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Hypertension - recientes

Correction to: Intracerebroventricular Infusion of the (Pro)renin Receptor Antagonist PRO20 Attenuates Deoxycorticosterone Acetate-Salt-Induced Hypertension [Corrections]
13/9/2017
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Clinical Implications [Clinical Implications]
13/9/2017
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Oxidative Stress, Inflammation, and Vascular Aging in Hypertension [Best Papers in Hypertension]
13/9/2017
Tomasz J. Guzik, Rhian M. Touyz
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Cardiovascular Risk Associated With White-Coat HypertensionResponse to Increased Cardiovascular Risk of White-Coat Hypertension: Pro Side of the Argument [Controversies in Hypertension]
13/9/2017
Giuseppe Mancia, Michele Bombelli, Cesare Cuspidi, Rita Facchetti, Guido Grassi
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Cardiovascular Risk Associated With White-Coat HypertensionResponse to Cardiovascular Risk Associated With White-Coat Hypertension:Con Side of the Argument [Controversies in Hypertension]
13/9/2017
Kei Asayama, Yan Li, Stanley S. Franklin, Lutgarde Thiȷs, Eoin O’Brien, Jan A. Staessen
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New Clinical Practice Guideline for the Management of High Blood Pressure in Children and Adolescents [Brief Reviews]
13/9/2017
Joseph T. Flynn, Bonita E. Falkner
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Hypertensive Kidney Injury and the Progression of Chronic Kidney Disease [Arthur C. Corcoran Memorial Lecture]
13/9/2017
Karen A. Griffin
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Next Steps for Gene Identification in Primary Hypertension Genomics [Editorial Commentary]
13/9/2017
Georg Ehret
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Chicken or the Egg? Hyperuricemia, Insulin Resistance, and Hypertension [Editorial Commentary]
13/9/2017
Jesse Dawson, Annick Wyss
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Unraveling the Role and Complexities of Inflammation in Hypertension [Editorial Commentary]
13/9/2017
Sean P. Didion
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Temporal Relationship Between Hyperuricemia and Insulin Resistance and Its Impact on Future Risk of HypertensionNovelty and Significance [Epidemiology/Population]
13/9/2017
Tianshu Han, Li Lan, Rongge Qu, Qian Xu, Ruyue Jiang, Lixin Na, Changhao Sun
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Although hyperuricemia and insulin resistance significantly correlated, their temporal sequence and how the sequence influence on future risk of hypertension are largely unknown. This study assessed temporal relationship between uric acid and insulin resistance and its impact on future risk of hypertension by examining a longitudinal cohort including 8543 subjects aged 20 to 74 years from China, with an average follow-up of 5.3 years. Measurements of fasting uric acid, as well as fasting and 2-hour serum glucose and insulin, were obtained at baseline and follow-up. Indicators of hepatic and peripheral insulin resistance were calculated. Cross-lagged panel and mediation analysis were used to examine the temporal relationship between uric acid and insulin resistance and its impact on follow-up hypertension. After adjusting for covariates, the cross-lagged path coefficients (β1 values) from baseline uric acid to follow-up insulin resistance indices were significantly greater than path coefficients (β2 values) from baseline insulin resistance indices to follow-up uric acid (β1=0.110 versus β2=0.017; P<0.001, for hepatic insulin resistance; β1=−0.208 versus β2=−0.021; P<0.001, for peripheral insulin resistance). The path coefficients from baseline uric acid to follow-up insulin resistance indices in the hypertensive group were significantly greater than that in the normotensive group (P<0.001 for the difference of β1 values in the 2 groups). Insulin resistance partially mediated the effect of uric acid on subsequent hypertension, and the mediation effect of peripheral insulin resistance was significantly greater than that of hepatic insulin resistance (31.3% versus 13.2%; P<0.001, for the difference of mediation effects). These findings provide evidence that higher uric acid levels probably precede insulin resistance, and peripheral insulin resistance likely plays a more important role in the development of hypertension than hepatic insulin resistance does.

Individual and Combined Effects of Dietary Factors on Risk of Incident HypertensionNovelty and Significance [Epidemiology/Population]
13/9/2017
Helene Lelong, Jacques Blacher, Julia Baudry, Solia Adriouch, Pilar Galan, Leopold Fezeu, Serge Hercberg, Emmanuelle Kesse-Guyot
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Dietary intake is pointed as one of the major determinants in hypertension development. Data in the area are mostly obtained from cross-sectional studies. We aimed to investigate the prospective association between (1) individual nutritional factors and (2) adherence to the Dietary Approach to Stop Hypertension and the risk of incident hypertension in a large cohort study. We prospectively examined the incidence of hypertension among 80 426 French adults participating in the NutriNet-Santé cohort study. Self-reported sociodemographic, lifestyle health questionnaires and dietary consumption assessed by three 24-hour records were completed at baseline and yearly thereafter. Associations between quartiles (Q) of nutrients and food groups and adherence to Dietary Approach to Stop Hypertension diet and hypertension risk were assessed by multivariable Cox proportional hazards models. During a mean follow-up of 3.4±2.1 years, 2413 cases of incident hypertension were documented. Dietary intakes of sodium (Q4 versus Q1): hazard ratio (HR)=1.17 (95% confidence interval [CI], 1.02–1.35), potassium: HR=0.82 (95% CI, 0.72–0.94), animal protein: HR=1.26 (95% CI, 1.11–1.43), vegetable protein: HR=0.85 (95% CI, 0.75–0.95), fiber: HR =0.81 (95% CI, 0.71–0.93), magnesium: HR=0.77 (95% CI, 0.67–0.89), fruit and vegetables: HR=0.85 (95% CI, 0.74–0.97), whole grain: HR=0.84(95% CI, 0.76–0.93), nuts: HR=0.72 (95% CI, 0.63–0.83), and red and processed meat: HR=1.25 (95% CI, 1.11–0.42) were associated with risk of hypertension. Besides, adherence to the Dietary Approach to Stop Hypertension was strongly inversely associated with incident hypertension: (Q4 versus Q1) HR=0.66 (95% CI, 0.58–0.75). Our results confirmed the association of several nutritional factors intake and incident hypertension and highlighted that adopting a global healthy diet could strongly contribute to the prevention of hypertension.

Increased Risk of New-Onset Hypertension After Shock Wave Lithotripsy in UrolithiasisNovelty and Significance [Epidemiology/Population]
13/9/2017
Shi-Wei Huang, Chung-You Tsai, Jui Wang, Yeong-Shiau Pu, Pei-Chun Chen, Chao-Yuan Huang, Kuo-Liong Chien
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Although shock wave lithotripsy is minimally invasive, earlier studies argued that it may increase patients’ subsequent risk of hypertension and diabetes mellitus. This study evaluated the association between shock wave lithotripsy and new-onset hypertension or diabetes mellitus. The Taiwanese National Health Insurance Research Database was used to identify 20 219 patients aged 18 to 65 years who underwent the first stone surgical treatment (shock wave lithotripsy or ureterorenoscopic lithotripsy) between January 1999 and December 2011. A Cox proportional model was applied to evaluate associations. Time-varying Cox models were applied to evaluate the association between the number of shock wave lithotripsy sessions and the incidence of hypertension or diabetes mellitus. After a median follow-up of 74.9 and 82.6 months, 2028 and 688 patients developed hypertension in the shock wave lithotripsy and ureterorenoscopic lithotripsy groups, respectively. Patients who underwent shock wave lithotripsy had a higher probability of developing hypertension than patients who underwent ureterorenoscopic lithotripsy, with a hazard ratio of 1.20 (95% confidence interval, 1.10–1.31) after adjusting for covariates. The risk increased as the number of shock wave lithotripsy sessions increased. However, the diabetes mellitus risk was similar in the shock wave lithotripsy and ureterorenoscopic lithotripsy groups. Furthermore, the hazard ratio did not increase as the number of shock wave lithotripsy sessions increased. Shock wave lithotripsy consistently increased the incidence of hypertension on long-term follow-up. Therefore, alternatives to urolithiasis treatment (eg, endoscopic surgery or medical expulsion therapy) could avoid the hypertension risk. Furthermore, avoiding multiple sessions of shock wave lithotripsy could also evade the hypertension risk.

Childhood Socioeconomic Status and Arterial Stiffness in AdulthoodNovelty and Significance [Epidemiology/Population]
13/9/2017
Elina Puolakka, Katȷa Pahkala, Tomi T. Laitinen, Costan G. Magnussen, Nina Hutri–Kahonen, Mika Kahonen, Terho Lehtimaki, Paivi Tossavainen, Eero Jokinen, Matthew A. Sabin, Tomi Laitinen, Marko Elovainio, Laura Pulkki–Raback, Jorma S.A. Viikari, Olli T. Raitakari, Markus Juonala
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Increasing evidence supports the importance of socioeconomic factors in the development of atherosclerotic cardiovascular disease. However, the association of childhood socioeconomic status (SES) with arterial stiffness in adulthood has not been reported. Our aim was to determine whether higher childhood family-level SES is associated with lower arterial stiffness in adulthood. The analyses were performed using data gathered within the longitudinal Young Finns Study. The sample comprised 2566 participants who had data concerning family SES at ages 3 to 18 years in 1980 and arterial pulse wave velocity and carotid artery distensibility measured 21 or 27 years later in adulthood. Higher family SES in childhood was associated with lower arterial stiffness in adulthood; carotid artery distensibility being higher (β value±SE, 0.029±0.0089%/10 mm Hg; P=0.001) and pulse wave velocity lower (β value±SE, −0.062±0.022 m/s; P=0.006) among those with higher family SES in a multivariable analysis adjusted with age, sex, and conventional childhood cardiometabolic risk factors. The association remained significant after further adjustment for participant’s SES in adulthood (β value±SE, 0.026±0.010%/10 mm Hg; P=0.01 for carotid artery distensibility and β value±SE, −0.048±0.023 m/s; P=0.04 for pulse wave velocity) but attenuated after adjustment for adulthood cardiometabolic risk factors (β value±SE, 0.015±0.008%/10 mm Hg; P=0.08 for carotid artery distensibility and β value±SE, −0.019±0.02 m/s; P=0.38 for pulse wave velocity). In conclusion, we observed an association between higher family SES in childhood and lower arterial stiffness in adulthood. Our findings suggest that special attention could be paid to children from low SES families to prevent cardiometabolic diseases primordially.

Trends in the Prevalence, Awareness, Treatment, and Control of Hypertension Among Young Adults in the United States, 1999 to 2014Novelty and Significance [Epidemiology/Population]
13/9/2017
Yiyi Zhang, Andrew E. Moran
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Overall hypertension prevalence has not changed in the United States in recent decades although awareness, treatment, and control improved. However, hypertension epidemiology and its temporal trends may differ in younger adults compared with older adults. Our study included 41 331 participants ≥18 years of age from 8 National Health and Nutrition Examination Surveys (1999–2014) and estimated temporal trends of hypertension, awareness, treatment, and control among young adults (age, 18–39 years) compared with middle-age (age, 40–59 years) and older adults (age, ≥60 years). In 2013 to 2014, 7.3% of the US young adults had hypertension. During 1999 to 2014, young adults saw larger increases in hypertension awareness, treatment, and control than did older adults. However, all of these components of hypertension control were lower among young adults compared with middle-aged or older adults (74.7% younger versus 81.9% middle versus 88.4% older for awareness; 50.0% versus 70.3% versus 83.0% for treatment; and 40.2% versus 56.7% versus 54.4% for control). Worse hypertension awareness, treatment, and control in young adults overall were mostly driven by worse measures in young adult men compared with young adult women. More frequent healthcare visits by young adult women explained ≈28% of the sex-related difference in awareness, 60% of the difference in treatment, and 52% of the difference in control. These findings suggest that improved access to and engagement in medical care might improve hypertension control in young adults, particularly young adult men, and reduce life-time cardiovascular risk.

Transcriptome-Wide Analysis Identifies Novel Associations With Blood PressureNovelty and Significance [Genomics]
13/9/2017
Tanȷa Zeller, Claudia Schurmann, Katharina Schramm, Christian Muller, Soonil Kwon, Philipp S. Wild, Alexander Teumer, David Herrington, Arne Schillert, Licia Iacoviello, Adelheid Kratzer, Annika Jagodzinski, Mahir Karakas, Jingzhong Ding, Johannes T. Neumann, Kari Kuulasmaa, Christian Gieger, Tim Kacprowski, Renate B. Schnabel, Michael Roden, Simone Wahl, Jerome I. Rotter, Francisco Oȷeda, Maren Carstensen–Kirberg, David–Alexandre Tregouet, Marcus Dorr, Thomas Meitinger, Karl J. Lackner, Petra Wolf, Stephan B. Felix, Ulf Landmesser, Simona Costanzo, Andreas Ziegler, Yongmei Liu, Uwe Volker, Walter Palmas, Holger Prokisch, Xiuqing Guo, Christian Herder, Stefan Blankenberg, Georg Homuth
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Hypertension represents a major cardiovascular risk factor. The pathophysiology of increased blood pressure (BP) is not yet completely understood. Transcriptome profiling offers possibilities to uncover genetics effects on BP. Based on 2 populations including 2549 individuals, a meta-analyses of monocytic transcriptome-wide profiles were performed to identify transcripts associated with BP. Replication was performed in 2 independent studies of whole-blood transcriptome data including 1990 individuals. For identified candidate genes, a direct link between long-term changes in BP and gene expression over time and by treatment with BP-lowering therapy was assessed. The predictive value of protein levels encoded by candidate genes for subsequent cardiovascular disease was investigated. Eight transcripts (CRIP1, MYADM, TIPARP, TSC22D3, CEBPA, F12, LMNA, and TPPP3) were identified jointly accounting for up to 13% (95% confidence interval, 8.7–16.2) of BP variability. Changes in CRIP1, MYADM, TIPARP, LMNA, TSC22D3, CEBPA, and TPPP3 expression associated with BP changes—among these, CRIP1 gene expression was additionally correlated to measures of cardiac hypertrophy. Assessment of circulating CRIP1 (cystein-rich protein 1) levels as biomarkers showed a strong association with increased risk for incident stroke (hazard ratio, 1.06; 95% confidence interval, 1.03–1.09; P=5.0×10–5). Our comprehensive analysis of global gene expression highlights 8 novel transcripts significantly associated with BP, providing a link between gene expression and BP. Translational approaches further established evidence for the potential use of CRIP1 as emerging disease-related biomarker.

Visit-to-Visit Office Blood Pressure Variability and Cardiovascular Outcomes in SPRINT (Systolic Blood Pressure Intervention Trial)Novelty and Significance [Blood Pressure Variability in SPRINT]
13/9/2017
Tara I. Chang, David M. Reboussin, Glenn M. Chertow, Alfred K. Cheung, William C. Cushman, William J. Kostis, Gianfranco Parati, Dominic Raj, Erik Riessen, Brian Shapiro, George S. Stergiou, Raymond R. Townsend, Konstantinos Tsioufis, Paul K. Whelton, Jeffrey Whittle, Jackson T. Wright, Vasilios Papademetriou
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Studies of visit-to-visit office blood pressure (BP) variability (OBPV) as a predictor of cardiovascular events and death in high-risk patients treated to lower BP targets are lacking. We conducted a post hoc analysis of SPRINT (Systolic Blood Pressure Intervention Trial), a well-characterized cohort of participants randomized to intensive (<120 mm Hg) or standard (<140 mm Hg) systolic BP targets. We defined OBPV as the coefficient of variation of the systolic BP using measurements taken during the 3-,6-, 9-, and 12-month study visits. In our cohort of 7879 participants, older age, female sex, black race, current smoking, chronic kidney disease, and coronary disease were independent determinants of higher OBPV. Use of thiazide-type diuretics or dihydropyridine calcium channel blockers was associated with lower OBPV whereas angiotensin-converting enzyme inhibitors or angiotensin receptor blocker use was associated with higher OBPV. There was no difference in OBPV in participants randomized to standard or intensive treatment groups. We found that OBPV had no significant associations with the composite end point of fatal and nonfatal cardiovascular events (n=324 primary end points; adjusted hazard ratio, 1.20; 95% confidence interval, 0.85–1.69, highest versus lowest quintile) nor with heart failure or stroke. The highest quintile of OBPV (versus lowest) was associated with all-cause mortality (adjusted hazard ratio, 1.92; confidence interval, 1.22–3.03) although the association of OBPV overall with all-cause mortality was marginal (P=0.07). Our results suggest that clinicians should continue to focus on office BP control rather than on OBPV unless definitive benefits of reducing OBPV are shown in prospective trials.Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT01206062

P2y12 Receptor Promotes Pressure Overload-Induced Cardiac Remodeling via Platelet-Driven Inflammation in MiceNovelty and Significance [Heart]
13/9/2017
Lujin Wu, Fujie Zhao, Meiyan Dai, Huaping Li, Chen Chen, Jiali Nie, Peihua Wang, Dao Wen Wang
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Inflammation plays a critical role in adverse cardiac remodeling and heart failure. The P2y12 receptor is one of the predominant activating receptors for platelets, thus initiating inflammatory responses under various diseases. In this study, we investigated the functional significance of P2y12-mediated platelet activation in pressure overload–induced cardiac remodeling. Notably, P2y12 knockout (P2y12−/−) mice exhibited suppressed transverse aortic constriction–induced changes in cardiac hypertrophy, collagen synthesis, inflammatory cell recruitment, and cardiac dysfunction. Activated platelets and platelet–leukocyte aggregates were markedly downregulated in P2y12 knockout mice compared with wild-type counterparts after transverse aortic constriction. Moreover, bone marrow chimera experiments revealed that wild-type recipients of P2y12 knockout bone marrow markedly improved cardiac function and attenuated cardiac remodeling, reversed by wild-type platelets reinjection. Platelet depletion and P-selectin inhibition mimicked these protective effects by limiting the interaction between activated platelets and leukocytes. Furthermore, activated wild-type platelets directly induced cardiomyocyte hypertrophy and collagen synthesis via α-granule exocytosis, vanished in P2y12 knockout platelets or those administered anti-NSF (N-ethlymalimide-sensitive factor) antibodies. The results suggest that P2y12-mediated platelet activation promotes cardiac remodeling by triggering a series of inflammatory changes and interacting with leukocytes and endotheliocytes.

Restoration of Circulating MFGE8 (Milk Fat Globule-EGF Factor 8) Attenuates Cardiac Hypertrophy Through Inhibition of Akt PathwayNovelty and Significance [Heart]
13/9/2017
Ke-Qiong Deng, Jing Li, Zhi-Gang She, Jun Gong, Wen-Lin Cheng, Fu-Han Gong, Xue-Yong Zhu, Yan Zhang, Zhihua Wang, Hongliang Li
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Cardiac hypertrophy occurs in response to numerous stimuli like neurohumoral stress, pressure overload, infection, and injury, and leads to heart failure. Mfge8 (milk fat globule-EGF factor 8) is a secreted protein involved in various human diseases, but its regulation and function during cardiac hypertrophy remain unexplored. Here, we found that circulating MFGE8 levels declined significantly in failing hearts from patients with dilated cardiomyopathy. Correlation analyses revealed that circulating MFGE8 levels were negatively correlated with the severity of cardiac dysfunction and remodeling in affected patients. Deleting Mfge8 in mice maintained normal heart function at basal level but substantially exacerbated the hypertrophic enlargement of cardiomyocytes, reprogramming of pathological genes, contractile dysfunction, and myocardial fibrosis after aortic banding surgery. In contrast, cardiac-specific Mfge8 overexpression in transgenic mice significantly blunted aortic banding–induced cardiac hypertrophy. Whereas MAPK (mitogen-activated protein kinase) pathways were unaffected in either Mfge8-knockout or Mfge8-overexpressing mice, the activated Akt/PKB (protein kinase B)–Gsk-3β (glycogen synthase kinase-3β)/mTOR (mammalian target of rapamycin) pathway after aortic banding was significantly potentiated by Mfge8 deficiency but suppressed by Mfge8 overexpression. Inhibition of Akt with MK-2206 blocked the prohypertrophic effects of Mfge8 deficiency in angiotensin II–treated neonatal rat cardiomyocytes. Finally, administering a recombinant human MFGE8 in mice in vivo alleviated cardiac hypertrophy induced by aortic banding. Our findings indicate that Mfge8 is an endogenous negative regulator of pathological cardiac hypertrophy and may, thus, have potential both as a novel biomarker and as a therapeutic target for treatment of cardiac hypertrophy.

Perivascular Adipose Tissue Angiotensin II Type 1 Receptor Promotes Vascular Inflammation and Aneurysm FormationNovelty and Significance [Aortic Aneurysm]
13/9/2017
Tomoki Sakaue, Jun Suzuki, Mika Hamaguchi, Chika Suehiro, Akiko Tanino, Tomoaki Nagao, Teruyoshi Uetani, Jun Aono, Hirotomo Nakaoka, Mie Kurata, Tomohisa Sakaue, Takafumi Okura, Takumi Yasugi, Hironori Izutani, Jitsuo Higaki, Shuntaro Ikeda
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Perivascular adipose tissue exhibits characteristics of active local inflammation, which contributes to the development of atherosclerotic disease as a complication of obesity/metabolic syndrome. However, the precise role of perivascular adipose tissue in the progression of abdominal aortic aneurysm remains unclear. To test the hypothesis that genetic deletion of angiotensin II type 1a (AT1a) receptor in perivascular visceral adipose tissue (VAT) can attenuate aortic aneurysm formation in apolipoprotein E–deficient (ApoE−/−) mice, we performed adipose tissue transplantation experiments by using an angiotensin II–induced aneurysm murine model, in which we transplanted VAT from ApoE−/− or ApoE−/− AT1a−/− donor mice onto the abdominal aorta of ApoE−/− recipient mice. Compared with ApoE−/− VAT transplantation, ApoE−/− AT1a−/− VAT transplantation markedly attenuated aortic aneurysm formation, macrophage infiltration, and gelatinolytic activity in the abdominal aorta. AT1a receptor activation led to the polarization of macrophages in perivascular VAT toward the proinflammatory phenotype. Moreover, osteopontin expression and gelatinolytic activity were considerably lower in ApoE−/− AT1a−/− perivascular VAT than in ApoE−/− perivascular VAT, and angiotensin II–induced osteopontin secretion from adipocytes was eliminated after deletion of AT1a receptor in adipocytes. Notably, induction of macrophage migration by conditioned medium from angiotensin II–stimulated wild-type adipocytes was suppressed by treatment with an osteopontin-neutralizing antibody, and ApoE−/− OPN−/− VAT transplantation more potently attenuated aortic aneurysm formation than ApoE−/− VAT transplantation. Our findings indicate a previously unrecognized effect of AT1a receptor in perivascular VAT on the pathogenesis of abdominal aortic aneurysm.







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