| author name | recommending | commenting | favorite | papers | recom. | cited | |
|---|---|---|---|---|---|---|---|
| 0 | 0 | 0 | 107 | 0 | 2828 | [Update] | |
| 0 | 0 | 0 | 96 | 0 | 997 | [Update] | |
| 0 | 0 | 0 | 1 | 0 | 5 | [Update] |
Latest Paper:
J Hypertens. 2012 Mar 20;:
22441350
David M Carty,
Lesley A Anderson,
Dilys J Freeman,
Paul I Welsh,
Janet E Brennand,
Anna F Dominiczak,
Christian Delles
aInstitute of Cardiovascular and Medical Sciences, University of Glasgow bDepartment of Obstetrics, Southern General Hospital, Glasgow, UK.
OBJECTIVE:: Circulating biomarkers of endothelial dysfunction and inflammation are elevated in late pregnancy in women with preeclampsia. We examined plasma levels of inflammatory cytokines and adhesion molecules in early pregnancy, to assess their ability to predict preeclampsia. METHODS:: In a prospective longitudinal study, 2600 women with singleton pregnancies and no history of hypertension were recruited at their antenatal hospital (booking) visit at gestational week 12-16. Of these, 49 (1.9%) developed preeclampsia, whereas 74 women matched for age and BMI with uncomplicated pregnancies were selected as controls. A subset of women with risk factors for preeclampsia were sampled again at gestational weeks 16 and 28 (11 cases, 39 controls) and postnatally (six cases, 36 controls). RESULTS:: From multiplex analysis, soluble E-selectin concentrations were higher at 12-16 weeks in women who subsequently developed preeclampsia (15.1 ± 4.9 versus 12.9 ± 4.5 ng/ml, P = 0.02). At gestational week 28, E-selectin concentrations were again higher in women who went on to develop preeclampsia compared with controls (14.4 ± 5.6 versus 10.7 ± 3.5 ng/ml, P = 0.010), whereas levels were not different between the two groups in postpartum samples. CONCLUSION:: Changes in soluble E-selectin concentration in early pregnancy may reflect underlying pathophysiological processes, potentially providing mechanistic insights into preeclampsia.
Eur J Pain. 2012 Jan 26;:
22337623
Aberdeen Pain Research Collaboration (Musculoskeletal Research), University of Aberdeen, UK.
Chronic pain is pathological, persisting beyond normal tissue healing time. Previous work has suggested ∼50% variation in chronic pain development is heritable. No data are currently available on the heritability of pain categorized using the Chronic Pain Grade (CPG). Furthermore, few existing studies have accounted for potential confounders that may themselves be under genetic control or indeed 'heritable' non-genetic traits. This study aimed to determine the relative contributions of genetic, measured and shared environmental and lifestyle factors to chronic pain. Chronic pain status was determined and CPG measured in participants from Generation Scotland: the Scottish Family Health Study, a large cohort of well-characterized, extended families from throughout Scotland, UK. Heritability estimates (h (2)) for 'any chronic pain' and 'severe' chronic pain (CPG 3 or 4) were generated using SOLAR software, with and without adjustment for shared household effects and measured covariates age, body mass index, gender, household income, occupation and physical activity. Data were available for 7644 individuals in 2195 extended families. Without adjustment, h (2) for 'any chronic pain' was 29%[standard errors (SE) 6%; p < 0.001], and for 'severe' chronic pain was 44%(SE 3%; p <0.001). After adjustment,'any chronic pain' h (2) = 16%(SE 7%; p = 0.02) and 'severe' chronic pain h (2) = 30%(SE 13%; p = 0.007). Co-heritability of both traits was 11%(SE 76%). This study supports the use of chronic pain as a phenotype in genetic studies, with adequate correction for confounders to specifically identify genetic risk factors for chronic pain.
Fadi J Charchar,
Lisa D S Bloomer,
Timothy A Barnes,
Mark J Cowley,
Christopher P Nelson,
Yanzhong Wang,
Matthew Denniff,
Radoslaw Debiec,
Paraskevi Christofidou,
Scott Nankervis,
Anna F Dominiczak,
Ahmed Bani-Mustafa,
Anthony J Balmforth,
Alistair S Hall,
Jeanette Erdmann,
Francois Cambien,
Panos Deloukas,
Christian Hengstenberg,
Chris Packard,
Heribert Schunkert,
Willem H Ouwehand,
Ian Ford,
Alison H Goodall,
Mark A Jobling,
Nilesh J Samani,
Maciej Tomaszewski
School of Health Sciences, University of Ballarat, Ballarat, VIC, Australia.
BACKGROUND A sexual dimorphism exists in the incidence and prevalence of coronary artery disease--men are more commonly affected than are age-matched women. We explored the role of the Y chromosome in coronary artery disease in the context of this sexual inequity. METHODS We genotyped 11 markers of the male-specific region of the Y chromosome in 3233 biologically unrelated British men from three cohorts: the British Heart Foundation Family Heart Study (BHF-FHS), West of Scotland Coronary Prevention Study (WOSCOPS), and Cardiogenics Study. On the basis of this information, each Y chromosome was tracked back into one of 13 ancient lineages defined as haplogroups. We then examined associations between common Y chromosome haplogroups and the risk of coronary artery disease in cross-sectional BHF-FHS and prospective WOSCOPS. Finally, we undertook functional analysis of Y chromosome effects on monocyte and macrophage transcriptome in British men from the Cardiogenics Study. FINDINGS Of nine haplogroups identified, two (R1b1b2 and I) accounted for roughly 90% of the Y chromosome variants among British men. Carriers of haplogroup I had about a 50% higher age-adjusted risk of coronary artery disease than did men with other Y chromosome lineages in BHF-FHS (odds ratio 1·75, 95% CI 1·20-2·54, p=0·004), WOSCOPS (1·45, 1·08-1·95, p=0·012), and joint analysis of both populations (1·56, 1·24-1·97, p=0·0002). The association between haplogroup I and increased risk of coronary artery disease was independent of traditional cardiovascular and socioeconomic risk factors. Analysis of macrophage transcriptome in the Cardiogenics Study revealed that 19 molecular pathways showing strong differential expression between men with haplogroup I and other lineages of the Y chromosome were interconnected by common genes related to inflammation and immunity, and that some of them have a strong relevance to atherosclerosis. INTERPRETATION The human Y chromosome is associated with risk of coronary artery disease in men of European ancestry, possibly through interactions of immunity and inflammation. FUNDING British Heart Foundation; UK National Institute for Health Research; LEW Carty Charitable Fund; National Health and Medical Research Council of Australia; European Union 6th Framework Programme; Wellcome Trust.
Hypertension. 2011 Dec 19;:
22184331
Monica Flores-Munoz,
Lorraine M Work,
Kirsten Douglas,
Laura Denby,
Anna F Dominiczak,
Delyth Graham,
Stuart A Nicklin
Institute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, United Kingdom.
The renin-angiotensin system regulates cardiovascular physiology via angiotensin II engaging the angiotensin type 1 or type 2 receptors. Classic actions are type 1 receptor mediated, whereas the type 2 receptor may counteract type 1 receptor activity. Angiotensin-converting enzyme 2 metabolizes angiotensin II to angiotensin-(1-7) and angiotensin I to angiotensin-(1-9). Angiotensin-(1-7) antagonizes angiotensin II actions via the receptor Mas. Angiotensin-(1-9) was shown recently to block cardiomyocyte hypertrophy via the angiotensin type 2 receptor. Here, we investigated in vivo effects of angiotensin-(1-9) via the angiotensin type 2 receptor. Angiotensin-(1-9)(100 ng/kg per minute) with or without the angiotensin type 2 receptor antagonist PD123 319 (100 ng/kg per minute) or PD123 319 alone was infused via osmotic minipump for 4 weeks into stroke-prone spontaneously hypertensive rats. We measured blood pressure by radiotelemetry and cardiac structure and function by echocardiography. Angiotensin-(1-9) did not affect blood pressure or left ventricular mass index but reduced cardiac fibrosis by 50%(P<0.01) through modulating collagen I expression, reversed by PD123 319 coinfusion. In addition, angiotensin-(1-9) inhibited fibroblast proliferation in vitro in a PD123 319-sensitive manner. Aortic myography revealed that angiotensin-(1-9) significantly increased contraction to phenylephrine compared with controls after N-nitro-l-arginine methyl ester treatment, an effect abolished by PD123 319 coinfusion (area under the curve: angiotensin-(1-9) N-nitro-l-arginine methyl ester=98.9±11.8%; control+N-nitro-l-arginine methyl ester=74.0±10.4%; P<0.01), suggesting that angiotensin-(1-9) improved basal NO bioavailability in an angiotensin type 2 receptor-sensitive manner. In summary, angiotensin-(1-9) reduced cardiac fibrosis and altered aortic contraction via the angiotensin type 2 receptor supporting a direct role for angiotensin-(1-9) in the renin-angiotensin system.
Hypertension. 2011 Dec 19;:
22184326
Erika Salvi,
Zoltán Kutalik,
Nicola Glorioso,
Paola Benaglio,
Francesca Frau,
Tatiana Kuznetsova,
Hisatomi Arima,
Clive Hoggart,
Jean Tichet,
Yury P Nikitin,
Costanza Conti,
Jitka Seidlerova,
Valérie Tikhonoff,
Katarzyna Stolarz-Skrzypek,
Toby Johnson,
Nabila Devos,
Laura Zagato,
Simonetta Guarrera,
Roberta Zaninello,
Andrea Calabria,
Benedetta Stancanelli,
Chiara Troffa,
Lutgarde Thijs,
Federica Rizzi,
Galina Simonova,
Sara Lupoli,
Giuseppe Argiolas,
Daniele Braga,
Maria C D'Alessio,
Maria F Ortu,
Fulvio Ricceri,
Maurizio Mercurio,
Patrick Descombes,
Maurizio Marconi,
John Chalmers,
Stephen Harrap,
Jan Filipovsky,
Murielle Bochud,
Licia Iacoviello,
Justine Ellis,
Alice V Stanton,
Maris Laan,
Sandosh Padmanabhan,
Anna F Dominiczak,
Nilesh J Samani,
Olle Melander,
Xavier Jeunemaitre,
Paolo Manunta,
Amnon Shabo,
Paolo Vineis,
Francesco P Cappuccio,
Mark J Caulfield,
Giuseppe Matullo,
Carlo Rivolta,
Patricia B Munroe,
Cristina Barlassina,
Jan A Staessen,
Jacques S Beckmann,
Daniele Cusi
Department of Medicine, Surgery, and Dentistry, Graduate School of Nephrology, University of Milano, Division of Nephrology, San Paolo Hospital, Milano, Italy; Filarete Foundation, Genomic and Bioinformatics Unit, Milano, Italy; Department of Medical Genetics, University of Lausanne, Lausanne, Switzerland; Swiss Institute of Bioinformatics, Lausanne, Switzerland; Hypertension and Related Diseases Centre-Azienda Ospedaliero-Universitaria, University of Sassari, Sassari, Italy; Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Diseases, University of Leuven, Leuven, Belgium; George Institute for Global Health, University of Sydney and the Royal Prince Alfred Hospital, Sydney, New South Wales, Australia; Department of Epidemiology and Biostatistics, School of Public Health, Imperial College of London, London, United Kingdom; Institut inter Régional pour la Santé, Tours, France; Institute of Internal Medicine, Siberian Branch of the Russian Academy of Medical Sciences, Novosibirsk, Russian; I Milano, Italy; 2nd Department of Internal Medicine, Charles University, Medical Faculty, Pilsen, Czech Republic; Department of Clinical and Experimental Medicine, University of Padova, Padova, Italy; First Department of Cardiology and Hypertension, Jagiellonian University Medical College, Krakow, Poland; Clinical Pharmacology and Genome Centre, William Harvey Research Institute, Barts and London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom; Institut National de la Santé et de la Recherche Médicale, UMRS-970, Paris Cardiovascular Research Center, Paris France; Chair of Nephrology, Università Vita Salute San Raffaele, Nephrology, Dialysis and Hypertension Unit, San Raffaele Scientific Institute, Milan, Italy; Human Genetics Foundation, Turin, Italy; Department of Medicine, University of Catania, Catania, Italy; KOS Genetic, Milano, Italy; Department of Genetics, Biology and Biochemistry, University of Torino and Human Genetics Foundation, Torino, Italy; Genomics Platform, National Center of Competence in Research "Frontiers in Genetics" University Medical Center University of Geneva, Geneva, Switzerland; Center of Transfusion Medicine and Immunohematology, Department of Regenerative Medicine, Foundation Istituto di Ricovero e Cura a Carattere Scientifico Ca' Granda Ospedale Maggiore Policlinico, Milano, Italy; Department of Physiology, University of Melbourne, Melbourne, Victoria, Australia; 2nd Medical Department, Cardiology and Angiology, 1st Medical Faculty, Charles University, Prague, Czech Republic; Institute of Social and Preventive Medicine, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland; Research Laboratories "John Paul II" Centre for High Technology Research and Education in Biomedical Sciences, Catholic University, Campobasso, Italy; Murdoch Childrens Research Institute, Department of Physiology, University of Melbourne, Melbourne, Victoria, Australia; Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland; Institute of Molecular and Cell Biology, University of Tartu, Tartu, Estonia; British Heart Foundation Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, United Kingdom; Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom; Hypertension and Cardiovascular Disease, Department of Clinical Sciences, Lund University, Malmö, Sweden; Centre of Emergency Medicine, Skåne University Hospital, Malmö, Sweden; University Paris Descartes, Paris, France; Assistance Publique Hopitaux de Paris, Department of Genetics, Hopital Europeen Georges Pompidou, Paris, France; IBM Haifa Research Lab, Haifa University Mount Carmel, Haifa, Israel; University of Warwick, Warwick Medical School, Coventry, United Kingdom; Genetic Epidemiology Unit, Department of Epidemiology, Maastricht University, Maastricht, The Netherlands; Service of Medical Genetics, Centre Hospitalier Universitaire Vaudois, University Hospital, Lausanne, Switzerland.
Essential hypertension is a multifactorial disorder and is the main risk factor for renal and cardiovascular complications. The research on the genetics of hypertension has been frustrated by the small predictive value of the discovered genetic variants. The HYPERGENES Project investigated associations between genetic variants and essential hypertension pursuing a 2-stage study by recruiting cases and controls from extensively characterized cohorts recruited over many years in different European regions. The discovery phase consisted of 1865 cases and 1750 controls genotyped with 1M Illumina array. Best hits were followed up in a validation panel of 1385 cases and 1246 controls that were genotyped with a custom array of 14 055 markers. We identified a new hypertension susceptibility locus (rs3918226) in the promoter region of the endothelial NO synthase gene (odds ratio: 1.54 [95% CI: 1.37-1.73]; combined P=2.58 · 10(-13)). A meta-analysis, using other in silico/de novo genotyping data for a total of 21 714 subjects, resulted in an overall odds ratio of 1.34 (95% CI: 1.25-1.44; P=1.032 · 10(-14)). The quantitative analysis on a population-based sample revealed an effect size of 1.91 (95% CI: 0.16-3.66) for systolic and 1.40 (95% CI: 0.25-2.55) for diastolic blood pressure. We identified in silico a potential binding site for ETS transcription factors directly next to rs3918226, suggesting a potential modulation of endothelial NO synthase expression. Biological evidence links endothelial NO synthase with hypertension, because it is a critical mediator of cardiovascular homeostasis and blood pressure control via vascular tone regulation. This finding supports the hypothesis that there may be a causal genetic variation at this locus.
J Hypertens. 2011 Nov 30;:
22134387
Ulf Neisius,
Grzegorz Bilo,
Chiara Taurino,
John D McClure,
Markus P Schneider,
Kalina Kawecka-Jaszcz,
Katarzyna Stolarz-Skrzypek,
Lukasz Klima,
Jan A Staessen,
Tatiana Kuznetsova,
Josep Redon,
Fernando Martinez,
Enrico A Rosei,
Maria L Muiesan,
Olle Melander,
Faiez Zannad,
Patrick Rossignol,
Stéphane Laurent,
Cedric Collin,
Laura Lonati,
Alberto Zanchetti,
Anna F Dominiczak,
Christian Delles
aBHF Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK bIstituto Auxologico Italiano, Milan, Italy cFirst Department of Cardiology and Hypertension, Jagiellonian University Medical College, Krakow, Poland dThe Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Diseases, University of Leuven, Leuven, Belgium eHypertension Clinic, Internal Medicine, Hospital Clinico, University of Valencia, Valencia, Spain fClinica Medica, Department of Medical and Surgical Sciences, University of Brescia, Brescia, Italy gDepartment of Clinical Sciences in Malmö, Lund University, Lund, Sweden hINSERM, Centre d'Investigation Clinique 9501 and Unité 961, Centre Hospitalier Universitaire, and the Department of Cardiology, Nancy University iPharmacology Department, Hopital Europeen Georges Pompidou, Paris, France jUniversity of Milan, Milan, Italy *Ulf Neisius and Grzegorz Bilo contributed equally to the writing of this article.
OBJECTIVE: We assessed the relationship between pulse pressure and intermediate cardiovascular phenotypes in a middle-aged cohort with high prevalence of hypertension. BACKGROUND: It has been suggested that central pulse pressure (cPP) is a better predictor of cardiovascular outcome than peripheral pulse pressure (pPP), particularly in the elderly. Yet, it is unclear if cPP provides additional prognostic information to pPP in younger individuals. METHODS: In 535 individuals we assessed cPP and pPP as well as the intermediate cardiovascular phenotypes pulse wave velocity (PWV; SphygmoCor, Complior, PulsePen), carotid intima-media thickness (C-IMT; carotid ultrasound), left-ventricular mass index (LVMI; echocardiography) and urinary albumin : creatinine ratio (ACR). cPP was derived noninvasively from brachial blood pressure by pulse wave analysis (PWA; SphygmoCor) based on radial pulse wave tonometry and a validated transfer function. RESULTS: The cohort contained 331 hypertensive participants of whom 84% were treated. The average age was 46 ± 16 years. When compared to pPP, cPP had stronger associations with PWV (r = 0.471 vs. r = 0.372; P < 0.01), C-IMT (r = 0.426 vs. r = 0.235; P < 0.01) and LVMI (r = 0.385 vs. r = 0.189; P < 0.01), but equal association with ACR (r = 0.236 vs. r = 0.226; P = n.s.). In contrast, after adjustment for age, mean arterial pressure, heart rate and hypertension status there was no significant difference between cPP and pPP for prediction of PWV (adjusted R, 0.399 vs. 0.413; P = 0.066), C-IMT (adjusted R, 0.399 vs. 0.413; P = 0.487) and LVMI (adjusted R, 0.181 vs. 0.170; P = 0.094) in multivariate analysis. CONCLUSION: In our middle-aged cohort with high prevalence of hypertension cPP is more closely correlated with cardiovascular phenotypes than pPP. When adjusted for relevant cofactors, however, cPP does not provide additional information beyond pPP.
Toby Johnson,
Tom R Gaunt,
Stephen J Newhouse,
Sandosh Padmanabhan,
Maciej Tomaszewski,
Meena Kumari,
Richard W Morris,
Ioanna Tzoulaki,
Eoin T O'Brien,
Neil R Poulter,
Peter Sever,
Denis C Shields,
Simon Thom,
Sasiwarang G Wannamethee,
Peter H Whincup,
Morris J Brown,
John M Connell,
Richard J Dobson,
Philip J Howard,
Charles A Mein,
Abiodun Onipinla,
Sue Shaw-Hawkins,
Yun Zhang,
George Davey Smith,
Ian N M Day,
Debbie A Lawlor,
Alison H Goodall,
F Gerald Fowkes,
Gonçalo R Abecasis,
Paul Elliott,
Vesela Gateva,
Peter S Braund,
Paul R Burton,
Christopher P Nelson,
Martin D Tobin,
Pim van der Harst,
Nicola Glorioso,
Hani Neuvrith,
Erika Salvi,
Jan A Staessen,
Andrea Stucchi,
Nabila Devos,
Xavier Jeunemaitre,
Pierre-François Plouin,
Jean Tichet,
Peeter Juhanson,
Elin Org,
Margus Putku,
Siim Sõber,
Gudrun Veldre,
Margus Viigimaa,
Anna Levinsson,
Annika Rosengren,
Dag S Thelle,
Claire E Hastie,
Thomas Hedner,
Wai K Lee,
Olle Melander,
Björn Wahlstrand,
Rebecca Hardy,
Andrew Wong,
Jackie A Cooper,
Jutta Palmen,
Li Chen,
Alexandre F R Stewart,
George A Wells,
Harm-Jan Westra,
Marcel G M Wolfs,
Robert Clarke,
Maria Grazia Franzosi,
Anuj Goel,
Anders Hamsten,
Mark Lathrop,
John F Peden,
Udo Seedorf,
Hugh Watkins,
Willem H Ouwehand,
Jennifer Sambrook,
Jonathan Stephens,
Juan-Pablo Casas,
Fotios Drenos,
Michael V Holmes,
Mika Kivimaki,
Sonia Shah,
Tina Shah,
Philippa J Talmud,
John Whittaker,
Chris Wallace,
Christian Delles,
Maris Laan,
Diana Kuh,
Steve E Humphries,
Fredrik Nyberg,
Daniele Cusi,
Robert Roberts,
Christopher Newton-Cheh,
Lude Franke,
Alice V Stanton,
Anna F Dominiczak,
Martin Farrall,
Aroon D Hingorani,
Nilesh J Samani,
Mark J Caulfield,
Patricia B Munroe
Clinical Pharmacology and Barts and The London Genome Centre, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, UK. t.johnson@qmul.ac.uk
Raised blood pressure (BP) is a major risk factor for cardiovascular disease. Previous studies have identified 47 distinct genetic variants robustly associated with BP, but collectively these explain only a few percent of the heritability for BP phenotypes. To find additional BP loci, we used a bespoke gene-centric array to genotype an independent discovery sample of 25,118 individuals that combined hypertensive case-control and general population samples. We followed up four SNPs associated with BP at our p < 8.56 × 10(-7) study-specific significance threshold and six suggestively associated SNPs in a further 59,349 individuals. We identified and replicated a SNP at LSP1/TNNT3, a SNP at MTHFR-NPPB independent (r(2)= 0.33) of previous reports, and replicated SNPs at AGT and ATP2B1 reported previously. An analysis of combined discovery and follow-up data identified SNPs significantly associated with BP at p < 8.56 × 10(-7) at four further loci (NPR3, HFE, NOS3, and SOX6). The high number of discoveries made with modest genotyping effort can be attributed to using a large-scale yet targeted genotyping array and to the development of a weighting scheme that maximized power when meta-analyzing results from samples ascertained with extreme phenotypes, in combination with results from nonascertained or population samples. Chromatin immunoprecipitation and transcript expression data highlight potential gene regulatory mechanisms at the MTHFR and NOS3 loci. These results provide candidates for further study to help dissect mechanisms affecting BP and highlight the utility of studying SNPs and samples that are independent of those studied previously even when the sample size is smaller than that in previous studies.
Department of Endocrinology, Western Infirmary, Glasgow G11 6NT, UK.
Catecholamines (epinephrine and norepinephrine) are synthesised and produced by the adrenal medulla and postganglionic nerve fibres of the sympathetic nervous system. It is known that essential hypertension has a significant neurogenic component, with the rise in blood pressure mediated at least in part by overactivity of the sympathetic nervous system. Moreover, novel therapeutic strategies aimed at reducing sympathetic activity show promise in the treatment of hypertension. This article reviews recent advances within this rapidly changing field, particularly focusing on the role of genetic polymorphisms within key catecholamine biosynthetic enzymes, cofactors, and storage molecules. In addition, mechanisms linking the sympathetic nervous system and other adverse cardiovascular states (obesity, insulin resistance, dyslipidaemia) are discussed, along with speculation as to how recent scientific advances may lead to the emergence of novel antihypertensive treatments.
J Hypertens. 2012 Jan ;30 (1):117-23
22052066
David M Carty,
Lesley A Anderson,
Catherine N Duncan,
David P Baird,
Laura K Rooney,
Anna F Dominiczak,
Christian Delles
BHF Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary & Life Sciences, University of Glasgow, Glasgow, UK.
OBJECTIVE Endothelial dysfunction is known to play a key role in the pathogenesis of preeclampsia, but the majority of methods for its detection are too invasive to be used in pregnancy. In this study we report a novel method - peripheral arterial tonometry (PAT)- for examining microcirculatory function in pregnancy. METHODS One hundred and eighty women with at least two risk factors for preeclampsia were examined at gestational weeks 16 and 28; 80 women were examined at 6-9 months postnatally. Twenty-four women developed preeclampsia or pregnancy-induced hypertension (cases), 156 remained normotensive (controls). PAT was measured using fingertip pneumatic probes; after baseline recordings the study arm was occluded with a blood pressure cuff then released after 5 min, causing reactive hyperaemia. PAT recordings pre and post occlusion were used to generate the reactive hyperaemia index (RHI). RESULTS RHI was significantly lower at gestational week 28 compared to week 16, both in cases and controls. Baseline pulse amplitude was significantly higher at week 28 compared to week 16. There was no difference in RHI at either week 16 or 28 between cases and controls. Postnatally, there was no difference in RHI between cases and controls, but baseline pulse amplitude was lower in affected women. CONCLUSION PAT and other methods which rely on flow-mediated dilatation for detection of endothelial dysfunction are less likely to be reliable in later pregnancy, when women are more vasodilated. PAT did not predict the development of hypertensive pregnancy complications, but demonstrated a relative peripheral vasoconstriction in affected women postnatally.
|
FP7 Partner
Add BioInfo.PL bioinformatics lab
to Your FP7 application bioinfo.pl
|