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Manabu Ogita,
Katsumi Miyauchi,
Tadashi Miyazaki,
Ryo Naito,
Hirokazu Konishi,
Shuta Tsuboi,
Tomotaka Dohi,
Takatoshi Kasai, Takayuki Yokoyama,
Shinya Okazaki,
Takeshi Kurata,
Hiroyuki Daida
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ABSTRACT: Diabetes mellitus is recognized an independent risk factor for coronary artery disease (CAD) and mortality. Clinical trials have shown that statins significantly reduce cardiovascular events in diabetic patients. However, residual cardiovascular risk persists despite the achievement of target low-density lipoprotein cholesterol (LDL-C) levels with statin. High-density lipoprotein cholesterol (HDL-C) is an established coronary risk factor that is independent of LDL-C levels. We evaluated the impact of HDL-C on long-term mortality in diabetic patients with stable CAD who achieved optimal LDL-C. We enrolled 438 consecutive diabetic patients who were scheduled for percutaneous coronary intervention between 2004 and 2007 at our institution. We identified 165 patients who achieved target LDL-C <100 mg/dl. Patients were stratified into two groups according to HDL-C levels (low HDL-C group, baseline HDL-C <40 mg/dl; high HDL-C group, ≥40 mg/dl). Major adverse cardiac events (MACE) that included all-cause death, acute coronary syndrome, and target lesion revascularization were evaluated between the two groups. The median follow-up period was 946 days. The rate of MACE was significantly higher in diabetic patients with low-HDL-C who achieved optimal LDL-C (6.9 vs 17.9 %, log-rank P = 0.030). Multivariate Cox regression analysis showed that HDL-C is significantly associated with clinical outcomes (adjusted hazard ratio for MACE 1.33, 95 % confidence interval 1.01-1.75, P = 0.042). Low HDL-C is a residual risk factor that is significantly associated with long-term clinical outcomes among diabetic patients with stable CAD who achieve optimal LDL-C levels.
Heart and Vessels 03/2013; · 2.05 Impact Factor
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ABSTRACT: Although coagulase-negative staphylococci (CoNS) is a frequent cause of prosthetic valve endocarditis, native valve endocarditis (NVE) caused by CoNS is not commonly seen. Its high mortality is well known; however, there are no systematic reports published in Japan. We herein report the cases of two Japanese patients with CoNS NVE who were admitted to our hospital located in Tokyo and conduct literature searches on CoNS NVE in Japan from 1983 to March 2012 using PubMed and ICHUSHI WEB (Japan Medical Abstract Society). We also summarize the features of 22 Japanese patients with CoNS NVE, including our patients.
Internal Medicine 01/2013; 52(5):567-72. · 0.94 Impact Factor
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Manabu Ogita,
Katsumi Miyauchi,
Tomotaka Dohi,
Shuta Tsuboi,
Tadashi Miyazaki, Takayuki Yokoyama,
Ken Yokoyama,
Kazunori Shimada,
Takeshi Kurata,
Meizi Jiang,
Hideaki Bujo,
Hiroyuki Daida
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ABSTRACT: BACKGROUND: LR11 is a novel marker of intimal smooth muscle cell (SMC) proliferation. Vascular SMCs play important roles in the development of atherosclerosis interacting with macrophages in vulnerable plaque of patients with acute coronary syndrome (ACS).The present study determines whether soluble LR11 (sLR11) is associated with ACS. METHODS: We studied 100 patients with coronary artery disease (CAD) comprising 50 consecutive patients with acute coronary syndrome (ACS; mean age 62.3±13.0 y; male 78.0%) who were successfully treated with percutaneous coronary intervention and 50 age- and sex-matched stable angina pectoris (SAP) patients as control. Concentration of sLR11 was measured by sandwich enzyme-linked immunosorbent assay method. RESULTS: Circulating sLR11 was significantly increased in patients with ACS compared with SAP (9.88±2.78 vs. 8.18±1.11ng/ml, p<0.01). Multivariate logistic regression analysis indicated that sLR11 was independently associated with ACS (odds ratio (OR), sLR11 quartile increment, 2.18, 95% confidence interval (CI) 1.21-4.19, p<0.01). Among various biomarkers of acute coronary syndrome, hsCRP were significantly correlated with LR11 (r=0.480, p<0.01). CONCLUSIONS: There is a statistical significant association between LR11 and ACS and may be a useful biomarker for the development of acute coronary syndrome.
Clinica chimica acta; international journal of clinical chemistry 11/2012; · 2.54 Impact Factor
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Shuta Tsuboi,
Katsumi Miyauchi,
Takatoshi Kasai,
Manabu Ogita,
Tomotaka Dohi,
Tadashi Miyazaki, Takayuki Yokoyama,
Takahiko Kojima,
Ken Yokoyama,
Takeshi Kurata,
Hiroyuki Daida
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ABSTRACT: Background: Red blood cell distribution width (RDW) is a novel prognostic marker that reflects oxidative stress and chronic inflammation in patients with cardiovascular disease. Diabetes mellitus increases oxidative stress and vascular inflammation, which accelerate atherosclerosis. However, the relationship between RDW and long-term outcome in diabetic patients with coronary artery disease (CAD) is unclear. Methods and Results: Subjects comprised 560 consecutive diabetic patients (mean age, 66.6 years; male, 80%) with stable CAD who had undergone elective percutaneous coronary intervention (PCI). Patients were divided into 2 groups according to median RDW at baseline (13.1%): a high RDW group (mean RDW, 14.0%; interquartile range, 13.3-14.2%); and a low RDW group (mean RDW, 12.6%; interquartile range, 12.4-12.9%). All-cause mortality rates were compared between groups. Mean duration of follow up was 3.9 years. Patients with high RDW were more likely to be older, show dyslipidemia and have a lower ejection fraction and decreased hemoglobin level. Twenty-nine patients (5.2%) died during follow up. The cumulative incidence of all-cause death was significantly higher in the high RDW group than in the low RDW group (log-rank P=0.0015). Multivariate analysis identified high RDW as being associated with all-cause mortality (hazard ratio, 2.56; 95% confidence interval, 1.12-6.62; P=0.025). Conclusions: Increased RDW was significantly associated with increased long-term all-cause mortality in diabetic patients after PCI.
Circulation Journal 10/2012; · 3.77 Impact Factor
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Tomotaka Dohi,
Katsumi Miyauchi,
Shinya Okazaki, Takayuki Yokoyama,
Ryunosuke Ohkawa,
Kazuhiro Nakamura,
Naotake Yanagisawa,
Shuta Tsuboi,
Manabu Ogita,
Ken Yokoyama,
Takeshi Kurata,
Yutaka Yatomi,
Hiroyuki Daida
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ABSTRACT: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a vascular-specific inflammatory enzyme, of which increases are associated with cardiovascular events. However, the relationship between circulating Lp-PLA2 levels and coronary plaque volume has not been clarified in patients with acute coronary syndrome (ACS).
We studied 40 patients with ACS (age, 61.4 ± 8.0 years; male, 87.5%; statin use, 45.0%) who had undergone successful percutaneous coronary intervention (PCI). Plaque volume (PV) in non-culprit sites of PCI lesions was precisely determined using grayscale intravascular ultrasound (IVUS) at onset and at six months later. We then analyzed associations among PV, lipid profiles and Lp-PLA2 levels.
Circulating Lp-PLA2 levels and PV significantly decreased between baseline and six months of follow-up (458.6 ± 166.7 IU/L vs. 378.4 ± 158.5 IU/L, p < 0.001 and 82.2 ± 34.8mm(3) vs. 77.3 ± 33.1mm(3), p < 0.001, respectively). The % change in PV positively and significantly correlated with % change in LDL-C and in the LDL-C/HDL-C ratio (r = 0.444, p = 0.004 and r = 0.462, p = 0.003, respectively). Furthermore, % changes in Lp-PLA2 and in PV correlated even more closely (r = 0.496, p = 0.001). The absolute change in PV also significantly correlated with the change in Lp-PLA2 levels (r = 0.404, p = 0.009).
Circulating Lp-PLA2 levels are associated with changes in coronary plaque determined by IVUS in patients with ACS.
Atherosclerosis 12/2011; 219(2):907-12. · 3.79 Impact Factor
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ABSTRACT: Metabolic syndrome (MS) plays a crucial role in the long-term prognosis and primary or secondary prevention of coronary artery disease, regardless of the presence or absence of diabetes mellitus (DM). We previously reported that after percutaneous coronary intervention (PCI), patients with MS had worse long-term outcome. However, there is no evidence indicating the importance of MS with and without DM on re-revascularization procedures in Japanese patients undergoing PCI.
We hypothesized that MS patients without DM have an increased risk of re-revascularization following PCI.
We classified 748 consecutive Japanese patients who had undergone PCI into 4 groups as follows: neither DM nor MS, DM alone, MS alone, and both DM and MS. Post-hoc analyses were conducted using prospectively collected clinical data. Multivariate Cox regression was used to evaluate the risk within each group for subsequent revascularization (repeat PCI and bypass surgery), adjusting for baseline covariates.
The progress of 321 (42.9%) patients without DM or MS, 109 (14.6%) patients with DM alone, 129 (17.2%) patients with MS alone, and 189 (25.3%) patients with both DM and MS was followed up for a mean duration of 12.0 ± 3.6 years. Patients with MS alone (hazard ratio: 1.38, 95% confidence interval: 1.01-1.89, P = 0.04) and those with both DM and MS (hazard ratio: 1.36, 95% confidence interval: 1.02-1.81, P = 0.04) had a significantly increased risk for revascularization.
The presence of MS significantly increased the risk for subsequent revascularization among Japanese patients who underwent PCI, regardless of the presence or absence of DM.
Clinical Cardiology 10/2011; 34(10):610-6. · 2.15 Impact Factor
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ABSTRACT: In-stent restenosis (ISR) after bare-metal stent (BMS) implantation is thought to be clinically benign, although this notion remains controversial. The long-term clinical outcomes of ISR with BMS have not been established.
Among 983 consecutive patients (1,227 lesions) implanted with a BMS between 1999 and 2004 at the authors' institution, 746 underwent routine follow-up angiography. Angiographic ISR (ISR group) was evident in 215 patients (28.8%) and 136 of them underwent repeat revascularization. The incidence of major adverse cardiac events (MACE), acute coronary syndrome (ACS), target lesion revascularization and all-cause death were evaluated between patients with and without ISR (non-ISR group). Patients in the ISR group were older and more likely to have diabetes. The median follow-up period was 2,031 days. The rates of MACE and ACS were significantly higher in the ISR group compared with the non-ISR group (33.5% vs. 13.7%, P<0.0001 and 11.2% vs. 7.0%, P<0.05, respectively). Multivariate Cox regression analysis demonstrated that ISR was significantly associated with clinical outcomes (adjusted hazard ratio [HR] for MACE, 2.81; 95% confidence interval [CI]: 2.01-3.94, P<0.01; adjusted HR for ACS, 1.84; 95%CI: 1.08-3.13, P<0.05).
ISR with BMS was significantly associated with long-term adverse clinical outcomes. Risk of future cardiovascular events due to ISR must be carefully considered.
Circulation Journal 08/2011; 75(11):2566-72. · 3.77 Impact Factor
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Takahiko Kojima,
Katsumi Miyauchi, Takayuki Yokoyama,
Ken Yokoyama,
Takeshi Kurata,
Satoru Suwa,
Masaki Kawamura,
Hiroshi Tamura,
Shinya Okazaki,
Kenji Inoue,
Yasumasa Fujiwara,
Masataka Sumiyoshi,
Kosei Tanimoto,
Yuji Nakazato,
Shinichiro Yamagami,
Takafumi Hiro,
Nobuyuki Komiyama,
Hiroyuki Daida
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ABSTRACT: A previous study reported that amlodipine retarded coronary plaque progression in patients with coronary artery disease. The goal of this multicenter study was to determine which calcium-channel blockers (CCBs) other than amlodipine attenuated the progression of plaque volume (PV) accessed by intravascular ultrasound (IVUS).
ALPS-J was a prospective, randomized open-label study conducted at 5 centers. Patients who had hypertension and were scheduled for coronary intervention were enrolled. Subjects were randomly assigned to receive 16 mg/day of azelnidipine or 5mg/day of amlodipine administered for 48 weeks. The primary endpoint was the percent change in coronary PV measured by IVUS. Between 2007 and 2009, 199 patients were enrolled; 115 had evaluable IVUS images at both baseline and after 48 weeks of treatment. Blood pressure significantly reduced to 128/68 mmHg at follow-up. The lipid profiles in the 2 groups were comparable (low-density lipoprotein cholesterol: 97 mg/dl). The %change in PV showed a significant regression of 4.67 and 4.85% in the azelnidipine and amlodipine groups, respectively. The upper limit of the 95% confidence interval of the mean difference in %change PV between the 2 groups (0.18%, 95% confidence interval 4.62 to 4.98%) did not exceed the pre-defined non-inferiority margin of 6.525%.
ALPS-J demonstrated that azelnidipine was not inferior to amlodipine for primary efficacy. In addition to standard medical therapy, dihydropyridine CCBs will retard PV progression in hypertensive patients.
Circulation Journal 04/2011; 75(5):1071-9. · 3.77 Impact Factor
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ABSTRACT: Sirolimus-eluting stents (SES) are widely used in coronary artery disease as revascularization therapy. Although endothelial dysfunction induced by implanted SES can become a major clinical concern, therapeutic strategies to overcome this disorder remain unclear. The aim of the present study was therefore to identify effective therapies in a clinically relevant animal model.
Twenty-one pigs were randomized to control, candesartan (CAN) and candesartan plus pioglitazone (CAN+PIO) groups. Drugs were administered orally for 7 days before SES implantation until the time of death. Forty-two SES were used in porcine coronary arteries. Early inflammatory cell adhesion in SES evaluated on scanning electron microscopy at 3 days was significantly suppressed in the CAN and CAN+PIO groups compared with controls. Bradykinin-induced endothelium-dependent relaxation at an adjacent segment distal to the SES evaluated using organ chambers was reduced compared with intact segments in control coronaries at 28 days. Endothelial dysfunction was reversed by CAN and even more obviously improved in the CAN+PIO group.
Candesartan protected against vascular inflammation and restored endothelial function after SES implantation. The combination of candesartan and pioglitazone was more effective than candesartan monotherapy and might confer vascular protection when administered before SES implantation.
Circulation Journal 03/2011; 75(5):1098-106. · 3.77 Impact Factor
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ABSTRACT: Accumulating evidence shows that chronic kidney disease (CKD) is an independent risk factor for major adverse cardiac and cerebrovascular events (MACCE) after acute coronary syndrome (ACS). However, it is not known whether mild renal insufficiency affects long-term clinical outcomes.
This is a post-hoc analysis from the Extended-ESTABLISH trial, which was designed to estimate the impact of renal insufficiency on patients with ACS after percutaneous coronary intervention over the long term. One hundred and eighty patients were divided into three groups based on the estimated glomerular filtration rate (eGFR) at time of ACS: moderate-to-severe CKD, <60 mL/min/1.73 m(2) (n = 31, 17.2%); mild CKD, 60-90 mL/min/1.73 m(2) (n = 100, 55.6%) and non-CKD, ≥90 mL/min/1.73 m(2) (n = 47, 26.1%). The eGFR was calculated using the new Japanese equation. Long-term outcomes were compared over a follow-up period of 1538 ± 707 days.
Cumulative incidence rates of MACCE did not significantly differ between groups 1 year after ACS onset (P = 0.384), whereas significant differences appeared during the long-term follow-up (10.6 versus 27.0% versus 35.4% in the non-CKD, mild CKD and moderate-to-severe CKD groups, respectively; log-rank test, P = 0.022). In a multivariate Cox hazard regression model, moderate-to-severe CKD and mild CKD were associated with a higher rate of MACCE after adjusting for confounding variables (hazard ratios = 3.46 and 2.67, respectively; P = 0.043).
The presence of mild CKD at ACS occurrence is associated with a worse outcome in the long term, but not the short term.
Nephrology Dialysis Transplantation 02/2011; 26(9):2906-11. · 3.40 Impact Factor
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Manabu Ogita,
Katsumi Miyauchi,
Tomotaka Dohi,
Hideki Wada,
Shuta Tuboi,
Tadashi Miyazaki,
Akihisa Nishino, Takayuki Yokoyama,
Takahiko Kojima,
Ken Yokoyama,
Takeshi Kurata,
Hiroyuki Daida
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ABSTRACT: Diabetes mellitus has a greater effect on mortality rates due to coronary artery disease in women than in men. Although women undergoing coronary intervention in general have a higher frequency of adverse outcomes than men, the effect of gender among diabetic patients on clinical outcomes after percutaneous coronary intervention (PCI) has not been well established in the drug-eluting stent (DES) era. We have investigated the impact of gender on long-term clinical outcome in these high risk populations. We enrolled 404 consecutive patients (74 women and 330 men) with diabetes mellitus who underwent elective PCI (85% with DES). We evaluated the incidence of major adverse cardiac events (MACE), which is a composite of total all-cause death, acute coronary syndrome (ACS), and target lesion revascularization (TLR) during a period of 4 years after coronary intervention. The women were significantly older, more likely to have dyslipidemia, and had significantly higher systolic blood pressure and LDL-C values than men. The use of insulin and angiotensin receptor blockers was more frequent among the women (32.4% versus 21.0%, P = 0.04 and 60.8% versus 39.8%, P < 0.01, respectively). The angiographic profiles of both were comparable. At four-year clinical follow-up, cumulative incidence of MACE was identical between the women and the men (16.2% versus 15.5%, P = 0.90; adjusted HR 1.23, 95% CI 0.61-2.50, P = 0.56). Although the baseline characteristics of the women were worse, clinical outcomes did not significantly differ between women and men among diabetic patients after elective PCI.
International Heart Journal 01/2011; 52(6):348-52. · 1.16 Impact Factor
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ABSTRACT: The usefulness of drugs to treat plaque regression is assessed by intravascular ultrasound (IVUS); however, the impact of plaque regression on clinical outcomes in patients with acute coronary syndrome (ACS) has not been established; therefore, we investigated the relationship between coronary plaque regression and long-term clinical outcomes.
We analyzed data from 86 patients who underwent percutaneous coronary intervention (PCI) and who were assessed in detail at baseline and at 6 months of follow-up by measuring proximal non-culprit sites of PCI lesions using volumetric IVUS. Patients were divided according to changes in plaque volume over 6 months into one group with plaque regression (n =55; 64.0%) and another with progression (n =31; 36.0%). They were followed up observationally for a mean of 1,736 days.
Baseline characteristics at the time of ACS were similar between the groups. The probability of event-free survival was significantly higher in the regression group than in the progression group as estimated by the Kaplan-Meier method (Log-rank test, p =0.032). Furthermore, the Cox hazards model revealed the relative contribution of plaque regression as a predictor of cardiovascular events (hazard ratio: 0.26; 95% CI, 0.07 to 0.83; p =0.023).
Plaque regression determined by volumetric IVUS over a period of 6 months was associated with a lower rate of cardiovascular events among patients with ACS. This study also demonstrated that plaque regression could be a surrogate marker of future cardiovascular events.
Journal of atherosclerosis and thrombosis 12/2010; 18(3):231-9. · 2.69 Impact Factor
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ABSTRACT: An equation that accurately estimates the glomerular filtration rate (GFR) in the Japanese population has been proposed; however, the prognostic significance of estimated GFR (eGFR) defined according to this equation has not been reported. In addition, the prognostic significance of eGFR during long-term follow-up after complete coronary revascularization remains unclear. We assessed the prognostic significance of eGFR values, estimated by the new Japanese equation, in a cohort of patients following complete coronary revascularization. We studied consecutive patients with complete revascularization from 1984 to 1992. Patients on dialysis were excluded. A novel Japanese equation was used to estimate the GFR: eGFR=194×(serum creatinine)(-1.094)×(age)(-0.287)(×0.739 if female). Multivariate Cox proportional hazards regression analyses were performed to determine all-cause and cardiac mortality. We analyzed data of 1809 patients, of whom 571 (31.6%) had an eGFR of ≥90 mlmin(-1) per 1.73 m(2), 917 (50.7%) had an eGFR of 60-89 mlmin(-1) per 1.73 m(2), 298 (16.5%) had an eGFR of 30-59 mlmin(-1) per 1.73 m(2) and 23 (1.3%) had an eGFR of <30 mlmin(-1) per 1.73 m(2). During follow-up (11.4±2.9 years), there were 397 (22.0%) all-cause and 123 (6.8%) cardiac deaths overall. Patients with an eGFR of 30-59 mlmin(-1) per 1.73 m(2), and <30 mlmin(-1) per 1.73 m(2) revealed significantly greater risk of all-cause mortality than those with eGFR of ≥90 mlmin(-1) per 1.73 m(2) (hazard ratio (HR) 1.91, P<0.001, HR 3.35, P<0.001, respectively). Furthermore, incidence of cardiac death was higher in patients with an eGFR of 30-59 mlmin(-1) per 1.73 m(2) than those with an eGFR of ≥90 mlmin(-1) per 1.73 m(2) (HR 2.89, P<0.001). GFR as estimated using the new Japanese equation had a prognostic significance among patients with complete coronary revascularization.
Hypertension Research 12/2010; 34(3):378-83. · 2.58 Impact Factor
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ABSTRACT: Some randomized studies have shown a delay of up to a few years in the statin-related survival advantage, whereas others have demonstrated an early survival benefit for some patients. We examined the short-term effects of statins in patients with acute coronary syndrome (ACS), stratified according to baseline LDL-C.
Patients with ACS (n = 180) were randomized to receive 6 months of atorvastatin (20 mg) in the Extended-ESTABLISH trial. Six months after ACS onset, all patients were treated with statins to achieve an LDL-C value of < 100 mg/dL. Patient outcomes were analyzed with respect to LDL-C at the time of ACS onset: high baseline (≥ 100 mg/dL, n = 124) or low baseline (< 100 mg/dL, n = 56) LDL-C.
The cumulative incidence rates of major adverse cardiac and cerebrovascular events (MACCE) did not significantly differ between the early-statin and control groups in the high baseline groups at 6 months (p = 0.158), whereas a significant benefit of early intensive statins appeared 1 year (p = 0.034) later. In contrast, we found no significant short-term benefits of statins after either 6 months or 1 year in the low baseline group. Multivariate analysis showed that early intensive atorvastatin therapy was associated with a lower risk of MACCE at 1 year in the high baseline group (OR, 0.25; 95% CI, 0.05 to 0.83; p = 0.035).
The effects of 6 months of intensive lipid-lowering therapy appear after 1 year in patients with ACS and baseline LDL-C ≥ 100 mg/dL.
Journal of atherosclerosis and thrombosis 10/2010; 18(1):42-8. · 2.69 Impact Factor
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ABSTRACT: The ESTABLISH trial found using volumetric intravascular ultrasound that atorvastatin therapy started early and continued for 6 months significantly reduced plaque volume in patients with acute coronary syndrome (ACS). However, the benefits of early statin administration on long-term outcomes remain unclear. We therefore examined whether the early initiation of statin in patients with ACS improves long-term prognosis.
The Extended-ESTABLISH trial included 180 patients with ACS who underwent emergency percutaneous coronary intervention (PCI). These patients were randomized here to groups given either early intensive lipid-lowering therapy (n=90; atorvastatin 20 mg/day) or standard care (control, n=90) within 48 h of events. Baseline characteristics between the two groups did not significantly differ at the time of ACS onset. Six months after PCI, all patients were treated with statins to achieve an LDL-C value of <100 mg/dL. We compared the first occurrence of major adverse cardiac and cerebrovascular events (MACCE). Prognostic data were fully documented during the entire follow-up period (mean, 1538+/-707 days). Cumulative event-free survival was significantly higher in the atorvastatin, than in the control group (p=0.041; log-rank test). Furthermore, by adjusting for validated prognosticators, early statin administration was identified as a good predictor of MACCE (HR 0.46, 95%CI 0.23-0.86; p=0.015).
In-hospital initiation of statin therapy immediately after ACS conferred long-term benefits and 6 months of intensive lipid-lowering therapy improved long-term clinical outcomes after PCI in patients with ACS.
Atherosclerosis 06/2010; 210(2):497-502. · 3.79 Impact Factor
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Katsumi Miyauchi,
Takahiko Kojima, Takayuki Yokoyama,
Takeshi Kurata,
Ken Yokoyama,
Masaki Kawamura,
Satoru Suwa,
Shinya Okazaki,
Kenji Inoue,
Yasumasa Fujiwara,
Masataka Sumiyoshi,
Kosei Tanimoto,
Yuji Nakazato,
Shinichiro Yamagami,
Hiroyuki Daida
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ABSTRACT: Many trials have shown that calcium channel blockers (CCBs) can reduce the cardiovascular (CV) events in patients with coronary artery disease (CAD). The mechanisms of this effect could be associated with plaque regression due to the anti-atherosclerotic properties of CCBs. The goal of this study is to determine the effects of CCB on volumetric quantitative changes of coronary plaques accessed by intravascular ultrasound (IVUS). To confirm this hypothesis, a multicenter randomized trial of CCBs treatment with azelnidipine or amlodipine will be conducted in hypertensive CAD patients undergoing elective percutaneous coronary intervention (PCI).
Patients who have hypertension and are scheduled for PCI will be enrolled. Subjects will be randomized to azelnidipine or amlodipine and observed for 48 weeks. The primary endpoint will be the percent change of coronary plaque volume. The secondary endpoint will include inflammatory markers, antioxidant activity, and incidence of composite cardiovascular events.
In this study, we will investigate the improvement of coronary plaque with IVUS by treatment with two dihydropyridine CCBs in hypertensive patients undergoing elective PCI. This result will lead to the discovery of more effective drug therapy for inhibition of coronary events.
Cardiovascular Drugs and Therapy 09/2009; 23(5):409-13. · 3.13 Impact Factor
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Tomotaka Dohi,
Katsumi Miyauchi,
Takatoshi Kasai,
Kan Kajimoto,
Naozumi Kubota,
Hiroshi Tamura, Takayuki Yokoyama,
Takahiko Kojima,
Ken Yokoyama,
Takeshi Kurata,
Hiroyuki Daida
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ABSTRACT: Metabolic syndrome (MetS) is a risk factor and prognosticator for ischemic heart disease, but its actual effect on long-term mortality after acute coronary syndrome (ACS) remains unknown.
All-cause death and cardiovascular death were investigated among patients with ACS upon admission who underwent complete revascularization by either percutaneous coronary intervention or bypass surgery between 1984 and 1992. MetS was defined according to the NCEP/ATPIII criteria modified for waist circumference. From among 1,836 patients who underwent complete revascularization during the study period, 384 (21.0%) with ACS were enrolled, of whom 163 (42.5%) had MetS. During a mean follow-up of 10.4 +/-3.4 years, the total number of deaths was 83 (21.6%), of which 38 (9.9%) were from cardiovascular causes. Cox proportional hazard analysis revealed that MetS increased the risk of mortality by a ratio of 1.62 (95% confidence interval (CI) 1.01-2.59, P=0.046) and of cardiovascular death by 2.40 (95%CI 1.16-4.94, P=0.018) in patients with ACS.
MetS is a powerful determinant of long-term all-cause and cardiovascular death after ACS. Furthermore, MetS and ACS might jointly exacerbate poor long-term outcomes.
Circulation Journal 07/2009; 73(8):1454-8. · 3.77 Impact Factor
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ABSTRACT: Recent studies have demonstrated the quantitative ability of contrast-enhanced multidetector computed tomography (MDCT) to evaluate not only the vessel lumen but also coronary plaque. The aim of this study was to assess the association between coronary wall thickness quantified by 64-slice MDCT and cardiovascular risk factors.
A total of 149 subjects with suspected coronary artery disease were scanned by contrast-enhanced 64-slice MDCT. The maximum coronary wall thickness of each proximal segment was measured and associations with baseline coronary risk factors were analyzed. The mean maximum wall thickness of all 149 patients was 0.7+/-0.3 mm and there was a significant positive correlation with age (P<0.001) and hemoglobin (Hb) A1c (P=0.001). Patients with hypertension (0.8+/-0.3 vs 0.7+/-0.3 mm, P=0.024) and diabetes (0.9+/-0.4 vs 0.7+/-0.3 mm, P=0.002) had thicker walls than those without. Multivariate linear regression analysis demonstrated that both risk factors were independently correlated with mean maximum wall thickness.
Coronary wall thickness measured by 64-slice MDCT is associated with age and HbA1c, so may add useful information to cardiovascular risk stratification.
Circulation Journal 02/2009; 73(4):681-5. · 3.77 Impact Factor
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ABSTRACT: Enhanced early inflammatory response accelerated the neointimal hyperplasia after vascular injury. Pioglitazone has antiatherogenic property through the inhibition of inflammation. Thus, we hypothesized that pioglitazone might inhibit the early inflammatory response, resulting in reduced neointimal hyperplasia in porcine coronary stenting model. Pioglitazone (5mg/kg/day) or placebo was administered orally to 10 pigs (20 coronaries) in each, from 7 days before stenting until the time of euthanasia at 3 or 28 days after stenting. The coronary artery of the pigs was injured with an oversized bare metal stent. Early inflammatory cell infiltration on the vessel surface was evaluated by scanning electron microscopy and was significantly suppressed in pioglitazone-treated group comparing with the control (% of site occurring greater infiltration: 40.8% versus 60.9%; P=0.002). Immunohistochemistry revealed that activated NF-kappaB and MCP-1 expression in the vessel was of significantly less in the pioglitazone-treated group. On day 28, morphometric assessment of stent-section showed significant reduction of neointimal thickness in the pioglitazone-treated group comparing with the control (neointimal thickness: 386.5+/-78.2mm versus 591.7+/-238.6mm; P=0.0051), whereas there was no difference in the injury score between two groups. Pioglitazone inhibited neointimal hyperplasia after stenting through a reduction of early inflammatory response.
Atherosclerosis 05/2008; 197(2):612-9. · 3.79 Impact Factor
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ABSTRACT: Constrictive remodeling and intimal hyperplasia play a prominent role in restenosis after angioplasty. It has been reported that the severity of constrictive remodeling and intimal hyperplasia correlate with adventitial angiogenesis and inflammation. Experimental evidence indicates that inflammation participates in angiogenesis, and therefore inhibition of inflammation may impair neovascularization. We tested whether fenofibrate, peroxisome proliferative activated receptors (PPAR)-alpha specific ligand, inhibits the early inflammation, adventitial angiogenesis, constrictive remodeling and intimal hyperplasia after angioplasty using porcine coronary arteries. Fenofibrate was tested in vivo, in 30 coronary arteries of 10 pigs (1g/day, orally) and was compared to placebo. Quantitative intravascular ultrasound and histopathologic assessment showed that fenofibrate increased lumen (6.28 mm(2) versus 5.15 mm(2)), vessel area (7.34 mm(2) versus 6.69 mm(2)) and inhibited constrictive remodeling. Inflammatory cell infiltration was evaluated with scanning electron microscopy 3 days after angioplasty and was significantly decreased in the treated vessels compared to control. Adventitial angiogenesis 3 days after angioplasty was significantly reduced in the injured vessels derived from the fenofibrate treated group compared to placebo. In conclusion, pharmacological activation of PPAR-alpha inhibited constrictive remodeling and neointimal hyperplasia after angioplasty through inhibition of inflammation and adventitial neovascularization.
Atherosclerosis 11/2006; 188(2):274-80. · 3.79 Impact Factor
