Psychological stress has the potential to cause a decline in the epidermal permeability barrier function of the horny layer.

OBJECTIVE: Psychological stress is known to have a negative effect on a large number of skin diseases. However, there is little research on the relationship between psychological stress and the epidermal permeability barrier function (EPBF) of healthy individuals. We hypothesize that psychological stress deteriorates EPBF and aimed to investigate this relationship. METHODS: Psychological stress was assessed using salivary alpha-amylase (sAmy; KIU L(-1) ), and chromogranin A level corrected with total protein (CgAP; pmol mg(-1) protein) as psychological stress biomarkers. Measurements were obtained from 16 healthy female students during two periods of presumed higher stress (final examinations and returning from a long vacation), and a period considered as a control. The EPBF level was evaluated by measuring transepidermal water loss (TEWL; g m(-2)  h(-1) ). The TEWL was measured three times: just before (TEWL [Intact]), immediately after (TEWL [Str]) and 4 h after (TEWL [4 h]) barrier disruption by tape stripping. The rate of barrier disruption was evaluated by comparing the difference between the TEWL [Intact] and the TEWL [Str] (delta-BD: g m(-2)  h(-1) ). The recovery was assessed by comparing the difference between the TEWL [Intact] and TEWL [4 h] (delta-RE: g m(-2)  h(-1) ). RESULTS: The subjects demonstrated a significant increase in the sAmy value after the long vacation compared with the control. There was no change in the CgAP value between the groups. Meanwhile, the EPBF level showed significant deterioration during both higher stress periods. There was a significant increase in delta-BD and delta-RE after the long vacation. CONCLUSIONS: The results indicate the possibility that psychological stress causes a decline in EPBF and deterioration in barrier disruption and recovery. Furthermore, it implies a relationship between psychological stress and the exacerbation or protracted healing of skin disease.

Impact of glucose fluctuation and monocyte subsets on coronary plaque rupture.

BACKGROUND AND AIMS: It remains unclear whether glycemic fluctuation can affect plaque rupture in acute myocardial infarction (AMI). Here we investigate the impact of glucose fluctuation on plaque rupture, as observed by optical coherence tomography (OCT), and monocyte subsets in patients with AMI. METHODS AND RESULTS: We studied 37 consecutive patients with AMI. All patients underwent OCT examination, which revealed 24 patients with plaque rupture and 13 patients without plaque rupture at the culprit site. Peripheral blood sampling was performed on admission. Three monocyte subsets (CD14(+)CD16(-), CD14(bright)CD16(+), and CD14(dim)CD16(+)) were assessed by flow cytometry. Glycemic variability, expressed as the mean amplitude of glycemic excursion (MAGE), was determined by a continuous glucose monitoring system 7 days after the onset of AMI. MAGE was significantly higher in the rupture patients than in the non-rupture patients (P=0.036). Levels of CD14(bright)CD16(+) monocytes from the rupture patients were significantly higher than those from the non-rupture patients (P=0.042). Of interest, levels of CD14(bright)CD16(+) monocytes correlated positively and significantly with MAGE (r=0.39, P=0.02). CONCLUSION: Dynamic glucose fluctuation may be associated with coronary plaque rupture, possibly through the preferential increase in CD14(bright)CD16(+) monocyte levels.

A recurring translocation, t(3;6)(q27;p21), in non-Hodgkin's lymphoma results in replacement of the 5' regulatory region of BCL6 with a novel H4 histone gene.

3q27 translocations affecting the BCL6 gene can involve not only immunoglobulin genes (IG) but also other as yet uncharacterized chromosomal loci as partners. Here, we describe cloning of the junctional area of a recurring translocation, t(3;6)(q27;p21), in non-Hodgkin's lymphoma of B-cell type and isolation of clones from 6p21; high resolution fluorescence in situ hybridization mapped the clones to sub-band 6p21.3. Nucleotide sequence analysis of a fragment from the junctional area of 6p21 revealed the presence of a novel H4 histone gene that was included in the histone gene cluster on this particular region, and the same fragment detected approximately 380-bp transcripts in hematological tumor cells. Breakpoints on 3q27 of two cases carrying t(3;6) were immediately 3' of the BCL6 exon 1, and the H4 histone gene was substituted for the 5' regulatory elements of BCL6. Because H4 gene expression is tightly coupled to DNA replication, this study suggested an immediate mechanism for deregulated expression of BCL6, leading to the development of non-Hodgkin's lymphoma.

Molecular anatomy of BCL6 translocations revealed by long-distance polymerase chain reaction-based assays.

BCL6 translocations involve not only immunoglobulin (IG) genes but also a number of non-IG loci as partners. Junctional sequences of three IG/BCL6 translocations were readily obtained by long-distance PCR. In cases where partner loci were not determined, we developed a long-distance inverse PCR method, which amplifies unknown fragments flanked by known BCL6 sequences. Using these two long-distance PCR-based approaches, we cloned junctional areas of BCL6 translocations from a total of 58 cases of B-cell tumors. Nucleotide sequencing and database searches revealed that 30 cases involved IGs as partners: IG heavy chain gene in 22, IG kappa light chain gene in 1, and IG lambda light chain gene in 7. In contrast, 23 cases affected non-IG loci, including the H4 histone gene, heat shock protein genes HSP89alpha and HSP90beta, and PIM-1 proto-oncogene. On der(3) chromosomes, complete sets of the promoters of these partner genes replaced that of BCL6 in the same transcriptional orientation. These results suggest that BCL6 gene affected by the translocation is transcriptionally activated by a variety of stimuli, including cell cycle control, changes in the physical environment, and response to cytokines. Break points on BCL6 occurred within the major translocation cluster, and we identified a 120-bp hyper-cluster region a short distance from the 3' end of exon 1. Gel mobility-shift assay suggested the presence of a protein(s) that bound to this particular region.

Molecular features of a new human lymphoma cell line carrying both BCL2 and BCL6 gene rearrangements.

Chromosomal translocations and/or their molecular equivalents involving the BCL6 gene on 3q27 band have been suggested to be involved in the development of non-Hodgkin's lymphoma of B-cell type (B-NHL). The rearrangement of BCL6 sometimes coexists with other translocations specific to B-NHL. Here, we report a novel B-cell lymphoma cell line, YM, established from a patient with diffuse large cell lymphoma. The YM cells expressed B-cell-associated antigens in addition to mu delta/kappa monoclonal immunoglobulin. Southern blot analysis of DNA from YM cells demonstrated rearrangement of the BCL2 gene within the 5' flanking region (5'-BCL2). Polymerase chain reaction (PCR) using primer pairs for the BCL2 exons 1 and 2, and for the constant region of the immunoglobulin kappa light chain gene (IGkappa) revealed PCR products encompassing the 5'-BCL2/IGkappa fusion, indicating that the YM cells had a t(2;18)(p11;q21) translocation. The BCL6 gene was rearranged at a point within the first intron, and cloning of the rearranged BCL6 revealed unidentified sequences juxtaposed to the 5' side of the gene. The isolated clones were mapped to 16p11.2 by high resolution fluorescence in situ chromosomal hybridization. Thus, the YM cells carried a 3q27 translocation involving 16p11.2 as a partner. Chromosome painting of metaphase spreads confirmed that the YM cells had both t(2;18) and t(3;16). Northern blot analysis using a fragment immediately adjacent to the breakpoint on 16p11.2 revealed transcriptional activity within this locus. The YM cells expressed abundant transcripts with aberrant sizes from BCL2 and BCL6, indicating deregulated overexpression of the two genes resulting from the t(2;18) and t(3;16). The YM cell line will therefore be useful to study whether BCL2 and BCL6 genes collaborate in the pathogenesis of B-NHL.

Relation of phasic coronary flow velocity characteristics with TIMI perfusion grade and myocardial recovery after primary percutaneous transluminal coronary angioplasty and rescue stenting.

BACKGROUND: A residual stenosis and/or microvascular damage have been proposed as mechanisms of TIMI 2 flow for acute myocardial infarction. Coronary flow dynamics were assessed in patients with TIMI 2 flow to predict whether additional intervention would improve TIMI grade. METHODS AND RESULTS: In 35 patients who had a successfully recanalized anterior acute myocardial infarction using angioplasty or rescue stenting, coronary flow patterns were compared with corresponding TIMI grade and regional left ventricular wall motion (LVWM) 1 month after the intervention. After angioplasty, the time-averaged peak velocity (APV) was lower in patients with TIMI 2 flow (n=22) than in those with TIMI 3 flow (n=13; 7.9+/-3.9 versus 20.6+/-5.1 cm/s; P<0.001). Two different flow patterns were recorded in patients with TIMI 2 flow (versus TIMI 3, P<0.001); patients with type 1 TIMI 2 flow (n=15) had a reduced diastolic APV (8.3+/-4.8 versus 24.2+/-7.4 cm/s), prolonged diastolic deceleration time (1176+/-455 versus 728+/-205 ms), and a small diastolic/systolic APV ratio (1.3+/-0.6 versus 2.1+/-0.7); patients with type 2 TIMI 2 flow (n=7) had systolic flow reversal (systolic APV, -7.9+/-4.6 versus 11. 7+/-4.5 cm/s), a rapid diastolic deceleration time (221+/-84 versus 728+/-205 ms), and a negative diastolic/systolic APV ratio (-2.1+/-1. 4 versus 2.1+/-0.7). A significantly lower mean chord LVWM (-3.0+/-0. 2 versus -1.9+/-0.8; P<0.001) and a greater number of chords <-2SD (50+/-2 versus 28+/-18; P<0.001) were present in patients with type 2 versus type 1 TIMI 2 flow. Stenting increased TIMI 2 flow to TIMI 3 flow more in patients with type 1 than type 2 flow (67% versus 0%; P=0.003). Patients with TIMI 2 flow after stenting continued to demonstrate a type 2 pattern, and they had poor LVWM recovery. CONCLUSIONS: The differentiation between 2 types of TIMI 2 flow can predict the improvement of TIMI grade and LVWM recovery after additional stenting.

Can coronary blood flow velocity pattern after primary percutaneous transluminal coronary angioplasty [correction of angiography] predict recovery of regional left ventricular function in patients with acute myocardial infarction?

BACKGROUND: In the era of primary percutaneous transluminal coronary angioplasty (PTCA), it is important to judge whether myocardium within acute ischemic injury is viable. This study sought to investigate parameters derived from the coronary blood flow velocity spectrum immediately after primary PTCA in patients with acute myocardial infarction and to elucidate the clinical value of coronary blood flow measurement in predicting myocardial viability. METHODS AND RESULTS: Using a Doppler guidewire, we measured coronary blood flow velocity after successful completion of primary PTCA in 23 consecutive patients with acute anterior myocardial infarction. Regional wall motion was analyzed to estimate anterior wall motion score index (A-WMSI) by echocardiography before PTCA and 1 month after the onset of symptoms. Average systolic peak velocity (ASV) and deceleration time of diastolic flow velocity (DDT) significantly correlated to 1-month A-WMSI (r=-0.54, P=0.007 and r=-0.62, P=0.002, respectively), and optimal cutoff values to predict viable myocardium (defined as 1-month A-WMSI

Molecular and clinical features of non-Burkitt's, diffuse large-cell lymphoma of B-cell type associated with the c-MYC/immunoglobulin heavy-chain fusion gene.

PURPOSE: t(8;14)(q24;q32) and/or c-MYC/immunoglobulin heavy-chain (IGH) fusion gene have been observed not only in Burkitt's lymphoma (BL) but also in a proportion of non-BL, diffuse large-cell lymphoma of B-cell type (DLCL). We explored molecular features of DLCL with c-MYC/IGH fusion and the impact of this genetic abnormality on clinical outcome of DLCL. PATIENTS AND METHODS: A total of 203 cases of non-BL DLCL were studied. Genomic DNA extracted from tumor tissues was subjected to long-distance polymerase chain reaction (LD-PCR) using oligonucleotide primers for exon 2 of c-MYC and for the four constant region genes of IGH. RESULTS: Twelve cases (5.9%) showed positive amplification; one had a c-MYC/Cmicro, nine had a c-MYC/Cgamma, and two had a c-MYC/Calpha fusion sequence. Restriction and sequence analysis of the LD-PCR products, ranging from 2.3 to 9.4 kb in size, showed that breakage in the 12 cases occurred within a 1.5-kb region that included exon 1 of c-MYC in combination with breakpoints at the switch regions of IGH (10 of 12). In 10 cases, Myc protein encoded by the fusion genes demonstrated mutations and/or deletions. Six cases had additional molecular lesions in BCL-2 or BCL-6 and/or p53 genes. The age range of the 12 patients was 44 to 86 years, with a median age of 65.5 years. Five patients had stage I/II disease, and seven had stage III/IV disease. Lactate dehydrogenase was elevated in nine of 11 subjects. Seven showed involvement of the gastrointestinal tract. All patients were treated by surgery and/or chemoradiotherapy; six died of the disease within 1 year, resulting in the poorest 1- and 2-year survival rates among DLCL subgroups. CONCLUSION: The c-MYC/IGH fusion gene of DLCL is identical to that of the sporadic type of BL (sBL). DLCL with c-MYC/IGH shares clinical features with sBL but is characterized further by an older age distribution.

Noninvasive assessment of left internal mammary artery graft patency using duplex Doppler echocardiography from supraclavicular fossa.

OBJECTIVES: The purpose of this study was to clarify the usefulness of duplex Doppler echocardiography from the supraclavicular fossa for assessment of left internal mammary artery graft patency. BACKGROUND: A noninvasive method to assess coronary artery bypass graft patency would be useful for clinical diagnosis and long-term follow-up of graft outcome. METHODS: Duplex Doppler echocardiography from the supraclavicular fossa was performed in 56 consecutive patients who underwent postoperative cardiac catheterization studies, including quantitative angiography. All patients underwent coronary artery bypass graft surgery using the left internal mammary artery graft to the left anterior descending coronary artery. RESULTS: The left internal mammary artery graft and its flow were detected in 55 (98%) of the 56 patients with duplex Doppler echocardiography from the supraclavicular fossa. According to the quantitative angiographic data, the patients were assigned to three groups: group A (36 patients) with a normal left internal mammary artery graft (< 50% diameter stenosis), group B (9 patients) with intermediate (50% to 75% diameter) graft stenosis and group C (10 patients) with severe (> 75% diameter) graft stenosis. The diastolic/systolic peak velocity ratio was smaller in group C than in groups A and B (p < 0.05), but there was no significant difference between groups A and B. A diastolic/systolic peak velocity ratio < 0.6 predicted severe left internal mammary artery graft stenosis (> 75% diameter stenosis) with a sensitivity and specificity of 100% and 80%, respectively. The diastolic fraction of time-velocity integral was smaller in group C than in groups A and B (p < 0.05), but there was no significant difference between groups A and B. A diastolic fraction < 0.5 predicted significant left internal mammary artery graft stenosis (> 75% diameter stenosis) with a sensitivity and specificity of 90% and 100%, respectively. CONCLUSIONS: Duplex Doppler echocardiography from the supraclavicular fossa is useful for noninvasive assessment of left internal mammary artery graft patency.

Direct visualization of ruptured chordae tendineae by transesophageal two-dimensional echocardiography.

To determine the value of transesophageal echocardiography in the detection of ruptured chordae tendineae, 28 patients who had surgical therapy for pure mitral regurgitation were evaluated prospectively by conventional transthoracic and transesophageal two-dimensional echocardiography. Seventeen patients (Group I) had ruptured chordae tendineae and 11 (Group II) had intact chordae tendineae. Transthoracic echocardiography detected ruptured chordae tendineae in 6 patients from Group I (sensitivity 35%) and flail leaflets in 11 patients from Group I (sensitivity 65%). Transesophageal echocardiography disclosed ruptured chordae tendineae in all 17 Group I patients (sensitivity 100%); the sensitivity was significantly higher than that of transthoracic echocardiography. No abnormal chordal echoes were visualized in any patient from Group II by either transthoracic or transesophageal echocardiography (specificity 100%). Transesophageal echocardiography is a highly sensitive method for detecting ruptured chordae tendineae and is superior to transthoracic echocardiography in establishing its diagnosis.

Value of acceleration flow signals proximal to the leaking orifice in assessing the severity of prosthetic mitral valve regurgitation.

To test the value of acceleration flow signals proximal to the leaking orifice in assessing the severity of prosthetic mitral valve regurgitation, 39 consecutive patients undergoing left ventriculography were examined by Doppler color flow imaging. Acceleration flow signals proximal to the regurgitant orifice were detected in 27 of the 31 patients who had prosthetic mitral regurgitation by left ventriculography (sensitivity 87%). All four patients without acceleration flow signals had mild prosthetic mitral regurgitation by angiography. No acceleration flow signals were detected in any patient without prosthetic regurgitation by left ventriculography (specificity 100%). Individual values of the maximal area of acceleration flow signals obtained from three orthogonal planes in seven patients with mild prosthetic mitral regurgitation by angiography ranged from 0 to 17 mm2 (mean 4 +/- 6). In 8 patients with moderate prosthetic mitral regurgitation by angiography, the maximal area of acceleration flow signals ranged from 21 to 58 mm2 (mean 33 +/- 15), whereas the maximal area of acceleration flow signals in 16 patients with severe prosthetic regurgitation ranged from 20 to 173 mm2 (mean 102 +/- 41). The maximal area of the acceleration flow signals from three planes correlated well with the angiographic grade of prosthetic mitral regurgitation. There was a significant difference in the maximal area of acceleration flow signals between mild and moderate (p less than 0.001), moderate and severe (p less than 0.001) and mild and severe (p less than 0.001) prosthetic mitral regurgitation. Thus, measurement of acceleration flow signals by Doppler color flow imaging is useful in assessing the severity of prosthetic mitral regurgitation.

Temporal resolution of mitral regurgitation in patients with mitral valve prolapse: a phonocardiographic and Doppler echocardiographic study.

To assess the timing and duration of mitral regurgitation in mitral valve prolapse, 20 patients with a mid-systolic click or late systolic murmur, or both (Group 1) and 16 patients with a pansystolic murmur with late systolic accentuation (Group 2) were studied with phonocardiography and echocardiography including various Doppler techniques. The subjects' ages ranged from 15 to 73 years. Mitral valve prolapse with mitral regurgitation was observed in 15 of 20 patients in Group 1 and in all 16 patients in Group 2. M-mode Doppler color echocardiography demonstrated a mitral regurgitant signal throughout systole and isovolumic relaxation in all but 1 of these 31 patients regardless of the pattern of the systolic murmur. The regurgitant signal was recorded after the click in only one patient with mitral valve prolapse in Group 1. Two of the five patients in Group 1 without two-dimensional echocardiographic findings of mitral valve prolapse had the early systolic signal of mitral regurgitation. The timing and duration of the mitral regurgitant signal detected in patients in Group 1 with pulsed or continuous wave Doppler ultrasound varied with the site of the sample volume or beam direction. In the patients in Group 2, however, the signal was demonstrated throughout systole and isovolumic relaxation by both Doppler methods. Compared with M-mode Doppler color echocardiography, therefore, pulsed and continuous wave Doppler methods were less sensitive and thus inadequate to investigate the timing and duration of mitral regurgitation in mitral valve prolapse, especially in patients with a mid-systolic click or a late systolic murmur, or both, who had mild or eccentric mitral regurgitant jets.(ABSTRACT TRUNCATED AT 250 WORDS)

Planimetry and transthoracic two-dimensional echocardiography in noninvasive assessment of aortic valve area in patients with valvular aortic stenosis.

OBJECTIVES: The aim of this study was to evaluate the reliability of transthoracic two-dimensional echocardiography in measuring aortic valve area (AVA) by planimetry. BACKGROUND: Planimetry of AVA using two-dimensional transesophageal echocardiographic images has been reported to be a reliable method for measuring AVA in patients with aortic stenosis. Recent advances in resolution of two-dimensional echocardiography permit direct visualization of an aortic valve orifice from the transthoracic approach more easily than before. METHODS: Forty-two adult patients with valvular aortic stenosis were examined. A parasternal short-axis view of the aortic valve was obtained with transthoracic two-dimensional echocardiography. AVA was measured directly by planimetry of the inner leaflet edges at the time of maximal opening in early systole. AVA was also measured by planimetry using transesophageal echocardiography, by the continuity equation and by cardiac catheterization (Gorlin formula). RESULTS: In 32 (76%) of the 42 study patients, AVA could be detected by using the transthoracic planimetry method. There were good correlations between results of transthoracic two-dimensional echocardiographic planimetry and the continuity equation (y = 0.90x + 0.09, r = 0.90, p < 0.001, SEE = 0.09 cm2), transesophageal echocardiographic planimetry (y = 1.05x - 0.02, r = 0.98, p < 0.001, SEE = 0.04 cm2) and the Gorlin formula (y = 1.02x + 0.05, r = 0.89, p < 0.001, SEE = 0.10 cm2). CONCLUSIONS: Transthoracic two-dimensional echocardiography provides a feasible and reliable method in measuring AVA in patients with aortic stenosis.

Valvular regurgitation in heart-lung transplant recipients: a Doppler color flow study.

To assess the frequency and degree of valvular regurgitation in combined heart and lung transplant recipients, 50 patients were investigated using Doppler color flow echocardiography 20 to 909 days (mean 369) after heart-lung transplantation. The mean age (+/- SD) of the patients was 25 +/- 9 years. No patient had evidence of rejection at the time of the study. Fifty normal volunteers acted as control subjects. Tricuspid, mitral and pulmonary regurgitation were commonly observed in the patients undergoing heart-lung transplantation (78%, 52% and 68%, respectively), but were not significantly more frequent than in the normal subjects (68%, 42% and 70%, respectively). Aortic regurgitation was uncommon in both groups (4% and 2%, respectively). However, tricuspid and mitral regurgitant jet areas were significantly greater (p less than 0.01) in heart-lung transplant recipients than in normal subjects (156 +/- 120 and 84 +/- 52 mm2 compared with 40 +/- 38 and 28 +/- 26 mm2, respectively); pulmonary regurgitant jet area was not significantly different in the two groups (32 +/- 26 and 28 +/- 26 mm2, respectively). Regurgitant jet area was not significantly correlated with patient or donor age, donor organ total ischemic time, time after operation, use of steroids for immunosuppression or total number of rejection episodes. These results show that valvular regurgitation is not significantly more frequent after heart-lung transplantation than in normal subjects, but atrioventricular (AV) valve regurgitation, when present, is significantly greater in degree. This suggests that the degree but not the frequency of AV valve regurgitation is related to transplantation.

Troglitazone reduces neointimal tissue proliferation after coronary stent implantation in patients with non-insulin dependent diabetes mellitus: a serial intravascular ultrasound study.

OBJECTIVES: The aim of the present study was to determine whether troglitazone reduces neointimal tissue proliferation after coronary stent implantation in patients with non-insulin dependent diabetes mellitus (NIDDM). BACKGROUND: Increased in-stent restenosis in patients with diabetes mellitus is due to accelerated neointimal tissue proliferation after coronary stent implantation. Troglitazone inhibits intimal hyperplasia in experimental animal models. METHODS: We studied 62 stented lesions in 52 patients with plasma glucose levels (PG) > or = 11.1 mmol/liter at 2 h after 75 g oral glucose load. The study patients were randomized into two groups: the troglitazone group of 25 patients with 29 stents, who were treated with 400 mg of troglitazone, and the control group of 27 patients with 33 stents. All patients underwent oral glucose tolerance tests before and after their six-month treatment period. The sum of PG (sum of PG) and the sum of insulin levels (sum of IRI) were measured. Serial (postintervention and at six-month follow-up) intravascular ultrasound studies were performed. Cross-sectional images within stents were taken at every 1 mm, using an automatic pullback. Stent areas (SA), lumen areas (LA), and intimal areas (IA = SA - LA) were measured and averaged over a number of selected image slices. The intimal index was calculated as intimal index = averaged IA/averaged SA x 100%. RESULTS: There were no differences between the two groups before treatment in sum of PG (31.35 +/- 3.07 mmol/liter vs. 32.89 +/- 4.87 mmol/liter, respectively, p = 0.2998) and sum of IRI (219.6 +/- 106.2 mU/liter vs. 209.2 +/- 91.6 mU/liter, respectively, p = 0.8934). However, reductions in sum of PG at the six-month follow-up in the troglitazone group were significantly greater than those in the control group (-21.4 +/- 8.8% vs. -4.5 +/- 7.4%, respectively, p < 0.0001). Likewise, decreases in sum of IRI were greater in the troglitazone-treated group (-31.4 +/- 17.9% vs. -1.9 +/- 15.1%, respectively, p < 0.0001). Although, there were no differences between the two groups in SA at postintervention (7.4 +/- 2.2 mm2 vs. 7.3 +/- 1.7 mm2, respectively, p = 0.9482) and at follow-up (7.3 +/- 2.3 mm2 vs. 7.3 +/- 1.8 mm2, respectively, p = 0.2307), the LA at follow-up in the troglitazone group was significantly greater than that in the control group (5.3 +/- 1.7 mm2 vs. 3.7 +/- 1.7 mm2, respectively, p = 0.0002). The IA at follow-up in the troglitazone group was significantly smaller than that in the control group (2.0 +/- 0.9 mm2 vs. 3.5 +/- 1.8 mm2, respectively, p < 0.0001). This was also true for intimal index (27.1 +/- 11.5% vs. 49.0 +/- 14.4%, respectively, p < 0.0001). CONCLUSIONS: Serial intravascular ultrasound assessment shows that administration of troglitazone reduces neointimal tissue proliferation after coronary stent implantation in patients with NIDDM.