Amir Lerman

Sun Yat-Sen University, Shengcheng, Guangdong, China

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Publications (590)4495.52 Total impact

  • Circulation Cardiovascular Imaging 12/2015; 8(1). DOI:10.1161/CIRCIMAGING.114.002636 · 6.75 Impact Factor
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    ABSTRACT: Myocardial perfusion scintigraphy (MPS) is used widely to assess cardiovascular risk in patients with chest pain. The utility of carotid intima-media thickness (CIMT) and endothelial function as assessed by reactive hyperemia-peripheral arterial tonometry index (RHI) in risk stratifying patients with angina-like symptoms needs to be defined. We investigated whether the addition of CIMT and RHI to Framingham Cardiovascular Risk Score (FCVRS) and MPS improves comprehensive cardiovascular risk prediction in patients presenting with angina-like symptoms. We enrolled 343 consecutive patients with angina-like symptoms suspected of having stable angina. MPS, CIMT, and RHI were performed and patients were followed for cardiovascular events for a median of 5.3years (range 4.4-6.2). Patients were stratified by FCVRS and MPS. During the follow-up, 57 patients (16.6%) had cardiovascular events. Among patients without perfusion defect, low RHI was significantly associated with cardiovascular events in the intermediate and high FCVRS groups (hazard ratio (HR) [95% confidence interval (CI)] of RHI≤2.11 was 6.99 [1.34-128] in the intermediate FCVRS group and 6.08 [1.08-114] in the high FCVRS group). Furthermore, although MPS did not predict, only RHI predicted hard cardiovascular events (cardiovascular death, myocardial infarction, and stroke) independent from FCVRS, and adding RHI to FCVRS improved net reclassification index (20.9%, 95% CI 0.8-41.1, p=0.04). Especially, RHI was significantly associated with hard cardiovascular events in the high FCVRS group (HR [95% CI] of RHI≤1.93 was 5.66 [1.54-36.4], p=0.007). Peripheral endothelial function may improve discrimination in identifying at-risk patients for future cardiovascular events when added to FCVRS-MPS-based risk stratification. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    International journal of cardiology 07/2015; 190. DOI:10.1016/j.ijcard.2015.04.124 · 6.18 Impact Factor
  • Journal of the American College of Cardiology 06/2015; 65(23):2478-2480. DOI:10.1016/j.jacc.2015.04.032 · 15.34 Impact Factor
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    ABSTRACT: Obesity and hypertension are major risk factors for cardiovascular diseases, and their growing coexistence accounts for an increase in adverse cardiac events, but the mechanisms are yet to be determined. We hypothesized that obesity exacerbates mitochondrial dysregulation imposed by hypertension and augments left ventricular dysfunction. Obesity-prone Ossabaw pigs were randomized to lean (standard diet) and obese (high-fat diet), without (Lean-sham and Obese-sham) or with renovascular hypertension (Lean-hypertension and Obese-hypertension), induced after 12 weeks of diet (n=7 each). Cardiac function, myocardial perfusion and oxygenation, and microvascular remodeling were assessed 4 weeks later. Mitochondrial biogenesis signals and structural proteins, respiratory chain complex activities, and mitochondrial self-degradation were examined, as was fibrosis. Obesity alone exerted no apparent effect on mitochondrial dynamics, but aggravated in hypertensive hearts the reduction of mitochondrial proteins, deoxyribonucleic acid content, and respiratory chain complex IV subunits activity, and amplified mitochondrial self-degradation. Synergistic interaction of obesity with hypertension also exacerbated myocardial fibrosis and left ventricular diastolic dysfunction. Mitochondrial content, respiratory chain complex IV subunits activity, and mitophagy were correlated with myocardial fibrosis. These findings suggest that obesity aggravates in renovascular hypertension cardiac mitochondrial aberrations. Mitochondrial function may regulate the progression of cardiac injury and functional deterioration in hypertension concomitant with obesity. © 2015 American Heart Association, Inc.
    Hypertension 06/2015; DOI:10.1161/HYPERTENSIONAHA.115.05478 · 7.63 Impact Factor
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    ABSTRACT: Cardiac rehabilitation (CR) following myocardial infarction is vastly underused. As such, the aim of this study was to test a digital health intervention (DHI) as an adjunct to CR. Patients undergoing standard Mayo Clinic CR were recruited prior to CR (n = 25) or after 3 months CR (n = 17). Changes in risk factors and rehospitalizations plus emergency department (ED) visits were assessed after 3 months. Patients assigned to DHI during CR had significant reductions in weight (-4.0 ± 5.2 kg, P = .001), blood pressure (-10.8 ± 13.5 mmHg, P = .0009), and the group using DHI after 3 months of CR had significant reductions in weight (-2.5 ± 3.8 kg, P = .04) and systolic BP (-12.6 ± 12.4 mmHg, P = .001) compared to the control groups. Both DHI groups also displayed significant reductions in rehospitalizations/ED visits (-37.9 %, P = 0.01 and -28 %, P = .04, respectively). This study suggests that a guideline-driven DHI CR program can augment secondary prevention strategies during usual CR by improving risk factors for repeat events.
    Journal of Cardiovascular Translational Research 05/2015; DOI:10.1007/s12265-015-9629-1 · 2.69 Impact Factor
  • JACC. Cardiovascular Interventions 05/2015; 8(6):834-6. DOI:10.1016/j.jcin.2014.12.245 · 7.44 Impact Factor
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    ABSTRACT: The purpose of this study was to assess the diagnostic accuracy of the instantaneous wave-free ratio (iFR) to characterize, outside of a pre-specified range of values, stenosis severity, as defined by fractional flow reserve (FFR) ≤0.80, in a prospective, independent, controlled, core laboratory-based environment. Studies with methodological heterogeneity have reported some discrepancies in the classification agreement between iFR and FFR. The ADVISE II (ADenosine Vasodilator Independent Stenosis Evaluation II) study was designed to overcome limitations of previous iFR versus FFR comparisons. A total of 919 intermediate coronary stenoses were investigated during baseline and hyperemia. From these, 690 pressure recordings (n = 598 patients) met core laboratory physiology criteria and are included in this report. The pre-specified iFR cut-off of 0.89 was optimal for the study and correctly classified 82.5% of the stenoses, with a sensitivity of 73.0% and specificity of 87.8% (C statistic: 0.90 [95% confidence interval (CI): 0.88 to 0.92, p < 0.001]). The proportion of stenoses properly classified by iFR outside of the pre-specified treatment (≤0.85) and deferral (≥0.94) values was 91.6% (95% CI: 88.8% to 93.9%). When combined with FFR use within these cut-offs, the percent of stenoses properly classified by such a pre-specified hybrid iFR-FFR approach was 94.2% (95% CI: 92.2% to 95.8%). The hybrid iFR-FFR approach obviated vasodilators from 65.1% (95% CI: 61.1% to 68.9%) of patients and 69.1% (95% CI: 65.5% to 72.6%) of stenoses. The ADVISE II study supports, on the basis rigorous methodology, the diagnostic value of iFR in establishing the functional significance of coronary stenoses, and highlights its complementariness with FFR when used in a hybrid iFR-FFR approach. (ADenosine Vasodilator Independent Stenosis Evaluation II-ADVISE II; NCT01740895). Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
    JACC. Cardiovascular Interventions 05/2015; 8(6):824-33. DOI:10.1016/j.jcin.2015.01.029 · 7.44 Impact Factor
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    ABSTRACT: We currently face a myriad of grand global challenges in fields such as poverty, the environment, education, science, and medicine. However, our current means of dealing with such challenges has fallen short, and ingenious solutions are required to overcome the inherent resistance to progress toward ameliorating such difficulties. Here, we highlight the promises and challenges of international collaboration in achieving success toward these trials. We note prior successes in fields such as education, medicine, science, and environmental issues made to date, yet at the same time we do note deficiencies and shortcomings in these efforts. Hence, the notion of international collaboration should be strengthened and encouraged by governments, non-profit organizations, and others moving forward using creative means to bring talented teams together to tackle these challenges across the globe.
    04/2015; 6(2):e0012. DOI:10.5041/RMMJ.10196
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    ABSTRACT: Left ventricular (LV) hypertrophy (LVH) plays an important role in hypertensive heart disease, and may be accompanied by myocardial autophagy. However, the pattern of autophagy during evolution of LVH is unclear. We hypothesized that autophagy activation indicates advancing cardiac LVH with tissue remodeling. Ten domestic pigs with a 10-week unilateral renovascular hypertension (HTN) were classified as mild or moderate HTN (n = 5 each group) based on the degree of renal artery stenosis (above or below 75%). Seven normal pigs served as controls. Left ventricular remodeling, function, and microvascular density were assessed using multi-detector- and micro-computed tomography and histology. Markers of myocardial autophagic and endoplasmic reticulum (ER) stress-related unfolded protein response (UPR), apoptosis, and fibrosis were examined ex vivo. Both HTN groups had increased myocyte cross-sectional area, but it was greater in moderate HTN, accompanied by elevated LV muscle-mass. Moderate, but not mild HTN, also showed impaired microvascular density and impaired myocardial perfusion. Autophagy mediators were unaltered in mild HTN but UPR markers were increased, while in moderate HTN they were all upregulated, whereas UPR markers were suppressed. Myocardial apoptosis and fibrosis were also greater in moderate HTN. Autophagic proteins were correlated with LVH and fibrosis. Autophagic activity is stimulated during the exacerbation of LVH, following a transient early increase in ER stress, and may be involved in the progression of cardiac remodeling in renovascular hypertensive heart disease. © American Journal of Hypertension, Ltd 2015. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
    American Journal of Hypertension 04/2015; DOI:10.1093/ajh/hpv057 · 3.40 Impact Factor
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    ABSTRACT: To assess the potential benefit of digital health interventions (DHIs) on cardiovascular disease (CVD) outcomes (CVD events, all-cause mortality, hospitalizations) and risk factors compared with non-DHIs. We conducted a systematic search of PubMed, MEDLINE, EMBASE, Web of Science, Ovid, CINHAL, ERIC, PsychINFO, Cochrane, and Cochrane Central Register of Controlled Trials for articles published from January 1, 1990, through January 21, 2014. Included studies examined any element of DHI (telemedicine, Web-based strategies, e-mail, mobile phones, mobile applications, text messaging, and monitoring sensors) and CVD outcomes or risk factors. Two reviewers independently evaluated study quality utilizing a modified version of the Cochrane Collaboration risk assessment tool. Authors extracted CVD outcomes and risk factors for CVD such as weight, body mass index, blood pressure, and lipid levels from 51 full-text articles that met validity and inclusion criteria. Digital health interventions significantly reduced CVD outcomes (relative risk, 0.61; 95% CI, 0.46-0.80; P<.001; I(2)=22%). Concomitant reductions in weight (-2.77 lb [95% CI, -4.49 to -1.05 lb]; P<.002; I(2)=97%) and body mass index (-0.17 kg/m(2) [95% CI, -0.32 kg/m(2) to -0.01 kg/m(2)]; P=.03; I(2)=97%) but not blood pressure (-1.18 mm Hg [95% CI, -2.93 mm Hg to 0.57 mm Hg]; P=.19; I(2)=100%) were found in these DHI trials compared with usual care. In the 6 studies reporting Framingham risk score, 10-year risk percentages were also significantly improved (-1.24%; 95% CI, -1.73% to -0.76%; P<.001; I(2)=94%). Results were limited by heterogeneity not fully explained by study population (primary or secondary prevention) or DHI modality. Overall, these aggregations of data provide evidence that DHIs can reduce CVD outcomes and have a positive impact on risk factors for CVD. Copyright © 2015 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved.
    Mayo Clinic Proceedings 04/2015; 90(4):469-480. DOI:10.1016/j.mayocp.2014.12.026 · 5.81 Impact Factor
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    ABSTRACT: Objectives: This study sought to evaluate adventitial vasa vasorum (VV) in vivo with novel imaging technique of optical coherence tomography (OCT). Methods:To verify OCT methods for quantification of VV, we first studied 2 swine carotid arteries in a model of focal angiogenesis by autologous blood injection, and compared microchannel volume (MCV) by OCT and VV by m-CT, and counts of those. In OCT images, adventitial MC was identified as signalvoiding areas which were located within 1 mm from the lumen-intima border. After manually tracing microchannel areas and the boundaries of lumen-intima and media-adventitial in all slices, we reconstructed 3D images. Moreover, we performed with OCT imaging in 8 recipients referred for evaluation of cardiac allograft vasculopathy at 1 year after heart transplantation. MCV and plaque volume (PV) were assessed with 3D images in each 10-mm-segment. Results: In the animal study, among the 16 corresponding 1-mm-segments, there were significant correlations of count and volume between both the modalities (count r(2) = 0.80, P < 0.01; volume r(2) = 0.50, P < 0.01) and a good agreement with a systemic bias toward underestimation with m-CT. In the human study, there was a significant positive correlation between MCV and PV (segment number = 24, r(2) = 0.63, P < 0.01). Conclusion: Our results suggest that evaluation of MCV with 3D OCT imaging might be a novel method to estimate the amount of adventitial VV in vivo, and further has the potential to provide a pathophysiological insight into a role of the VV in allograft vasculopathy.
    Atherosclerosis 03/2015; 239(1). DOI:10.1016/j.atherosclerosis.2015.01.016 · 3.97 Impact Factor
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    ABSTRACT: Medically refractory angina remains a significant health concern despite major advances in revascularization techniques and emerging medical therapies. We aimed to determine the safety and efficacy of extracorporeal shockwave myocardial therapy (ESMT) in managing angina pectoris. A single-arm multicenter prospective study was designed aiming to determine the safety and efficacy of ESMT. Patients of functional Canadian Cardiovascular Society class II-IV, despite stable and optimal medical management, with documented myocardial segments with reversible ischemia and/or hibernation on the basis of echocardiography/single-photon emission computerized tomography (SPECT) were enrolled from 2010 to 2012. A total of 111 patients were enrolled, 33 from Indonesia, 21 from Malaysia, and 57 from Philippines. Patients underwent nine cycles of ESMT over 9 weeks. Patients were followed up for 3-6 months after ESMT treatment. During follow-up, patients were subjected to clinical evaluation, the Seattle Angina Questionnaire, assessment of nitrate intake, the 6-min walk test, echocardiography, and SPECT. The mean age of the population was 62.9±10.9 years. The summed difference score on pharmacologically induced stress SPECT improved from 9.53±17.87 at baseline to 7.77±11.83 at follow-up (P=0.0086). Improvement in the total Seattle Angina Questionnaire score was seen in 83% of patients (P<0.0001). Sublingual nitroglycerin use significantly decreased (1.14±1.01 tablets per week at baseline to 0.52±0.68 tablets per week at follow-up; P=0.0215). There were no changes in left ventricular function on echocardiography (0.33±9.97, P=0.93). The Canadian Cardiovascular Society score improved in 74.1% of patients. This multicenter prospective trial demonstrated that ESMT is both a safe and an efficacious means of managing medically refractory angina.
    Coronary Artery Disease 03/2015; 26(3). DOI:10.1097/MCA.0000000000000218 · 1.30 Impact Factor
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    ABSTRACT: Over the past decades, secondary prevention of cardiovascular (CV) disease has improved and considerably reduced mortality rates. However, there remains a high-rate of new or recurrent CV events in those with established atherosclerotic vascular diseases. Although most of the prevailing therapies target the conventional risk factors, there is notable interindividual heterogeneity in adaptation to risk factors and response to therapies, which affects efficacy. It is desirable to have a methodology for directly assessing the functional significance of atherogenesis, and for managing individual patients based on their comprehensive vascular health. Endothelial function plays a pivotal role in all stages of atherosclerosis, from initiation to atherothrombotic complication. Endothelial function reflects the integrated effect of all the atherogenic and atheroprotective factors present in an individual, and is therefore regarded as an index of active disease process and a significant risk factor for future CV events. Moreover, improvement in endothelial function is associated with decreased risk of CV events, even in the secondary prevention setting. The introduction of endothelial function assessment into clinical practice may trigger the development of a more tailored and personalized medicine and improve patient outcomes. In this review, we summarize current knowledge on the contribution of endothelial dysfunction to atherosclerotic CV disease in the secondary prevention setting. Finally, we focus on the potential of an endothelial function-guided management strategy in secondary prevention.
    Circulation Journal 02/2015; 79(4). DOI:10.1253/circj.CJ-15-0068 · 3.69 Impact Factor
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    ABSTRACT: Heart valve tissue engineering is a promising alternative to prostheses for the replacement of diseased or damaged heart valves, because tissue-engineered valves have the ability to remodel, regenerate and grow. To engineer heart valves, cells are harvested, seeded onto or into a three-dimensional (3D) matrix platform to generate a tissue-engineered construct in vitro, and then implanted into a patient's body. Successful engineering of heart valves requires a thorough understanding of the different types of cells that can be used to obtain the essential phenotypes that are expressed in native heart valves. This article reviews different cell types that have been used in heart valve engineering, cell sources for harvesting, phenotypic expression in constructs and suitability in heart valve tissue engineering. Natural and synthetic biomaterials that have been applied as scaffold systems or cell-delivery platforms are discussed with each cell type. Copyright © 2015 John Wiley & Sons, Ltd. Copyright © 2015 John Wiley & Sons, Ltd.
    Journal of Tissue Engineering and Regenerative Medicine 02/2015; DOI:10.1002/term.2010 · 4.43 Impact Factor
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    ABSTRACT: Background:Patients with heart failure (HF) have abnormal endothelial function. Although use of a continuous flow left ventricular assist device (CF-LVAD) results in significant hemodynamic improvement, the effects on systemic endothelial function are unclear.Methods and Results:Eighteen HF patients with CF-LVAD implantation were included in this prospective observational study. We measured reactive hyperemia index (RHI) before and after CF-LVAD implantation to evaluate sequential changes in endothelial function. Patients were followed clinically for the occurrence of adverse cardiovascular events, a composite of death, thrombosis, bleeding, HF, renal failure, and arrhythmia. Preoperative RHI was 1.77±0.39. Early in the postoperative period (7-14 days after operation) RHI significantly decreased to 1.19±0.31 (P<0.001, compared with preoperative RHI). At first and second follow-up (4-6 weeks and 3-7 months after operation) RHI remained lower at 1.48±0.50 (P=0.030) and 1.26±0.37 (P=0.002), respectively, compared with preoperative RHI. The decrease in early postoperative RHI relative to preoperative RHI was significantly associated with adverse cardiovascular events after CF-LVAD (age-adjusted risk ratio for 0.25 decrease in RHI, 1.35; 95% confidence interval: 1.13-1.62, P=0.001).Conclusions:Peripheral endothelial function had a significant and persistent decline up to 5 months following implantation of CF-LVAD, and this decline was associated with adverse cardiovascular events. These findings may provide insight into some of the vascular complications following CF-LVAD in HF patients.
    Circulation Journal 01/2015; 79(4). DOI:10.1253/circj.CJ-14-1079 · 3.69 Impact Factor
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    ABSTRACT: Percutaneous transluminal renal angioplasty (PTRA) fails to fully improve cardiac injury and dysfunction in patients with renovascular hypertension (RVH). Mesenchymal stem cells (MSCs) restore renal function, but their potential for attenuating cardiac injury after reversal of RVH has not been explored. We hypothesized that replenishment of MSCs during PTRA would improve cardiac function and oxygenation, and decrease myocardial injury in porcine RVH. Pigs were studied after 16 weeks of RVH, RVH treated 4 weeks earlier with PTRA with or without adjunct intra-renal delivery of MSC (10^6 cells), and controls. Cardiac structure, function (fast-computed tomography (CT)), and myocardial oxygenation (Blood-Oxygen-Level-Dependent- magnetic resonance imaging) were assessed in-vivo. Myocardial microvascular density (micro-CT) and myocardial injury were evaluated ex-vivo. Kidney venous and systemic blood levels of inflammatory markers were measured and their renal release calculated. PTRA normalized blood pressure, yet stenotic-kidney glomerular filtration rate, similarly blunted in RVH and RVH + PTRA, normalized only in PTRA + MSC-treated pigs. PTRA attenuated left ventricular remodeling, whereas myocardial oxygenation, subendocardial microvascular density, and diastolic function remained decreased in RVH + PTRA, but normalized in RVH + PTRA-MSC. Circulating isoprostane levels and renal release of inflammatory cytokines increased in RVH and RVH + PTRA, but normalized in RVH + PTRA-MSC, as did myocardial oxidative stress, inflammation, collagen deposition, and fibrosis. Intra-renal MSC delivery during PTRA preserved stenotic-kidney function, reduced systemic oxidative stress and inflammation, and thereby improved cardiac function, oxygenation, and myocardial injury four weeks after revascularization, suggesting a therapeutic potential for adjunctive MSC delivery to preserve cardiac function and structure after reversal of experimental RVH.
    Stem Cell Research & Therapy 01/2015; 6(1):7. DOI:10.1186/scrt541 · 4.63 Impact Factor
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    ABSTRACT: The ubiquitin-proteasome system (UPS) is an integral part of the protein metabolism and protein quality control in eukaryotic cells. It is involved in a number of biological processes of significance for vascular biology and pathology such as oxidative stress, inflammation, foam cell formation, and apoptosis. This review summarizes both indirect and direct lines of evidence for a role of the UPS in atherosclerosis from the initiation to the progression and complication stage and concludes with a future perspective.
    01/2015; 5(1):83-100.
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    ABSTRACT: Over the last 50 years medicine and technology have progressed to the point where it has become commonplace to safely replace damaged or diseased heart valves with mechanical and biological prostheses. Despite the advancements in technology current valve substitutes continue to have significant limitations with regards to thrombogenicity, durability, and inability to grow or remodel. In an attempt to overcome the limitations of currently available valve prosthesis, heart valve tissue engineering has emerged as a promising technique to produce biological valve substitutes. Currently, the field of tissue engineering is focused on delivering complex matrices which include scaffolds and cells separately or together to the damaged site. Additional functional enhancement of the matrices by exposing encoded biological signals to their residing cells in a controlled manner has the potential to augment the tissue engineering approach. This review provides an overview of the delivery of biological reagents to guide and regulate heart valve tissue engineering.
    Journal of Controlled Release 12/2014; 196. DOI:10.1016/j.jconrel.2014.10.009 · 7.26 Impact Factor
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    ABSTRACT: Occlusive renovascular disease and hypertension may progress to CKD. Circulating levels of several biomarkers, including fibroblast growth factor (FGF)-23, Klotho, and soluble urokinase plasminogen activator receptor (suPAR), are altered in patients with CKD, but their role in essential hypertension (EH) and renovascular hypertension (RVH) remains unclear. Levels of FGF-23, Klotho, suPAR, plasminogen activator inhibitor (PAI)-1, tissue factor, and tissue factor pathway inhibitor (TFI) were measured in the inferior vena cava and renal vein of hypertensive patients with atherosclerotic renal artery stenosis (n=12) or age-matched participants with EH (n=12) and relatively preserved renal function. Single-kidney blood flow was measured to calculate renal release of markers. For control, peripheral vein levels were measured in healthy volunteers (HVs; n=12). FGF-23 levels did not differ among the groups, whereas Klotho levels were lower in participants with RVH and EH than in HVs, and suPAR levels were elevated in patients with RVH compared with HVs and patients with EH (6.1±1.5 versus 4.4±1.9 and 3.2±1.2 ng/ml, P<0.05). PAI-1 levels were higher in patients with RVH than in patients with EH, but tissue factor and TFI levels were not statistically significantly different. After adjustment for GFR, Klotho levels remained decreased in both RVH and EH, and suPAR and PAI-1 levels remained elevated in RVH. eGFR correlated inversely with systemic and renal vein suPAR levels, and directly with systemic Klotho levels. Klotho levels are low in hypertensive patients, whereas suPAR and PAI-1 levels are specifically elevated in RVH, correlating with GFR. Klotho, PAI-1, and suPAR may be markers of kidney injury in hypertensive patients. Copyright © 2014 by the American Society of Nephrology.
    Clinical Journal of the American Society of Nephrology 12/2014; 10(3). DOI:10.2215/CJN.07290714 · 5.25 Impact Factor
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    ABSTRACT: Autoimmune rheumatic diseases can affect the cardiac vasculature, valves, myocardium, pericardium, and conduction system, leading to a plethora of cardiovascular manifestations that can remain clinically silent or lead to substantial cardiovascular morbidity and mortality. Although the high risk of cardiovascular pathology in patients with autoimmune inflammatory rheumatological diseases is not owing to atherosclerosis alone, this particular condition contributes substantially to cardiovascular morbidity and mortality-the degree of coronary atherosclerosis observed in patients with rheumatic diseases can be as accelerated, diffuse, and extensive as in patients with diabetes mellitus. The high risk of atherosclerosis is not solely attributable to traditional cardiovascular risk factors: dysfunctional immune responses, a hallmark of patients with rheumatic disorders, are thought to cause chronic tissue-destructive inflammation. Prompt recognition of cardiovascular abnormalities is needed for timely and appropriate management, and aggressive control of traditional risk factors remains imperative in patients with rheumatic diseases. Moreover, therapies directed towards inflammatory process are crucial to reduce cardiovascular disease morbidity and mortality. In this Review, we examine the multiple cardiovascular manifestations in patients with rheumatological disorders, their underlying pathophysiology, and available management strategies, with particular emphasis on the vascular aspects of the emerging field of 'cardiorheumatology'.
    Nature Reviews Cardiology 12/2014; 12(3). DOI:10.1038/nrcardio.2014.206 · 10.15 Impact Factor

Publication Stats

22k Citations
4,495.52 Total Impact Points

Institutions

  • 2013–2015
    • Sun Yat-Sen University
      • Department of Vascular Surgery
      Shengcheng, Guangdong, China
    • Capital Medical University
      • Department of Cardiology
      Beijing, Beijing Shi, China
  • 1991–2015
    • Mayo Clinic - Rochester
      • • Department of Cardiovascular Diseases
      • • Department of Internal Medicine
      • • Department of Cardiovascular Surgery
      Рочестер, Minnesota, United States
  • 2012
    • University of California, Los Angeles
      Los Angeles, California, United States
  • 2004–2012
    • Rochester College
      Rochester, New York, United States
  • 2011
    • University of Florida
      Gainesville, Florida, United States
  • 2010
    • Gachon University
      Sŏngnam, Gyeonggi Province, South Korea
  • 2002–2009
    • University of Minnesota Rochester
      Rochester, Minnesota, United States
  • 2008
    • Duke University Medical Center
      Durham, North Carolina, United States
    • Vanderbilt University
      Нашвилл, Michigan, United States
  • 2006–2008
    • Boston University
      Boston, Massachusetts, United States
    • Konyang University Hospital
      Gaigeturi, Jeju-do, South Korea
    • University of Southern California
      • Division of Cardiovascular Medicine
      Los Angeles, CA, United States
  • 2007
    • University of Mississippi
      • Department of Physiology and Biophysics
      Mississippi, United States
    • Minnesota State University, Mankato
      • Department of Biological Sciences
      MKT, Minnesota, United States
  • 2003–2007
    • Università degli Studi di Salerno
      Fisciano, Campania, Italy
    • Technion - Israel Institute of Technology
      H̱efa, Haifa District, Israel
  • 2003–2006
    • Aarhus University
      Aarhus, Central Jutland, Denmark
  • 2005
    • University of Birmingham
      Birmingham, England, United Kingdom
  • 2002–2003
    • University of California, San Diego
      • Department of Medicine
      San Diego, California, United States
    • Second University of Naples
      Caserta, Campania, Italy
  • 1998–2000
    • Mayo Foundation for Medical Education and Research
      • • Department of Internal Medicine
      • • Division of Cardiovascular Diseases
      Rochester, MI, United States
    • University of Zurich
      Zürich, Zurich, Switzerland
    • University of Rome Tor Vergata
      Roma, Latium, Italy
  • 1999
    • Yonsei University
      • Department of Internal Medicine
      Seoul, Seoul, South Korea
  • 1995
    • Tel Aviv University
      Tell Afif, Tel Aviv, Israel