SwinGar: Spectrum-Inspired Neural Dynamic Deformation for Free-Swinging Garments.

Our work presents a novel spectrum-inspired learning-based approach for generating clothing deformations with dynamic effects and personalized details. Existing methods in the field of clothing animation are limited to either static behavior or specific network models for individual garments, which hinders their applicability in real-world scenarios where diverse animated garments are required. Our proposed method overcomes these limitations by providing a unified framework that predicts dynamic behavior for different garments with arbitrary topology and looseness, resulting in versatile and realistic deformations. First, we observe that the problem of bias towards low frequency always hampers supervised learning and leads to overly smooth deformations. To address this issue, we introduce a frequency-control strategy from a spectral perspective that enhances the generation of high-frequency details of the deformation. In addition, to make the network highly generalizable and able to learn various clothing deformations effectively, we propose a spectral descriptor to achieve a generalized description of the global shape information. Building on the above strategies, we develop a dynamic clothing deformation estimator that integrates graph attention mechanisms with long short-term memory. The estimator takes as input expressive features from garments and human bodies, allowing it to automatically output continuous deformations for diverse clothing types, independent of mesh topology or vertex count. Finally, we present a neural collision handling method to further enhance the realism of garments. Our experimental results demonstrate the effectiveness of our approach on a variety of free-swinging garments and its superiority over state-of-the-art methods.

The combination of the neutrophil-to-lymphocyte and platelet-to-lymphocyte ratios as a novel predictor of intravenous immunoglobulin resistance in patients with Kawasaki disease: a multicenter study.

INTRODUCTION: The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) have been reported to be a predictor for intravenous immunoglobulin (IVIG) resistance in patients with Kawasaki disease (KD) recently. The objective of the present study was to elucidate the predictive validity of this new marker in a multicenter study. MATERIALS AND METHODS: We retrospectively reviewed the clinical records of 520 consecutive KD patients (development data set) and 332 subsequent patients (validation data set) at 7 hospitals in Japan. RESULTS: Both NLR and PLR were significantly higher in the IVIG-resistant group than in the IVIG-responsive group. When we set the cut-off point as NLR ≥ 4.11 and PLR ≥ 119, multiple logistic regression analyses showed that a high NLR and PLR before initial IVIG were independent predictors of IVIG resistance, and their combination was a stronger predictor than either alone. The sensitivity and specificity of the combination of NLR ≥ 4.11 and PLR ≥ 119 were 0.58 and 0.73 in the development data set. Validated using an independent data set, they were 0.54 and 0.72 in the validation data set. On comparing the AUC of this predictor with those of the Gunma and Kurume scores, the AUC was highest for this predictor, followed by the Gunma score and Kurume score (0.70, 0.68, and 0.64, respectively). DISCUSSION: The predictive validity of the combination of a high NLR and PLR, which is a simple and convenient indicator, was equal to or better than that of the existing scoring systems. The new predictive marker may be a suitable indicator for predicting IVIG resistance in KD patients.

Enhanced formation of neutrophil extracellular traps in Kawasaki disease.

BACKGROUND: Neutrophils contribute to the clearance of pathogens through the formation of neutrophil extracellular traps (NETs) in a process known as NETosis, but the excessive release of NETs has been reported to be involved in the pathogenesis of various diseases, including vasculitis, by inducing tissue injury. The aim of the present study was to investigate whether or not NETosis is enhanced in the acute phase of Kawasaki disease (KD). METHODS: After neutrophils isolated from the peripheral blood of patients with KD and healthy control (HC) were cultured in vitro, the degree of spontaneous NETosis was evaluated by measuring the number of NETs formed and the titers of cell-free DNA (cfDNA) and neutrophil elastase (NE)-DNA complex. RESULTS: Spontaneous NET formation in vitro was observed in neutrophils isolated from KD patients, and the number of NET formations was significantly higher in acute KD than in convalescent KD and HC. The increased levels of cfDNA and NE-DNA complexes in the acute phase of KD tended to decrease in the convalescent phase. CONCLUSIONS: Spontaneous NET formation was enhanced in neutrophils from patients with acute KD, suggesting that circulating neutrophils may be primed to undergo NETosis in KD vasculitis.

Angioscopic differences of coronary intima between diffuse and focal coronary vasospasm: Comparison of optical coherence tomography findings.

BACKGROUND: Coronary artery vasospasm (CS) can be identified as either a diffuse type or focal type; however, the difference in endothelial characteristics between these spasm types remains unclear. The features of coronary intima associated with diffuse spasm and focal spasm using coronary angioscopy (CAS) were evaluated and the optical coherence tomography (OCT) findings were compared. METHODS: CAS and/or OCT observational analysis was performed in 55 patients (mean age: 61.4 years, 31 men) who had acetylcholine-provoked CS (diffuse CS, 31 patients; focal CS, 24 patients). The yellowness of the intima, presence of thrombus in CAS, and intimal characteristics based on the OCT results were evaluated. RESULTS: CAS showed more atherosclerotic yellow plaques at the focal spasm segment than at the diffuse spasm segment (p=0.032). Moreover, there were more thrombi at the focal spasm segment (p=0.039). In addition, OCT results revealed that the intima area, maximum intima thickness, and lipid content in the focal CS group were larger than the diffuse CS group (4.22±1.67mm2 vs. 3.45±2.36mm2; 0.71±0.29mm vs. 0.53±0.30mm; 55.9% vs. 32.0%, p<0.001, respectively). CONCLUSIONS: These results indicate that the presence of atherosclerotic plaques at the spasm site is likely to be related to the occurrence of a focal vasospasm. This may support the difference of features between focal CS and diffuse CS and contribute to precise treatment for each spasm type.

A comparison of the predictive validity of the combination of the neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio and other risk scoring systems for intravenous immunoglobulin (ivig)-resistance in Kawasaki disease.

BACKGROUND: We recently reported that the combination of the neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR) is a novel and useful predictor of intravenous immunoglobulin (IVIG)-resistance in Kawasaki disease (KD). In the present study, to evaluate the effectiveness of the new risk score, we compared its predictive validity to that of previously reported risk scores. MATERIALS AND METHODS: The laboratory records of 437 patients with KD before IVIG therapy were retrospectively analyzed, and the IVIG-responsive (n = 344) and IVIG-resistant (n = 93) patients were compared. The validity of the new score (the combination of NLR≥3.83 and PLR≥150) for predicting IVIG resistance in KD was compared to that of the Kobayashi, Egami and Sano risk scores. RESULTS: The new score and the Kobayashi score displayed high sensitivity (0.72 and 0.70 respectively) and specificity (0.67 and 0.68 respectively), while the Egami and Sano scores showed high specificity (0.71 and 0.81 respectively) but relatively low sensitivity (0.56 and 0.45 respectively). The odds ratios (ORs) for the new score, the Kobayashi score, the Egami score and the Sano score were 5.34 (95% confidence interval [CI] 3.22-8.85), 4.87 (95% CI 2.96-8.01), 3.14 (95% CI 1.96-5.03) and 3.53 (95% CI 2.17-5.77) respectively. CONCLUSIONS: The predictive validity of the combination of NLR≥3.83 and PLR≥150, which is a simple and convenient indicator, was equal to or higher than that of the other risk scores. This suggests that the new score could be a widely available marker for predicting IVIG resistance in KD.

Urinary Lactate Dehydrogenase Activity and Its Isozyme Patterns in Kawasaki Disease.

Abnormal urinary findings, such as sterile pyuria, proteinuria, and microscopic hematuria, are often seen in the acute phase of Kawasaki disease (KD). We investigated the potential significance of urinary lactate dehydrogenase (U-LDH) activity and its isozyme patterns in KD. Total U-LDH activity and its isozymes (U-LDH1-5) levels were compared among 120 patients with KD, 18 patients with viral infection (VI), and 43 patients with upper urinary tract infection (UTI) and additionally compared between intravenous immunoglobulin (IVIG) responders (n = 89) and nonresponders (n = 31) with KD. Total U-LDH activity was higher in KD (35.4 ± 4.8 IU/L, P < 0.05) and UTI patients (66.0 ± 8.0 IU/L, P < 0.01) than in VI patients (17.0 ± 6.2 IU/L). In the isozyme pattern analysis, KD patients had high levels of U-LDH1 and U-LDH2, while UTI patients had high levels of U-LDH3, U-LDH4, and U-LDH5. Furthermore, IVIG nonresponders of KD had significantly higher levels of total U-LDH activity (45.1 ± 4.7 IU/L, P < 0.05), especially U-LDH1 and U-LDH2 (P < 0.05), than IVIG responders (32.0 ± 2.8 IU/L). KD patients have increased levels of total U-LDH activity, especially U-LDH-1 and U-LDH2, indicating a unique pattern of U-LDH isozymes different from that in UTI patients.

The Combined Usefulness of the Neutrophil-to-Lymphocyte and Platelet-to-Lymphocyte Ratios in Predicting Intravenous Immunoglobulin Resistance with Kawasaki Disease.

The laboratory records of 405 patients with Kawasaki disease before and after intravenous immunoglobulin (IVIG) therapy were compared between the IVIG-responsive (n = 320) and IVIG-resistant (n = 85) groups. A high neutrophil-to-lymphocyte ratio and a high platelet-to-lymphocyte ratio before IVIG, especially when combined, were useful predictors for IVIG resistance in Kawasaki disease.

Soluble sortilin is released by activated platelets and its circulating levels are associated with cardiovascular risk factors.

OBJECTIVE: Sortilin is involved multilaterally in the development of atherosclerosis. Here, we examine the release of soluble sortilin (sSortilin) from platelets and assess the association between circulating levels of sSoritlin and atherothrombosis such as coronary artery disease (CAD). METHODS AND RESULTS: sSortilin levels measured in healthy subjects were higher in serum than in plasma (38.4 ± 8.7 vs. 15.8 ± 2.9 ng/mL; p < 0.0001). Platelets were shown to contain both membrane-bound sortilin and its soluble form lacking the cytoplasmic tail. Stimulation of platelet-rich plasma with collagen induced sSortilin release concomitantly with platelet aggregation, and the release was suppressed by aspirin. In clinical evaluation, plasma sSortilin was detected at significantly higher levels in cardiovascular risk patients with hypertension, dyslipidemia, and/or diabetes without CAD (non-CAD, 18.7 ± 3.3 ng/mL) than in patients with CAD under aspirin therapy (17.1 ± 3.6 ng/mL; p < 0.01) or in healthy controls (16.8 ± 2.9 ng/mL; p < 0.01). In these patients, plasma sSortilin levels were significantly correlated with platelet counts (rs = 0.33; p = 0.0085) and showed significant positive associations with cardiovascular risk factors: low-density lipoprotein cholesterol (rs = 0.37; p = 0.0023), triglycerides (rs = 0.28; p = 0.023), and serum uric acid (rs = 0.30; p = 0.017) in non-CAD, and γ-glutamyltransferase (rs = 0.43; p = 0.020) and high-sensitivity C-reactive protein (rs = 0.33, p = 0.0022) in CAD. CONCLUSION: Elevated plasma sSortilin levels may be associated with in vivo platelet activation and could be a risk factor for atherothrombosis.

Improvements in Augmentation Index and Urinary Albumin Excretion With Benidipine in Hypertensive Patients With Chronic Kidney Disease.

Although calcium channel blockers (CCB) are expected to improve the augmentation index (AI) in CKD patients, the potential effect of benidipine on AI has been poorly studied.The present study aimed to compare the effect of benidipine and amlodipine in the treatment of CKD patients as measured through AI and urinary albumin excretion (UAE). Eligible patients with CKD were randomized to either the benidipine group or amlodipine group. Changes in UAE and AI were compared with target blood pressure level set at < 130/80 mmHg. A total of 108 patients were enrolled; 88 patients who were followed up were included in the analysis. Although no significant change in renal function was noted in either group, there was a significant improvement in AI only in the benidipine group (85.7 ± 13.3% to 81.4 ± 15.2%; P = 0.021) A subgroup analysis of 64 patients who achieved SBP < 140 mmHg at the end of follow-up (31 on amlodipine and 33 on benidipine) was carried out. Significant improvement in AI was noted only in the benidipine group (84.5 ± 13.6% to 79.5 ± 15.2%; P = 0.0138). In another subgroup of patients with UAE ≥ 300 mg/g Cr, a significant improvement in UAE in the benidipine group was found compared with the amlodipine group (-25 ± 46, 51 ± 60%, P = 0.031, respectively).These results suggest that benidipine might reduce significantly AI and might have potentially greater improvements in UAE than amlodipine in advanced CKD patients receiving RAS inhibitors.

Association between the epicardial adipose tissue thickness and the presence of multivessel disease in patients with acute myocardial infarction.

AIM: Epicardial adipose tissue (EAT) is implicated in the development of coronary atherosclerosis.We sought to investigate the association between the EAT thickness and presence of multivessel disease (MV) in patients with acute myocardial infarction (AMI). METHODS: We enrolled 45 consecutive patients with AMI who underwent primary percutaneous coronary intervention (PCI). The EAT thickness was measured on echocardiography. A follow-up study was performed using coronary angiography with coronary angioscopy two weeks after primary PCI. RESULTS: Based on the angiographic findings, 21 patients had single-vessel disease (SV) and 24 patients had MV. The EAT thickness in the patients with SV was significantly smaller than that in the patients with MV (1.9±0.9 mm vs 2.8±1.3 mm, p=0.005, respectively). A multivariate logistic analysis demonstrated that the EAT thickness was the only independent predictor of MV (odds ratio=1.987, 95% confidence interval: 1.089-3.626, p=0.025). An EAT thickness of 2.3 mm was determined to be the optimal cut-off value for predicting MV, with a sensitivity of 70.8% and specificity of 71.4%. Between the thin EAT (＜2.3 mm) and the thick EAT (≥2.3 mm) groups, there were no difference in the number of intense yellow plaques in the non-infarct-related artery evaluated on angioscopy (2.0±2.2 vs 1.8±2.0, p=0.365, respectively). CONCLUSIONS: The EAT thickness is closely associated with the presence of MV, but not vessel vulnerability in the non-infarct-related artery, in patients with AMI. Measuring the EAT provides important information for treating patients with AMI.

[Use of the urinary trypsin inhibitor ulinastatin for acute Kawasaki disease].

Intravenous immunoglobulin (IVIG) therapy is widely recognized as standard treatment for Kawasaki disease(KD). However, about 20 % of KD patients are resistant to IVIG and are considered to be a high risk group for coronary artery lesions (CAL). Ulinastatin(UTI) is one of the neutrophil elastase inhibitors used for patients with pancreatitis or circulatory shock, and several studies have shown its efficacy for KD. Recently, we demonstrated that initial UTI treatment combined with IVIG decreased the number of patients requiring addi- tional rescue treatment and the occurrence of CAL. In this study, no severe adverse events occurred. Further research and a prospective trial are needed to prove the clinical efficacy and demonstrate the limits of UTI in patients with KD.

Impact of coronary plaque burden and composition on periprocedural myocardial infarction and coronary flow reserve after percutaneous coronary intervention.

Periprocedural myocardial infarction (PMI) is one of the major complications of percutaneous coronary intervention (PCI). We investigated the influence of coronary plaque burden and characteristics on PMI using intravascular ultrasound (IVUS) with radiofrequency-based tissue characterization technology (iMAP). The study population consisted of 33 consecutive patients with stable angina pectoris who underwent PCI. IVUS images were recorded before and after PCI for offline analysis, and coronary flow reserve (CFR) was measured after PCI. PMI was defined as a post-PCI cardiac troponin T elevation > 5 × 99(th) percentile of the upper reference limit (0.014 ng/mL). Plaque volume in patients with PMI (n = 12) was significantly greater than that in patients without PMI (n = 21) (240.4 ± 106.0 mm(3) versus 152.1 ± 76.9 mm(3), P = 0.0096). The iMAP-IVUS analysis demonstrated that the fibrotic, lipidic, and necrotic tissue volume within culprit lesions were also greater in patients with PMI than in patients without PMI (129.4 ± 52.2 mm(3) versus 94.6 ± 40.8 mm(3), P = 0.041; 26.8 ± 10.5 mm(3) versus 15.8 ± 11.5 mm(3), P = 0.011; and 81.3 ± 48.4 mm(3) versus 40.2 ± 33.6 mm(3), P = 0.0071, respectively). Multivariate logistic analysis demonstrated that necrotic tissue volume was the only independent predictor of PMI. Multiple regression analysis demonstrated that the post-PCI CFR values signifi cantly correlated with percent plaque burden, and there were no correlations with the percent tissue burden of each plaque component. In conclusion, the iMAP-IVUS analyses demonstrate that necrotic tissue volume is a potent predictor of PMI. Microcirculatory disturbance after PCI is significantly influenced by percent plaque burden, regardless of plaque compositions.

Un tratamiento nuevo para una enfermedad antigua: tratamiento de la hipertensión arterial resistente mediante denervación simpática renal percutánea / New treatment for old disease: management of resistant hypertension by percutaneous renal sympathetic denervation

La hipertensión es un importante factor de riesgo que contribuye a que ocurran eventos cardiovasculares como el ictus y el infarto de miocardio; en su patogenia está involucrada la actividad nerviosa simpática acelerada. Sin embargo, no se controla adecuadamente la hipertensión de muchos pacientes a pesar de disponerse de múltiples fármacos para tratarla. Se han desarrollado nuevas estrategias basadas en intervenciones y en dispositivos, como la terapia de denervación simpática renal percutánea, para mejorar el control de la presión arterial en estos pacientes refractarios. La denervación simpática renal proporciona una disminución no sólo de la presión arterial, sino también de la actividad nerviosa simpática sistémica. La reducción de la presión arterial parece mantenerse 3 años tras la intervención, lo cual implica que en este tiempo no se produce ningún mecanismo de contrarregulación ni reinervación de los nervios simpáticos renales aferentes. Se espera que la denervación simpática renal sea un tratamiento prometedor para los pacientes con hipertensión arterial, insuficiencia cardiaca congestiva, enfermedad renal crónica y síndrome metabólico, eventos que intervienen en la patogenia de la potenciación de la actividad nerviosa simpática. Esta revisión se centra en los dispositivos e intervenciones actuales, sus resultados y las perspectivas que abren en el tratamiento de la hipertensión(AU)

Hypertension is a major contributor to cardiovascular events, such as stroke and myocardial infarction, with accelerated sympathetic nerve activity implicated in its pathogenesis. However, hypertension in many patients is not adequately controlled, despite the availability of numerous medication classes. Novel procedure—as well as device-based strategies, such as percutaneous renal sympathetic nerve denervation therapy—have been developed to improve blood pressure in these refractory patients. Renal sympathetic denervation delivers not only a decrease in blood pressure levels but also renal as well as systemic sympathetic nerve activity. The reduction in blood pressure appears to be sustained over 3 years after the procedure, which implies no counterregulatory mechanism or re-innervation of afferent renal sympathetic nerve so far. Renal sympathetic denervation is expected to be a promising treatment for patients with hypertension, congestive heart failure, chronic kidney disease, and metabolic syndrome implicated in the pathogenesis of potentiated sympathetic nerve activity. This review will focus on the current devices and procedures, their outcomes and prospects in the treatment of hypertension(AU)

Technical note: Quantification of neurocranial shape variation using the shortest paths connecting pairs of anatomical landmarks.

Three-dimensional geometric morphometric techniques have been widely used in quantitative comparisons of craniofacial morphology in humans and nonhuman primates. However, few anatomical landmarks can actually be defined on the neurocranium. In this study, an alternative method is proposed for defining semi-landmarks on neurocranial surfaces for use in detailed analysis of cranial shape. Specifically, midsagittal, nuchal, and temporal lines were approximated using Bezier curves and equally spaced points along each of the curves were defined as semi-landmarks. The shortest paths connecting pairs of anatomical landmarks as well as semi-landmarks were then calculated in order to represent the surface morphology between landmarks using equally spaced points along the paths. To evaluate the efficacy of this method, the previously outlined technique was used in morphological analysis of sexual dimorphism in modern Japanese crania. The study sample comprised 22 specimens that were used to generate 110 anatomical semi-landmarks, which were used in geometric morphometric analysis. Although variations due to sexual dimorphism in human crania are very small, differences could be identified using the proposed landmark placement, which demonstrated the efficacy of the proposed method.

New treatment for old disease: management of resistant hypertension by percutaneous renal sympathetic denervation.

Hypertension is a major contributor to cardiovascular events, such as stroke and myocardial infarction, with accelerated sympathetic nerve activity implicated in its pathogenesis. However, hypertension in many patients is not adequately controlled, despite the availability of numerous medication classes. Novel procedure-as well as device-based strategies, such as percutaneous renal sympathetic nerve denervation therapy-have been developed to improve blood pressure in these refractory patients. Renal sympathetic denervation delivers not only a decrease in blood pressure levels but also renal as well as systemic sympathetic nerve activity. The reduction in blood pressure appears to be sustained over 3 years after the procedure, which implies no counterregulatory mechanism or re-innervation of afferent renal sympathetic nerve so far. Renal sympathetic denervation is expected to be a promising treatment for patients with hypertension, congestive heart failure, chronic kidney disease, and metabolic syndrome implicated in the pathogenesis of potentiated sympathetic nerve activity. This review will focus on the current devices and procedures, their outcomes and prospects in the treatment of hypertension.

Serial change and its determinants of residual plaque characteristics under sirolimus-eluting stent: a coronary angioscopic study.

OBJECTIVES: To examine serial change in the residual plaque behind the sirolimus-eluting stent (SES) using coronary angioscopy in patients with SES implantation and to identify its baseline determinants. BACKGROUND: Previous coronary angioscopic studies have demonstrated that SES enhances the yellow grade of residual plaque during follow-up period. METHODS: A total of 42 patients with stable angina pectoris or silent ischemic heart disease, who had a successful SES implantation were examined by coronary angioscopy both at the baseline (SES implantation) and the follow-up period (9-14 month follow-up). The patients were divided into three groups as: worsened group (WS: yellow color grade of coronary plaque at the follow-up period was worsened compared to the baseline period, n=15), no change group (NP: no change compared to the baseline, n=16), and improved group (IP: improved compared to the baseline, n=11). Then, the determinants of the nominal change of yellow color grade were examined by multiple regression analysis. RESULTS: The low-density lipoprotein cholesterol (LDL-C) level in IP group at the follow-up was significantly decreased compared to baseline (from 120.0±29.8mg/dl to 74.3±16.7mg/dl, p=0.0005), and was the lowest among three groups (WS: 103.5±16.4mg/dl, NC: 105.7±18.7mg/dl, and IP: 74.3±16.7mg/dl). Multiple regression analysis revealed that family history, statin administration, baseline serum creatinine, baseline 'in-stent' thrombus, and follow-up LDL-C were significant determinants to the nominal change of yellow color grade after the SES implantation (p<0.0001). CONCLUSIONS: Serial change in tissue characteristics within residual plaque under SES is determined by several factors, especially LDL-C level as well as statin administration. Adequate management of LDL-C by statins might be crucial for stabilizing residual plaque after SES implantation.

Three-dimensional visualization of scoring mechanism of 'AngioSculpt' balloon for calcified coronary lesions using optical coherence tomography.

Despite developments in coronary interventional cardiology, plaque calcification is a critical issue of stent expansion. AngioSculpt Scoring Balloon Catheter® (AngioSculpt; AngioScore Inc., Fremont, CA, USA) can produce more 'scoring' marks, which leads to prevention of 'plaque shift' and 'balloon slippage'; moreover, the 'scoring' produces some cutting effect, leading to successful stent implantation even on severe calcified lesions. We have applied AngioSculpt on severe calcified lesions to achieve its adequate expansion, and report the mechanism of the 'scoring' and its efficacy evaluated by three-dimensional stereoscopic reconstruction (3-D) of optical coherence tomography (OCT; LightLab Imaging, Inc., Westford, MA, USA). The patient is a 64-year-old male, who had diffuse stenosis in the left circumflex coronary artery (LCX) with severe calcifications, and was treated using AngioSculpt. AngioSculpt predilatation with a high pressure led to successful stent implantation. The radial scores were clearly imaged by 3-D OCT, demonstrating that radial nitinol wires made spiral indents from the relative weak points at the surface adjacent to calcification, which resulted in a less traumatic and safe dilatation although the scoring mark was not recognized clearly in intravascular ultrasound. This report suggests AngioSculpt might become one of the options for a severe calcified lesion.

Ulinastatin, a urinary trypsin inhibitor, for the initial treatment of patients with Kawasaki disease: a retrospective study.

BACKGROUND: Markedly activated neutrophils or higher plasma levels of neutrophil elastase are involved in the poor response to intravenous immunoglobulin (IVIG) and the formation of coronary artery lesions (CAL) in patients with acute Kawasaki disease. We hypothesized that ulinastatin (UTI), by both direct and indirect suppression of neutrophils, would reduce the occurrence of CAL. METHODS AND RESULTS: We retrospectively analyzed the clinical records of patients with Kawasaki disease between 1998 and 2009. Three hundred sixty-nine patients were treated with a combination of UTI, aspirin, and IVIG as an initial treatment (UTI group), and 1178 were treated with a conventional initial treatment, and IVIG with aspirin (control group). The baseline characteristics did not demonstrate notable differences between the two groups. The occurrence of CAL was significantly lower in the UTI group than in the control group (3% versus 7%; crude odds ratio [OR], 0.46; 95% confidence interval [CI], 0.25-0.86; P=0.01). The OR adjusted for sex, Gunma score (the predictive score for IVIG unresponsiveness), and dosage of initial IVIG (1 or 2 g/kg) was 0.32 (95% CI, 0.17-0.60; P<0.001). In addition, most CAL occurred in patients requiring additional rescue treatment and the proportion of those patients was significantly lower in the UTI group than in the control group (13% versus 22%; crude OR, 0.52; 95% CI, 0.38-0.73; P<0.001). The adjusted OR was 0.30 (95% CI, 0.20-0.44; P<0.001). CONCLUSIONS: UTI was associated with fewer patients requiring additional rescue treatment and reduction of CAL in this retrospective study.