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Digital, Background: Two glucagon-like peptide-1 (GLP-1) receptor agonists reduced renal outcomes in people with type 2 diabetes at risk for cardiovascular disease. We assessed the long-term effect of the GLP-1 receptor agonist dulaglutide on renal outcomes in an exploratory analysis of the REWIND trial of the effect of dulaglutide on cardiovascular disease. Methods: REWIND was a multicentre, randomised, double-blind, placebo-controlled trial at 371 sites in 24 countries. Men and women aged at least 50 years with type 2 diabetes who had either a previous cardiovascular event or cardiovascular risk factors were randomly assigned (1:1) to either weekly subcutaneous injection of dulaglutide (1·5 mg) or placebo and followed up at least every 6 months for outcomes. Urinary albumin-to-creatinine ratios (UACRs) and estimated glomerular filtration rates (eGFRs) were estimated from urine and serum values measured in local laboratories every 12 months. The primary outcome (first occurrence of the composite endpoint of non-fatal myocardial infarction, non-fatal stroke, or death from cardiovascular causes), secondary outcomes (including a composite microvascular outcome), and safety outcomes of this trial have been reported elsewhere. In this exploratory analysis, we investigate the renal component of the composite microvascular outcome, defined as the first occurrence of new macroalbuminuria (UACR >33·9 mg/mmol), a sustained decline in eGFR of 30% or more from baseline, or chronic renal replacement therapy. Analyses were by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT01394952. Findings: Between Aug 18, 2011, and Aug 14, 2013, 9901 participants were enrolled and randomly assigned to receive dulaglutide (n=4949) or placebo (n=4952). At baseline, 791 (7·9%) had macroalbuminuria and mean eGFR was 76·9 mL/min per 1·73 m2 (SD 22·7). During a median follow-up of 5·4 years (IQR 5·1-5·9) comprising 51 820 person-years, the renal outcome developed in 848 (17·1%) participants at an incidence rate of 3·5 per 100 person-years in the dulaglutide group and in 970 (19·6%) participants at an incidence rate of 4·1 per 100 person-years in the placebo group (hazard ratio [HR] 0·85, 95% CI 0·77-0·93; p=0·0004). The clearest effect was for new macroalbuminuria (HR 0·77, 95% CI 0·68-0·87; p, Ciencias Médicas y de la Salud

Digital, Background Three different glucagon-like peptide-1 (GLP-1) receptor agonists reduce cardiovascular outcomes in people with type 2 diabetes at high cardiovascular risk with high glycated haemoglobin A1c (HbA1c) concentrations. We assessed the effect of the GLP-1 receptor agonist dulaglutide on major adverse cardiovascular events when added to the existing antihyperglycaemic regimens of individuals with type 2 diabetes with and without previous cardiovascular disease and a wide range of glycaemic control. Methods This multicentre, randomised, double-blind, placebo-controlled trial was done at 371 sites in 24 countries. Men and women aged at least 50 years with type 2 diabetes who had either a previous cardiovascular event or cardiovascular risk factors were randomly assigned (1:1) to either weekly subcutaneous injection of dulaglutide (1·5 mg) or placebo. Randomisation was done by a computer-generated random code with stratification by site. All investigators and participants were masked to treatment assignment. Participants were followed up at least every 6 months for incident cardiovascular and other serious clinical outcomes. The primary outcome was the first occurrence of the composite endpoint of non-fatal myocardial infarction, non-fatal stroke, or death from cardiovascular causes (including unknown causes), which was assessed in the intention-to-treat population. This study is registered with ClinicalTrials.gov, number NCT01394952. Findings Between Aug 18, 2011, and Aug 14, 2013, 9901 participants (mean age 66·2 years [SD 6·5], median HbA1c 7·2% [IQR 6·6–8·1], 4589 [46·3%] women) were enrolled and randomly assigned to receive dulaglutide (n=4949) or placebo (n=4952). During a median follow-up of 5·4 years (IQR 5·1–5·9), the primary composite outcome occurred in 594 (12·0%) participants at an incidence rate of 2·4 per 100 person-years in the dulaglutide group and in 663 (13·4%) participants at an incidence rate of 2·7 per 100 person-years in the placebo group (hazard ratio [HR] 0·88, 95% CI 0·79–0·99; p=0·026). All-cause mortality did not differ between groups (536 [10·8%] in the dulaglutide group vs 592 [12·0%] in the placebo group; HR 0·90, 95% CI 0·80–1·01; p=0·067). 2347 (47·4%) participants assigned to dulaglutide reported a gastrointestinal adverse event during follow-up compared with 1687 (34·1%) participants assigned to placebo (p, Ciencias Médicas y de la Salud

Introduction Shift work is known to have a negative impact on a wide range of health problems such as sleep disturbance, cognitive impairment, and emotional disorders (e.g., anxiety and depression). It is important to understand underlying mechanisms for negative impact of shift work on health problems. This study aimed to investigate psychological and neural mechanisms associated with shift work. Methods Thirty six shift workers (28 females, age = 29.9 ± 7.4) and 35 non-shift workers (20 females, age = 30.5 ± 5.5) participated in this study. They were performing the word Stroop task during fMRI scanning. This task included sleep-related words and negative words to investigate neural substrates associated with sleep-related information and emotional information processing. Neutral words were included as control stimuli. The participants also completed questionnaires assessing sleep-related problems such as Pittsburgh Sleep Quality Index (PSQI) and Epworth Sleepiness Scale, and emotion-related problems such as Beck Depression Inventory and Beck Anxiety Inventory. Two-sample t-tests were conducted to find group differences in self-report measures and neural response to sleep-related words and negative words compared to neutral words. Results Relative to non-shift workers, shift workers showed greater sleep disturbance (i.e., higher PSQI), but they did not show any evidence of emotion-related problems. Shift workers also demonstrated greater neural response to negative words (vs. neutral words) in several prefrontal regions (e.g., dorsal anterior cingulate cortex and dorsolateral prefrontal cortex), anterior insula and caudate compared to non-shift workers. However, shift workers did not show significantly different neural response to sleep-related words (vs. neutral words) compared to non-shift workers. Conclusion The result from this study provides supporting evidence that shift work is associated with subjective sleep disturbance. Shift workers’ heightened neural response to negative information may reflect their increased sensitivity to negative information, that may contribute to sleep disturbance. Support Brain Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (Study No.: 2016M3C7A1904338 and NRF-2018R1D1A1B07049704).

Lipid lowering agents and anti-oxidants are known to improve endothelial dysfunction in hypercholesterolemic patients, respectively. The objective of this study is to investigate whether vitamin C has additional benefit on endothelial function of statin-treated hypercholesterolemic patients. The endothelial function was estimated using venous occlusion plethysmography (VOP) in 13 hypercholesterolemic patients and 9 healthy volunteers. The patients in the HC group were treated with the statin, then examined again. The change of the forearm blood flow (FBF) was measured with the acetylcholine infusion through brachial artery and also with intra-arterial vitamin C. Endothelium-dependent vasodilatation was significantly impaired in the HC group compared to the control group (p < 0.01). The FBF increased significantly after statin therapy (8.4 ± 1.3 → 25.2 ± 3.1 ml/min/100 mg forearm tissue, p < 0.01). Vitamin C infusion in these patients results in additional improvement in FBF (25.2 ± 3.1 → 31.9 ± 4.9, p < 0.05). Vitamin C seems to have additional benefit on the endothelial function of statin-treated hypercholesterolemic patients.

Extracorporeal membrane oxygenator (ECMO) as a rescue therapy is widely implicated to provide circulatory support. Yet, factors that predict clinical outcomes of ECMO therapy for cardiogenic shock in AMI have not been elucidated. This study aimed to assess the specific factors for potential

Objective— There is hope that molecular imaging can identify vulnerable atherosclerotic plaques. However, there is a paucity of clinical translational data to guide the future development of this field. Here, we cross-correlate cathepsin-B or matrix metalloproteinase-2/-9 molecular optical imaging data of human atheromata or emboli with conventional imaging data, clinical data, and histopathologic data. Methods and Results— Fifty-two patients undergoing carotid endarterectomy (41 atheromata) or carotid stenting (15 captured emboli) were studied with protease-activatable imaging probes. We show that protease-related fluorescent signal in carotid atheromata or in emboli closely reflects the pathophysiologic alterations of plaque inflammation and statin-mediated therapeutic effects on plaque inflammation. Inflammation-related fluorescent signal was observed in the carotid bifurcation area and around ulcero-hemorrhagic lesions. Pathologically proven unstable plaques had high cathepsin-B–related fluorescent signal. The distribution patterns of the mean cathepsin-B imaging signals showed a difference between the symptomatic vs asymptomatic plaque groups. However, the degree of carotid stenosis or ultrasonographic echodensity was weakly correlated with the inflammatory proteolytic enzyme-related signal, suggesting that molecular imaging yields complimentary new information not available to conventional imaging. Conclusion— These results could justify and facilitate clinical trials to evaluate the use of protease-sensing molecular optical imaging in human atherosclerosis patients.

A combination of a charcoal pack during irradiation and α -tocopherol addition into ground beef was applied to eliminate an irradiation characteristic off-odor and to retard the lipid oxidation caused by the irradiation process. Ground beef was mixed with 200 ppm α -tocopherol and gamma irradiated with 0, 5, and 10 kGy with or without a charcoal pack present during the irradiation treatment. The pH of the control group was lower than that of α -tocopherol and charcoal pack treatment initially but increased rapidly and showed higher pH at day 7. Addition of α -tocopherol with or without charcoal pack addition showed lower 2-thiobarbituric acid reactive substances values in irradiated ground beef at days 3 and 7 compared to those without addition. The color of ground beef was not significantly affected by the treatment. However, odor preference result showed that 10 kGy-irradiated ground beef with a combination of charcoal pack and α -tocopherol addition had higher scores than the control group regardless of irradiation. Solid-phase microextraction (SPME) gas chromatograph/mass spectrometry (GC/MS) analysis identified various volatile compounds that were created by irradiation of ground beef. These compounds were reduced or eliminated when a charcoal pack was used during the irradiation process. The results of the present study imply that combination of packaging with a charcoal pack during the irradiation process and addition of α -tocopherol into ground beef is a good method to effectively eliminate an irradiation off-odor and retard the lipid oxidation development in ground beef caused by irradiation.

Background We compared sirolimus-eluting stent (SES) implantation and intracoronary brachytherapy (ICBT) for diffuse bare metal in-stent restenosis (ISR) to identify more effective treatment modality. Methods Patients ( n =129) with diffuse ISR (lesion length≥10 mm) were randomly assigned to either SES implantation ( n =65, group I) or beta-radiation with 188 Re–MAG 3 -filled balloon ( n =64, group II). The radiation dose was 20 Gy at a depth of 1.0 mm into the vessel wall. The primary end point was late loss in analysis segment at 6 months. The secondary end points were 6-month angiographic restenosis and 1-year major adverse cardiac events (MACE) including myocardial infarction (MI), cardiac death, and target lesion revascularization (TLR). Results Baseline characteristics were similar between two groups. The lesion length was 27.52±13.98 mm in group I and 27.75±14.25 mm in group II ( p =0.927). Late loss in analysis segment at 6 months was smaller in group I than in group II (0.15±0.62 vs. 0.55±0.69 mm, p =0.003). Angiographic restenosis for analysis segment at 6 months was 8.0% (4/50) in group I and 30.2% (16/53) in group II ( p =0.006). One MI and two deaths (all from group I) occurred during follow-up. TLR (4.6% vs. 18.8%, p =0.014) and MACEs (7.7% vs. 18.8%, p =0.073) were lower in group I than group II at 1 year. Conclusion Compared to ICBT, SES implantation for diffuse bare metal ISR showed less late loss, lower restenosis, and a trend toward lower 1-year MACEs. SES implantation appears to be superior to ICBT for treating diffuse ISR.

The effects of various doses of electron-beam irradiation on the changes in microbiological attributes of fermented sausage and the combined effect of electron-beam irradiation and various antioxidants on the oxidative stability and sensory properties during cold storage were investigated. Results indicated that 2 kGy of irradiation was the most effective in manufacturing a fermented sausage, and the addition of rosemary extracts was effective in controlling the production of off-flavor and development of lipid oxidation during cold storage.

Objectives This study sought to compare the nephrotoxicity of iodixanol and ioxaglate in patients with renal impairment undergoing coronary angiography. Background Iodixanol, a nonionic, dimeric, iso-osmolar contrast medium (IOCM), may be less nephrotoxic than low-osmolar contrast media (LOCM) in high-risk patients. Methods In a prospective, randomized trial in 300 adults with creatinine clearance (CrCl) ≤60 ml/min, patients received either iodixanol or ioxaglate and underwent coronary angiography with or without percutaneous coronary intervention. The primary end point was the incidence of contrast-induced nephropathy (CIN) (an increase in serum creatinine [SCr] ≥25% or ≥0.5 mg/dl [≥44.2 μmol/l]). The incidence of CIN in patients with severe renal impairment at baseline (CrCl Results The incidence of CIN was significantly lower with iodixanol (7.9%) than with ioxaglate (17.0%; p = 0.021), corresponding to an odds ratio (OR) of CIN of 0.415 (95% confidence interval [CI] 0.194 to 0.889) for iodixanol. The incidence of CIN was also significantly lower with iodixanol in patients with severe renal impairment (p = 0.023) or concomitant diabetes (p = 0.041), or in patients given ≥140 ml of contrast media (p = 0.038). Multivariate analysis identified use of ioxaglate (OR 2.65, 95% CI 1.11 to 6.33, p = 0.028), baseline SCr, mg/dl (OR 2.0, 95% CI 1.04 to 3.85, p = 0.038), and left ventricular ejection fraction, % (OR 0.97, 95% CI 0.94 to 0.99, p = 0.019) as independent risk factors for CIN. Conclusions The IOCM iodixanol was significantly less nephrotoxic than ioxaglate, an ionic, dimeric LOCM. (The RECOVER Trial; http://clinicaltrials.gov; NCT00247325)

Background: Clopidogrel is a prodrug requiring metabolism by cytochrome P450 3A (CYP3A) isoenzymes, including CYP3A5, in order to be active. It is controversial whether clopidogrel interacts with CYP3A inhibitors. We investigated the influence of CYP3A5 polymorphism on the drug interaction of clopidogrel. Methods: In phase 1 of the study, we administered clopidogrel to 16 healthy volunteers who had the CYP3A5 non-expressor genotype (*3 allele) and 16 who had the CYP3A5 expressor genotype (*1 allele) with and without pretreatment with itraconazole, a potent CYP3A inhibitor. A platelet aggregation test was performed at baseline, 4 hours, 24 hours and 6 days after clopidogrel administration. In phase 2, we compared clinical outcomes of 348 patients treated with clopidogrel after successful coronary angioplasty with bare-metal stent implantation according to their CYP3A5 genotype; the primary end point was a composite of atherothrombotic events (cardiovascular death, myocardial infarction and non-hemorrhagic stroke) within 1 and 6 months after stent implantation. Results: In phase 1, the change in platelet aggregation after clopidogrel administration and pretreatment with itraconazole was greater among the subjects with the CYP3A5 expressor genotype than among those with the non-expressor genotype: 24.9% (standard deviation [SD] 13.9%) v. 6.2% (SD 13.5%) at 4 hours ( p p p p = 0.023). Multivariable analysis showed that the CYP3A5 polymorphism was a predictor of atherothrombotic events in clopidogrel users. Interpretation: People with the CYP3A5 non-expressor genotype are vulnerable to drug interactions between clopidogrel and CYP3A inhibitors. This phenomenon may be associated with worse outcomes in patients with the non-expressor genotype who are given clopidogrel after coronary angioplasty and implantation of bare-metal stents.

Objective— β-Catenin plays a critical role in directing cell fate during embryogenesis, and uncontrollable activation leads to cancers, suggesting its importance in cell survival and proliferation. However, little is known regarding its role in endothelial cell (EC) and skeletal muscle proliferation and progenitor cell mobilization. Methods and Results— β-Catenin enhanced ECs proliferation, protected ECs from apoptosis, and increased the capillary forming capabilities, which was completely blocked by inhibition of its nuclear translocation. In addition, the increased proliferation by β-catenin was associated with increased expression of cyclin E2. In skeletal myocytes, β-catenin overexpression increased proliferation with cyclin D1 expression, decreased apoptosis, and induced hypertrophy. Furthermore, β-catenin induced the expression of vascular endothelial growth factor (VEGF) in skeletal myocytes, resulting in EC proliferation. In a mouse hindlimb ischemia model, β-catenin significantly increased recovery of blood perfusion, capillary density along with enhanced VEGF expression, and the number of proliferating ECs and myocytes. Local delivery of β-catenin also promoted angiogenic progenitor cell mobilization and increased the number of satellite cells. Conclusions— β-Catenin may be an important modulator of angiogenesis and myocyte regeneration not only by directly enhancing proliferation and survival of ECs and skeletal myocytes but also by inducing VEGF expression and promoting angiogenic progenitor cell mobilization and muscle progenitor cell activation.

Objective: This study compared the efficacy of the sirolimus-eluting stent (SES), the paclitaxel-eluting stent (PES), and the bare metal stent (BMS) for long coronary lesions. Background: The outcome of drug-eluting stent (DES) implantation in long coronary lesions remains unclear. Methods: The study involved 527 patients with de novo long coronary lesions (≥24 mm), which were treated with long (≥28 mm) SESs (223 lesions), PESs (194 lesions), or BMSs (201 lesions). Results: Lesions in the SES (36.0 ± 14.9 mm, P < 0.001) and PES (36.3 ± 14.5 mm, P < 0.001) groups were longer than those in the BMS group (32.0 ± 12.3 mm), meaning the two DES groups had longer stented segments than did the BMS group. Six-month angiographic follow-up showed the SES (9.3%, P < 0.001) and PES (21.3%, P < 0.001) groups had lower in-segment restenosis rates than that of the BMS group (42.5%). The rate of major adverse cardiac events (MACE) including death, myocardial infarction, and target lesion revascularization at 9 months was higher in the BMS group (26.6%) than that in the SES (13.0%, P < 0.001) and PES (15.7%, P < 0.001) groups. Posthoc analysis of the two DES groups showed that the in-segment restenosis rate was lower for the SES than that for the PES group (P = 0.002), while the MACE rate was similar. Conclusions: The use of DESs for long coronary lesions appears to be safe and more effective than the use of BMSs in terms of restenosis and adverse clinical events. SES use was associated with lower late luminal loss and a lower angiographic restenosis rate compared with PES use. © 2006 Wiley-Liss, Inc.

Intracoronary radiation with a rhenium-188 ((188)Re)-filled balloon is safe and efficiently reduces restenosis, but there is a potential risk of a (188)Re-filled balloon induced dissection. Little is known about the effect of radiation on dissection resolution and the late clinical outcome of dissection after brachytherapy.After successful catheter-based treatments of de novo or restenotic lesion, 256 patients were randomly assigned to the radiation or control group. The (188)Re-filled balloon system was designed to deliver 17.6 Gy in 1.0-mm tissue depth.Dissections were identified in 15 patients among the 138 patients of the radiation group (10.9%). Additional stents were deployed in 10 patients to cover the flow-limiting dissection. Binary restenosis rate (53.3% vs. 16.3%, p=0.001) and target vessel revascularization (TVR) rate (53.3% vs. 11.1%, p0.001) were significantly higher in patients with the dissection at 9 months. Geographic miss (GM) was identified in 4 of the 10 patients who underwent additional stenting. Binary restenosis rate in the GM group (100%; 4 of 4 patients) was significantly higher than the non-GM group (33.3%; 2 of 6 patients, p=0.02). Long-term follow-up of the patients with dissections who had not undergone TVR (n=7, mean follow-up duration: 640.7+/-387.3 days) has demonstrated persistent unhealed dissections.Intracoronary radiation impairs the healing process after vessel injury and residual dissection after brachytherapy leads to adverse clinical outcomes, which was mainly due to GM in case of stent implantation.

ObjectivesThis study was performed to evaluate the feasibility of the physiologic assessment of jailed side branches using fractional flow reserve (FFR) and to compare the measured FFR with the stenosis severity assessed by quantitative coronary angiography (QCA).BackgroundIt is not well-known which side branches should be treated after stent implantation at main branches and how to assess the functional significance of these lesions.MethodsNinety-seven jailed side branch lesions (vessel size >2.0 mm, percent stenosis >50% by visual estimation) after stent implantation at main branches were consecutively enrolled. The FFR was measured using a pressure wire at 5 mm distal and proximal to the ostial lesion of the jailed side branch.ResultsThe FFR measurement was successful in 94 lesions. Mean FFRs were 0.94 ± 0.04 and 0.85 ± 0.11 at the main branches and jailed side branches, respectively. There was a negative correlation between the percent stenosis and FFR (r = −0.41, p < 0.001). However, no lesion with

Due to the lower level of the traditional lipid profiles in Koreans than in the series of patients from the western countries, the need to investigate other lipid parameters to help identify the individuals at high risk of CAD has been emphasized.To investigate whether apolipoprotein B (apo B), apolipoprotein A-I (apo A-I) and their ratio give additional information to the traditional lipid risk factors for discriminating the individuals at high-risk for coronary artery disease (CAD), 544 subjects, who met the lipid criteria of total cholesterol (TC)230 mg/dl, low-density lipoprotein cholesterol (LDL-C)120 mg/dl and high-density lipoprotein cholesterol (HDL-C)40 mg/dl were recruited. Patients were considered to be CAD(+) if they hador =50% stenosis in at least one coronary artery.In men, TC and apo B/apo A-I ratio were significantly different between groups with and without CAD after adjusting for age and diabetes (P = 0.037 and 0.035), and in women, triglyceride (TG), HDL-C and apo B/apo A-I ratio were significantly different after adjusting for age, diabetes and smoking status (P = 0.006, 0.007 and 0.030, respectively). In the lowest quartile of TC, TG and LDL-C, and the highest quartile of HDL-C, only apo B/apo A-I ratio was associated with CAD in both men and women. The only variable showing a significant difference between patients with and without CAD was apo B/apo A-I ratio. In models assessing whether apolipoproteins give additional information to traditional lipid risk factors, HDL-C, LDL-C, apo B/apo A-I ratio and in women but not in men, TG and apo B were all independent markers for the presence of CAD. Among the nontraditional lipid factors, only apo B/apo A-I ratio showed its additional value for identifying the presence of CAD.Apo B/apo A-I ratio is the only variable that differentiates the patients with CAD from those without and, furthermore, gives additional information to that supplied by traditional lipid risk factors in a low-risk Korean population.

5-HT2A is one of major serotonin receptor that is involved in the action of serotonin-targeting drugs. Previous clinical studies have shown an unexpected association between lower cholesterol level and psychiatric diseases, in which T102C polymorphism of HTR2A, gene of 5-HT2A serotonin receptor, might be involved. Therefore, we hypothesized a potential association between lower cholesterol level and T102C polymorphism. The effect of the T102C polymorphism on the serum lipid profiles of 646 subjects without specific psychiatric disease was investigated. Genotype was determined by polymerase chain reaction and restriction fragment length polymorphism analysis. There were significantly lower levels of total cholesterol (193.6 +/- 35.0 versus 202.1 +/- 45.5 mg/dl, p = 0.016) and HDL-cholesterol (42.7 +/- 11.6 versus 46.3 +/- 12.7 mg/dl, p = 0.004) in CC genotype than non-CC genotypes. Moreover, multivariate analysis showed that the CC genotype is a strong predictor of a lower HDL-cholesterol level (p < 0.001). In conclusion, this study shows that the CC genotype of the HTR2A gene is related to lower HDL-cholesterol level in Koreans. This is the first demonstration showing the potential genetic relationship between the serotonin receptor gene polymorphism and the HDL-cholesterol level.

Background Various methods are used to induce maximal hyperemia for physiologic studies, but the feasibility and efficacy of continuous intracoronary (IC) infusion of adenosine for measurement of fractional flow reserve (FFR) has not been well-defined. Methods and Results Patients with intermediate coronary artery stenosis were consecutively enrolled. In the phase I study, FFR was measured after 3 dosages of IC adenosine infusion (180, 240 and 300μg/min) in 30 patients. The phase II study was performed to compare the hyperemic efficacy of IC infusion (240μg/min) with IC bolus injection (40, 80μg) and intravenous (IV) infusion (140μg·kg‐1 ·min ‐1 ) of adenosine in 20 patients. In the phase I study, no significant differences in FFR were observed with the 3 different doses of IC infusion (p=0.06). In the phase II study, FFR after an IC bolus injection (0.83±0.06) was significantly higher than with IV (0.79± 0.07) or IC (0.78±0.09) infusion (p

Introduction: Fasciculoventricular (FV) pathways are rare variants of preexcitation, and their ECGs may be misinterpreted as Wolff-Parkinson-White syndrome with anteroseptal accessory pathways (WPW-AS). We analyzed the electrocardiographic characteristics of the patients with FV pathways to find out the different findings from WPW-AS. Methods and Results: Five patients with FV pathways and four patients with WPW-AS who underwent electrophysiologic studies were evaluated. Intervals and amplitudes of each wave and QRS morphologies were analyzed in standard 12-lead ECGs of these patients by two independent cardiologists without the information of the electrophysiologic findings. PR intervals were longer in FV pathways (122 ± 11.0 vs 83 ± 21 ms, FV pathways vs WPW-AS, P = 0.017). In lead V1, narrower width of R waves (25 ± 6 vs 45 ± 13 ms, P = 0.037) and smaller amplitude of S waves (12.8 ± 8.3 vs 26.6 ± 7.4 mm, P = 0.037) were observed in FV pathways. The polarity of delta waves in V1 was flat or negative in contrast with the cases of WPW-AS in which the polarity was positive. Three of five patients had notching in the descending limb of S waves in V1, which was not observed in WPW-AS. Conclusion: FV pathways have different ECG characteristics from WPW-AS in PR interval and morphology of QRS complexes in lead V1 of the standard 12-lead ECG.

Background There is a paucity of information regarding the impact of the coronary collaterals on prognosis in type 2 diabetic (T2DM) patients. We developed a novel index, which considers not only the degree of collateral circulation but also the stimulus of collateral development, and investigated its prognostic value in T2DM patients with coronary artery disease (CAD). Methods and Results One hundred and ninety four consecutive T2DM patients were analyzed and followed for an average of 30 months. We measured the diameter stenosis (DS; %), corrected TIMI frame count (CTFC) and Rentrop score at 3 major epicardial coronary arteries. The collateral development (CD) score was calculated by: (ΣRentrop score +1)/Σ [DS (%) × CTFC] ×1,000. During the follow-up, acute cardiovascular events occurred in 49 patients. By multivariate analysis, the CD score was an independent predictor of adverse events not only in the total population (p

The biologic mechanisms for the success and failure of intravascular radiation therapy after angioplasty have not been well studied. We investigated the molecular mechanism of radiation-induced cell cycle arrest in vascular smooth muscle cell (VSMC) and examined whether p21 knock-out is a cause of radiation failure. Using different dosages of gamma radiation, we evaluated the effect of radiation on VSMC apoptosis and cell cycle progression, and its action mechanism. Irradiation significantly retarded the growth of cultured VSMC, which was not due to induction of apoptosis but mainly due to cell cycle arrest. Radiation showed remarkable cell cycle arrest at G1 and G2 phase (G0/G1:S:G2/M phases = 61%:34%:5% with 0 Gy versus 61%:9%:30% with 16 Gy, 12 h after radiation). In immunoblot analysis and kinase assay, radiation increased the expression of p21 and decreased the expression and activity of CDK2 and 1. In contrast, radiation did not affect the expression and activity of CDK4 and 6, nor the expression of p27 and p16. When p21 was knocked out, cell cycle of VSMC was not arrested by radiation, leading to increased proliferation. These finding provide the evidence that radiation inhibits VSMC proliferation through cell cycle arrest by enhancing p21 expression and suppressing CDK1 and 2. This observation supports the key role of p21 in radiation-induced cell cycle arrest and the degree of p21 expression may be the possible mechanism of radiation failure and delayed restenosis.

Antioxidative potential of lyophilized citrus (Citrus unshiu) peel extract in raw and cooked meat systems was investigated. Beef pork, chicken, and salmon patties were prepared without (control), with lyophilized citrus peel extract (0.1%, NICP), and with 20 kGy-irradiated, lyophilized citrus peel extract (0.1%, ICP). TBARS value showed that the addition of lyophilized citrus peel (NICP or ICP) inhibited the development of lipid oxidation of raw and cooked meat patties during storage for 8 days at 20C (P

Summary Background Bone-marrow stem-cell transplantation has been shown to improve cardiac function in patients with myocardial infarction. We examined the feasibility and efficacy of granulocyte-colony stimulating factor (G-CSF) therapy and subsequent intracoronary infusion of collected peripheral blood stem-cells (PBSCs) in such patients. Methods We prospectively randomised 27 patients with myocardial infarction who underwent coronary stenting for the culprit lesion of infarction into three groups; cell infusion (n=10), G-CSF alone (n=10), and control group (n=7). Changes in left ventricular systolic function and perfusion were assessed after 6 months. By December, 2003, seven patients from the cell infusion group, three from the G-CSF group, and one from the control group had been assessed. Findings G-CSF injection and intracoronary infusion of the mobilised PBSC did not aggravate inflammation and ischaemia during the periprocedural period. Exercise capacity (mean treadmill exercise time: 450 s [SD 178] at baseline vs 578 s [168] at 6 months’ follow-up, p=0·004), myocardial perfusion (perfusion defect 11·6% [9·6] vs 5·3% [5·0], p=0·020) and systolic function (left ventricular ejection fraction 48·7% [8·3] vs 55·1% [7·4], p=0·005) improved significantly in patients who received cell infusion. However, we noted an unexpectedly high rate of in-stent restenosis at culprit lesion in patients who received G-CSF, and therefore we stopped enrolment. Interpretation G-CSF therapy with intracoronary infusion of PBSC showed improved cardiac function, and promoted angiogenesis in patients with myocardial infarction. However, aggravation of restenosis could be a serious problem. In future studies with G-CSF based stem-cell therapy, patients should be carefully monitored for unexpected effects.

Background— Endothelial progenitor cells (EPCs) play a pivotal role in repair and regeneration of damaged vessels. We investigated the role of mobilized EPCs in the healing process after intravascular radiation therapy. Methods and Results— One iliac artery of hypercholesterolemic rabbits was subjected to balloon injury and intravascular radiation with a Re-188 balloon and the contralateral iliac artery to balloon injury only. Rabbits received granulocyte-macrophage colony-stimulating factor (recombinant human GM-CSF) (60 μg/d subcutaneously) daily for 1 week, either 7 days before the angioplasty or at the time of angioplasty. Control rabbits received human albumin. GM-CSF significantly increased the double-positive (CD31+ and KDR+) fraction in peripheral blood monocytes and showed a higher number of EPCs than albumin after culture and, furthermore, enhanced migration and incorporation of EPCs. In the albumin group, intravascular radiation therapy reduced neointimal hyperplasia but delayed reendothelialization and aggravated monocyte infiltration. GM-CSF treatment significantly accelerated the reendothelialization and inhibited monocyte infiltration (reendothelialization index, 81±13% in the GM-CSF radiation [n=7] versus 30±11% in the control radiation [n=9] at 2 weeks, P P Conclusions— GM-CSF treatment mobilizes EPCs, accelerates reendothelialization, and reduces monocytes infiltration after intravascular radiation therapy, suggesting that stem cell mobilization is a promising strategy for enhancing the vascular healing process after cytotoxic angioplasty.

Slow pathways are used as both antegrade and retrograde conduction pathway in slow/slow atrioventricular nodal reentrant tachycardia (SS-AVNRT), and patients with SS-AVNRT have tachycardia ECGs mimicking atrioventricular reentrant tachycardia using concealed posteroseptal accessory pathway (PS-AVRT). Therefore, SS-AVNRT can be misdiagnosed as PS-AVRT, and the differential diagnosis is clinically important. Standard 12-lead ECGs during tachycardia were analyzed in patients with SS-AVNRT (n = 10) and PS-AVRT (n = 10). All these patients were diagnosed by electrophysiological study and underwent successful catheter ablation. Differences of the RP' intervals (dRP') between V1 and the inferior leads were evaluated. SS-AVNRT had significantly longer RP' intervals measured in V1 (167 +/- 25.2 vs 137 +/- 26.8 ms, SS-AVNRT vs PS-AVRT, respectively, P = 0.02), longer dRP' between V1 and II (dRP'[V1-II], 37 +/- 14 vs 17 +/- 6.7 ms, P = 0.0007), longer dRP'[V1-III] (39 +/- 14 vs 17 +/- 9.9 ms, P = 0.0011), and longer dRP'[V1-aVF] (39 +/- 13 vs 20 +/- 9.5 ms, P = 0.0008). The following criteria were suggested for differential diagnosis of SS-AVNRT from PS-AVRT: dRP'[V1-II] >25 ms (sensitivity and specificity: 80% and 100%, respectively), dRP'[V1-III] >23 ms (90% and 90%), dRP'[V1-aVF] >30 ms (90% and 90%). Differences of the RP' intervals between V1 and the inferior leads in the tachycardia ECGs were useful for differential diagnosis of SS-AVNRT from PS-AVRT.

Naringin, a flavonoid found in citrus species and grapes, has anti-inflammatory, anti-oxidative properties. In this study, we investigated whether naringin protects vascular smooth muscle cells (VSMCs) from the mitogenic effect of lysophosphatidylcholine. Lysophosphatidylcholine, an atherogenic lysophospholipid of oxidized low density lipoprotein (LDL), is known to impair endothelial release of nitric oxide, up-regulate the expression of adhesion molecules, and promote the proliferation of VSMCs. VSMCs were prepared from the aortas of Sprague-Dawley rats, and cultured in DMEM/F12 media. Near-confluent cells were incubated with 0, 10, or 100 μM of naringin for 24 hours, and then incubated with 0, 10, 20, or 100 μM of lysophosphatidylcholine. Lysophosphatidylcholine promoted the growth of VSMCs, whereas naringin suppressed its mitogenic effect on VSMCs. In an MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide) assay, lysophosphatidylcholine promoted cell proliferation by 63 ± 24% and 89 ± 17% at 10 μM and 20 μM respectively, when compared with the control group (p < 0.01). [H3]-thymidine incorporation assay showed that the degree of DNA replication also increased by 61 ± 25% and 92 ± 25% at 10 μM and 20 μM of lysophosphatidylcholine (p < 0.01). Naringin at 100 μM significantly suppressed the mitogenic effect of lysophosphatidylcholine on VSMCs by 34 ± 5% (MTT assay), and 35 ± 5% ([H3]-thymidine incorporation assay) (p = 0.01). This study demonstrates that naringin suppresses the mitogenic effect of lysophosphatidylcholine on VSMCs, whereas lysophosphatidylcholine promotes the proliferation of VSMCs.

Various blends of spent hen meat and grains (potato starch, corn starch, and rice flour) were popped using a popping machine. Lowest bulk density was observed in the snack with 1:2 ratio of meat and potato starch. Except for the popped snack with meat and rice flour, as the starch content increased, bulk density decreased gradually. Popped snacks with grains only were higher in L* value than those with meat and grains. The a* and b* values increased with increasing meat content. All popped snacks were significantly different (P

Background Determinants of exercise capacity have not been clearly defined in hypertensive patients. Doppler tissue imaging (DTI), a recently developed echocardiographic modality, is useful for evaluating left ventricular (LV) function regardless of loading conditions. The present study was performed to identify the determinants of exercise capacity in hypertensive patients using DTI. Methods We studied 48 hypertensive patients (26 men; mean age, 57 ± 9 years) with normal LV ejection fraction (>50%). Conventional echocardiographic indexes were measured before and after symptom-limited treadmill exercise. Also, longitudinal systolic (SL′) and diastolic myocardial velocities (EL′ and AL′) and radial velocities (SR′, ER′, AR′) were measured using DTI with the sample volume at the LV basal posterior wall. Results Mean exercise time was 525 ± 135 sec. Mean LV ejection fraction was 61% ± 6%. Mean LV mass index was 110.9 ± 24.4 g/m2. On univariate analysis, SL′, EL′, AL′ and percentage increase of SR′ velocity after exercise showed significant correlation with exercise time. However, only EL′ and percentage increase of SR′ remained significant after multivariate analysis. Conclusions Left ventricular contractile reserve and relaxation property are important cardiac factors determining exercise capacity. Early diastolic longitudinal myocardial velocity might be useful for identifying hypertensive patients with poor exercise capacity.

Hepatic lipase is a key enzyme that is involved in HDL-C metabolism. The goal of this study was to find out the frequency of the hepatic lipase C514T polymorphism, and evaluate its relationship with plasma HDL-C levels and coronary artery disease (CAD) in Koreans. Two hundred and twenty four subjects with no previous history of lipid-lowering therapy, 118 patients with significant CAD, and 106 controls were examined with respect to their genotypes, lipid profiles, and other risk factors for CAD. The frequency of the -514T allele was 0.37 in men and 0.35 in women, which were higher than the frequency that was reported in Caucasians, but lower than the frequency that was reported in African-Americans. The -514T allele was associated with significantly higher HDL-C levels in women. After controlling for age, gender, BMI, DM, and smoking, the non-CC genotype was significantly associated with HDL-C levels, and explained 6% of the HDL-C variation in this study. When the genotypes-distribution was compared between the CAD and non-CAD patients, the hepatic lipase C-514T polymorphism was not associated with the presence of CAD. Koreans have a higher frequency of the hepatic lipase gene 514T allele than Caucasians, and the -514T allele is associated with higher plasma HDL-C levels in Korean women, and perhaps non-smoking men. However, our data does not suggest an association between the polymorphism and an increased risk of CAD.

Background : The effects of antihypertensive agents on endothelial function have not been fully evaluated in human hypertension and data on the forearm circulation of humans are controversial. The aim of this study was (1) to evaluate the endothelial function in hypertensive patients (2) to investigate whether vitamin C administration has any benefit on the endothelial function and (3) to determine whether treatment with calcium antagonist improves endothelial dysfunction in hypertensive patients. Methods : The endothelial function was estimated using venous occlusion plethysmography (VOP) in 8 hypertensive patients and 8 healthy volunteers. The patients in the hypertension group were treated with amlodipine, then examined again. The change of forearm blood flow (FBF) was measured with acetylcholine infusion through brachial artery and also with intra-arterial vitamin C. Results : Forearm blood flow response to acetylcholine was significantly enhanced with intra-arterial infusion of vitamin C in hypertensive group before antihypertensive treatment. Co-infusion of L-NMMA, an inhibitor of nitric oxide synthase, blunted forearm blood flow response to acetylcholine. After treatment with amlodipine for 2 months in hypertensive group, endothelium-dependent vasorelaxation to acetylcholine was significantly improved compared to pretreatment, and vitamin C did not affect the improved endothelial function by amlodipine treatment. Conclusion : Vitamin C (acutely) and amlodipine (chronically) improved endothelial function in hypertensive patients. These results suggest that increased oxidative stress, at least in part, may be involved in the decreased endothelial function in hypertension.

The endothelium plays an important role in maintaining vascular tone and function. Essential hypertension is associated with alterations in endothelial function. The effects of antihypertensive agents on endothelial function have not been fully evaluated in human hypertension and data on the forearm circulation of humans are controversial. The aim of this study was to determine whether treatment with an angiotensin converting enzyme (ACE) inhibitor or a calcium antagonist improves endothelial dysfunction in hypertensive patients and whether the mechanism involved could be related to antioxidant activity. Endothelial function was estimated using venous occlusion plethysmography in 18 hypertensive patients and 11 healthy volunteers. The patients in the hypertension group were treated with enalapril or amlodipine. The change of forearm blood flow (FBF) was measured during acetylcholine infusion through the brachial artery and also during intra-arterial vitamin C infusion to explore the effects of vitamin C on responses to acetylcholine. FBF response to acetylcholine was significantly enhanced by intra-arterial infusion of vitamin C in the hypertensive group before antihypertensive treatment. Co-infusion of L-NMMA(NG-monomethyl-L-arginine), an inhibitor of nitric oxide synthase, blunted forearm blood flow response to acetylcholine. After antihypertensive treatment with enalapril or amlodipine for 2 months in the hypertensive group, endothelium-dependent vasorelaxation (vasodilatory response to acetylcholine) was significantly improved. Even though the mechanisms leading to depressed endothelial function in essential hypertension remain to be elucidated, our study shows that treatment with an ACE inhibitor or a calcium antagonist resulted in demonstrable improvement by a mechanism that is probably related to antioxidant activity. (Hypertens Res 2002; 25: 365-371)

1. Doroghazi RM, Slater EE, DeSanctis RW, Buckley MJ, Austen WG, Rosenthal S. Long-term survival of patients with treated aortic dissection. J Am Coll Cardiol 1984;3:1026–1034. 2. Glower DD, Fann JI, Speier RH, Morrison L, White WD, Smith LR, Rankin JS, Miller DC, Wolfe WG. Comparison of medical and surgical therapy for uncomplicated descending aortic dissection. Circulation 1990;82(suppl IV):IV39–IV-46. 3. Glower DD, Speier RH, White WD, Smith LR, Rankin JS, Wolfe WG. Management and long-term outcome of aortic dissection. Ann Surg 1991;214: 31–41. 4. Masuda Y, Yamada Z, Morooka N, Watanabe S, Inagaki Y. Prognosis of patients with medically treated aortic dissections. Circulation 1991;84(suppl III):III-7–III-13. 5. Elefteriades JA, Hartleroad J, Gusberg RJ, Slazar AM, Black HR, Kopf GS, Baldwin JC, Hammond GL. Long-term experience with descending aortic dissection: the complication-specific approach. Ann Thorac Surg 1992;53:11–21. 6. Elefteriades JA, Lovoulos CJ, Coady MA, Tellides G, Kopf GS, Rizzo JA. Management of descending aortic dissection. Ann Thorac Surg 1999;67:2002– 2005. 7. Wheat ME, Palmer RJ, Bartley TB, Seelman RC. Treatment of dissecting aneurysm of the aorta without surgery. J Thorac Cardiovasc Surg 1965;50:364– 373. 8. Daily PO, Trueblood HW, Stinson EB, Wurflein RD, Shumway NE. Management of acute aortic dissections. Ann Thorac Surg 1970;10:237–247. 9. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, Evangelista A, Fattori R, Suzuki T, Oh JK, Moore AG, Malouf JF, Pape LA, Gaca C, Sechtem U, Lenferink S, Deutsch HJ, Diedrichs H, Marcos y Robles J, Llovet A, Gilon D, Das SK, Armstrong WF, Deeb GM, Eagle KA. The international registry of acute aortic dissection (IRAD): new insights into an old disease. JAMA 2000;283:897–903.

Both hypercholesterolemia and vascular injury have been reported to induce macrophage infiltration, but their combined effect and the mechanism by which hypercholesterolemia enhances the infiltration remain to be clarified in vivo. To evaluate the effect of hypercholesterolemia on macrophage infiltration after vascular injury, the iliac arteries of hypercholesterolemic (HC) and normocholesterolemic (NC) rabbits were examined 2h, 1 day, 3 days, 7 days, and 14 days after balloon injury using immunohistochemical staining for macrophages, intercellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1. Nuclear factor kappa-B (NF-kappaB) activation was also evaluated in fresh frozen iliac arteries using the electrophoretic mobility shift assay method. The fundamental difference between HC and NC was the amount of macrophage infiltration seen in HC from 7 days after balloon injury. Two out of 4 HC iliac arteries on the 7th day, and 3 out of 4 HC iliac arteries on the 14th day were positively stained with ICAM-1 in regenerated endothelium and neointima, whereas there were no positively stained NC iliac arteries. Neither HC nor NC tissues showed positive staining with VCAM-1. NF-kappaB was activated in HC 7 and 14 days after balloon injury, but not in NC. In conclusion, in vivo hypercholesterolemia induces macrophage infiltration after balloon injury and it is mediated by increased NF-kappaB activation promoting ICAM-1 expression.

A restrictive left ventricular filling pattern is generally recognized as an ominous prognostic sign in patients with congestive heart failure. Recently, this filling pattern has been further categorized into reversible and irreversible groups according to the changes in the mitral inflow pattern after preload reduction; furthermore, the prognosis is reported to be different for the two groups. Forty-two patients with a restrictive left ventricular filling pattern who could adequately perform Valsalva's maneuver were studied. Baseline peak early (E) and late (A) mitral inflow velocities, E/A ratio, deceleration time of E velocity, peak early (E') and late (A') diastolic mitral annulus velocities, and E'/A' ratio were obtained. During Valsalva's maneuver, the E/A ratio reversed (1) in fifteen patients (15/42, 36%). These patients were categorized as belonging to the reversible group. Among the baseline mitral inflow and mitral annulus velocity parameters, A'0.05 m/s best discriminated between the reversible and irreversible restrictive left ventricular filling patterns, with a sensitivity of 80% and a specificity of 85%.

Abstract —To verify that apoptosis is one of the possible mechanisms of neonatal vascular remodeling during the transition from fetal to neonatal circulation, we assayed for apoptosis and evaluated the expression of apoptosis-regulatory proteins in umbilical vessel versus ascending aorta, ductus arteriosus (DA) versus adjacent pulmonary artery and aorta, or aorta versus its branching arteries. Twenty-two umbilical cords (UCs), 6 DAs with adjacent aortas and pulmonary arteries, and 4 aortic arches with their branching great arteries were obtained from neonates. Smooth muscle cell (SMC) apoptosis in umbilical vessels was identified in all UCs. The expressions of Bax and Bcl-X were stronger in umbilical artery than in the neonatal aorta, but Bcl-2 was weak in both arteries in immunohistochemistry. In the immunoblot analysis of UCs, the expression of the proapoptotic short isoform of Bcl-X was stronger than in other tissue, and caspase-3 was selectively activated, whereas it was not in the other components of the cardiovascular system. In contrast, the expression patterns of the FasAg and Fas ligand were similar in umbilical artery and aorta. Regulation of Bcl-2 family proteins was also observed in other vascular sites at which SMCs undergo apoptosis on hemodynamic changes during birth, such as the DA and the branching points of the great arteries from the aortic arch. Apoptosis is involved in the regression of human umbilical vessels and the DA and in the remodeling of the branching great arteries during the neonatal period, when Bcl-2 family proteins are likely to play a key role.

The aim of this study was to analyze sequential change of angiotensinogen (Ao) mRNA expression in rat liver and noninfarcted myocardium after myocardial infarction (MI). Female sprague-Dawley rats were subjected either to left coronary artery occlusion or sham operation. Three weeks after MI, coronary artery ligation resulted in comparable infarct sizes. A hypokinetic thin anterior wall and remarkable dilatation of the left ventricle, as well as decreased contractility (left ventricular end-systolic dimension = 6.0+/-0.4, 3.3+/-0.2, LV end-diastolic dimension = 7.9+/-0.3, 5.9+/-0.2 mm, and fractional shortening = 25.3+/-3.1%, 45.1+/-3.3%) were shown in the MI and sham group, respectively, by echocardiography (P0.01). Experimental MI caused a significant fall in systolic blood pressure (MI 90+/-5.0, vs sham 130+/-7.5 mmHg; P0.01) and significantly higher left ventricular end-diastolic pressure (MI 21+/-1.5, vs sham 11+/-1.0 mmHg: P0.01). At 4, 18, and 24h after MI, liver Ao mRNA levels, as shown by Northern blot analysis, had increased by up to four times (Ao/glyceraldehyde-3-phosphate dehydrogenase (GAPDH) = 1.4+/-0.1 and 6.0+/-0.2 at baseline and 4h after MI, respectively (P0.01). After sham surgery, however, the corresponding increase was slight (maximal 1.5-fold). Three days after MI, liver mRNA had returned to the baseline level. In contrast, ATG mRNA expression in noninfarcted myocardium, as shown by reverse transcription-polymerase chain reaction and Southern blotting, decreased transiently during the acute phase. It returned to its baseline level within 3 days, and then increased further (Ao/ GAPDH = 2.9+/-0.6, 0.3+/-0.1, 3.2+/-0.8, and 3.7+/-0.8 at baseline, 24h, 3 days, and 3 weeks after MI, respectively). In conclusion, it can be stated that after MI, the Ao gene contributes, acutely in the liver and chronically in the myocardium, to the maintenance of hemodynamic homeostasis during the acute phase and ventricular remodeling during the chronic phase.

The predictability of brachial-ankle pulse wave velocity (baPWV) for the presence and severity of coronary artery disease (CAD) was investigated by measuring baPWV in 501 subjects scheduled for coronary angiography. Severity of CAD was measured using modified Gensini stenosis score (GSS) and classified as a vessel disease score (VDS) of 0-3. The presence of CAD was defined as diameter stenosis50%. Subjects were grouped in tertile by level of baPWV (14, 14-17, 17 m/s). Subjects with CAD showed higher mean age, prevalence of men and diabetes, and systolic blood pressure. The prevalence of hypertension, use of antihypertensive medications and use of statin was not different. Subjects with CAD had higher baPWV than subjects without CAD (16.70 ± 3.46 versus 15.21 ± 3.19 m/s, p0.001). Multiple linear regression analysis showed significant correlation of baPWV and modified GSS (p=0.0337). ANCOVA adjusted with age, gender, body mass index, presence of hypertension or diabetes, status of smoking, use of antihypertensive medications and risk of hypercholesterolemia showed a statistically significant association of baPWV with VDS (p0.0001). Highest tertile of baPWV had a statistically significant effect on the severity of CAD from an ANCOVA model. The predictive power of highest tertile of baPWV for the presence of CAD was 3.600 [95% confidence interval (CI) 1.884-6.881, p0.0001]. It is concluded that increased baPWV is a reliable predictor of the presence and severity of CAD, suggesting that baPWV17 m/s may be a threshold value for the presence and severity of CAD.

AlGaN/GaN heterostructures have very superior material properties such as high breakdown field and high saturation current. Especially, AlGaN/GaN HEMTs have received much attention for next-generation high-frequency and high-power devices, particularly at high temperature and voltage operation [1]. Although significant progresses have been made in the past few years, additional efforts are needed in regard to current collapse effects and reliability issues [2]. To reduce current collapse, proper surface passivation is needed in AlGaN/GaN HEMTs [3]. Moreover, N2 plasma pretreatment has been recently reported to supperssion current collapse prior to the SiN passivation [3]-[5]. In this study, we tried to use SiN prepassivation for additional effects; preventing nitrogen desorption at the GaN surface during high temperature ohmic alloy and early protection of surface open to the process flow. Furthermore, this work focuses on the in situ N2 plasma treatment just prior to the SiN prepassivation to further mitigate current collapse.

Korean red ginseng (KRG) improves endothelial function and lower blood pressure (BP), which may affect arterial stiffness. The present study evaluated whether KRG treatment could improve arterial stiffness in subjects with hypertension.Eighty (80) participants with hypertension who were treated with antihypertensive agents were randomly assigned to an active (KRG 3 g/day) or a placebo treatment group in a double-blind manner. Participants were not allowed to change their antihypertensive medications. Systolic BP (SBP) and diastolic BP (DBP) were measured at baseline, and at 1, 2, and 3 months. Arterial stiffness was assessed by the measurement of brachial-ankle pulse wave velocity (baPWV) at baseline, and at 1 and 3 months.Thirty (30) subjects in the active group (AG) and 34 subjects in the placebo group (PG) completed 3 months of treatment and then a per-protocol analysis was done. SBP and DBP at baseline, and at 1, 2, and 3 months were not different between the AG and PG (p0.05). After 3 months of treatment, SBP of AG was not changed from SBP at baseline. However, DBP of AG, and SBP and DBP of PG after 3 months of treatment were significantly reduced (p0.05). baPWV of both groups was significantly reduced at 1 and 3 months (p0.05), but was not different between the groups at each time point. Analysis after adjustment for age, time-dependent mean arterial BP, heart rate, and levels of fasting blood glucose and triglycerides showed no significant difference between AG and PG in changes of baPWV from baseline to 1 and 3 months (p0.05).Three (3) months' treatment with KRG did not improve arterial stiffness in subjects with hypertension.

A intramural hematoma (IMH) was first described by Krukenberg in 19201 and is characterized by the absence of an intimal tear and false lumen that are the main characteristics of classic aortic dissection. This variant form of aortic dissection can not be diagnosed by angiography.2 Magnetic resonance imaging (MRI),3,4 computed tomography (CT),5,6 and transesophageal echocardiography (TEE)7,8 represent recent advances in the noninvasive diagnosis of aortic dissection. However, without recognition of this variant form of aortic dissection, one could erroneously make the diagnosis of aortic aneurysm with mural thrombus. Despite these challenging aspects of diagnosis, once the diagnosis is established, the recommended treatment strategy is not very different from classic aortic dissection. Surgical treatment has been recommended for type A and medical treatment for type B IMH.9–12 • • • Between July 1995 and December 1999, as a prospective study, IMH without associated surgical complications was treated medically in our hospital regardless of the involvement of the ascending aorta. TEE was used in the initial diagnosis and MRI or CT used complementarily when necessary. Patients were hospitalized for 2 weeks and TEE was repeated just before discharge. Late follow-up TEE was performed at 6 months and 1 year based on the patient’s acceptance. TEE was performed in the echocardiography laboratory or intensive care unit with local anesthesia and mild sedation (midazolam 3 to 6 mg). All transesophageal echocardiographic images were stored on a super VHS videotape. IMH was defined as a maximal crescentic or circular thickness of the aortic wall $7 mm associated with the absence of a dissection flap and flow communication with true lumen, with supportive echocardiographic characteristics (i.e., the displacement of intimal calcification and the presence of echolucent areas). In defining the extent of involvement, the segment with wall thickening ,7 mm was regarded as the involved segment when follow-up examination showed complete absorption. Furthermore, when the luminal surface showed an irregularity due to atheromatous change, in contrast to the typical smooth luminal surface of the IMH, the presence of an echolucent area or IMH with a smooth luminal surface in the proximal, intervening, or distal sites were required to define the segment involved by IMH. Conventional computer tomographic imaging was obtained with a General Electric CT/T 9800 scanner (Milwaukee, Wisconsin), spiral computer tomographic examinations with a Somatom Plus S scanner (Siemens, Erlangen, Germany), and MRI with a 2.0-T MRI system (Spectro-20000; Goldstar, Seoul, Korea). Sixteen patients (25%) with IMH were enrolled from among the 64 acute aortic dissections observed during the study period. Twelve patients were men (mean age of 65 6 6 years). There were 6 patients with type A and 10 patients with type B IMH. All patients with type A IMH were treated medically during a mean follow-up period of 30 6 17 months; no deaths occurred during this period. During the initial examination, fluid accumulations around the descending aorta were noted in 6 patients (38%), pleural effusion in 3 patients (19%, 2 with type A and 1 with type B), and pericardial effusions in 2 patients (16%, all with type A), which spontaneously disappeared during follow-up. During follow-up, the IMH was observed to have been completely absorbed in 2 patients (13%) and partially absorbed (a certain extent of complete absorption or the presence of segments with a .5 mm decrease in thickness) in 8 patients (50%). A limited extent IMH showed intimal tear and flow communication with true lumen in 4 patients (25%). No significant change was observed in the remaining patients. • • • Before beginning this study, we retrospectively analyzed 143 patients with acute aortic dissections admitted to our hospital before July 1995. There were 20 IMHs (14%) with 9 type A and 11 type B IMHs. In patients with type A IMH, only 2 patients underwent surgery. The remaining 7 patients were treated medically and there was no deaths during the mean follow-up of 36 6 4 months. This unexpected finding led us to perform this prospective study. Because of the relatively low incidence of IMH, its prognosis and treatment strategy have not been firmly established. Most opinions concur that IMH should be considered a precursor of classic aortic dissection and that type A IMH has an unfavorable prognosis if medically treated.9–13 Mohr-Kahaly et al9 have suggested the location of the hematoma as a possible reason for poor prognosis. Rupture of the vasa vasorum,14 which is considered to be the most frequent cause of IMH, is likely to occur in the outer layer of media close to the adventitia. This deeply seated hematoma is less likely to lead to a tearing of intima with a high propensity to rupture. Expressing another point From the Departments of Internal Medicine and Radiology, Clinical Research Institute and Division of Cardiology, Seoul National University College of Medicine, Seoul, Korea. Dr. Sohn’s address is: Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, 28 Yungun-Dong, Chongno-Gu, Seoul 110-744, Korea. Manuscript received August 30, 2000; revised manuscript received and accepted November 13, 2000.