Larger Plaque Area Research Articles

INTRAVASCULAR ULTRASOUND ASSESSMENT OF BORDERLINE CORONARY ARTERY DISEASE OF PATIENTS WITH CORONARY HEART DISEASE AND DIABETES

INTRAVASCULAR ULTRASOUND ASSESSMENT OF BORDERLINE CORONARY ARTERY DISEASE OF PATIENTS WITH CORONARY HEART DISEASE AND DIABETES

Cadmium exposure is accompanied by increased prevalence and future growth of atherosclerotic plaques in 64‐year‐old women

There is currently widespread exposure to the toxic metal cadmium through the diet as well as through smoking, and it has been suggested that cadmium exposure may increase the risk of cardiovascular disease. Here we examined whether cadmium exposure is associated with prevalence and growth of atherosclerotic plaques in the carotid arteries. The analyses were performed in a screening-based cohort of 64-year-old Caucasian women with stratified, random selection to groups with normal glucose tolerance, impaired glucose tolerance and diabetes (n=599). We measured cadmium concentrations in blood and urine at baseline. In addition, we performed ultrasound examination to determine the prevalence and area of atherosclerotic plaques in the carotid arteries and assessed smoking history and other cardiovascular risk factors at baseline and at a follow-up examination after a mean of 5.4years. At baseline, blood cadmium levels were associated with increased risk of plaque and a large plaque area after adjustment for confounders. In women who had never smoked, blood cadmium levels correlated positively with plaque area at baseline. The occurrence of large plaques and the change in plaque area at follow-up were associated with blood and creatinine-corrected urinary cadmium concentrations at baseline after adjustment for confounders. Blood and urine cadmium levels added information to established cardiovascular risk factors in predicting progress of atherosclerosis. We have shown that cadmium levels in blood and urine are independent factors associated with the development of atherosclerotic plaques at baseline as well as prospectively. This novel observation emphasizes the need to consider cadmium as a pro-atherogenic pollutant.

Assessment of Echo-Attenuated Plaque by Optical Coherence Tomography and its Impact on Post-Procedural Creatine Kinase-Myocardial Band Elevation in Elective Stent Implantation

This study examined morphological characteristics of echo-attenuated plaques by optical coherence tomography (OCT) and evaluated their influence on creatine kinase-myocardial band (CK-MB) elevation after percutaneous coronary intervention (PCI) in patients with elective stent implantation. Recent intravascular ultrasound studies have described atherosclerotic plaques with echo attenuation (EA) without associated bright echoes that are correlated with no-reflow phenomenon after PCI. We studied 135 native de novo culprit coronary lesions in 135 patients with normal pre-PCI CK-MB levels (28 with unstable angina; 107 with stable angina) who underwent intravascular ultrasound and OCT examinations before elective stent implantation. The lesions were divided into 2 groups based on the presence or absence of EA, and OCT findings were compared. We then determined predictors of post-PCI CK-MB elevation. EA was found in 47 (34.8%) lesions and was associated with the presence of OCT-derived thin-capped fibroatheroma, ruptured plaques, greater lipid content, intravascular ultrasound-derived large reference and plaque area, lesion eccentricity, and microcalcification. Elevated CK-MB levels were observed in 36 (26.7%) lesions, and significantly more frequently in lesions with EA than without. In multivariable analysis, EA (odds ratio [OR]: 3.49; 95% confidence interval [CI]: 1.53 to 7.93; p = 0.003) and OCT-derived ruptured plaque (OR: 2.92; 95% CI: 1.21 to 7.06; p = 0.017) were independent predictors of post-PCI CK-MB elevation. Atherosclerotic plaques with EA were associated with characteristics considered to be high risk or unstable. OCT examination showed an additive predictive value to the presence of EA for post-PCI CK-MB elevation.

Remodeling is a more important determinant of lumen size than atheroma burden in left main coronary artery disease

Left main coronary artery (LMCA) disease influences survival; however, the predictors of LMCA changes over time are incompletely understood. Paired intravascular ultrasound (IVUS) and core laboratory analyses were performed in a standardized fashion in 207 subjects (mean +/- SD age 58 +/- 10 years, 80% men). The average follow-up duration was 18 months (range 12-24 months). The IVUS measurements were first obtained at the smallest lumen area and the largest plaque area at follow-up and the corresponding positions in the LMCA were then measured at baseline. The LMCA percentage of atheroma area at baseline was 38.2% +/- 11.8%, and 133 patients (64%) experienced an increase in percentage of atheroma area. Change in lumen area correlated positively with change in total vessel area (R = 0.85, P < .0001) and negatively with change in percentage of atheroma area (R = -0.58, P < .0001). Change in plaque area correlated well with change in total vessel area (R = 0.64, P < .0001) but only weakly with change in lumen area (r = 0.14, P = .039). Although LMCA length correlated negatively with baseline lumen area and total vessel area, it did not correlate with their changes over time. On multivariable analyses, current smoking predicted an increase in percentage of atheroma area (P = .0013) and plaque area (P = .0041). Height negatively predicted change in percentage of atheroma area (P = .001). The LMCA lumen dimensions are more tightly linked with remodeling than with atheroma progression/regression.

ORIGINAL ARTICLE: Morphometric evaluation for relationship of atherosclerosis developed in coronary and peripheral muscular arteries: An autopsy study

Background and aims: Atherosclerosis is a systemic disorder that develops in any blood vessel of the body. Atherosclerosis can result in fatal complications such as myocardial infarction or stroke. The aim of this study was to compare the severity of atherosclerosis between the coronary arteries and other peripheral arteries. To our knowledge, no such morphometric tissue studies through autopsy samples so far are available in Korea. Methods: The left anterior descending artery, right coronary artery and bilateral carotid, renal and femoral arteries were obtained from 50 autopsies during the period from June to October 2008. Detailed gross examination of the each arteries was performed to look for the most severe site of luminal narrowing. Results: There was a significant correlation between the maximal carotid artery intima-media thickness and the largest plaque area of the coronary artery (P < 0.05). However, some discordant cases were also noted. Seven cases had more severe coronary atherosclerosis compared to the carotid artery. Conclusions: The careful examination of peripheral arteries including the carotid artery can be helpful in clinical prediction of coronary artery disease. However, such prediction should include other risk factors such as age, hypertension, diabetes and dyslipidemia and other relevant clinical conditions.

In vivo Detection of Vulnerable Atherosclerotic Plaque by MRI in a Rabbit Model

Background— The ability to identify atherosclerotic plaques with a high risk for sudden disruption before stroke or myocardial infarction would be of great utility. We used a rabbit model of controlled atherothrombosis to test whether in vivo MRI can noninvasively distinguish between plaques that disrupt after pharmacological triggering (vulnerable) and those that do not (stable). Methods and Results— Atherosclerosis was induced in male New Zealand White (n=17) rabbits by cholesterol diet and endothelial denudation of the abdominal aorta. After baseline (pretrigger) MRI with and without gadolinium contrast, the rabbits underwent 2 pharmacological triggerings to induce atherothrombosis, followed by another MRI 48 hours later (post-triggering). Atherosclerosis was identified by the pretriggered images in all rabbits, and thrombosis was identified in 9 of 17 animals (53%) by post-trigger MRI. After the animals were euthanized, 95 plaques were analyzed; 28 (29.5%) had thrombi (vulnerable) and 67 did not (stable) (70.5%). Pretriggered MRI revealed comparable stenosis in stable and vulnerable plaques, but vulnerable plaques had a larger plaque area (4.8�1.6 versus 3.0�1.0 mm 2 ; P =0.01), vessel area (9.2�3.0 versus. 15.8�4.9 mm 2 ; P =0.01), and higher remodeling ratio (1.16�0.2 versus 0.93�0.2; P =0.01) compared with stable plaques. Furthermore, vulnerable plaques more frequently exhibited (1) positive remodeling (67.8% versus 22.3%; P =0.01), in which the plaque is hidden within the vessel wall instead of occluding the lumen; and (2) enhanced gadolinium uptake (78.6% versus 20.9%; P =0.01) associated with histological findings of neovascularization, inflammation, and tissue necrosis. Conclusions— We demonstrate that in vivo MRI at 3.0 T detects features of vulnerable plaques in an animal model of controlled atherothrombosis. These findings suggest that MRI may be used as a noninvasive modality for localization of plaques that are prone to disruption.

Adrenomedullin ameliorates the development of atherosclerosis in apoE−/− mice

Adrenomedullin (ADM) is a multifunctional peptide regulating cardiovascular homeostasis. We studied the role of ADM in the pathogenesis of atherosclerosis by investigating changes in ADM and its receptors – calcitonin receptor-like receptor (CRLR) and receptor activity-modifying proteins (RAMPs) – in aorta of apoE−/− mice and the effect of exogenous ADM administration. ApoE−/− mice were fed an atherogenic diet for 4 weeks, and apoE−/− + ADM mice were additionally given subcutaneous injections of ADM, 300 ng/kg/h, for 4 weeks. ApoE−/− mice fed an atherogenic diet showed hyperlipidemia, a large plaque area and increased vessel wall thickness. The mRNA expression and protein level of ADM/ADM receptors were increased in the aorta, compared with C57BL/6J mice. The elevated mRNA level of CRLR and RAMPs correlated positively with ADM mRNA level. Radioimmunoassay revealed a higher plasma and aorta ADM content, by 61.6% and 285% (both P < 0.01), respectively, in apoE−/− mice than that in C57BL/6J mice. Exogenous ADM significantly ameliorated dyslipidemia in apoE−/− mice. ADM-treated mice showed fewer aortic plaques, decreased plaque area, by 76% ( P < 0.01), and reduced ratio of plaque area to luminal area, by 65% ( P < 0.01), and ultrasonography revealed significantly reduced intima-media thickness of the ascending branch and abdominal aorta. The results suggest that atherosclerotic apoE−/− mice fed an atherogenic diet showed upregulated endogenous ADM and its receptors, and exogenous ADM treatment ameliorated the dyslipidemia and vascular atherosclerotic lesions. ADM/ADM receptors might be an important protective system against atherosclerosis and could become a new target of prevention and therapy for atherosclerosis.

Abstract 907: Plaque Burden at Left Main Coronary Artery of Patients Undergoing Percutaneous Coronary Intervention with Metabolic Syndrome

Background: The left main coronary artery (LMCA) is an important target of atherosclerotic plaque accumulation. The purpose of this study is to investigate the relationship between metabolic syndrome and plaque characteristics at LMCA. Methods: We enrolled 63 consecutive patients with stable angina who underwent percutaneous coronary intervention (PCI). Using intravascular ultrasound (IVUS), cross-sectional area (CSA), lumen area and plaque area were checked at LMCA undergoing PCI for the left anterior descending coronary artery or left circumflex coronary artery but not LMCA. Total plaque volume at LMCA was also checked by IVUS. The tissue characteristics of coronary plaque at LMCA was analyzed and quantified using integrated backscatter (IB) IVUS. The patients were devided into the two groups who had metabolic syndrome (n = 34) or not (n = 39). We evaluated the relationship between plaque burden at LMCA and metabolic syndrome. Results: Patients with metabolic syndrome had significantly larger plaque area and CSA at minimum lumen area (MLA) of LMCA than patients without metabolic syndrome (10.8 ± 3.7mm2 vs 8.2 ± 4.4 mm2, p = 0.01, 25.8 ± 5.0mm2 vs 23.1 ± 5.4 mm2, p = 0.04, respectively). About total plaque volume at LMCA, patients with metabolic syndrome had also significantly larger volume than patients without metabolic syndrome (53.8 ± 24.7mm3 vs 39.8 ± 21.2 mm3, p = 0.021, respectively). Furthermore, the lipid component of plaque volume at LMCA using IB-IVUS was significantly larger in patients with metabolic syndrome than without metabolic syndrome (25.7 ± 12.1mm3 vs 19.3 ± 11.6 mm3, p = 0.038, respectively). Conclusion: These findings suggest that patients with metabolic syndrome have not only larger plaque but also lipid-rich plaque at LMCA than without metabolic syndrome. IVUS and IB-IVUS Parameter at LMCA

Plaque in superficial femoral arteries indicates generalized atherosclerosis and vulnerability to coronary death: An autopsy study

Risk factors for atherosclerosis have limited ability to identify persons at high risk of coronary heart disease. Assessment of subclinical atherosclerosis in peripheral arteries might improve this limitation. We studied the relationship between atherosclerotic plaques in peripheral arteries, coronary plaques, and coronary death. Predefined segments from the left anterior descending coronary artery, the right coronary artery, bilateral carotid, and superficial femoral arteries (SFA) were obtained from 100 autopsies (20-82 years, 30 females, 27 coronary deaths). Based on microscopic examination of 4756 sections, the extension of atherosclerosis (plaque burden) and the largest plaque area in each segment were quantified. Plaque burden in all arteries increased with age and was larger in coronary death (P < .05). SFA plaques occurred later than coronary and carotid plaques. When SFA plaque had developed, coronary plaque was also present. SFA plaque (odds ratio, 95% confidence interval: 7.07 [2.40-20.81]), but not carotid plaque, was significantly associated with coronary death, also after age and gender adjustment (21.25 [5.02-89.97]). The area under the receiver operating characteristic curves for the identification of coronary death individuals was 0.72 (95% confidence interval: 0.62-0.83) for coronary plaque, and 0.80 (0.72-0.89) for SFA plaque (age and gender adjusted). Atherosclerosis develops slower in SFA compared with coronary and carotid arteries. In persons with plaque in the SFA, plaque is always present in the coronary arteries. In younger persons, the presence of SFA plaque indicates a generalized susceptibility to atherosclerosis and vulnerability to coronary death.

Intravascular Ultrasonic Study of Gender Differences in Ruptured Coronary Plaque Morphology and Its Associated Clinical Presentation

Coronary plaque rupture is a phenomenon underlying most acute coronary events. Although gender is an important determinant of the incidence and clinical course of coronary atherosclerosis, its relation to plaque rupture is unknown. Therefore, we assessed gender differences in native artery plaque rupture characteristics and their related clinical presentations. There were 468 intravascular ultrasound (IVUS) preintervention images of ruptured plaques retrospectively identified. There were 328 men (81.6%) with 387 plaque ruptures and 74 women (18.4%) with 81 plaque ruptures. Patient demographics, angiographic characteristics, and qualitative and quantitative IVUS analyses of ruptured plaques were assessed. On average women were older than men (67.6 +/- 11.8 vs 62.6 +/- 11.4 years, p = 0.001) and more often presented with an acute coronary syndrome (89.2% vs 72.9%, p = 0.003). Older women had smaller vessel areas at the rupture site (p = 0.001), minimum lumen site (p = 0.002), and reference segments (p = 0.002) and smaller lumen areas at the rupture site (p = 0.026) and reference segments (p = 0.03). Ruptured plaques in older women were more often associated with IVUS-evident thrombus (48.1% vs 34.6%, p = 0.022). Independent predictors of acute clinical presentation were female gender (p = 0.006), smoking (p = 0.013), and presence of thrombus (p = 0.049). Independent predictors of the presence of thrombus were female gender (p = 0.025), smaller lumen area (p = 0.023) and larger plaque area (p = 0.008) at the rupture site, longer plaque ruptures (p = 0.016), and smoking (p = 0.045). In conclusion, coronary plaque ruptures are more often associated with thrombus and acute presentations in women than in men.

In-Vivo Coronary Plaque Composition in Patients with Acute Coronary Syndrome: A Virtual Histology Intravascular Ultrasound Study

Background and Objectives：Rupture-prone plaque, characterized by a large necrotic core, thin fibrous cap and large number of inflammatory cells, is known to be associated with acute coronary syndrome (ACS) from several autopsy and animal studies. We sought to assess in-vivo lesion characteristics of culprit lesions in patients with ACS. Subjects and Methods：One hundred consecutive patients (mean age 60.4 years, 70 males), who underwent percutaneous coronary intervention, were analyzed for intravascular ultrasound (IVUS) radiofrequency information using IVUS-virtual histology (VH) software. Results：Patients with ACS (n=44, mean 59.7 years, 34 males) had a lower prevalence of hypertension (45.5% vs. 67.9%, p=0.024), higher level of high-sensitivity C-reactive protein (0.36±0.36 mg/dL vs. 0.22±0.27, p=0.043), longer lesion length (22.6±8.6 mm vs. 19.3±6.9 mm, p=0.036), and more plaque rupture (63.6% vs. 10.7%, p<0.001) than those without ACS (mean 61.0 years 36 males). The lesion analysis, at a minimal luminal area, revealed that patients with ACS had a larger plaque area (12.5±5.8 mm

Absence of the protease inhibitor cystatin C in inflammatory cells results in larger plaque area in plaque regression of apoE-deficient mice

Matrix remodelling plays an important role in regulating plaque stability. Cystatin C, an inhibitor of the elastin-degrading cysteine proteases of the cathepsin family, is believed to be one of the key protease inhibitors in this process. The aim of the present study was to investigate the role of leukocyte-specific cystatin C expression under conditions that favour plaque regression. Apolipoprotein E-deficient mice (apoE −/−) were given a Western-type diet 15 weeks prior transplantation with bone marrow from mice lacking cystatin C (cysC −/−) or cystatin C positive (cysC +/+) mice, in both cases apoE +/+ to create conditions favouring plaque regression. Transplantations were verified with PCR and Western analyses. Transplanted mice showed a 70% decrease in lipid content and reduction in plaque area compared to baseline ApoE −/− mice, demonstrating plaque regression due to apoE expression in macrophages. apoE −/− mice transplanted with cysC −/− bone marrow were then compared to mice transplanted with cysC +/+ bone marrow. Mice receiving cysC −/− bone marrow had a 30% larger plaque area, despite absence of significant differences in plasma cholesterol and lipid contents in plaque. Unexpectedly, mice transplanted with cystatin C-deficient bone marrow cells had increased elastin and collagen content in lesions. These observations suggest that leukocyte-specific expression of cystatin C is actively involved in matrix remodelling associated with plaque regression.

Extent and direction of arterial remodeling in stable versus unstable coronary syndromes : an intravascular ultrasound study.

The morphological characteristics of coronary plaques in patients with stable versus unstable coronary syndromes have been described in vivo with intravascular ultrasound, but the relationship between arterial remodeling and clinical presentation is not well known. We studied 85 patients with unstable and 46 patients with stable coronary syndromes using intravascular ultrasound before coronary intervention. The lesion site and a proximal reference site were analyzed. The remodeling ratio (RR) was defined as the ratio of the external elastic membrane (EEM) area at the lesion to that at the proximal reference site. Positive remodeling was defined as an RR >1.05 and negative remodeling as an RR <0.95. Plaque area (13.9+/-5.5 versus 11.1+/-4.8 mm(2); P=0.005), EEM area (16.1+/-6.2 versus 13.0+/-4.8 mm(2); P=0. 004), and the RR (1.06+/-0.2 versus 0.94+/-0.2; P=0.008) were significantly greater at target lesions in patients with unstable syndromes than in patients with stable syndromes. Positive remodeling was more frequent in unstable than in stable lesions (51. 8% versus 19.6%), whereas negative remodeling was more frequent in stable lesions (56.5% versus 31.8%) (P=0.001). Positive remodeling and larger plaque areas were associated with unstable clinical presentation, whereas negative remodeling was more common in patients with stable clinical presentation. This association between the extent of remodeling and clinical presentation may reflect a greater tendency of plaques with positive remodeling to cause unstable coronary syndromes.

Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodeling paradox.

To relate local arterial geometry with markers that are thought to be related to plaque rupture. Plaque rupture often occurs at sites with minor luminal stenosis and has retrospectively been characterized by colocalization of inflammatory cells. Recent studies have demonstrated that luminal narrowing is related with the mode of atherosclerotic arterial remodeling. We obtained 1,521 cross section slices at regular intervals from 50 atherosclerotic femoral arteries. Per artery, the slices with the largest and smallest lumen area, vessel area and plaque area were selected for staining on the presence of macrophages (CD68), T-lymphocytes (CD45RO), smooth muscle cells (alpha-actin) and collagen. Inflammation of the cap or shoulder of the plaque was observed in 33% of all cross sections. Significantly more CD68 and CD45RO positive cells, more atheroma, less collagen and less alpha-actin positive staining was observed in cross sections with the largest plaque area and largest vessel area vs. cross sections with the smallest plaque area and smallest vessel area, respectively. No difference in the number of inflammatory cells was observed between cross sections with the largest and smallest lumen area. Intraindividually, pathohistologic markers previously reported to be related to plaque vulnerability were associated with a larger plaque area and vessel area. In addition, inflammation of the cap and shoulder of the plaque was a common finding in the atherosclerotic femoral artery.

Intravascular Ultrasound Assessment of the Prevalence and Causes of Angiographic “Haziness” Following High-Pressure Coronary Stenting

Haziness at sites of balloon angioplasty is believed to represent plaque fractures or platelet deposition. The etiology of haziness adjacent to coronary stents remains uncertain. This study examines the prevalence and etiology of “peri-stent” haziness following high-pressure deployment. Consecutive patients undergoing coronary stenting and intravascular ultrasound imaging were included. Haziness was defined as nonhomogeneous contrast density and/or indistinct vessel borders by consensus of 2 observers. Patients were excluded if angiography revealed an obvious cause of haziness (thrombus, dissection). Matched control segments without haziness were selected for comparison. The most diseased site within the reference segment was identified by ultrasound. Lumen and plaque areas, percent plaque area, and plaque echo density were assessed. Haziness was identified within 31 segments in 30 patients (15% of 201 angiograms examined). At hazy sites, ultrasound revealed a large percent plaque area in 15, dissections in 14, and near-normal findings in 2 segments. In the absence of dissection, percent plaque area and lumen area step-down from the stent to the diseased reference were greater than controls (percent plaque area 64 ± 12% vs 56 ± 10%, p = 0.04 and lumen step-down 35 ± 20% vs 13 ± 25%, p = 0.006). With dissections, percent plaque area and lumen step-down were not different from controls (p = 0.13 and 0.30, respectively), but underlying plaques were more frequently echolucent (64% vs 23%, p = 0.02). Thus, in this study, peri-stent haziness was evident in 15% of patients after high-pressure coronary stent deployment. Etiologies identified by intravascular ultrasound included unrecognized reference plaque and angiographically occult dissections.

Atherosclerotic arterial remodeling in the superficial femoral artery. Individual variation in local compensatory enlargement response.

In previous studies on atherosclerotic arterial remodeling, compensatory enlargement of the artery in response to plaque accumulation was inferred from pooled data based on one cross section per artery. We assessed local arterial remodeling individually by analyzing 45 artery segments at 0.5-cm intervals over a length of 10 to 15 cm. Twenty patients were studied by 30-MHz intravascular ultrasound (IVUS) before balloon angioplasty of the superficial femoral artery (370 cross sections), and 25 femoral artery segments were studied postmortem (551 cross sections). In each cross section, the area surrounded by the internal elastic lamina (IEL area) and the plaque area were measured. The IEL area was larger in the cross section with the largest plaque area than in the cross section with the smallest plaque area (32.5+/-13.0 and 32.0+/-11.5 mm2 versus 28.9+/-9.7 [P=NS] and 26.7+/-10.1 [P<.05] mm2 for IVUS and histology, respectively [mean+/-SD]). A significant positive correlation was found between plaque area and IEL area for the pooled data (r=.61 and r=.47 and slope=1.07 and 0.90 for IVUS and histology, respectively; both P<.001). In 12 of 20 and 16 of 25 individual arterial segments, however, no significant correlation was observed between plaque area and IEL area for IVUS and histology, respectively. A large variation was found in the correlation of the regression of plaque to IEL area (IVUS, r=-.40 to .89; histology, r=-.13 to .91) and slope (IVUS, -0.28 to 1.29; histology, -0.18 to 1.32). In the majority of atherosclerotic femoral arteries, significant compensatory enlargement could not be determined. It is inferred that arterial remodeling in response to plaque formation may vary among individuals.

Subacute thrombotic complications after intracoronary implantation of Palmaz-Schatz stents

Despite excellent results as a bail-out procedure for the management of abrupt closure after balloon angioplasty and the potential beneficial effects on restenosis after angioplasty, intracoronary stenting is limited, especially by subacute stent thrombosis. In 100 consecutive patients with intracoronary implantation of 118 Palmaz-Schatz stents, 10 patients (10%) developed subacute stent thrombosis during their hospital course 3 to 9 days after implantation. Therapy included intravenous thrombolysis, mechanical recanalization by balloon angioplasty, and emergency bypass surgery. Although successful recanalization was maintained in eight of nine nonsurgically treated patients within 2 hours after the onset of symptoms, seven patients developed myocardial infarction, with two patients having Q wave myocardial infarction and five patients having non-Q wave myocardial infarction. By univariate analysis, several variables could be identified as risk factors for the development of subacute stent thrombosis: bail-out implantations (odds ratio: 6.42; 95% confidence interval: 1.53 to 26.38; p = 0.007), unstable angina (12.32; 1.50 to 101.37; p = 0.006), long (5.44; 1.31 to 22.65; p = 0.015) and complex (type C) lesions (8.17; 1.93 to 34.50; p = 0.002) with large plaque areas (9.85; 1.96 to 44.51; p = 0.002), symptomatic postangioplasty dissections (4.36; 1.10 to 16.90; p = 0.029), incomplete wrapping of the dissection after stenting (6.50; 1.10 to 42.30; p = 0.039), and vessel irregularities distal to the stented segment (21.70; 4.12 to 113.18; p < 0.001). These variables, except the variable large plaque area, were confirmed as independent predictors of subacute stent thrombosis by a stepwise multivariate logistic regression analysis.(ABSTRACT TRUNCATED AT 250 WORDS)