Intravascular ultrasound assessment of the presence of vascular remodeling in diseased human saphenous vein bypass grafts

Remodeling occurs in diseased human coronary arteries; however, reports of remodeling in diseased autologous saphenous vein bypass graft (SVG) stenoses are inconsistent. Preintervention intravascular ultrasound and quantitative coronary angiography were used to study 104 SVG stenoses in 93 consecutive patients. Lesion site and proximal and distal reference segment measurements included vein graft, external elastic membrane, lumen, wall (vein graft minus lumen), and plaque (external elastic membrane minus lumen) areas. Three indexes of remodeling were assessed: (1) lesion site SVG (or external elastic membrane) area was compared with the average reference segment, (2) SVG area was correlated with the wall area and external elastic membrane area was correlated with the plaque area, and (3) the impact of excess plaque accumulation (at the stenosis compared with the reference segment) on lumen compromise was calculated. Overall, the ratio of lesion/reference vein graft area was 1.07 +/- 0.25; however, 23 lesions were classified as negative remodeling (ratio <0.9), 37 as intermediate remodeling (ratio between 0.9 and 1.1), and 44 as positive remodeling (ratio >1.1). Reference segment vein graft area correlated with wall area (r = 0.906, p <0.0001), and external elastic membrane area correlated with plaque area (r = 0.703, p <0.0001). Similarly, lesion site vein graft area correlated with wall area (r = 0.978, p <0.0001), and external elastic membrane area correlated with plaque area (r = 0.961, p <0.0001). The regression line relating delta lumen area to delta wall area was y = -0.22 x - 6.2 (r = 0.451, p <0.0001) and the regression line relating delta lumen to delta plaque area was y = -0.47 x - 4.5 (r = 0.572, p <0.0001). (A slope of 0 would indicate perfect positive remodeling and a slope of 1.0 no positive remodeling.) Diseased SVGs undergo positive and negative remodeling similar to native coronary arteries.     

Association of plaque characterization by intravascular ultrasound virtual histology and arterial remodeling

Positive remodeling is more often observed in lesions of patients who have acute coronary syndromes or vulnerable (rupture-prone) plaques. However, there are few data that correlate plaque morphology, composition, and arterial remodeling in vivo. We evaluated coronary plaque characterization of lesions with positive remodeling using intravascular ultrasound (IVUS) radiofrequency data analysis. Seventy-seven nonbifurcation native coronary lesions (in 50 patients) were imaged in vivo using 30-MHz IVUS transducers. Lesions were classified into 4 plaque types, fibrous, fibrofatty, dense calcium, and necrotic core, by using processing of the radiofrequency signal validated in vitro. The remodeling index was calculated as the lesion external elastic membrane area divided by the proximal reference external elastic membrane area. Lesions were divided into 2 groups: positive remodeling (remodeling index>1.0, 26 lesions) and intermediate/negative remodeling (remodeling index相似文献   

Correlation of coronary arterial remodeling determined by intravascular ultrasound with angiographic diameter reduction of 20% to 60%

Negative remodeling is commonly observed in stenotic coronary lesions. It is unknown whether negative remodeling is an early or late event. This study was designed to elucidate when negative remodeling occurs in the development of coronary stenosis. Remodeling was assessed by preintervention intravascular ultrasound in 104 native coronary lesions with intermediate stenosis (20% to 60% of diameter stenosis measured by quantitative coronary angiography). Positive remodeling was defined as lesion external elastic membrane (EEM) cross-sectional area (CSA) greater than the proximal reference, intermediate remodeling as lesion EEM CSA between those of the proximal and distal references, and negative remodeling as lesion EEM CSA less than the distal reference. Positive, intermediate, and negative remodeling were observed in 18%, 32%, and 50%, respectively, of lesions with intermediate stenosis. Lesions with negative and intermediate remodeling had more hard plaque compared with those with positive remodeling (79% vs 70% vs 42%, p = 0.02). Calcium was more frequent in lesions with negative and intermediate remodeling than in those with positive remodeling (52% vs 55% vs 16%, p = 0.01). Lesions with negative remodeling had smaller EEM CSA (11.5 +/- 5.2 vs. 13.7 +/- 3.4 vs 14.5 +/- 5.6 mm(2), p = 0.03) and less plaque (7.9 +/- 4.6 vs 10.8 +/- 3.4 vs 10.8 +/- 4.9 mm(2), p = 0.004) compared with positive and intermediate remodeling lesions, although lumen CSA (3.7 +/- 1.7 vs 2.8 +/- 0.8 vs 3.6 +/- 1.3 mm(2), p = 0.1) and area stenosis (57 +/- 15% vs 59 +/- 14% vs 56 +/- 10%, p = 0.7) were similar. Negative remodeling is frequently observed in lesions with intermediate stenosis. This suggests that negative remodeling occurs early in lesion formation.     

Effect of simvastatin on coronary lesion site remodeling: a serial intravascular ultrasound study

BACKGROUND: Direct evidence of coronary artery remodeling can be derived only from serial changes in the external elastic membrane (EEM) and plaque area. The aim of the study was to assess the effect of simvastatin on coronary remodeling in serial intravascular ultrasound (IVUS) studies. METHODS: In 39 male patients ECG-triggered transducer pullback IVUS was performed at baseline, after 3 months on a lipid-lowering diet (control period), and after another 12 months of simvastatin 40 mg/day. The lesion site was the image slice with maximum plaque burden at 3 months. RESULTS: Absolute changes in the EEM area correlated significantly with changes in plaque area during the control period [B = 0.966, r = 0.792 (95% CI 0.71-1.22); p < 0.001] and during simvastatin treatment [B = 0.945, r = 0.822 (95% CI 0.73-1.16); p < 0.001], but there was no significant difference in the slope (delta EEM/delta plaque) between the two time intervals. After 12 months of simvastatin, there was a significant reduction in the lesion EEM area of 4.6% (p = 0.006) and in the lesion plaque area of 5.9% (p < 0.001), but there was no change in reference measurements. As a result, the remodeling index was reduced by simvastatin from 1.01 +/- 0.12 to 0.95 +/- 0.09 (p < 0.001). CONCLUSION: Simvastatin decreases the remodeling index by reducing lesion, but not reference plaque and EEM area. However, simvastatin does not affect direct evidence of remodeling (delta EEM/delta plaque) obtained using serial IVUS studies.     

Mechanisms of acute gain and late lumen loss after atherectomy in different preintervention arterial remodeling patterns

The main mechanism of restenosis after directional coronary atherectomy (DCA) remains obscure. We investigated mechanisms of restenosis after DCA in different coronary artery remodeling patterns. DCA was performed in 51 de novo lesions. The lesions were evaluated by intravascular ultrasound (IVUS) before, immediately after, and 6 months after the procedure. According to the IVUS findings before DCA, we classified the lesions into the following 3 groups: (1) positive (n = 10), (2) intermediate (n = 25), and (3) negative (n = 16) remodeling. We measured lumen area, vessel area, and plaque area using IVUS before DCA, immediately after DCA, and at follow-up. Lumen area increase after DCA was mainly due to plaque area reduction in the positive and intermediate remodeling groups (90 plus minus 15% and 80 plus minus 25% increase in lumen area, respectively), whereas that in the negative remodeling group was due to both plaque area reduction (57 plus minus 22% increase in lumen area) and vessel area enlargement (43 plus minus 33% increase in lumen area). The plaque area increase correlated strongly with late lumen area loss in the positive and intermediate remodeling groups (r = 0.884, p <0.001; r = 0.626, p <0.001, respectively), but the decrease in vessel area was not correlated with lumen area loss. In contrast, both an increase in plaque area and a decrease in vessel area were correlated with late lumen area loss (r = 0.632, p = 0.009; r = 0.515, p = 0.041) in the negative remodeling group. Coronary artery restenosis after atherectomy was primarily due to an increase in plaque in the positive and/or intermediate remodeling groups. However, in the negative remodeling group, late lumen loss might have been caused by both an increase in plaque and vessel shrinkage.     

Spectrum of remodeling behavior observed with serial long-term (>/=12 months) follow-up intravascular ultrasound studies in left main coronary arteries

Most intravascular ultrasound (IVUS) studies of arterial remodeling in native coronary arteries reported a remodeling index obtained at a single time point. We analyzed serial IVUS examinations, including the vessel cross-sectional area changes (remodeling behavior), of 60 hemodynamically nonstenotic left main lesions (baseline vs 18.4 +/- 9.4 months follow-up). Lumen reduction resulted from vessel reduction (sometimes despite plaque + media decrease), plaque + media increase (with or without vessel increase), or both. The percent annual changes in lumen area correlated strongly with changes in vessel (r = 0.84), but not with changes in plaque + media area. Plaques were classified as group A lesions, reflecting positive remodeling behavior (vessel changes >0), or group B lesions, reflecting negative (or intermediate) remodeling behavior (vessel changes <==0). Both groups did not differ significantly in demographics, laboratory data, and medications. Group A lesions (n = 40) more often showed plaque + media increase than group B lesions (32 of 40 [80%] vs 9 of 20 [45%]; p = 0.02). Group A lesions had, on average, mild annual lumen increase despite mild plaque + media increase, i.e, overcompensation of remodeling for plaque + media increase (vessel increase greater than plaque + media area increase, 19 of 40 [47%]). Conversely, group B lesions (n = 20) showed a significant lumen area reduction (-2.8 +/- 2.6 mm(2)/year) as a result of a decrease in vessel area only. Thus, serial long-term reduction of lumen size may result from vessel shrinkage (sometimes despite plaque decrease), plaque increase (with or without vessel increase), or both; overall, only the remodeling behavior has a significant relation to lumen changes. More than 30% of lesions show a negative remodeling behavior, which shows no relation to patient characteristics or initial plaque burden.     

Comparison of Men Versus Women in Cross-Sectional Area Luminal Narrowing, Quantity of Plaque, Presence of Calcium in Plaque, and Lumen Location in Coronary Arteries by Intravascular Ultrasound in Patients with Stable Angina Pectoris

Women have an increased mortality after coronary interventions compared with men, which may be partly explained by differences in comorbid clinical conditions. However, whether women also have quantitative differences in coronary atherosclerosis is not known. Preinterventional intravascular ultrasound (IVUS) was used to study de novo, nonostial native coronary lesions in 169 women and 549 men with chronic angina. The external elastic membrane (EEM), lumen, and plaque + media (P + M) areas, plaque burden, plaque eccentricity, and calcium were measured at the target lesion and at a proximal reference site. All cross-sectional IVUS measures were also corrected for body surface area. Results are reported as mean ± 1 SD. Women had significantly smaller reference site EEM (16.5 ± 5.3 vs 19.4 ± 6.3 mm², p <0.0001), lumen (8.7 ± 3.0 vs 9.9 ± 4.0 mm², p = 0.0020), and P + M areas (7.8 ± 3.7 vs 9.5 ± 4.2 mm², p = 0.0001). Women also had significantly smaller lesion site EEM (16.2 ± 5.9 vs 18.3 ± 6.7 mm², p = 0.0028), lumen (2.4 ± 1.7 vs 2.9 ± 2.6 mm², p = 0.0273), and P + M areas (13.6 ± 5.7 vs 15.3 ± 6.4 mm², p = 0.0112). However, when corrected for BSA, these differences were no longer significant. Women and men also had similar reference and lesion plaque burden, eccentricity, and calcium. Preinterventional IVUS analysis failed to detect any quantitative or qualitative differences in coronary atherosclerosis in men compared with women.

To determine whether there are quantitative differences in coronary atherosclerosis in men compared with women, preinterventional intravascular ultrasound (IVUS) was used to study de novo, nonostial native vessel lesions in 169 women and 549 men with chronic angina. Women had significantly smaller reference segment and target lesion external elastic membrane, lumen, and plaque cross-sectional areas; however, when corrected for body surface area, these differences were no longer significant. Women and men also had similar reference segment and target lesion plaque burden, eccentricity, and calcification. Preinterventional IVUS analysis failed to detect any quantitative differences in coronary atherosclerosis in men compared with women.     

Elevated homocysteine levels might be associated with coronary artery remodeling in patients with stable angina: an intravascular ultrasound study

BACKGROUND: The relationship between plasma biologic markers and coronary artery remodeling is unknown. Hypothesis: Plasma biologic markers are associated with coronary artery remodeling. METHODS: Preintervention intravascular ultrasound images were obtained in 44 patients with chronic stable angina. Plasma samples were collected 24 h before coronary intervention. The biologic markers included total cholesterol, low-density lipoprotein (LDL) cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, lipoprotein(a) [LP(a)], C-reactive protein (CRP), and homocysteine. The remodeling index (RI) was defined as a ratio of the (lesion/proximal reference) external elastic membrane cross-sectional area. Positive remodeling was defined as an RI > 1.05, negative remodeling as an RI <0.95, and intermediate remodeling as an RI between 0.95 and 1.05. RESULTS: Total cholesterol level (r = 0.092, p = 0.557), LDL cholesterol level (r = 0.123, p = 0.426), triglyceride level (r = 0.020, p = 0.901), HDL cholesterol level (r = 0.042, p = 0.789), LP(a) level (r = 0.062, p = 0.729), and CRP level (r = 0.266, p = 0.089) did not significantly correlate with the RI. However, the plasma homocysteine level positively correlated with the RI (r = 0.398, p = 0.008). The plasma homocysteine level was significantly lower in the lesions with negative remodeling and higher in the lesions with positive remodeling (10.8 +/- 0.7 micromol/l in negative remodeling, 13.1 +/- 0.6 micromol/l in intermediate remodeling, and 18.1 +/- 2.8 micromol/l in positive remodeling, p = 0.021). CONCLUSIONS: Elevated homocysteine levels might be associated with coronary artery remodeling in patients with stable angina.     

Relationship between coronary artery remodeling and plaque composition in culprit lesions: an intravascular ultrasound radiofrequency analysis.

BACKGROUND: The relationship between coronary artery remodeling and culprit plaque composition in vivo has not been fully evaluated by spectral analysis of intravascular ultrasound (IVUS) radiofrequency (RF) data. METHODS AND RESULTS: IVUS RF analyses were performed for 56 consecutive de novo culprit lesions of 52 patients undergoing percutaneous coronary intervention. Remodeling of culprit lesions was determined using the remodeling index (RI), calculated as the external elastic membrane area of the minimum lumen area (MLA) site divided by that of the proximal reference site. Positive remodeling was defined as RI >1.05, intermediate remodeling as 0.95< or = RI < or =1.05 and negative remodeling as RI <0.95. Among the 56 lesions, positive remodeling was detected in 24, intermediate remodeling in 16, and negative remodeling in 16. At MLA sites, positive remodeling lesions had a larger percentage of the fibrofatty component than negative remodeling lesions (22.5+/-10.3% vs 10.4+/-6.6%, p=0.0001), whereas the latter contained a larger percentage of the dense calcium component than the former (2.8+/-2.9% vs 8.4+/-7.0%, p=0.016). CONCLUSIONS: Culprit plaques with positive remodeling have a large lipid burden, whereas those with negative remodeling contain a large amount of calcium.     

左主干冠状动脉病变的血管内超声研究

目的 血管内超声评价非严蕈钙化性左主干病变的形态特点,探讨开口和非开口部位形成狭窄的不同机制.方法 2004年10月至2007年10月,共入选造影确诊或可疑的狭窄病变并行血管内超声检查的153例(开口47例,非开口106例)非严重钙化性左主干病变,定性和定量分析血管内超声图像;负性重构定义为重构指数＜0.95.结果 左主干参考节段平均管腔直径和血管(外弹力膜)直径为(4.1±0.8)mm和(5.3士0.8)mm.开口病变的纤维性、钙化性和软斑块分别为70.2%、19.2%和8.5%,而非开口病变为35.8%、43.4%和3.8%,两者差异有统计学意义(P=0.01).总体来说,31.1%病例的最小管腔面积＜6 mm2,其中开口组29.5%,非开口组31.9%(P=0.87).最小管腔面积在两组相似,但非开口组的斑块面积[(13.3±5.4)mm2比(10.8±4.5)mm2,P=0.007]和斑块负荷(61.9%±14.5%比54.8%±15.9%,P=0.020)均显著大于开口组,斑块负荷＞50%的比例更高(84.8%比61.3%,P=0.002).开口病变的重构系数显著低于非开口病变(0.9±0.2比1.0.±0.2,P=0.000),而且负性重构更多见(74.5%和34.9%,P=0.000).logistic回归分析发现,病变部位(OR=4.9,P=0.004)、斑块面积(OR=1.2,P=0.01)和斑块负荷(OR=0.003,P=0.000)是左主干发生重构的独立预测因素.结论 负性重构现象在左主干开口病变中更常见,可能是其狭窄形成的机制之一.狭窄程度不确定的冠状动脉左主干病变需要血管内超声精确评价.     

Prevention of positive coronary artery remodeling with statin therapy in patients with coronary artery diseases

Since positive coronary artery remodeling with large plaque burden is associated with subsequent coronary events, the authors tested their hypothesis that secondary prevention of coronary events by a statin may be associated with inhibition of the process of positive coronary artery remodeling in underlying coronary atherosclerotic lesions in patients with coronary artery diseases. They evaluated the intravascular ultrasound imaging in angiographically normal coronary lesions at baseline and after 6 months of therapy in 64 patients with coronary artery diseases. External elastic membrane area was defined as the vessel area, and the difference between the vessel and lumen area was calculated as plaque area. The relative echogenicity of coronary plaque to adventitia was evaluated as acoustic characteristics of coronary plaque. Twenty-five patients were treated with a statin and 39 patients did not receive a statin. In patients treated with a statin, plaque area decreased by 12% (p = 0.013) compared to an increase in plaque area of 13% (p = 0.023) in those who did not receive a statin. The vessel area was not enlarged in patients treated with a statin but did show positive remodeling in patients who had plaque progression without a statin. The relative echogenicity of plaque was unchanged in patients treated with a statin but significantly decreased in patients not receiving a statin. A statin may prevent positive coronary artery remodeling via inhibition of plaque progression in underlying coronary atherosclerotic lesions in patients with coronary artery diseases.     

Relation of myocardial perfusion defects and nonsignificant coronary lesions by angiography with insights from intravascular ultrasound and coronary pressure measurements

Several studies have demonstrated a correlation between myocardial ischemia and severity of coronary lesions as determined by intravascular ultrasound (IVUS) and fractional flow reserve (FFR) measurements. However, their value for the assessment of mild coronary stenoses that are associated with myocardial perfusion abnormalities has not been well studied. The objective of this study was to prospectively compare the results of myocardial perfusion as determined by exercise/dipyridamole myocardial single-photon emission computed tomography with IVUS and FFR measurements in patients who had angiographically mild coronary stenosis (< 50% diameter stenosis by quantitative coronary angiography). Forty-eight patients who had stable coronary disease (61 +/- 11 years of age; 6 women) were included. All had mild coronary stenosis in the proximal/middle segment of > or = 1 coronary artery and had undergone maximal exercise myocardial technetium-99m tetrofosmin single-photon emission computed tomography within 48 hours before coronary angiography. IVUS measurements included lesion lumen area, external elastic membrane area, lesion plaque burden (calculated as external elastic membrane minus lumen area, divided by external elastic membrane, and multiplied by 100), and lumen area stenosis (calculated as reference lumen area minus lesion lumen area, divided by reference lumen area, multiplied by 100). Fifty-three coronary lesions were studied, with a mean percent diameter stenosis of 34.9 +/- 7.9% on angiography. Myocardial perfusion defects were demonstrated by single-photon emission computed tomography in 11 patients (12 myocardial regions) with no differences in lesion percent diameter stenosis compared with those without perfusion defects. The presence of reversible perfusion defects was associated with a higher lesion plaque burden as evaluated by IVUS (67.4 +/- 8.1% vs 60.2 +/- 9.3%, p = 0.01). FFR values did not differ in the presence or absence of perfusion defects (0.90 +/- 0.06 vs 0.92 +/- 0.07, respectively; p = NS). In conclusion, plaque burden as determined by IVUS may partly explain the presence of myocardial perfusion defects in cases of angiographically nonsignificant coronary lesions. However, the high FFR values associated with these lesions suggest that other mechanisms, such as endothelial/microvascular dysfunction, might also account for perfusion abnormalities in these patients.     

Remodeling index compared to actual vascular remodeling in atherosclerotic left main coronary arteries as assessed with long-term (> or =12 months) serial intravascular ultrasound.

OBJECTIVES: We present the remodeling index (RI) versus serial intravascular ultrasound (IVUS) data. BACKGROUND: The RI, derived by comparing lesion external elastic membrane (EEM) cross-sectional area versus the reference at one time point, is used in various IVUS studies as a substitute of true remodeling (change in EEM over time), assuming that it represents true remodeling. METHODS: We studied 46 non-stenotic left main arteries using serial IVUS (follow-up 18 +/- 8 months). Plaques were divided into subgroups according to the follow-up RI: follow-up RI >1 (n = 27) versus follow-up RI < or =1 (n = 19). RESULTS: Lesions with a follow-up RI >1 had an increase in lumen despite an increase in plaque because of an increase in EEM. Conversely, lesions with a follow-up RI < or =1 had a reduction in lumen as a result of both a plaque increase and EEM decrease. Overall, the follow-up RI correlated directly with changes in lesion site EEM (baseline-to-follow-up). Although there was no correlation between the follow-up RI and changes in reference EEM area, changes in reference EEM area did correlate directly with changes in lesion EEM area. In nearly 90% of lesions with a follow-up RI >1, there was a previously documented increase in EEM area. Using multivariate linear regression analysis, the follow-up RI was dependent on the baseline RI, the increase in lesion EEM area, and the decrease in reference EEM area. The follow-up RI was not dependent on changes in lesion plaque area. CONCLUSIONS: The vast majority of left main lesions with a remodeling index >1 had evidence of a previous increase in lesion-site EEM area.     

Serial intravascular ultrasound analysis of edge recurrence after intracoronary gamma radiation treatment of native artery in-stent restenosis lesions

In the Washington Radiation for In-Stent restenosis Trial (WRIST), patients were first treated with conventional techniques and then randomized to either gamma-irradiation ((192)Ir) or placebo (dummy seeds). In the (192)Ir group with native coronary in-stent restenosis, we identified 8 patients with edge recurrence and compared them with 21 patients with no recurrence. Serial (postirradiation and follow-up) intravascular ultrasound analysis was performed according to conventional methods. When compared with nonrecurring lesions, lesions with distal edge recurrence had (1) greater decrease in mean distal lumen cross-sectional area (-3.0 +/- 1.2 vs -0.7 +/- 1.0 mm(2), p = 0.0002), (2) no change in mean distal external elastic membrane cross-sectional area versus an increase in mean distal cross-sectional area of 1.0 +/- 0.9 mm(2) in nonrecurring lesions (p = 0.0047), and (3) a greater increase in mean distal plaque + media cross-sectional area (2.9 +/- 1.2 mm vs 1.7 +/- 0.6 mm(2), p = 0.0103). Within the stented segment, the nonrecurring lesions had no decrease in mean lumen and no increase in mean intimal hyperplasia cross-sectional area. Conversely, lesions with distal edge recurrence had a significant decrease in mean intrastent lumen cross-sectional area (-1.7 +/- 1.7 mm(2)) and a significant increase in mean intrastent intimal hyperplasia cross-sectional area (1.6 +/- 1.6 mm(2)). Lesions with distal edge recurrence also had a greater decrease in mean proximal lumen cross-sectional area (-1.7 +/- 1.3 vs -0.3 +/- 0.8 mm(2), p = 0.0213), with a trend toward a greater increase in mean proximal plaque + media cross-sectional area. Thus, edge recurrence after (192)Ir treatment of in-stent restenosis is the result of neointimal hyperplasia (part of generalized treatment failure) and the absence of radiation-induced positive remodeling.     

Intravascular ultrasound assessment of the relation between early and late changes in arterial area and neointimal hyperplasia after percutaneous transluminal coronary angioplasty and directional coronary atherectomy.

Previous serial intravascular ultrasound (IVUS) analysis after percutaneous transluminal coronary angioplasty or directional coronary atherectomy showed (1) early (within 1 month) increase in arterial area, (2) late (1- to 6-month) decrease in arterial area, and (3) an increase in plaque area from immediately to 6 months after intervention. To further understand these findings, we used serial IVUS to study the relations between changes in arterial and plaque area during the follow-up period after coronary intervention. Serial IVUS was performed before intervention and immediately, 24 hours, 1 month, and 6 months after percutaneous transluminal coronary angioplasty (n = 35) or directional coronary atherectomy (n = 26) in 57 patients. Arterial, lumen, and plaque areas were measured at the lesion site with the smallest preintervention and follow-up lumen areas at all time points. The increase in plaque area in the first month after intervention was accompanied by an equal or greater increase in arterial area (r = 0.670, p <0.0001). There was a decrease in arterial area from 1 to 6 months after intervention, which correlated inversely with both the increase in plaque area (r = 0.434, p <0.0001) or arterial area (r = 0.515, p <0.0001) during the first month after intervention and directly with the 1- to 6-month increase in plaque area (r = 0.460, p <0.0001). Comparison of the late (1 to 6 months) and early (within 1 month) delta arterial versus delta plaque area regression lines suggested that the late decrease in arterial area was superimposed on the relation between delta arterial area and delta plaque area. These relations were especially strong in restenotic (vs nonrestenotic) lesions. The early increase and late decrease in stenosis arterial area and neointimal hyperplasia appear to be interrelated, especially in restenotic stenoses.     

冠状动脉造影显示造影剂排空滞缓段的血管内超声研究

目的:探讨造影剂排空滞缓的冠状动脉段的病变结构特点及其临床意义。方法:对23例冠状动脉造影(CAG)显示造影剂充盈缓慢且排空滞缓的血管行血管内超声检查,分析斑块性质、测量面积狭窄率及计算重构指数。结果:与参照血管段比较,病变处血管面积[(17·04±3·86)mm2vs(14·35±3·62)mm2,P<0·01]及血管腔面积[(13·72±2·38)mm2vs(11·86±2·57)mm2,P<0·01]均显著增加,并有软斑块,狭窄程度较轻(19·48%±5·23%)。23处病变20处为正重构,重构指数为1·21±0·07。结论:小的粥样硬化斑块及正重构是导致造影剂排空滞缓的原因,这种病变具有不稳定的结构特点。     

Comparison of clinical characteristics and arterial remodeling by intravascular ultrasonic imaging in three age groups (< or =55, 56 to 69 and > or =70 years) of Japanese patients with acute myocardial infarction

Recent epidemiologic, pathologic, and intravascular ultrasound (IVUS) studies have shown that there are differences in coronary risk factors or plaque morphology between younger and older patients with acute myocardial infarctions (AMIs). This study examined clinical background and plaque morphology using IVUS in younger and older adults with AMIs in Japan. The study population consisted of 96 patients with AMIs, for whom preinterventional IVUS images were obtained. Patients were classified into 3 groups: a young group (aged < or =55 years), a middle-aged group (aged 56 to 69 years), and an old group (aged > or =70 years). The remodeling index was defined as the ratio of the external elastic membrane area at the culprit lesion to the external elastic membrane area at the proximal reference site. Expansive remodeling was defined as a remodeling index >1.05 and constrictive remodeling as a remodeling index <0.95. The frequency of hypercholesterolemia was significantly different among the 3 age groups. Total cholesterol (p <0.001), low-density lipoprotein cholesterol (p <0.005), and triglyceride (p <0.05) levels and body mass index (p <0.001) in the young group were significantly higher than in the old group. On IVUS images, constrictive remodeling was most common in the young group, whereas expansive remodeling occurred most commonly in the middle-aged and old groups. In conclusion, this study demonstrated that patients with AMIs in the young group had higher levels of hypercholesterolemia, obesity, and constrictive remodeling compared with those in the old group. The differences in arterial remodeling of the culprit lesions between younger and older patients with AMIs may reflect different biologic mechanisms of plaque activation and destabilization.     

冠状动脉重构的血管内超声研究及基质金属蛋白酶和高敏C反应蛋白检测

目的用血管内超声(IVUS)对比研究不同类型冠心病患者的冠状动脉重构(remodeling)特点,探讨冠状动脉重构与临床表现、基质金属蛋白酶(MMPs)及高敏C反应蛋白(hs CRP)的关系。方法在行冠状动脉介入治疗前,应用IVUS研究38例急性冠状动脉综合征(ACS)和18例稳定性心绞痛(SA)患者,测量“罪犯”血管病变处及其近端、远端参考段的外弹力膜(EEM)面积、管腔面积,计算斑块面积和重构指数(RI),定义RI>1.05为正重构,RI<0.95为负重构。识别出高危斑块,检测外周血基质金属蛋白酶2(MMP2)、基质金属蛋白酶9(MMP9)和hs CRP水平。结果ACS组“罪犯”血管处的斑块面积大于SA组[(11.94±4.90)mm2比(9.17±3.36)mm2,P=0.035]。ACS组RI明显大于SA组(0.972±0.222比0.796±0.130,P=0.003)。两组正、负重构分布比率显著不同正重构在ACS组比SA组更常见(34.2%比5.6%,P=0.047),而负重构在SA组更常见(负重构在ACS组和SA组分别为52.6%与88.9%,P=0.003)。ACS组高危斑块发生率多于SA组(76.3%比50.0%,P=0.040)。ACS组患者血清MMP2高于SA组[(250.65±47.97)μg/L比(214.21±47.20)μg/L,P=0.029],前者的血浆MMP9也高于后者[(84.26±9.78)μg/L比(68.46±22.82)μg/L,P=0.038],前者的血清hs CRP亦高于后者[(3.62±3.37)mg/L比(1.48±1.52)mg/L     

Effect of disease eccentricity on compensatory remodeling of coronary arteries: evidence from intravascular ultrasound before interventions

BACKGROUND: Compensatory remodeling occurs to maintain lumen area in human coronary vessels. However, few data exist regarding the relationship between vessel remodeling and plaque distribution. Therefore, we studied coronary sites with or without remodeling by intravascular ultrasound and correlated with disease distribution. METHODS AND RESULTS: A total of 90 coronary sites with significant stenosis (>50%) from 80 patients were examined before interventions. For identifying the vessel remodeling, external elastic membrane (EEM) area was measured at the stenotic sites and the adjacent proximal and distal sites. The reference EEM area was calculated by averaging proximal and distal EEM areas, and percent enlargement of the EEM area was calculated by the formula: [(stenosis EEM area-reference EEM area)/reference EEM area]x100. Plaque area was determined by reducing the lumen from EEM areas. The maximal (max) and minimal (min) distances from the center of the lumen to the EEM were also measured, and the disease eccentricity index was calculated by the formula: [(max-min)/max]. The lesion was defined as eccentric if the index was >0.5 and as concentric if 相似文献   

Longitudinal plaque redistribution during stent expansion

The purpose of this study was to clarify the 3-dimensional behavior of plaque during coronary stent expansion. Serial intravascular ultrasound (IVUS) studies, preintervention, and poststenting were evaluated in 32 patients treated with a single-balloon expandable tubular stent. External elastic membrane (EEM), lumen, stent, and plaque + media cross-sectional area were measured at 1-mm intervals through the entire stent as well as proximal and distal reference segments 5 mm from the stent edge. Volumetric calculations were based on Simpson's rule. Overall, the plaque + media volume through the entire lesion did not change during stent expansion (218 +/- 51 vs 217 +/- 47 mm3, p = 0.69). However, EEM and lumen volume increased significantly (EEM volume, 391 +/- 84 vs 448 +/- 87 mm3 [p < 0.0001]; lumen volume, 173 +/- 52 vs 231 +/- 54 mm3 [p < 0.0001]). The change in lumen volume correlated strongly with the change in EEM volume (r = 0.85, p < 0.0001), but poorly with the change in plaque + media volume (r = 0.37, p = 0.03). Plaque + media volume decreased in the midstent zone (59 +/- 14 vs 53 +/- 11 mm3, p = 0.0005), and increased in the distal stent zone (40 +/- 11 vs 44 +/- 9 mm3, p = 0.003), but did not change in either the proximal stent zone or reference segments. The mechanism of stent expansion is a combination of vessel stretch and plaque redistribution, translating disease accumulation from the midstent zone to the distal stent zone.