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Aims: As part of the Toon Health Study, which is an ongoing population‐based cohort study, we aimed to develop a prediction model for N‐terminal pro‐brain natriuretic peptide (NT‐proBNP) in a general Japanese population. We sought to explore the influence of various demographic and clinical factors on NT‐proBNP levels and assess the model's performance. In addition, our objectives included internal validation and investigation of the diagnostic potential of the observed‐to‐predicted NT‐proBNP ratio (OPR) at baseline for predicting the risk of heart failure with preserved ejection fraction (HFpEF). Methods and results: In this prospective cohort study, participants were recruited from Toon City, Japan, as part of the larger Toon Health Study, focusing on cardiovascular risk factors. We measured the NT‐proBNP levels and used linear regression with penalization (ridge regression) to develop the model. The model incorporated 10 prespecified predictors (age, gender, body mass index, diastolic blood pressure, heart rate, haemoglobin, albumin, total cholesterol, haemoglobin A1c, and estimated glomerular filtration rate) and underwent assessment using R2 and root mean squared error (RMSE). Internal validation was conducted through bootstrapping. In a post hoc analysis, we explored the OPR's diagnostic potential using 5 year follow‐up data (n = 636) to predict the elevation of NT‐proBNP > 125 pg/mL at the 5 year follow‐up as the risk of HFpEF. A total of 2505 participants (age: 60.4 ± 12.9 years, men: 35%) were enrolled in this study. There was a linear relationship between the observed and predicted values of NT‐proBNP in which the logarithm of observed NT‐proBNP was <6, which corresponds to 403 pg/mL in NT‐proBNP. The prediction model demonstrated satisfactory performance (R2: 0.291, RMSE: 0.688), with age identified as a dominant predictor. The stability of the model was underscored by the internal validation. The OPR at baseline predicted NT‐proBNP > 125 pg/mL at the 5 year follow‐up with an area under the curve of 0.793. Conclusions: This study introduces the first prediction model for NT‐proBNP in a general Japanese population. Although the model has acceptable performance, ongoing refinement is essential. Our transparent approach to model development, alongside a web‐based interactive tool, lays the groundwork for further improvements and external validation. The OPR holds potential for predicting the future risk of HFpEF. This research contributes to understanding the nuanced influence of patient backgrounds on levels of NT‐proBNP in asymptomatic individuals within the context of a broader population‐based cohort study. [ABSTRACT FROM AUTHOR]

We evaluated the feasibility of myocardial perfusion ratio to the aorta (MPR) in static computed tomography perfusion (CTP) for detecting myocardial perfusion abnormalities assessed by single-photon emission computed tomography (SPECT). Twenty-five patients with suspected coronary artery disease who underwent dynamic CTP and SPECT were retrospectively evaluated. CTP images scanned at a sub-optimal phase for detecting myocardial perfusion abnormalities were selected from dynamic CTP images and used as static CTP images in the present study. The diagnostic accuracy of MPR derived from static CTP was compared to those of visual assessment and conventional quantitative parameters such as myocardial CT attenuation (HU) and transmural perfusion ratio (TPR). The area under the curve of MPR (0.84; 95% confidence interval [CI], 0.76–0.90) was significantly higher than those of myocardial CT attenuation (0.73; 95% CI, 0.65–0.79) and TPR (0.76; 95% CI, 0.67–0.83) (p < 0.05). Sensitivity and specificity were 67% (95% CI, 54–77%) and 90% (95% CI, 86–92%) for visual assessment, 51% (95% CI, 39–63%) and 86% (95% CI, 82–89%) for myocardial CT attenuation, 63% (95% CI, 51–74%) and 84% (95% CI, 80–88%) for TPR, and 78% (95% CI, 66–86%) and 84% (95% CI, 80–88%) for MPR, respectively. MPR showed higher diagnostic accuracy for detecting myocardial perfusion abnormality compared with myocardial CT attenuation and TPR. [ABSTRACT FROM AUTHOR]

Pseudoxanthoma elasticum (PXE) is a rare hereditary disorder that causes elastic tissue degeneration in the skin, eyes, and cardiovascular system. Gastrointestinal bleeding and fundus hemorrhage are serious complications associated with PXE prognosis as well as cardiovascular involvement. This is a rare case of acute coronary syndrome in a PXE patient with high bleeding risk. Pseudoxanthoma elasticum (PXE) resulting in acute coronary syndrome (ACS) is rare. Given PXE patients are generally at very high bleeding risk, antithrombotic therapy as secondary prevention after ACS onset should be taken into full consideration. [ABSTRACT FROM AUTHOR]

Pulmonary artery intimal sarcomas (PAIS) are often misdiagnosed as pulmonary embolisms (PE) as their clinical findings and imaging findings are similar. However, given the clinical outcome of both diseases is different in its prognosis, accurate and rapid diagnosis is mandatory. This is a case report of a histologically-proven PAIS which was initially treated as a PE. The color-coded iodine map using dual-energy computed tomography (dual-energy CT iodine map) well reflected the distribution of the tumor consistent with 18fluoro-2-deoxyglucose-uptake region using positron emission tomography/CT. This case demonstrates the potential of using dual-energy CT iodine map to differentiate PAIS from PE. Use of a dual-energy computed tomography iodine map to visualize a pulmonary artery intimal sarcoma may provide useful diagnostic information. [ABSTRACT FROM AUTHOR]

Aims: Cardiac amyloidosis (CA) is an infiltrative myocardial disease that occasionally mimics hypertrophic cardiomyopathy (HCM). The aim of this study is to investigate the discriminatory ability of visual assessment of left atrial (LA) function between CA and HCM on echocardiography. Methods and results: In total, 93 patients with cardiac magnetic resonance imaging (CMR)‐confirmed HCM and 34 with cardiac biopsy‐confirmed CA were retrospectively assessed. LA dilatation was assessed via echocardiography in an apical four‐chamber view. Visual assessment was performed to identify LA dilatation grade (preserved = 1, abnormal = 2, and restricted = 3) based on the extent of outward expansion in the LA reservoir phase. Regarding the reproducibility of visually assessing LA dilatation grade, the kappa values between intra‐ and inter‐observer measurements were 0.82 and 0.70, respectively. Of 127 participants, 57 (45%), 42 (33%), and 28 (22%) presented with LA dilatation Grades 1, 2, and 3, respectively. All 57 patients with preserved LA dilatation (Grade 1) had HCM, and 20 of 28 patients (71%) with restricted LA dilatation (Grade 3) presented with CA. Patients with CA had a higher LA dilatation grade than those with HCM (P < 0.01). LA emptying fraction and reservoir strain were also quantitatively evaluated. The area under the curves of LA dilatation grade (0.88) and LA emptying fraction (0.88) for differentiation of these two diseases were higher than that of LA reservoir strain (0.73) (P < 0.01, respectively). During follow‐up, nine patients with HCM and 16 with CA experienced cardiac event (cardiac death or hospitalization due to heart failure). In Kaplan–Meier analysis including both groups of HCM and CA, the incidence of cardiac events was higher in patients with restricted LA dilatation than in those with preserved or abnormal LA dilatation (log‐rank test, P < 0.01). Conclusions: Restricted LA dilatation is an indicator for the diagnosis of CA. Further, visual assessment of abnormal LA motion may facilitate diagnosis in patients with CA and high‐risk patients with HCM. [ABSTRACT FROM AUTHOR]

The management of systemic artery aneurysms secondary to Kawasaki disease (KD) in adults remains a therapeutic challenge. KD guidelines recommend the use of anticoagulation therapy with warfarin in addition to antiplatelet therapy when a giant coronary aneurysm or a history of thrombosis is documented. However, long-term use of warfarin presents several concerns. This case reports acute thrombotic occlusion due to the giant arterial aneurysm in an adult KD. A surgical resection of the aneurysm was performed because of recurrent thrombotic events, despite anticoagulant therapy with warfarin. Pathological examinations revealed a layered thrombus with inflammation in the aneurysm and Factor Xa expression mainly in newly formed thrombus. This study provides an insight into the anticoagulation therapy for cardiovascular sequelae after KD. < Learning objective: This study, along with pathological evidence, illustrates that Factor Xa might contribute to thrombotic events after Kawasaki disease.> [ABSTRACT FROM AUTHOR]

In extracardiac Fontan, an epicardial pacemaker implantation has many limitations, especially given that it is highly invasive and a high-risk procedure due to repeat thoracotomy. Herein we illustrate a case with the possibility of transvenous pacing in extracardiac Fontan being less invasive and lower risk transvenous dual-chamber pacemaker implantation by electrophysiological assessment. < Learning objective: Transvenous pacemaker implantation via left superior vena cava may be a viable alternative to epicardial pacing with a minimally invasive procedure in patients with extracardiac Fontan.> [ABSTRACT FROM AUTHOR]

Aims: Traditional criteria for heart transplantation by cardiopulmonary exercise testing (CPX) include peak oxygen uptake (VO2) < 14 mL/kg/min. Reaching a sufficient exercise load is challenging for patients with refractory heart failure (HF) because of their exercise intolerance. Recently, a substantial impact of right ventricular (RV) dysfunction was highlighted on urgent heart transplantation and mortality. This study aims to investigate the impact of RV contractile reserve, assessed by low‐load exercise stress echocardiography (ESE), on exercise intolerance defined as peak VO2 < 14 mL/kg/min, in patients with HF. Methods and results: We prospectively examined 67 consecutive patients hospitalized for HF who underwent ESE and CPX under a stabilized HF condition. Although low‐load ESE was defined as 25 W load exercise, an increment in RV systolic (s′) velocity was regarded as the preservation of RV contractile reserve. All patients completed low‐load ESE. During low‐load ESE, the variation in RV s′ velocity significantly correlated with peak VO2 (r = 0.787, P < 0.001). The change in RV s′ velocity during low‐load ESE accurately identified patients with peak VO2 < 14 mL/kg/min (area under the curve, 0.95; sensitivity, 92%; specificity, 85%). The intraclass correlation coefficient for intra‐observer and inter‐observer agreement for the change in RV s′ velocity was 0.96 (95% confidence interval, 0.88–0.99, P < 0.001) and 0.86 (95% confidence interval, 0.64–0.95, P < 0.001), respectively. The RV‐to‐pulmonary circulation (PC) coupling, which was assessed by the slope of the relationship between RV s′ velocity and pulmonary artery systolic pressure at rest and low‐load exercise, was worse in the low‐peak VO2 group (<14 mL/kg/min) than the preserved‐peak VO2 group (≥14 mL/kg/min). Conclusions: The change in RV s′ velocity during low‐load ESE could estimate the exercise capacity in HF patients. The assessments of RV contractile reserve and RV‐to‐PC coupling could be clinically beneficial to distinguish high‐risk HF patients. [ABSTRACT FROM AUTHOR]

Covalently-linked polyamine-polyhydroxy clusters are synthesized to model solvation shells for polar solutes in water for the three-dimensional encapsulation of a guest. The alkyalation of the octaaza macrocycle with a long-chain epoxy alcohol in DMF yields the octakis(dihydroxyalkyl) derivative. This compound behaves as a host, with a binding site consisting of an intramolecularly associated polyamine/ammonium-polyhydroxy cluster with a small quantity of water. Thus, the compound may also be considered as a unimolecular reversed micelle.

The Impella (Abiomed, Danvers, MA, USA) is a novel percutaneous heart pump device for left ventricular (LV) assistance; however, LV thrombus is a notable contraindication for this device. Contrast computed tomography assessment is useful for detecting LV thrombus and preventing thromboembolism in patients recommended for Impella use. < Learning objective: The Impella (Abiomed, Danvers, MA, USA) is a heart pump device which aspirates blood from a left ventricular (LV) cavity and ejects it into an ascending aorta. Therefore, LV thrombus should be explored before the Impella insertion to prevent systemic embolism. Generally, echocardiography is the first choice to detect LV thrombus. Given limited diagnostic sensitivity for detecting LV thrombus in echocardiography, contrast computed tomography might be a useful strategy for the patient targeting Impella insertion.> [ABSTRACT FROM AUTHOR]

Objectives This study evaluated the relationship between platelet reactivity and plaque morphology using grayscale and radiofrequency intravascular ultrasound (IVUS) virtual histology (VH). Background Recent studies have reported that high on-treatment platelet reactivity (HPR) is associated with higher plaque volume and the presence of multivessel disease; however, the association between HPR and plaque morphology has not been evaluated. Methods The ADAPT-DES (Dual AntiPlatelet Therapy With Drug Eluting Stents) intravascular ultrasound substudy was a prospective, multicenter, observational study of 8,582 patients undergoing percutaneous coronary intervention with drug-eluting stents in whom platelet reactivity on clopidogrel was assessed routinely. The current analysis included 909 culprit lesions from 773 patients with pre-intervention grayscale IVUS and IVUS-VH. HPR was defined as platelet reactivity >208 P2Y12 reaction unit in point-of-care P2Y12 testing by the VerifyNow assay, measured during steady-state platelet inhibition in patients receiving an antiplatelet agent. Results HPR was associated with 3-vessel coronary artery disease (31.0% vs. 24.4%; p = 0.04). The incidence of fibroatheroma was higher in patients with HPR than those without HPR (77.1% vs. 68.9%; p = 0.01). The HPR group had larger percent plaque and media volume (plaque and media/external elastic membrane volume: 58.1% [95% confidence interval (CI): 57.1% to 59.0%] vs. 56.6% [95% CI: 55.8% to 57.5%]; p = 0.03) and plaque burden at the minimum lumen site (76.7% [95% CI: 75.7% to 77.8%] vs. 75.0% [95% CI: 74.0% to 76.0%]; p = 0.02). Despite a similar prevalence of attenuated plaque, patients with HPR had longer culprit lesion attenuated plaque length (8.0 [95% CI: 7.0 to 9.1] mm vs. 6.5 [95% CI: 5.9 to 7.1] mm; p = 0.01). On multivariate analysis, the presence of angiographic calcium (odds ratio [OR]: 1.85: 95% CI: 1.33 to 2.56; p = 0.0002) and HPR (OR: 1.45; 95% CI: 1.05 to 2.01; p = 0.02) were independent predictors for a culprit lesion fibroatheroma. Conclusions HPR was associated with increased culprit lesion atherosclerotic burden and adverse plaque morphology among patients undergoing percutaneous coronary intervention. Platelet reactivity might be associated with not only blood clot formation, but also severity of atherosclerosis. (Assessment of Dual AntiPlatelet Therapy With Drug Eluting Stents [ADAPT-DES]; NCT00638794 ) [ABSTRACT FROM AUTHOR]

Objectives: This study investigated coronary artery remodeling patterns associated with clinical outcomes. Background: In the prospective, multicenter PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree: An Imaging Study in Patients With Unstable Atherosclerotic Lesions) study, reported predictors of nonculprit lesion (NCL) major adverse cardiac events (MACE) were an intravascular ultrasound (IVUS) minimal lumen area (MLA) ≤4 mm2, a plaque burden ≥70%, and a IVUS–virtual histology (VH) thin-cap fibroatheroma (TCFA), but not lesion site remodeling. Methods: Overall, 697 consecutive patients with an acute coronary syndrome were enrolled and underwent 3-vessel gray-scale and IVUS-VH; 3,223 NCLs were identified by IVUS. The remodeling index (RI) was calculated as the external elastic membrane area at the MLA site divided by the average of the proximal and distal reference external elastic membrane areas. First, one third of the patients were randomly selected to determine RI cutoffs related to NCL MACE (development cohort). Receiver-operating characteristic analysis showed that there were 2 separate cut points that predicted NCL MACE: RI = 0.8789 and RI = 1.0046 (area under the curve = 0.663). These cut points were used to define negative remodeling as an RI <0.88, intermediate remodeling as an RI of 0.88 to 1.00, and positive remodeling as an RI >1.00. Second, we used the remaining two-thirds of patients to validate these cut points with respect to lesion morphology and clinical outcomes (validation cohort). Results: Kaplan-Meier curve analysis in the validation cohort showed that NCL MACE occurred more frequent (and equally) in negative and positive remodeling lesions compared with intermediate remodeling lesions. In this cohort, negative remodeling lesions had the smallest MLA, positive remodeling lesions had the largest plaque burden, and VH TCFA, especially VH TCFA with multiple necrotic cores, was most common in negatively remodeling lesions. Conclusions: The present study showed the novel concept that positive and negative lesion site remodeling was associated with unanticipated NCL MACE in the PROSPECT study. (PROSPECT: An Imaging Study in Patients With Unstable Atherosclerotic Lesions [PROSPECT]; NCT00180466) [Copyright &y& Elsevier]

Background: Two-dimensional speckle tracking echocardiography (2D-STE) is a novel technology that directly measures regional left ventricular (LV) wall contraction. This study aimed to directly measure inner-layer thickening (radial strain) of the LV using 2D-STE, and to examine the relationship between radial strain and the degree of hypertrophy. Methods: The study enrolled 63 untreated hypertensive patients with normal geometry (N group, n = 32) or concentric hypertrophy (CH group, n = 31 ), classified according to LV mass index (LVMI) and relative wall thickness (RWT). Thirty normotensive subjects (C group, n = 30) served as controls. Radial strain (e) in the inner half (ei) and all layers of the LV wall (sa) were calculated from the LV short-axis view by 2D-STE. Results: LV ejection fraction did not differ significantly among the groups. However, ei and sa were significantly lower in the CH group compared with the C and N groups (p < 0.01 ). A ratio of ei to ea was significantly lower in the CH group compared with the C and N groups (p < 0.01 ). A multivariate regression model that included midwall fractional shortening, E/e', LVMI, RWT, and LV ejection fraction showed that LVMI (p = 0.002) and RWT (p = 0.014) were independent predictors (R2 = 0.59) of ei. Conclusion: Radial strain in the inner half layer of the LV wall decreases in parallel with the degrees of LV concentricity and hypertrophy in hypertensive patients. Radial strain in the inner half layer may identify subtle systolic dysfunction even in hypertensive patients with preserved LV chamber function. [ABSTRACT FROM AUTHOR]

BackgroundThe present study examined the inhibitory action of temporary treatment with an angiotensin type 1 (AT1) receptor blocker (ARB) on vascular remodeling using hypertensive mice with overexpression of the human renin (hRN) and angiotensinogen (hANG) genes.MethodshRN/hANG transgenic mice (hRN/hANG-Tg) were treated with an ARB, valsartan, from 4 weeks of age. In some mice, valsartan treatment was stopped at 8 weeks of age (temporary treatment). Inflammatory vascular injury was induced by polyethylene-cuff placement around the femoral artery at the age of 10 weeks.ResultsCompared with wild-type (WT) mice, hRN/hANG-Tg showed higher blood pressure (BP) and enhancement of oxidative stress and medial thickening even before cuff placement. Inflammatory vascular remodeling and oxidative stress after cuff placement were further enhanced in hRN/hANG-Tg. Temporary treatment with valsartan continuously lowered BP even after cessation of administration, and inhibited these changes. In contrast, administration of hydralazine lowered BP to a similar level to that with valsartan, but did not inhibit medial thickening and inflammatory vascular remodeling. In contrast to the valsartan treatment, BP immediately increased to the untreated level after cessation of hydralazine.ConclusionsThese results indicate that temporary ARB treatment leads to prolonged effect of BP lowering and prevents vascular remodeling in hypertensive mice induced by activation of the human renin-angiotensin system. The inhibitory action of valsartan is not due to the BP lowering but is at least in part due to a decrease in oxidative stress and inflammation.American Journal of Hypertension (2011). doi:10.1038/ajh.2011.6 [ABSTRACT FROM AUTHOR]

BackgroundTo explore the metabolic actions of nifedipine on diabetes, we examined glucose intolerance and white adipose tissue changes in type 2 diabetic KK-Ay mice.MethodsMale KK-Ay mice were treated with nifedipine (1.5 mg/kg/day in lab chow) for 5 weeks, which did not affect blood pressure or feeding of KK-Ay mice.ResultsAfter treatment with nifedipine, body weight tended to decrease and the weight of white adipose tissue was reduced. Without food restriction, nifedipine decreased plasma insulin level, while plasma glucose level tended to decrease. In oral glucose tolerance test, nifedipine suppressed the increase in glucose level after a glucose load without affecting plasma insulin concentration. Nifedipine also improved the result of insulin tolerance test. In white adipose tissue, nifedipine increased adipocyte number and the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and adipocyte fatty acid-binding protein related to adipocyte differentiation. In addition, expression of adiponectin, insulin receptor, insulin receptor substrate-1, and glucose transporter type-4 was also increased by nifedipine. Nifedipine also increased the expression of NO synthase in white adipose tissue. Nifedipine did not affect expression of angiotensin II type 1 (AT1) and type 2 (AT2) receptors in white adipose tissue. Such changes in white adipose tissue were apparent in retroperitoneal adipose tissue. Nifedipine did not change the expression of angiotensin receptors, renin receptor, and angiotensinogen in white adipose tissue. Moreover, nifedipine attenuated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and increased superoxide dismutase (SOD) activity in white adipose tissue.ConclusionThese results suggest that nifedipine can enhance insulin sensitivity and reduce white adipose tissue, possibly related to stimulation of adipocyte differentiation.American Journal of Hypertension (2011). doi:10.1038/ajh.2010.198 [ABSTRACT FROM AUTHOR]

BackgroundPrevious reports indicated that blockade of AT1 receptor stimulation attenuated adipocyte dysfunction. However, the effects of AT2 receptor stimulation on adipose tissue were not yet clear. In the present study, we examined the adipose tissue dysfunction in atherosclerotic apolipoprotein E knockout (ApoEKO) mice with AT2 receptor deficiency.MethodsMale ApoEKO and AT2 receptor/ApoE knockout (AT2/ApoEKO) mice at 6 weeks of age were treated with a normal diet or a high-cholesterol diet (HCD: 1.25% cholesterol). Markers for adipocyte differentiation and inflammation in adipose tissue were assayed with real-time reverse-transcription-PCR and western blot.ResultsCompared with ApoEKO mice, AT2/ApoEKO mice with a normal diet showed only a decrease in expression of adiponectin and CCAAT/enhancer binding protein δ (C/EBPδ) in epididymal adipose tissue without changes in body weight, adipose tissue weight, and adipocyte number even at 6 months of age. After HCD for 4 weeks, the weight of both epididymal and retroperitoneal adipose tissue in AT2/ApoEKO mice was greater than that in ApoEKO mice without a change in body weight. Plasma concentrations of cholesterol and fatty acids were higher in AT2/ApoEKO mice than in ApoEKO mice. In adipose tissue of AT2/ApoEKO mice, the adipocyte number was decreased and the expression of peroxisome proliferator–activated receptor γ (PPARγ), C/EBPα, and aP2 was lower than that in ApoEKO mice, in association with an increase in nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity.ConclusionsThese results suggest that AT2 receptor stimulation in adipose tissue is involved in the improvement of adipocyte differentiation and adipose tissue dysfunction in atherosclerotic model.American Journal of Hypertension 2009; doi:10.1038/ajh.2009.85American Journal of Hypertension 2009; 22, 7, 784–791. doi:10.1038/ajh.2009.85 [ABSTRACT FROM AUTHOR]

This article discusses the role of continuous activation of the renin-angiotensin system in the development of dementia and other cognitive disorders. Observed increases in superoxide anion production and decreases in the cerebral blood flow of mice with renin-angiotensin system disorders are noted. The relationship between treating the renin-angiotensin disorder and the recovery of cognitive function when these mice were treated with Tempol, olmesartan, and hydralazine is noted.

BackgroundA combination of different types of antihypertensive drugs is widely used for the treatment of hypertension. We examined the inhibitory effects of a combination of an AT1 receptor blocker (ARB), olmesartan, with various calcium channel blockers (CCBs) on inflammatory vascular remodeling.MethodsInflammatory vascular remodeling was induced by polyethylene-cuff placement around the femoral artery of C57BL/6J mice at 10 weeks of age. Olmesartan (0.5 mg/kg/day) was administered intraperitoneally using an osmotic minipump. CCBs (nifedipine 1.0 mg/kg/day, amlodipine 0.1 mg/kg/day, azelnidipine 0.1 mg/kg/day), and hydrochlorothiazide (HCTZ 0.5 mg/kg/day) were administered orally.ResultsIn the injured artery, superoxide anion production and expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits p47phox and Rac-1 were markedly increased, together with expression of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor (TNF)-α. Administration of a single drug alone at each concentration did not significantly inhibit these changes in the injured artery. However, a combination of olmesartan with various CCBs inhibited neointimal formation as well as oxidative stress and inflammatory markers in the injured artery. Moreover, among these CCBs, inhibition of these markers by olmesartan with azelnidipine was stronger than that caused by a combination with other CCBs. On the other hand, a combination of subeffective doses of olmesartan and HCTZ did not significantly affect vascular changes after cuff placement.ConclusionsThese results suggest that the combination of ARB with CCB synergistically inhibits vascular remodeling and that the inhibitory actions of ARB on vascular remodeling may vary depending on the combined CCB.American Journal of Hypertension (2009). doi:10.1038/ajh.2008.344American Journal of Hypertension (2009); 22, 2, 145–150. doi:10.1038/ajh.2008.344 [ABSTRACT FROM AUTHOR]