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Hypertension - recientes

Novel Blood Pressure Locus and Gene Discovery Using Genome-Wide Association Study and Expression Data Sets From Blood and the KidneyNovelty and Significance [Genomics]
9/8/2017
Louise V. Wain, Ahmad Vaez, Rick Jansen, Roby Joehanes, Peter J. van der Most, A. Mesut Erzurumluoglu, Paul F. O’Reilly, Claudia P. Cabrera, Helen R. Warren, Lynda M. Rose, Germaine C. Verwoert, Jouke–Jan Hottenga, Rona J. Strawbridge, Tonu Esko, Dan E. Arking, Shih–Jen Hwang, Xiuqing Guo, Zoltan Kutalik, Stella Trompet, Nick Shrine, Alexander Teumer, Janina S. Ried, Joshua C. Bis, Albert V. Smith, Naȷaf Amin, Ilȷa M. Nolte, Leo–Pekka Lyytikainen, Anubha Mahaȷan, Nicholas J. Wareham, Edith Hofer, Peter K. Joshi, Kati Kristiansson, Michela Traglia, Aki S. Havulinna, Anuȷ Goel, Mike A. Nalls, Siim Sober, Dragana Vuckovic, Jian’an Luan, Fabiola Del Greco M., Kristin L. Ayers, Jaume Marrugat, Daniela Ruggiero, Lorna M. Lopez, Teemu Niiranen, Stefan Enroth, Anne U. Jackson, Christopher P. Nelson, Jennifer E. Huffman, Weihua Zhang, Jonathan Marten, Ilaria Gandin, Sarah E. Harris, Tatiȷana Zemunik, Yingchang Lu, Evangelos Evangelou, Nabi Shah, Martin H. de Borst, Massimo Mangino, Bram P. Prins, Archie Campbell, Ruifang Li–Gao, Ganesh Chauhan, Christopher Oldmeadow, Goncalo Abecasis, Maryam Abedi, Caterina M. Barbieri, Michael R. Barnes, Chiara Batini, John Beilby, BIOS Consortium, Tineka Blake, Michael Boehnke, Erwin P. Bottinger, Peter S. Braund, Morris Brown, Marco Brumat, Harry Campbell, John C. Chambers, Massimiliano Cocca, Francis Collins, John Connell, Heather J. Cordell, Jeffrey J. Damman, Gail Davies, Eco J. de Geus, Renee de Mutsert, Joris Deelen, Yusuf Demirkale, Alex S.F. Doney, Marcus Dorr, Martin Farrall, Teresa Ferreira, Mattias Franberg, He Gao, Vilmantas Giedraitis, Christian Gieger, Franco Giulianini, Alan J. Gow, Anders Hamsten, Tamara B. Harris, Albert Hofman, Elizabeth G. Holliday, Jennie Hui, Marȷo–Riitta Jarvelin, Asa Johansson, Andrew D. Johnson, Pekka Jousilahti, Antti Jula, Mika Kahonen, Sekar Kathiresan, Kay–Tee Khaw, Ivana Kolcic, Seppo Koskinen, Claudia Langenberg, Marty Larson, Lenore J. Launer, Benȷamin Lehne, David C.M. Liewald, Li Lin, Lars Lind, Francois Mach, Chrysovalanto Mamasoula, Cristina Menni, Borbala Mifsud, Yuri Milaneschi, Anna Morgan, Andrew D. Morris, Alanna C. Morrison, Peter J. Munson, Priyanka Nandakumar, Quang Tri Nguyen, Teresa Nutile, Albertine J. Oldehinkel, Ben A. Oostra, Elin Org, Sandosh Padmanabhan, Aarno Palotie, Guillaume Pare, Alison Pattie, Brenda W.J.H. Penninx, Neil Poulter, Peter P. Pramstaller, Olli T. Raitakari, Meixia Ren, Kenneth Rice, Paul M. Ridker, Harriette Riese, Samuli Ripatti, Antonietta Robino, Jerome I. Rotter, Igor Rudan, Yasaman Saba, Aude Saint Pierre, Cinzia F. Sala, Antti–Pekka Sarin, Reinhold Schmidt, Rodney Scott, Marc A. Seelen, Denis C. Shields, David Siscovick, Rossella Sorice, Alice Stanton, David J. Stott, Johan Sundstrom, Morris Swertz, Kent D. Taylor, Simon Thom, Ioanna Tzoulaki, Christophe Tzourio, Andre G. Uitterlinden, Understanding Society Scientific Group, Uwe Volker, Peter Vollenweider, Sarah Wild, Gonneke Willemsen, Alan F. Wright, Jie Yao, Sebastien Theriault, David Conen, John Attia, Peter Sever, Stephanie Debette, Dennis O. Mook–Kanamori, Eleftheria Zeggini, Tim D. Spector, Pim van der Harst, Colin N.A. Palmer, Anne–Claire Vergnaud, Ruth J.F. Loos, Ozren Polasek, John M. Starr, Giorgia Girotto, Caroline Hayward, Jaspal S. Kooner, Cecila M. Lindgren, Veronique Vitart, Nilesh J. Samani, Jaakko Tuomilehto, Ulf Gyllensten, Paul Knekt, Ian J. Deary, Marina Ciullo, Roberto Elosua, Bernard D. Keavney, Andrew A. Hicks, Robert A. Scott, Paolo Gasparini, Maris Laan, YongMei Liu, Hugh Watkins, Catharina A. Hartman, Veikko Salomaa, Daniela Toniolo, Markus Perola, James F. Wilson, Helena Schmidt, Jing Hua Zhao, Terho Lehtimaki, Cornelia M. van Duiȷn, Vilmundur Gudnason, Bruce M. Psaty, Annette Peters, Rainer Rettig, Alan James, J. Wouter Jukema, David P. Strachan, Walter Palmas, Andres Metspalu, Erik Ingelsson, Dorret I. Boomsma, Oscar H. Franco, Murielle Bochud, Christopher Newton–Cheh, Patricia B. Munroe, Paul Elliott, Daniel I. Chasman, Aravinda Chakravarti, Joanne Knight, Andrew P. Morris, Daniel Levy, Martin D. Tobin, Harold Snieder, Mark J. Caulfield, Georg B. Ehret
ver resumen
Elevated blood pressure is a major risk factor for cardiovascular disease and has a substantial genetic contribution. Genetic variation influencing blood pressure has the potential to identify new pharmacological targets for the treatment of hypertension. To discover additional novel blood pressure loci, we used 1000 Genomes Project–based imputation in 150 134 European ancestry individuals and sought significant evidence for independent replication in a further 228 245 individuals. We report 6 new signals of association in or near HSPB7, TNXB, LRP12, LOC283335, SEPT9, and AKT2, and provide new replication evidence for a further 2 signals in EBF2 and NFKBIA. Combining large whole-blood gene expression resources totaling 12 607 individuals, we investigated all novel and previously reported signals and identified 48 genes with evidence for involvement in blood pressure regulation that are significant in multiple resources. Three novel kidney-specific signals were also detected. These robustly implicated genes may provide new leads for therapeutic innovation.

Moving Beyond Office Blood Pressure to Achieve a Personalized and More Precise Hypertension Management [Role of Office Blood Pressure in Diagnosis and Treatment of Hypertension]
9/8/2017
Gianfranco Parati, Juan Eugenio Ochoa, Grzegorz Bilo
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Correction to: Case of Asymptomatic Carotid Artery Stenosis in a Hypertensive Patient [Corrections]
9/8/2017
ver resumen

Clinical Implications [Clinical Implications]
9/8/2017
ver resumen

Acknowledgment of Reviewers [Acknowledgment of Reviewers]
9/8/2017
ver resumen

Recent Advances in Neurogenic Hypertension [Recent Advances in Hypertension]
9/8/2017
Sean D. Stocker, Brian J. Kinsman, Alan F. Sved
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Report of the National Heart, Lung, and Blood Institute Working Group on the Role of Microbiota in Blood Pressure Regulation [Brief Reviews]
9/8/2017
Mohan K. Raizada, Bina Joe, Nathan S. Bryan, Eugene B. Chang, Floyd E. Dewhirst, Gary G. Borisy, Zorina S. Galis, Wendy Henderson, Pedro A. Jose, Christian J. Ketchum, Johanna W. Lampe, Carl J. Pepine, Jennifer L. Pluznick, Dominic Raj, Douglas R. Seals, Rachel A. Gioscia-Ryan, W.H. Wilson Tang, Young S. Oh
ver resumen

Early-Life Detection of Hypertension Risks [Editorial Commentary]
9/8/2017
Daniel T. Lackland
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Expanding Clinical Phenotype of Fibromuscular Dysplasia [Editorial Commentary]
9/8/2017
Jeffrey W. Olin
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Development of PKG I{alpha} (Protein Kinase G I{alpha})-Dimerizing Antihypertensive Drugs [Editorial Commentary]
9/8/2017
Paula K. Bautista–Nino, Anton J.M. Roks, A.H. Jan Danser
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Pressure Paradox [Editorial Commentary]
9/8/2017
Michael F. O’Rourke, Audrey Adȷi
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Vitamin D, Hypertension, and Ischemic Stroke [Editorial Commentary]
9/8/2017
Ronen Levi-Vardi, Yoram Yagil
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Vitamin D, Hypertension, and Ischemic Stroke in 116 655 Individuals From the General PopulationNovelty and Significance [Epidemiology/Population]
9/8/2017
Shoaib Afzal, Borge G. Nordestgaard
ver resumen
Observational studies indicate that low concentrations of plasma 25-hydroxyvitamin D (25(OH)D) are associated with high blood pressure, hypertension, and ischemic stroke. However, whether these associations are causal remain unknown. A total of 116 655 white individuals of Danish descent from the general population were genotyped for genetic variants in DHCR7 and CYP2R1 affecting plasma 25(OH)D concentrations; 35 517 had plasma 25(OH)D measurements. Primary outcomes were blood pressure, hypertension, and ischemic stroke. Median follow-up for incident ischemic stroke was 9.3 years (range, 1 day–33.6 years). DHCR7/CYP2R1 allele score was as expected associated with lower 25(OH)D concentration (F=328 and R2=1.0%). A genetically determined 10 nmol/L lower 25(OH)D concentration was associated with a 0.68 (95% confidence interval [CI], 0.20–1.17) mm Hg higher systolic blood pressure and a 0.36 (95% CI, 0.08–0.63) mm Hg higher diastolic blood pressure with corresponding observational estimates of 0.58 (95% CI, 0.50–0.68) and 0.40 (95% CI, 0.35–0.45) mm Hg. The odds ratio for hypertension was 1.02 (95% CI, 0.97–1.08) for a genetically determined 10 nmol/L lower 25(OH)D with a corresponding observational odds ratio of 1.06 (95% CI, 1.05–1.07). The odds ratio for ischemic stroke was 0.98 (95% CI, 0.86–1.13) for a genetically determined 10 nmol/L decrease in 25(OH)D with a corresponding observational odds ratio of 1.03 (95% CI, 1.01–1.05). Genetic and observational low 25(OH)D concentrations were associated with higher blood pressure, as well as with hypertension consistent with causal relationships. Because observational but not genetic low 25(OH)D concentration was associated with ischemic stroke, and as the CIs overlapped, we can neither support nor exclude a causal relationship.

Blood Pressure Trajectories and the Risk of Intracerebral Hemorrhage and Cerebral InfarctionNovelty and Significance [Epidemiology/Population]
9/8/2017
Weijuan Li, Cheng Jin, Anand Vaidya, Yuntao Wu, Kathryn Rexrode, Xiaoming Zheng, Mahmut E. Gurol, Chaoran Ma, Shouling Wu, Xiang Gao
ver resumen
The association between long-term blood pressure (BP) patterns in community-dwelling adults and risk of intracerebral hemorrhage and cerebral infarction is not well characterized. This prospective study included 79 385 participants, free of stroke, myocardial infarction, and cancer in or before 2010 (baseline). Systolic BP trajectories were identified using latent mixture modeling with data from 2006, 2008, and 2010. Incident cases of intracerebral hemorrhage and cerebral infarction occurred during 2010 to 2014, confirmed by review of medical records, by 3 physicians. We identified 5 distinct systolic BP trajectories during 2006 to 2010. Each of the trajectories was labeled according to their BP range and pattern over time: normotensive-stable (n=26 740), prehypertension-stable (n=35 674), stage 1 hypertension-increasing (n=8215), stage 1 hypertension-decreasing (n=6422), and stage 2 hypertension-stable (n=2334). We documented 1034 incident cases of cerebral infarction and 187 cases of intracerebral hemorrhage. Although the prehypertension-stable trajectory exhibited systolic BP range within the normal range (120–140 mm Hg) during 2006 to 2010, this group had higher stroke risk relative to the normotensive-stable group (<120 mm Hg) (adjusted hazard ratio was 3.11 for intracerebral hemorrhage and 1.99 for cerebral infarction; P<0.001 for both), after adjusting for possible confounders. Individuals in the stage 2 hypertension-stable systolic BP trajectory (175–179 mm Hg) had the highest risk of intracerebral hemorrhage (adjusted hazard ratio was 12.4) and cerebral infarction (adjusted hazard ratio was 5.07), relative to the normotensive-stable group (P<0.001 for both). BP trajectories were associated with the risk of stroke and increasing BP trajectories within the currently designated normal range may still increase the risk for stroke.

Control of Pathological Cardiac Hypertrophy by Transcriptional Corepressor IRF2BP2 (Interferon Regulatory Factor-2 Binding Protein 2)Novelty and Significance [Heart]
9/8/2017
Jing Fang, Tianyu Li, Xuehai Zhu, Ke-Qiong Deng, Yan-Xiao Ji, Chun Fang, Xiao-Jing Zhang, Jun-Hong Guo, Peng Zhang, Hongliang Li, Xiang Wei
ver resumen
The transcription factor NFAT1 (nuclear factor of activated T-cells 1), with the aid of transcriptional coactivators, has been recognized for its necessity and sufficiency to drive pathological cardiac hypertrophy. However, how the transcriptional activity of NFAT1 in terms of cardiac hypertrophy is controlled at the transcriptional level has not been well defined. Herein, we showed that a cardiac-enriched protein IRF2BP2 (interferon regulatory factor-2 binding protein 2) was further upregulated in both human and mouse hypertrophied myocardium and negatively regulated cardiomyocyte hypertrophic response in vitro. By generating cardiomyocyte-specific Irf2bp2 knockout and Irf2bp2-transgenic mouse strains, our in vivo experiments showed that, whereas IRF2BP2 loss-of-function exacerbated both aortic banding- and angiotensin II infusion-induced cardiac hypertrophic response, IRF2BP2 overexpression exerted a strong protective effect against these maladaptive processes. Particularly, IRF2BP2 directly interacted with the C-terminal transactivation domain of NFAT1 by competing with myocyte enhancer factor-2C and disturbing their transcriptional synergism, thereby impeding NFAT1-transactivated hypertrophic transcriptome. As a result, the devastating effect of Irf2bp2 deficiency on cardiac hypertrophy was largely rescued by NFAT1 blockage. Our study, thus, defined IRF2BP2 as a novel negative regulator in controlling pathological cardiac hypertrophy at the transcriptional level.

Aortic Arch Pulse Wave Velocity Assessed by Magnetic Resonance Imaging as a Predictor of Incident Cardiovascular EventsNovelty and Significance [Arterial Stiffness]
9/8/2017
Yoshiaki Ohyama, Bharath Ambale-Venkatesh, Chikara Noda, Jang-Young Kim, Yutaka Tanami, Gisela Teixido-Tura, Atul R. Chugh, Alban Redheuil, Chia-Ying Liu, Colin O. Wu, W. Gregory Hundley, David A. Bluemke, Eliseo Guallar, Joao A.C. Lima
ver resumen
The predictive value of aortic arch pulse wave velocity (PWV) assessed by magnetic resonance imaging for cardiovascular disease (CVD) events has not been fully established. The aim of the present study was to evaluate the association of arch PWV with incident CVD events in MESA (Multi-Ethnic Study of Atherosclerosis). Aortic arch PWV was measured using magnetic resonance imaging at baseline in 3527 MESA participants (mean age, 62±10 years at baseline; 47% men) free of overt CVD. Cox regression was used to evaluate the risk of incident CVD (coronary heart disease, stroke, transient ischemic attack, or heart failure) in relation to arch PWV adjusted for age, sex, race, and CVD risk factors. The median value of arch PWV was 7.4 m/s (interquartile range, 5.6–10.2). There was significant interaction between arch PWV and age for outcomes, so analysis was stratified by age categories (45–54 and >54 years). There were 456 CVD events during the 10-year follow-up. Forty-five to 54-year-old participants had significant association of arch PWV with incident CVD independent of CVD risk factors (hazard ratio, 1.44; 95% confidence interval, 1.07–1.95; P=0.018; per 1-SD increase for logarithmically transformed PWV), whereas >54-year group did not (P=0.93). Aortic arch PWV assessed by magnetic resonance imaging is a significant predictor of CVD events among middle-aged (45–54 years old) individuals, whereas arch PWV is not associated with CVD among an elderly in a large multiethnic population.

Influence of Child and Adult Elevated Blood Pressure on Adult Arterial StiffnessNovelty and Significance [Arterial Stiffness]
9/8/2017
Heikki Aatola, Teemu Koivistoinen, Heikki Tuominen, Markus Juonala, Terho Lehtimaki, Jorma S.A. Viikari, Olli T. Raitakari, Mika Kahonen, Nina Hutri–Kahonen
ver resumen
Elevated blood pressure (BP) in childhood has been associated with increased adult arterial stiffness, the independent predictor of cardiovascular and all-cause mortality. The favorable BP change from childhood to adulthood and the risk of high adult arterial stiffness has not been reported. We examined the effect of child and adult BP on pulse wave velocity (PWV) assessed in adulthood among 1540 white adults followed-up for 27 years since baseline (1980, aged 6–18 years). Childhood elevated BP was defined according to the tables from the National High Blood Pressure Education Program. In adulthood, BP was classified as elevated if systolic BP ≥120 mm Hg, diastolic BP ≥80 mm Hg, or self-reported use of antihypertensive medications. PWV was measured in 2007 by whole-body impedance cardiography, and high PWV was defined as values at or above the age-, sex-, and heart rate–specific 80th percentile. Individuals with persistently elevated BP and individuals with normal child but elevated adult BP had increased risk of high adult PWV (relative risk [95% confidence interval], 3.18 [2.22–4.55] and 2.64 [1.79–3.88], respectively) in comparison with individuals with normal (both child and adult) BP. In contrast, individuals with elevated BP in childhood but not in adulthood did not have significantly increased risk of high PWV (relative risk [95% confidence interval], 1.26[0.80–1.99]). The results were consistent when different definitions for child and adult elevated BP were applied. These findings highlight the importance of BP control in the primary prevention of cardiovascular diseases.

Office Pulse Pressure Is a Predictor of Favorable Outcome in Young- to Middle-Aged Subjects With Stage 1 HypertensionNovelty and Significance [Pulse Pressure and Cardiovascular Events]
9/8/2017
Francesca Saladini, Claudio Fania, Lucio Mos, Adriano Mazzer, Edoardo Casiglia, Paolo Palatini
ver resumen
The role of pulse pressure in young individuals remains controversial. The aim of the present study was to investigate the clinical significance of elevated pulse pressure in young- to middle-aged subjects screened for stage 1 hypertension. We examined 1241 subjects (mean age, 33.1±8.4 years) from the HARVEST (Hypertension Ambulatory Recording Venetia Study), during a median follow-up of 12.1 years. To evaluate the predictive value of pulse pressure and mean blood pressure for future hypertension needing treatment and for cardiovascular events, participants were grouped into pressure tertiles. Significant determinants of pulse pressure were male sex (P=0.029), younger age (P<0.001), physical activity (P=0.003), heart rate (P<0.001), systolic white-coat effect (P<0.001), and stroke volume (n=829; P<0.001). During follow-up, 65.1% of participants developed hypertension requiring pharmacological treatment and 5.1% experienced a cardiovascular event. Participants in the highest pulse pressure tertile had a reduced risk of incident hypertension compared with those of the bottom tertile (hazard ratio, 0.75; 95% confidence interval, 0.62–0.91; P=0.003). In contrast, participants in the top mean blood pressure tertile had an increase in risk (1.91; 1.57–2.33; P<0.001). In addition, participants in the highest pulse pressure tertile had a reduced risk of cardiovascular events (0.35; 0.17–0.73; P=0.005) and those in the top mean blood pressure tertile had an increase in risk (3.06; 1.32–7.09; P=0.009). Our data show that in subjects <45 years, only mean blood pressure is a predictor of adverse outcome whereas high pulse pressure even carries a reduced risk.

Increased Perfusion Pressure Drives Renal T-Cell Infiltration in the Dahl Salt-Sensitive RatNovelty and Significance [Kidney]
9/8/2017
Louise C. Evans, Galina Petrova, Theresa Kurth, Chun Yang, John D. Bukowy, David L. Mattson, Allen W. Cowley, Jr
ver resumen
Renal T-cell infiltration is a key component of salt-sensitive hypertension in Dahl salt-sensitive (SS) rats. Here, we use an electronic servo-control technique to determine the contribution of renal perfusion pressure to T-cell infiltration in the SS rat kidney. An aortic balloon occluder placed around the aorta between the renal arteries was used to maintain perfusion pressure to the left kidney at control levels, ≈128 mm Hg, during 7 days of salt-induced hypertension, whereas the right kidney was exposed to increased renal perfusion pressure that averaged 157±4 mm Hg by day 7 of high-salt diet. The number of infiltrating T cells was compared between the 2 kidneys. Renal T-cell infiltration was significantly blunted in the left servo-controlled kidney compared with the right uncontrolled kidney. The number of CD3+, CD3+CD4+, and CD3+CD8+ T cells were all significantly lower in the left servo-controlled kidney. This effect was not specific to T cells because CD45R+ (B cells) and CD11b/c+ (monocytes and macrophages) cell infiltrations were all exacerbated in the hypertensive kidneys. Increased renal perfusion pressure was also associated with augmented renal injury, with increased protein casts and glomerular damage in the hypertensive kidney. Levels of norepinephrine were comparable between the 2 kidneys, suggestive of equivalent sympathetic innervation. Renal infiltration of T cells was not reversed by the return of renal perfusion pressure to control levels after 7 days of salt-sensitive hypertension. We conclude that increased pressure contributes to the initiation of renal T-cell infiltration during the progression of salt-sensitive hypertension in SS rats.

Hypertension and VEGF (Vascular Endothelial Growth Factor) Receptor Tyrosine Kinase InhibitionNovelty and Significance [Kidney]
9/8/2017
Brian C. Boursiquot, Emily C. Zabor, Ilya G. Glezerman, Edgar A. Jaimes
ver resumen
VEGF (vascular endothelial growth factor) receptor tyrosine kinase inhibitors have become first-line therapy for metastatic renal cell carcinoma. Their use commonly leads to hypertension, but their effects on long-term renal function are not known. In addition, it has been suggested that the development of hypertension is linked to treatment efficacy. The objective of this study was to determine the effects of these drugs on long-term renal function, especially in those with renal dysfunction at baseline, and to examine the role of hypertension on these effects. Serum creatinine measurements were used to calculate the estimated glomerular filtration rate for 130 renal cell carcinoma patients who were treated with this class of tyrosine kinase inhibitors. New or worsening hypertension was defined by documented start or addition of antihypertensive medications. Overall, the use of tyrosine kinase inhibitors in patients with estimated glomerular filtration <60 or ≥60 mL/min per 1.73 m2 was not associated with a decline in long-term renal function. During follow-up, 41 patients developed new or worsening hypertension within 30 days from first drug administration, and this was not linked to further reductions in glomerular filtration. These patients seemed to survive longer than those who did not develop hypertension within 30 days, although this was not statistically significant (P=0.07). Our findings suggest that the use of VEGF tyrosine kinase inhibitors does not adversely affect long-term renal function even in the setting of new-onset hypertension or reduced renal function at baseline.







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