation and again annually thereafter for 3 years. From 90 arteries, 304 sites were matched from baseline to the third year post-transplant. Based on the change in external elastic membrane (EEM) area +/-10% at 1 year, 304 sites were divided into three groups: sites with no remodelling (52%); early constrictive remodelling (26%); and early compensatory enlargement (22%). Greater intimal growth was seen at 1 year in sites with early compensatory enlargement, whereas there was no change in intimal area in sites with early constrictive remodelling. Over 3 years, the cumulative lumen loss was greater in sites with early constrictive remodelling than in sites with early compensatory enlargement or no remodelling (P<0.001). When luminal narrowing occurred for each annual interval, the contribution from the decrease in EEM area was greater than that due to intimal thickening (P<0.001). CONCLUSION: During the first 3 years post-transplant, the largest intimal growth occurs in the first year, mostly in sites with early compensatory enlargement. The contribution to luminal loss in TCAD is greater from constrictive remodelling than from intimal hyperplasia. The type of remodelling pattern that occurs in transplanted coronary arteries within the first year post-transplant may be a predictor of the progression of luminal narrowing during subsequent years.     

Coronary arterial remodeling studied by high-frequency epicardial echocardiography: an early compensatory mechanism in patients with obstructive coronary atherosclerosis

Coronary arterial remodeling is a compensatory mechanism that may limit the adverse effects of coronary obstructive lesions by expansion of the entire vascular segment. To determine if this compensatory anatomic change occurs in patients, high-frequency epicardial echocardiography using a 12 MHz transducer was performed during open heart surgery in 33 patients (10 with normal coronary arteries undergoing valvular surgery and 23 with coronary atherosclerosis). From stop-frame videotape high-frequency epicardial echocardiographic images, cross-sectional measurements of luminal area and total arterial area (lumen, intima, media and dense adventitia) were made in the patients with atherosclerosis at the site of arterial lesions and from the most proximal portion of the same artery. Remodeling was defined as enlargement of the total arterial area. In normal arteries measurements were made from proximal and midarterial locations. In the patients with normal coronary arteries, total arterial area, as determined by high-frequency echocardiography, decreased from the proximal site to the midportion of the artery (from 10.4 +/- 0.9 to 8.4 +/- 1.0 mm2, p less than 0.05); luminal area also decreased (from 6.0 +/- 0.6 to 4.5 +/- 0.7 mm2, p less than 0.05). In patients with coronary arterial lesions, luminal area also decreased from the proximal site to the arterial lesion site (from 5.3 +/- 0.6 to 2.3 +/- 0.3 mm2, p less than 0.05), but total arterial area increased (from 11.6 +/- 1.0 to 13.0 +/- 1.0 mm2, p less than 0.05). Of the 25 coronary arteries evaluated, only 4 had angiographic evidence of coronary collateral formation. These data indicate that coronary arterial remodeling is an important compensatory mechanism in obstructive coronary disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impact of compensatory enlargement of atherosclerotic coronary arteries on angiographic assessment of coronary artery disease

To determine whether compensatory enlargement of atherosclerotic coronary arteries occurs and to what degree it affects the angiographic assessment of coronary artery disease, we performed postmortem coronary angiography of 30 human hearts with suspected coronary artery disease and studied 70 histologic cross sections of the proximal left anterior descending artery and proximal right coronary artery. Angiographic and morphometric analyses of 50 stenoses in proximal and middle sections of the left anterior descending artery, right coronary artery, and left circumflex artery were performed. The control group of 10 human hearts without suspected coronary artery disease was evaluated in the same way. For this purpose, coronary arteries were filled with a methylmethacrylic radiopaque resin at a pressure of 100 mm Hg and closely embedded in a methylmethacrylic resin by use of which shrinkage and mechanical artifacts could be avoided. The area circumscribed by the internal elastic lamina was taken as a measure of the area of the arterial lumen if no plaque had been present. The angiographic and corresponding morphometric degree of stenosis was assessed. A significant correlation (r = 0.85, p less than or equal to 0.0001) was found between the internal elastic lamina area and the area of the plaque (lesion area), suggesting that coronary arteries may enlarge as lesion area increases. With the morphometric degree of stenosis, the expected anatomic diminution of the coronary artery was abolished (r = 0.79, p less than or equal to 0.0001), indicating compensatory enlargement in atherosclerotic segments. Accordingly, the degree of stenosis assessed from in vitro angiograms was underestimated. Compensatory coronary enlargement of the stenotic segment was the main reason for angiographic underestimation. The underestimation factor of up to 3.50 for very mild stenoses decreased to 1.37 at an angiographic degree of 50% area stenosis and 30% diameter stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intravascular ultrasound imaging in human peripheral and coronary arteries in vivo.

To determine the feasibility of intravascular ultrasound imaging in vivo, a miniaturized high frequency transducer catheter was introduced into human peripheral (n = 10) and coronary (n = 4) arteries. Cross-sectional ultrasound images were obtained from iliofemoral arteries in 10 patients using a 20 MHz transducer catheter (1.2 mm in diameter) and from coronary arteries in 4 patients using a 30 MHz transducer catheter 5 French size (Fr) following successful coronary angioplasty. Ultrasound images obtained from peripheral arteries showed a three-layered appearance (echo-reflective intima, echo-lucent media and echo-reflective adventitia) in the normal arteries. In diseased arteries, the location, amount and extent of atheromatous plaque were clearly documented. The arterial diameters measured by ultrasound closely correlated with the measurements by angiography (r = 0.91) in the peripheral arteries. Coronary angiograms obtained following balloon angioplasty revealed smooth edges at the dilatation sites without significant narrowing in all patients. However, a significant amount of residual atheromatous plaque was clearly observed on the ultrasound images at the previously dilated sites. Coronary dissection, which was identified as an echo-lucent area behind the plaque, was noted in 2 patients. Ultrasound images also revealed the presence of calcium in the plaque which was unrecognized on the angiograms in 3 patients. In addition, direct measurement of the lumen cross-sectional area was possible on the ultrasound images.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of atherosclerotic regression on total luminal size of coronary arteries as determined by intravascular ultrasound

We assessed vascular changes during atherosclerosis regression. Compensatory enlargement of coronary arteries accommodates plaque burden during atherosclerosis development. Lipid-lowering therapy has altered the natural history of coronary atherosclerosis, but the arterial changes that occur during disease regression need to be clarified. Intravascular ultrasound was performed at baseline and after approximately 18 months in 432 patients with coronary disease. Mean plaque, lumen, and total vessel area were computed in a 30-mm coronary segment of interest. Mean low-density lipoprotein cholesterol level was 2.4 mmol/L, and 88% of patients received statins. Overall, changes in plaque and total vessel areas were highly correlated (r = 0.82, p <0.0001). Among the 227 patients with plaque regression, the plaque area decrease was -0.58 +/- 0.54 mm(2), and changes in total vessel and lumen areas were -1.02 +/- 1.10 and -0.44 +/- 0.86 mm(2), respectively. The decrease in plaque area correlated better with the change in total vessel area (r = 0.64, p <0.0001) than with the change in lumen area (r = 0.20, p = 0.003). The relation between plaque regression and decrease in total vessel area was significantly better (p = 0.019) for patients with a >40% atheroma area (r = 0.72; p <0.0001) than for those with 相似文献   

Assessment of coronary compensatory enlargement by three-dimensional intravascular ultrasound

Several techniques have been used to demonstrate that human arteries respond to atherosclerosis by increasing their total arterial area to prevent a decrease in blood flow. Three-dimensional reconstructions of coronary arteries can document this compensatory response accurately and specifically. Seven human coronary arteries were reconstructed using intravascular ultrasound and biplane angiography, and vessel geometries were quantified. In all seven vessels, as plaque area increased, overall vessel area increased (R = 0.986, 0.933, 0.984, 0.678, 0.763, 0.963, and 0.830), but luminal cross-sectional area did not significantly decrease. Focal compensatory enlargement was identified in each vessel, and in some cases this response appeared to occur until the vessel was 65% occluded. Luminal enlargement near the proximal ends was attributed to the natural taper of the vessel. The semi-automated, three-dimensional segmentation technique used in this study allows reproducible quantification, as there is no subjective manual tracing involved. Following the intravascular ultrasound transducer in time and space with biplane angiography allows for accurate reconstruction with or without automated pullback devices. Information on the rate of change of vessel measurements is also presented, which, when combined with visualization of accurate 3D geometry, provides a unique assessment of coronary compensatory enlargement. This reconstruction technique can be applied in a clinical environment with no major modification.