Attenuated coronary flow reserve and vascular remodeling in patients with hypertension and left ventricular hypertrophy

OBJECTIVES: The purpose of this study was to evaluate the association between hypertension and left ventricular hypertrophy (LVH) with both coronary vascular remodeling and endothelial function. BACKGROUND: The association between endothelial and nonendothelial coronary flow reserve with vascular remodeling in patients with hypertension and LVH is still unclear. METHODS: One hundred and eleven patients with normal or mildly diseased coronary arteries at angiography underwent intravascular ultrasound examination of the left anterior descending coronary artery. Patients were divided into three groups: group 1: n = 13, hypertensive patients with LVH; group 2: n = 30, hypertensive patients without LVH; group 3: n = 68, normotensive patients. Vessel and lumen area and atherosclerotic plaque area were evaluated. Vascular reactivity was examined using intracoronary adenosine and acetylcholine. RESULTS: Vessel area in group 1 (with LVH) was significantly (p < 0.01) greater than that in group 2 (without LVH), whereas, vessel area in both groups 1 and 3 was similar (12.8 +/- 0.8 mm2, 10.7 +/- 0.4 mm2 and 11.5 +/- 0.3 mm2). Coronary blood flow at baseline for patients in group 1 (with LVH) was significantly greater than it was for patients in groups 2 and 3 (81.1 +/- 9.9 ml/min, 56.5 +/- 6.2 ml/min and 48.1 +/- 3.2 ml/min, both p < 0.05). In comparison with groups 2 and 3, the response to both acetylcholine and adenosine was significantly impaired in patients with LVH. CONCLUSIONS: The current study demonstrates that hypertension with LVH is associated with both coronary vascular remodeling and attenuated endothelial and nonendothelial coronary flow reserve.     

Association of coronary shear stress with endothelial function and vascular remodeling in patients with normal or mildly diseased coronary arteries

BACKGROUND: The relationship between coronary remodeling, shear stress and endothelial function remains unclear. OBJECTIVE: The present study investigated the effects of mechanical factors on structure and function of epicardial coronary arteries. METHODS: Patients (group 1: %area stenosis<40%, n=55; or group 2: %area stenosis>or=40%, n=17) with a discrete mildly stenotic lesion (%diameter stenosis<30%) underwent intravascular ultrasound examination of the left anterior descending coronary artery for determination of vessel area, lumen area, plaque area, cross-sectional areas at reference segments, and remodeling index (the ratio of vessel area at the culprit lesion to vessel area at the proximal reference site). Further, vascular reactivity was examined using intracoronary administration of acetylcholine, papaverine, and nitroglycerin. RESULTS: Vessel area significantly correlated with plaque area in both groups (r=0.65, P<0.0001 and r=0.85, P<0.0001). Group 1 showed significantly greater acetylcholine-induced percentage changes in coronary blood flow (67+/-70 vs. 16+/-75%, P<0.05) and coronary artery diameter (-7+/-18 vs.-32+/-31%, P<0.01) and also significantly smaller coronary wall shear stress (65+/-27 vs. 81+/-32 dynes/cm, P<0.05) than group 2. The percentage increase in coronary blood flow induced by acetylcholine was significantly and positively correlated with remodeling index in group 1 (r=0.64, P<0.0001) but not in group 2 (r=-0.03, P=0.90) and was also significantly and positively correlated with coronary wall shear stress in group 1 (r=0.46, P<0.001) but not in group 2 (r=-0.33, P=0.19). CONCLUSIONS: Endothelium-dependent vasodilation in the resistance coronary artery correlates with remodeling via increased wall shear stress when target lesions %area stenosis is <40%.     

Advancing age is associated with diminished vascular remodeling and impaired vasodilation in resistance coronary arteries

BACKGROUND: Compensatory enlargement of the coronary arterial wall has been described in the early stages of native atherosclerosis. However, little is known about the specific effect of aging on this adaptive process in atherosclerosis. The purpose of the current study was to characterize the effects of advancing age on vascular remodeling and endothelium-dependent and -independent coronary vasodilation in patients without coronary artery disease risk factors. METHODS: Twenty-six patients without coronary risk factors and with normal and mildly diseased coronary arteries were studied. Vessel, lumen and atherosclerotic plaque areas were evaluated by intravascular ultrasound and coronary flow response was assessed using papaverine and acetylcholine in the left anterior descending coronary artery. RESULTS: There was a weak but significant correlation between plaque area and age (r = 0.29, P<0.01). Vessel area was also weakly but significantly correlated with age (r = 0.22, P<0.05). However, lumen area had no correlation with age. Vessel area in the younger group (<50 years) and the older group (> or =50 years) increased 1.64 and 0.55 mm2 for every 1 mm2 increase in plaque area (r = 0.62, P<0.0001 and r = 0.39, P<0.05, respectively). With regard to vascular reactivity, there was an inverse correlation between the percentage increases in coronary blood flow (CBF) evoked by acetylcholine and aging (r = -0.49, P<0.05). The percentage increases in CBF evoked by papaverine also inversely correlated with aging (r=-0.53, P<0.01). However, the percentage changes in coronary artery diameter evoked with acetylcholine did not correlate with aging. CONCLUSION: This study suggests that endothelium-dependent and -independent vasodilation of the resistance coronary artery are impaired with advancing age, which may be in association with attenuated coronary vascular remodeling with aging.     

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   

Art und Ausma? des vaskul?ren Remodelings kritischer Koronarstenosen.?Eine Studie mit intravaskul?rem Ultraschall

The purpose of this study was to assess the dimension of regional vascular remodeling and its influence on lumen narrowing in vivo. Sixty-three patients with 68 coronary lesions were imaged by intravascular ultrasound before transcatheter therapy. Quantitative measurements of lumen area, vessel area, and plaque area were performed at the lesion site and at the proximal and distal reference site. Area stenosis was calculated as plaque area/vessel area. 100. The extent of remodeling was quantified by a remodeling index (RI = stenosis vessel area - mean reference vessel area/mean reference vessel area. 100). Additionally, three different groups of vascular remodeling were defined: 1) positive remodeling = stenosis vessel area > maximal reference vessel area; 2) intermediate remodeling = maximal reference vessel area >/= stenosis vessel area >/= minimal reference vessel area; 3) negative remodeling = stenosis vessel area < minimal reference vessel area. In 57% of lesions stenosis vessel area was not in between the proximal and distal reference area: 29% of lesions (20/68) had positive, 28% (19/68) negative, and 43% (29/68) intermediate remodeling. Overall remodeling index averaged -0.8+/-19.7%. In the negative remodeling group, reduction of vessel area contributed to 40+/-21% of lumen narrowing, in the positive remodeling group, stenosis vessel area was 21+/-12% enlarged (p<0.001). Lesions with negative remodeling exhibit a lesser plaque area, lesions with positive remodeling a larger than other vessels (8.2+/-2.4 mm(2), 13.8+/-3.7 mm(2), 10. 8+/-3.7 mm(2); p <0.001). Distinct vascular remodeling occurred in the majority of atherosclerotic lesions and is a bidirectional process. Overall, the extent and the frequency of positive and negative remodeling was almost balanced. In lesions with negative remodeling the plaque area was significantly lesser than in other lesions.     

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.     

Sex differences in coronary atherosclerosis: coronary angiography and intravascular ultrasonography

OBJECTIVES: Women have higher mortality and frequency of complications compared with men after coronary intervention. Possible differences in coronary atherosclerosis between men and women were investigated. METHODS: The left anterior descending arteries of 214 patients (164 men, mean age 62.3 +/- 9.10 years; 50 women, mean age 67.8 +/- 7.76 years) were examined. Lesion length, reference diameter, percentage diameter stenosis and minimal lumen diameter were measured by quantitative coronary angiography. Vessel area, lumen area, percentage area stenosis, and remodeling index were measured by intravascular ultrasonography, and presence of calcification in the lesion was classified. These parameters were compared between men and women. RESULTS: There were no significant differences in quantitative coronary angiography, but intravascular ultrasonography showed calcification was more severe in women, vessel area was significantly smaller in women (13.25 +/- 4.21 vs 15.91 +/- 4.35 mm2, p = 0.004), and remodeling index was significantly lower in women (0.95 +/- 0.13 vs 1.04 +/- 0.18, p = 0.015). CONCLUSIONS: Vessel area measured by intravascular ultrasonography was significantly smaller in women, and calcification was more severe in women. Such factors may be involved in the higher mortality in women.     

Comparison of ruptured plaques in native coronary arteries and in saphenous vein grafts: an intravascular ultrasound study

Intravascular ultrasound (IVUS) has been used to describe ruptured plaques in saphenous vein grafts (SVGs) and native coronary arteries. We compared clinical, angiographic, and IVUS features of ruptured atherosclerotic plaques in SVGs and native coronary arteries. We identified 95 plaque ruptures in 76 SVGs in 73 patients. These lesions and patients were matched with 95 lesions and patients from a database of 468 native artery ruptures. The matching criterion was IVUS mean reference lumen area. Patients with ruptured SVG plaques were older (68.4 +/- 10.1 vs 65.0 +/- 10.6 years, p = 0.021), more often had hypercholesterolemia (92% vs 74%, p = 0.015) and hypertension (78% vs 62%, p = 0.059), and more often had a history of a remote myocardial infarction (57% vs 32%, p = 0.002). In contrast, anginal symptoms were similar in the 2 groups (70% to 75% of each group had an acute coronary syndrome). Most (90% to 95%) ruptured plaques in each group were classified as angiographically complex. However, ruptured SVG lesions more often had an angiographically visible intimal flap (71% vs 38%, p <0.001). More than 70% of lesions in the 2 groups had positive arterial remodeling by IVUS, but there was a tendency for a higher remodeling index in ruptured plaque SVG lesions (1.18 +/- 0.30 vs 1.11 +/- 0.20, p = 0.085). The site of the initial tear occurred mainly (in approximately 70%) at the plaque shoulders in the 2 groups. In conclusion, although patients with SVG plaque ruptures are older and have more co-morbidities, the clinical presentation and angiographic and IVUS features are remarkably similar to those of native artery plaque ruptures.     

Impact of histological plaque characteristics on intravascular ultrasound parameters at culprit lesions in coronary artery disease

Prior intravascular ultrasound (IVUS) studies have demonstrated that a positive remodeling pattern of a culprit lesion is observed more frequently in acute coronary syndrome (ACS) than stable angina (SA). However, the relationship between the plaque morphology detected by IVUS and the histological type of atherosclerotic plaque has not been well defined. This is a prospective study on 37 consecutive patients who underwent directional coronary atherectomy. The 37 patients were divided into 2 groups; 21 patients with SA and 16 with ACS. Vessel and plaque cross sectional area were measured at the culprit lesion and the remodeling index (RI) was calculated by IVUS. The plaque tissue was assessed for the presence of inflammatory cells and lipids, and the presence of each was scored as 0 (absent), 1 (sparse), 2 (dense), or 3 (predominant). The RI of the patients with ACS was higher than that of SA. Inflammatory cells were present to a greater extent in patients with ACS. Inflammatory cells and lipids were significantly correlated with the RI (Inflammatory cell score grade > or = 2 patients; 1.14 +/- 0.13 versus grade 0 patients; 0.87 +/- 0.24, and grade 1 patients; 0.93 +/- 0.17, P < 0.01 and lipid score grade > or = 2 patients; 1.13 +/- 0.17 versus grade 0 patients; 0.85 +/- 0.18, P < 0.001 and grade 1 patients; 0.95 +/- 0.19, P < 0.05). The results clearly indicate that the evaluation of vessel morphology by vascular imaging is an important indicator of plaque instability.     

Randomized evaluation of atorvastatin in patients with coronary heart disease: a serial intravascular ultrasound study.

BACKGROUND: It is unclear whether a marked reduction of low-density lipoprotein-cholesterol (LDL-C) in patients with coronary heart disease (CHD) and mild hypercholesterolemia leads to less progression of atherosclerosis. METHODS AND RESULTS: Patients with CHD and hypercholesterolemia (100相似文献   

Intravascular ultrasound evaluation of coronary plaque regression by low density lipoprotein-apheresis in familial hypercholesterolemia: the Low Density Lipoprotein-Apheresis Coronary Morphology and Reserve Trial (LACMART)

OBJECTIVES: We sought to assess the effects of low density lipoprotein (LDL)-apheresis (LDL-A) for regression of coronary plaque in familial hypercholesterolemia (FH), we set up a one-year follow-up multicenter trial using coronary angiography and intravascular ultrasound (IVUS). BACKGROUND: It is still unclear whether aggressive lipid-lowering therapy by LDL-A leads to the regression of coronary plaque in patients with FH. METHODS: Eighteen patients with FH were assigned to one of two groups: medication + LDL-A (LDL-A group, n = 11) and medication only (medication group, n = 7). Total cholesterol, triglycerides, high density lipoprotein cholesterol and LDL cholesterol were measured in all subjects at the outset of treatment (baseline) and every three months thereafter. Coronary angiography and IVUS were performed at the outset and after the one-year follow-up period to measure minimal lumen diameter (MLD) by coronary angiogram and plaque area (PA) by IVUS. RESULTS: The LDL-A group showed 28.4% reduction in total cholesterol (from 275 +/- 27 mg/dl to 197 +/- 19 mg/dl) and 34.3% reduction in LDL cholesterol (from 213 +/- 25 mg/dl to 140 +/- 27 mg/dl) after one-year follow-up, while the medication group showed no changes in cholesterol levels. There were significant interactions between both treatments in total cholesterol (p = 0.0001), LDL cholesterol (p = 0.0001), MLD (p = 0.008) and PA (p = 0.017) using two-way repeated-measures analysis of variance by the SAS system (SAS Institute Inc., Cary, North Carolina). Significant differences were seen in net change in MLD (p = 0.004) and PA (p = 0.008) during the one-year follow-up period between both groups. CONCLUSIONS: These results suggest that aggressive lipid-lowering therapy using the combination of LDL-A and lipid-lowering drugs may induce regression of coronary atherosclerotic plaque in FH patients.     

Simvastatin treatment is associated with improvement in coronary endothelial function and decreased cytokine activation in patients after heart transplantation

OBJECTIVES: This study was designed to assess the association between 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition, coronary endothelial function and cytokine activation in heart transplant recipients without angiographically detectable disease. BACKGROUND: Coronary endothelial dysfunction contributes to cardiac allograft vasculopathy. The vasoprotective effects of statins in heart transplant recipients may include restoration of endothelial function and suppression of allograft inflammatory activity. METHODS: Heart transplant recipients (one to three years after heart transplant) were divided into three groups based on the total cholesterol levels: group 1 (n = 21), patients with a history of hypercholesterolemia adequately controlled with simvastatin; group 2 (n = 19), patients with hypercholesterolemia not adequately treated with simvastatin; and group 3 (n = 40), patients without hypercholesterolemia. Coronary vasomotor function and intimal thickness as well as coronary sinus and aortic cytokine concentrations (tumor necrosis factor [TNF]-alpha, interleukin [IL]-6 and soluble IL-2 receptor) were investigated. In a prospective one-year follow-up study, changes in coronary endothelial function and cytokine levels were compared between 11 hypercholesterolemic patients treated with simvastatin and 9 controls. RESULTS: Epicardial and microvascular endothelial functions were better in groups 1 and 3 than they were in group 2 (p < 0.01 and p < 0.05). Transcardiac IL-6 and TNF-alpha gradients were significantly increased in groups 2 and 3 compared with group 1 (IL-6: p < 0.05; TNF-alpha: p < 0.01). Plaque areas were significantly increased in groups 1 and 2 (p < 0.05 vs. group 3), whereas lumen area was increased in group 2 compared with group 1 (p < 0.05), demonstrating adaptive vascular remodeling. In patients treated with simvastatin, coronary endothelial function and cardiac cytokine activity significantly improved during the one-year follow-up. CONCLUSIONS: Inhibition of allograft inflammatory activity and attenuation of the coronary endothelial dysfunction observed in cardiac transplant recipients during treatment with simvastatin may represent an important mechanism by which HMG-CoA reductase inhibitors protect against the development of cardiac allograft vasculopathy.     

Vascular remodeling in atherosclerotic coronary arteries is affected by plaque composition

BACKGROUND: Narrowing of lumen in atherosclerotic lesions is determined not solely by accumulation of plaque but also by constrictive or expansive vascular remodeling. Underlying mechanisms and determinants of these bidirectional processes are not known. OBJECTIVES: To elucidate the response of vascular remodeling to progressive atherosclerosis by analyzing its potential association with composition of plaque. METHODS: Seventy patients with 77 de-novo coronary artery lesions underwent intravascular ultrasound imaging before coronary intervention. Target lesions were defined as soft, fibrous/mixed, and calcified plaques. Quantitative measurements of area of lumen (A(L)), total area of vessel (A(TV)) and area of plaque (A(P) = A(TV)-A(L)) were performed at the lesion site and at the proximal and distal reference sites. Remodeling was determined by using a remodeling index [I(R) = (stenosis of A(TV)/mean reference A(TV)) x 100]. RESULTS: Overall vascular remodeling was balanced with a mean remodeling index of 100.2+/-19.3% and a high interlesion range (60.2-152.4%). The remodeling index for soft lesions was significantly higher than those for fibrous/mixed and calcified lesions (110+/-18.8 versus 96.2+/-14.4 and 85.9+/-15.1%, P < 0.01). Calcified lesions exhibited lower remodeling indexes than did uncalcified lesions (85.9+/-15.1 versus 104.6+/-18.4%, P < 0.01). CONCLUSIONS: Processes involved in vascular remodeling are affected by composition of plaque insofar as there is a higher prevalence of constrictive remodeling among calcified plaques and a higher prevalence of expansive remodeling among soft lesions. These findings indicate that constrictive remodeling is a late manifestation in atherogenesis. Future studies are warranted in order to enhance the understanding of progression of atherosclerosis, and of mechanisms of vascular remodeling and their impacts on interventional therapy.     

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     

Greater late lumen loss after successful coronary balloon angioplasty in the proximal left anterior descending coronary artery is not explained by extent of vessel wall damage or plaque burden

OBJECTIVES: We investigated whether the greater late lumen loss after coronary balloon angioplasty in the proximal left anterior descending artery (P-LAD) compared with that in other segments might be related to differences in vascular dimensions or morphology as determined by angiography and intravascular ultrasound imaging. BACKGROUND: The greater late lumen loss after angioplasty in the P-LAD that has been observed in several studies has not been explained. METHODS: We studied 178 patients and 194 coronary artery lesions by quantitative angiography and 30 MHz intravascular ultrasound imaging after successful balloon angioplasty. Vessel wall morphology was compared among three proximal and three nonproximal segments. Follow-up quantitative angiography for late lumen loss calculation was performed in 168 lesions. Multivariate analysis was used to determine predictors of late lumen loss. RESULTS: Absolute and relative late loss were significantly greater at the P-LAD compared with the pooled group of other segments (0.42 +/- 0.60 mm vs. 0.10 +/- 0.48 mm, p = 0.0008 and 0.14 +/- 0.24 vs. 0.03 +/- 0.17, p < 0.001). Also, a greater percentage of calcific lesions (65% vs. 44%, p = 0.034), a lower incidence of rupture (51% vs. 74%, p = 0.009) and a larger reference segment plaque area (5.4 +/- 2.2 mm2 vs. 4.7 +/- 1.9 mm2, p = 0.05) were found in the P-LAD. In multivariate analysis however, these variables were not predictive of late loss. CONCLUSIONS: Greater late lumen loss after coronary balloon angioplasty of the P-LAD is not explained by differences in atherosclerotic plaque burden or in vessel wall damage.     

Impact of preinterventional arterial remodeling on in-stent neointimal hyperplasia and in-stent restenosis after coronary stent implantation.

BACKGROUND: Patterns of arterial remodeling during the course of plaque development have been shown to play an important role in both the progression of de novo atherosclerosis and in the restenotic process following coronary intervention. The aim of the present prospective study was to evaluate the effect of pre-interventional arterial remodeling on in-stent neointimal hyperplasia (NIH) and in-stent restenosis (ISR) after stenting. METHODS AND RESULTS: Pre-interventional arterial remodeling was assessed in 85 native coronary lesions by using intravascular ultrasound (IVUS). The remodeling index (RI) was 1.09+/-0.20 in the positive remodeling (PR)/intermediate remodeling (IR) group and 0.84+/-0.12 in the negative remodeling (NR) group. The plaque plus media cross sectional area (P&M CSA) at pre-intervention and NIH CSA at follow-up in the minimal lumen CSA were significantly larger in the PR/IR group (9.2+/-2.9 mm2 vs 6.2+/-1.8 mm2, 3.3+/-1.2 mm2 vs 1.5+/-0.9 mm2; p = 0.001, p = 0.001, respectively). On 3-dimensional analysis of IVUS images at follow-up, the lumen volume was significantly smaller in the PR/IR group than that in the NR group (62+/-15 mm3 vs 75 +/-20 mm3; p = 0.001), and neointima hyperplasia volume was significantly larger in the PR/IR group than that in the NR group (46+/-15 mm3 vs 26+/-10 mm3; p = 0.001). A significant positive correlation was found between pre-interventional RI and follow-up NIH CSA (r = 0.25, p = 0.022). The incidence of ISR and repeat intervention was significantly higher in the PR/IR group (30.8% vs 18.2%, 28.8% vs 15.2%; p = 0.032, 0.035, respectively). CONCLUSION: Measuring pre-interventional arterial remodeling patterns by IVUS may be helpful to stratify lesions at high-risk of ISR.     

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.     

Serial intravascular ultrasound evidence of both plaque stabilization and lesion progression in patients with ruptured coronary plaques: effects of statin therapy on ruptured coronary plaque

Using serial intravascular ultrasound (IVUS), we evaluated the natural evolution of non-culprit/non-target lesion ruptured coronary plaques and assessed the impact of statin therapy. Twenty-eight patients with non-stenotic ruptured plaques underwent baseline and 12-month follow-up IVUS studies; half were treated with statins. Standard IVUS analyses were performed. Complete healing of ruptured plaques was observed in four (29%) statin-treated patients and no non-statin-treated patients (p=0.049). Statin-treated patients had an increase in lumen area of 0.4+/-0.8 mm2 (versus a decrease in lumen area of -0.6+/-1.0 mm2 in non-statin-treated patients, p=0.007) and no change in plaque area (versus an increase in plaque area of 0.6+/-0.9 mm2, p=0.051). During 1-year follow-up, target lesion revascularization was performed in three non-statin-treated patients (21%) and no statin-treated patient (p=0.11). Compared to lesions that did not require revascularization, lesions requiring revascularization had a decrease in lumen area (-1.7+/-1.4 mm2 versus 0.1+/-0.8 mm2, p=0.001) as well as an increase in plaque area (1.6+/-1.0 mm2 versus 0.1+/-0.7 mm2, p=0.002). In conclusion, the current observational follow-up IVUS study showed beneficial effects of statin treatment on reduction of revascularization rates and stabilization of non-culprit/non-target lesion plaque ruptures without significant stenosis. Conversely, healing of non-statin-treated non-culprit/non-target lesion plaque ruptures can be responsible for lesion progression requiring revascularization.     

The influence of plaque orientation (pericardial or myocardial) on coronary arterial remodeling

BACKGROUND: Many systemic, regional and lesion factors have been identified which may influence arterial remodeling, but little is known about the importance of extravascular resistance to vessel enlargement. As myocardial systolic splinting may significantly affect vessel expansion the effect of plaque orientation on arterial remodeling in eccentric coronary atherosclerotic lesions was examined. METHODS: Using intravascular ultrasound imaging to obtain cross-sectional vessel area (VA), plaque area (PA) and lumen area (LA), remodeling in eccentric left anterior descending coronary artery lesions was compared which predominantly involved the pericardial or free arc (P, n=25) and the myocardial side (M, n=40) of the vessel wall. Normalized vessel area (NVA, VA(lesion)/VA(reference)) was compared as a continuous and categorical variable (positive>1.05, intermediate 0.95-1.05, negative<0.95) as well as remodeling index (RI, VA(lesion)-VA(reference)/PA(lesion)-PA(reference)). RESULTS: The two groups were well matched for clinical and lesion characteristics known to affect remodeling. Reference segments areas were similar in the two groups; while lesion LA was also similar, in the pericardial group there was significantly greater lesion PA (P 12.78+/-0.72, M 10.26+/-0.50 mm(2), P<0.05) and VA (P 15.71+/-0.90, M 12.82+/-0.57 mm(2), P<0.05) demonstrating enhanced compensatory remodeling. Outward remodeling was significantly greater in P than in M by both NVA (P 1.03+/-0.03, M 0.86+/-0.03, P<0.01) and RI (P 0.02+/-0.07, M -1.10+/-0.32, P<0.01). Positive, intermediate and negative remodeling occurred in nine, nine and seven lesions in P and in four, ten and 26 lesions in M (P<0.01). CONCLUSIONS: Remodeling compensates more for plaque growth in eccentric coronary lesions which are surrounded by the pericardium than those surrounded by the myocardium. Extravascular resistance appears to influence arterial remodeling.     

Volumetric remodeling of the proximal left coronary artery: early versus late after heart transplantation.

OBJECTIVES: The aim of this study was to characterize progression of cardiac allograft vasculopathy (CAV) with special respect to coronary artery geometry. BACKGROUND: As previously shown by intravascular ultrasound (IVUS), CAV is characterized by a multifocal intimal hyperplasia. Little is known, however, about vascular remodeling processes influencing vessel geometry and luminal narrowing. METHODS: In 30 heart transplant recipients serial IVUS studies were performed at baseline (BL) and after a mean follow-up period of 12.5+/-2.5 months. Changes in plaque, lumen and vessel volume were assessed in the proximal left anterior descending artery. Pattern of remodeling was analyzed in patients "early" (n = 15, BL study 1.4+/-0.7 months after heart transplantation [HTX]) compared with "late" after HTX (n = 15, BL 46.1+/-29.1 months). RESULTS: Plaque volume was found to increase by a mean of 23.8+/-25.9 mm3, not significantly different within and beyond the 1st year after HTX. Significant differences, however, were observed in changes in vessel volume with a mean decrease of -52.8+/-70.9 mm3 in the early group, whereas late follow-up group presented with an enlargement of 32.3+/-46.0 mm3. Based on these changes, lumen volume decreased by -73.2+/-69.8 mm3 early, in contrast to a slight increase of 5.2+/-32.6 mm3 in the late group. CONCLUSIONS: Progression of CAV is a complex process, modified by changes in the vascular geometry. Especially within the 1st year after HTX, luminal loss is influenced not only by an increase in plaque area but by a decrease in total vessel volume as well.