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Cardiovascular biomarkers predict fragility fractures in older adults.

https://arctichealth.org/en/permalink/ahliterature299736
Source
Heart. 2019 03; 105(6):449-454
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
03-2019
Author
Madeleine Johansson
Fabrizio Ricci
Giuseppe Di Martino
Cecilia Rogmark
Richard Sutton
Viktor Hamrefors
Olle Melander
Artur Fedorowski
Author Affiliation
Department of Clinical Sciences, Faculty of Medicine, Clinical Research Center, Lund University, Malmö, Sweden.
Source
Heart. 2019 03; 105(6):449-454
Date
03-2019
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Adrenomedullin - blood
Aged
Atrial Natriuretic Factor - blood
Biomarkers - blood
Body mass index
Cardiovascular System - metabolism
Cohort Studies
Correlation of Data
Endothelin-1 - blood
Female
Fractures, Bone - blood
Humans
Independent Living - statistics & numerical data
Male
Middle Aged
Peptide Fragments - blood
Prospective Studies
Protein Precursors - blood
Reproducibility of Results
Risk assessment
Risk factors
Sweden
Vasopressins - blood
Abstract
To assess the role of four biomarkers of neuroendocrine activation and endothelial dysfunction in the longitudinal prediction of fragility fractures.
We analysed a population-based prospective cohort of 5415 community-dwelling individuals (mean age, 68.9±6.2 years) enrolled in the Malmö Preventive Project followed during 8.1±2.9 years, and investigated the longitudinal association between C-terminal pro-arginine vasopressin (CT-proAVP), C-terminal endothelin-1 precursor fragment (CT-proET-1), the mid-regional fragments of pro-adrenomedullin (MR-proADM) and pro-atrial natriuretic peptide (MR-proANP), and incident vertebral, pelvic and extremity fractures.
Overall, 1030 (19.0%) individuals suffered vertebral, pelvic or extremity fracture. They were older (70.7±5.8 vs 68.4±6.3 years), more likely women (46.9% vs 26.3%), had lower body mass index and diastolic blood pressure, were more often on antihypertensive treatment (44.1% vs 38.4%) and had more frequently history of fracture (16.3% vs 8.1%). Higher levels of MR-proADM (adjusted HR (aHR) per 1 SD: 1.51, 95% CI 1.01 to 2.28, p
Notes
CommentIn: Heart. 2019 Mar;105(6):427-428 PMID 30361269
PubMed ID
30322844 View in PubMed
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Pharmacogenetic implications for eight common blood pressure-associated single-nucleotide polymorphisms.

https://arctichealth.org/en/permalink/ahliterature125023
Source
J Hypertens. 2012 Jun;30(6):1151-60
Publication Type
Article
Date
Jun-2012
Author
Viktor Hamrefors
Marketa Sjögren
Peter Almgren
Björn Wahlstrand
Sverre Kjeldsen
Thomas Hedner
Olle Melander
Author Affiliation
Department of Clinical Sciences, Lund University, Malmö, Norway. Viktor.Hamrefors@med.lu.se
Source
J Hypertens. 2012 Jun;30(6):1151-60
Date
Jun-2012
Language
English
Publication Type
Article
Keywords
Aged
Antihypertensive Agents - therapeutic use
Blood Pressure - genetics
Female
Humans
Hypertension - drug therapy - genetics - physiopathology
Male
Middle Aged
Pharmacogenetics
Polymorphism, Single Nucleotide
Sweden
Abstract
We aimed to test whether eight common recently identified single-nucleotide polymorphisms (SNPs), strongly associated with blood pressure (BP) in the population, also have impact on the degree of BP reduction by antihypertensive agents with different mechanisms.
In 3863 Swedish hypertensive patients, we related number of unfavorable alleles of each SNP (i.e. alleles associated with higher baseline BP) to the magnitude of BP reduction during 6 months of monotherapy with either a beta-blocker, a thiazide diuretic or diltiazem.
For six SNPs (rs16998073, rs1378942, rs3184504, rs1530440, rs16948048, rs17367504) no pharmacogenetic interactions were suggested, whereas two SNPs showed nominal evidence of association with treatment response: PLCD3-rs12946454 associated with more SBP (beta?=?1.53?mmHg per unfavorable allele; P?=?0.010) and DBP (beta?=?0.73?mmHg per unfavorable allele; P?=?0.014) reduction in patients treated with diltiazem, in contrast to those treated with beta-blockers or diuretics wherein no treatment response association was found. CYP17A1-rs11191548 associated with less DBP reduction (beta?=?-1.26?mmHg per unfavorable allele; P?=?0.018) in patients treated with beta-blockers or diuretics, whereas there was no treatment response association in diltiazem-treated patients. However, if accounting for multiple testing, the significant associations for rs12946454 and rs11191548 were attenuated.
For a majority of these, eight recently identified BP-associated SNPs, there are probably no important pharmacogenetic interactions for BP reduction with use of beta-blockers, diuretics or diltiazem. Whether the nominally significant associations for rs12946454 and rs11191548 are true signals and could be of possible clinical relevance for deciding treatment of polygenic essential hypertension should be further tested.
PubMed ID
22525200 View in PubMed
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Smoking modifies the associated increased risk of future cardiovascular disease by genetic variation on chromosome 9p21.

https://arctichealth.org/en/permalink/ahliterature259037
Source
PLoS One. 2014;9(1):e85893
Publication Type
Article
Date
2014
Author
Viktor Hamrefors
Bo Hedblad
George Hindy
J Gustav Smith
Peter Almgren
Gunnar Engström
Marketa Sjögren
Klas Gränsbo
Marju Orho-Melander
Olle Melander
Source
PLoS One. 2014;9(1):e85893
Date
2014
Language
English
Publication Type
Article
Keywords
Aged
Cardiovascular Diseases - etiology - genetics - mortality
Chromosomes, Human, Pair 9 - genetics
Educational Status
Female
Gene Frequency
Genetic Predisposition to Disease - etiology - genetics
Genotype
Humans
Incidence
Male
Middle Aged
Polymorphism, Single Nucleotide
Proportional Hazards Models
Prospective Studies
Questionnaires
Registries - statistics & numerical data
Risk factors
Smoking - adverse effects
Survival Rate
Sweden - epidemiology
Abstract
Genetic predisposition for cardiovascular disease (CVD) is likely to be modified by environmental exposures. We tested if the associated risk of CVD and CVD-mortality by the single nucleotide polymorphism rs4977574 on chromosome 9p21 is modified by life-style factors.
A total of 24,944 middle-aged subjects (62% females) from the population-based Malm?-Diet-and-Cancer-Cohort were genotyped. Smoking, education and physical activity-levels were recorded. Subjects were followed for 15 years for incidence of coronary artery disease (CAD; N?=?2309), ischemic stroke (N?=?1253) and CVD-mortality (N?=?1156). Multiplicative interactions between rs4977574 and life-style factors on endpoints were tested in Cox-regression-models. We observed an interaction between rs4977574 and smoking on incident CAD (P?=?0.035) and CVD-mortality (P?=?0.012). The hazard ratios (HR) per risk allele of rs4977574 were highest in never smokers (N?=?9642) for CAD (HR?=?1.26; 95% CI 1.13-1.40; P
Notes
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PubMed ID
24465769 View in PubMed
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