Peter M Nilsson

Skåne University Hospital, Malmö, Skåne, Sweden

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Publications (492)2663.89 Total impact

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    ABSTRACT: Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone with extrapancreatic effects beyond glycemic control. Here we demonstrate unexpected effects of GIP signaling in the vasculature. GIP induces the expression of the pro-atherogenic cytokine osteopontin (OPN) in mouse arteries, via local release of endothelin-1 (ET-1) and activation of cAMP response element binding protein (CREB). Infusion of GIP increases plasma OPN levels in healthy individuals. Plasma ET-1 and OPN levels are positively correlated in patients with critical limb ischemia. Fasting GIP levels are higher in individuals with a history of cardiovascular disease (myocardial infarction, stroke) when compared to controls. GIP receptor (GIPR) and OPN mRNA levels are higher in carotid endarterectomies from patients with symptoms (stroke, transient ischemic attacks, amaurosis fugax) than in asymptomatic patients; and expression associates to parameters characteristic of unstable and inflammatory plaques (increased lipid accumulation, macrophage infiltration and reduced smooth muscle cell content). While GIPR expression is predominantly endothelial in healthy arteries from human, mouse, rat and pig; remarkable up-regulation is observed in endothelial and smooth muscle cells upon culture conditions yielding a "vascular disease-like" phenotype. Moreover, a common variant rs10423928 in the GIPR gene associated with increased risk of stroke in type 2 diabetes patients.
    Diabetes 09/2015; DOI:10.2337/db15-0122 · 8.10 Impact Factor
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    ABSTRACT: BACKGROUND/OBJECTIVE:Genome-wide-association studies have identified numerous BMI-associated variants, but it is unclear how these relate to weight gain in adults at different ages. METHODS: We examined the association of a genetic risk score (GRS), consisting of 31 BMI-associated variants, with an annual weight gain (AWG) and a substantial weight gain (SWG) of 10% by comparing self-reported weight at 20 years (y) with baseline weight (mean: 58 y; standard deviation (s.d.): 8y) in 21407 participants from the Malmö Diet and Cancer Study (MDCS), and comparing baseline weight to weight at follow-up (mean: 73y; s.d.: 6y) among 2673 participants. Association between GRS and AWG and SWG was replicated in 4327 GLACIER participants (mean: 45y; s.d.: 7y) with 10y follow-up. Cohort-specific results were pooled by fixed-effect meta-analyses. RESULTS: In MDCS, the GRS was associated with increased AWG (β: 0.003; s.e: 0.01; P: 7 × 10-8) and increased odds for SWG (odds ratio (OR) 1.01 (95% confidence interval (CI): 1.00, 1.02); P: 0.013) per risk-allele from age 20y, but unexpectedly with decreased AWG (β: -0.006; s.e: 0.002; P: 0.009) and decreased odds for SWG OR 0.96 (95% CI: 0.93, 0.98); P: 0.001) between baseline and follow-up. Effect estimates from age 20y to baseline differed significantly from those from baseline to follow-up (P: 0.0002 for AWG and P: 0.0001 for SWG). Similar to MDCS, the GRS was associated with decreased odds for SWG OR 0.98 (95% CI: 0.96, 1.00); P: 0.029) from baseline to follow-up in GLACIER. In meta-analyses (n=7000), the GRS was associated with decreased AWG (β: -0.005; s.e: 0.002; P: 0.002) and decreased odds for SWG OR 0.97 (95% CI: 0.96, 0.99); P: 0.001) per risk-allele. CONCLUSION: Our results provide convincing evidence for a paradoxical inversed relationship between a high number of BMI-associated risk-alleles and less weight gain during and after middle-age, in contrast to the expected increased weight gain seen in younger age.
    International Journal of Obesity 09/2015; 10.1038/ijo.2015.180. DOI:10.1038/ijo.2015.180 · 5.00 Impact Factor
  • Journal of Clinical Hypertension 09/2015; DOI:10.1111/jch.12671 · 2.85 Impact Factor
  • International journal of cardiology 09/2015; 194. DOI:10.1016/j.ijcard.2015.05.081 · 4.04 Impact Factor
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    ABSTRACT: Substitution of carbohydrates with fat in a diet for type 2 diabetes patients is still debated. This study aimed to investigate the association between dietary carbohydrate intake and isocaloric substitution with (i) total fat, (ii) saturated fatty acids (SFA), (iii) mono-unsaturated fatty acids (MUFA) and (iv) poly-unsaturated fatty acids (PUFA) with all-cause and cardiovascular (CVD) mortality risk and 5-year weight change in patients with type 2 diabetes. The study included 6192 patients with type 2 diabetes from 15 cohorts of the European Prospective Investigation into Cancer and Nutrition (EPIC). Dietary intake was assessed at recruitment with country-specific food-frequency questionnaires. Cox and linear regression were used to estimate the associations with (CVD) mortality and weight change, adjusting for confounders and using different methods to adjust for energy intake. After a mean follow-up of 9.2 y ± SD 2.3 y, 791 (13%) participants had died, of which 268 (4%) due to CVD. Substituting 10 g or 5 energy% of carbohydrates by total fat was associated with a higher all-cause mortality risk (HR 1.07 [1.02-1.13]), or SFAs (HR 1.25 [1.11-1.40]) and a lower risk when replaced by MUFAs (HR 0.89 [0.77-1.02]). When carbohydrates were substituted with SFAs (HR 1.22 [1.00-1.49]) or PUFAs (HR 1.29 [1.02-1.63]) CVD mortality risk increased. The 5-year weight was lower when carbohydrates were substituted with total fat or MUFAs. These results were consistent over different energy adjustment methods. In diabetes patients, substitution of carbohydrates with SFAs was associated with a higher (CVD) mortality risk and substitution by total fat was associated with a higher all-cause mortality risk. Substitution of carbohydrates with MUFAs may be associated with lower mortality risk and weight reduction. Instead of promoting replacement of carbohydrates by total fat, dietary guideline should continue focusing on replacement by fat-subtypes; especially SFAs by MUFAs. Copyright © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.
    Clinical nutrition (Edinburgh, Scotland) 08/2015; DOI:10.1016/j.clnu.2015.08.003 · 4.48 Impact Factor
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    ABSTRACT: Background/objective: The present study tested the hypothesis that obesity-related changes in carotid intima-media thickness (IMT) might represent not only preclinical atherosclerosis but an adaptive remodeling meant to preserve circumferential wall stress (CWS) in altered hemodynamic conditions characterized by body size-dependent increase in stroke volume (SV) and blood pressure (BP). Subjects/methods: Common carotid artery (CCA) luminal diameter (LD), IMT and CWS were measured in three different populations in order to study: (A) cross-sectional associations between SV, BP, anthropometric parameters and CCA LD (266 healthy subjects with wide range of body weight (24-159 kg)); (B) longitudinal associations between CCA LD and 3-year IMT progression rate (ΔIMT; 571 healthy non-obese subjects without increased cardiovascular (CV) risk); (C) the impact of obesity on CCA geometry and CWS (88 obese subjects without CV complications and 88 non-obese subjects matched for gender and age). Results: CCA LD was independently associated with SV that was determined by body size. In the longitudinal study, baseline LD was an independent determinant of ΔIMT, and ΔIMT of subjects in the highest LD quartile was significantly higher (28±3 μm) as compared with those in the lower quartiles (8±3, 16±4 and 16±3 μm, P=0.001, P<0.05 and P=0.01, respectively). In addition, CCA CWS decreased during the observational period in the highest LD quartile (from 54.2±8.6 to 51.6±7.4 kPa, P<0.0001). As compared with gender- and age-matched lean individuals, obese subjects had highly increased CCA LD and BP (P<0.0001 for both), but only slightly higher CWS (P=0.05) due to a significant increase in IMT (P=0.005 after adjustment for confounders). Conclusions: Our findings suggest that in obese subjects, the CCA wall thickens to compensate the luminal enlargement caused by body size-induced increase in SV, and therefore, to normalize the wall stress. CCA diameter in obesity could represent an additional biomarker, depicting the impact of altered hemodynamics on arterial wall.
    Nutrition & Diabetes 08/2015; 5(8):e177. DOI:10.1038/nutd.2015.26 · 2.65 Impact Factor
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    Emma von Wowern · Gerd Östling · Peter M Nilsson · Per Olofsson
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    ABSTRACT: Arterial stiffness is an independent risk factor for cardiovascular morbidity and can be assessed by applanation tonometry by measuring pulse wave velocity (PWV) and augmentation index (AIX) by pressure pulse wave analysis (PWA). As an inexpensive and operator independent alternative, photoelectric plethysmography (PPG) has been introduced with analysis of the digital volume pulse wave (DPA) and its second derivatives of wave reflections. The objective was to investigate the repeatability of arterial stiffness parameters measured by digital pulse wave analysis (DPA) and the associations to applanation tonometry parameters. 112 pregnant and non-pregnant individuals of different ages and genders were examined with SphygmoCor arterial wall tonometry and Meridian DPA finger photoplethysmography. Coefficients of repeatability, Bland-Altman plots, intraclass correlation coefficients and correlations to heart rate (HR) and body height were calculated for DPA variables, and the DPA variables were compared to tonometry variables left ventricular ejection time (LVET), PWV and AIX. No DPA variable showed any systematic measurement error or excellent repeatability, but dicrotic index (DI), dicrotic dilatation index (DDI), cardiac ejection elasticity index (EEI), aging index (AI) and second derivatives of the crude pulse wave curve, b/a and e/a, showed good repeatability. Overall, the correlations to AIX were better than to PWV, with correlations coefficients >0.70 for EEI, AI and b/a. Considering the level of repeatability and the correlations to tonometry, the overall best DPA parameters were EEI, AI and b/a. The two pansystolic time parameters, ejection time compensated (ETc) by DPA and LVET by tonometry, showed a significant but weak correlation. For estimation of the LV function, ETc, EEI and b/a are suitable, for large artery stiffness EEI, and for small arteries DI and DDI. The only global parameter, AI, showed a high repeatability and the overall best correlations with AIX and PWV.
    PLoS ONE 08/2015; 10(8):e0135659. DOI:10.1371/journal.pone.0135659 · 3.23 Impact Factor
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    ABSTRACT: In experimental studies, enkephalins (ENKs) and related opioids have been implicated as negative regulators of breast cancer development by enhancing immune-mediated tumoral defense as well as directly inhibiting cancer cells. We hypothesized that plasma levels of ENKs are predictive of the long-term breast cancer risk. Therefore, our objective was to measure pro-ENK A, a surrogate for mature ENK, and evaluate its predictive value for the development of breast cancer in a large population of middle-aged women and an independent study population. We related pro-ENK in fasting plasma samples from 1,929 healthy women (mean age, 57.6 ± 5.9 years) of the Malmö Diet and Cancer study to breast cancer incidence (n = 123) during a median follow-up of 14.7 years. For replication, pro-ENK was related to risk of breast cancer (n = 130) in an older independent sample from the Malmö Preventive Project consisting of 1,569 women (mean age, 70.0 ± 4.4 years). In the Malmö Diet and Cancer study, pro-ENK was inversely related to the risk of incident breast cancer, with a hazard ratio per each standard deviation increment of logarithm-transformed pro-ENK of 0.72 (95% CI, 0.62 to 0.85; P < .001). The linear elevation of risk over pro-ENK quartiles 3, 2, and 1, with the fourth quartile as a reference, was 1.38 (95% CI, 0.73 to 2.64), 2.29 (95% CI, 1.26 to 4.15), and 3.16 (95% CI, 1.78 to 5.60; for the trend, P < .001), respectively. These results were replicated in the Malmö Preventive Project, where the continuous odds ratio for incident breast cancer was 0.63 (95% CI, 0.52 to 0.76; P < .001) and the risk over pro-ENK quartiles 3, 2, and 1, where the fourth quartile was the reference, was 2.48 (95% CI, 1.25 to 4.94), 2.94 (95% CI, 1.50 to 5.77), and 4.81 (95% CI, 2.52 to 9.18; for the trend, P < .001), respecitvely. Low fasting plasma concentration of the opioid precursor peptide pro-ENK is associated with an increased risk of future breast cancer in middle-aged and postmenopausal women. © 2015 by American Society of Clinical Oncology.
    Journal of Clinical Oncology 07/2015; 33(24). DOI:10.1200/JCO.2014.59.7682 · 18.43 Impact Factor
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    ABSTRACT: Obesity is a disorder that develops from the interaction between genotype and environment involving social, behavioral, cultural, and physiological factors. Obesity increases the risk for type 2 diabetes mellitus, hypertension, cardiovascular disease, cancer, musculoskeletal disorders, chronic kidney and pulmonary disease. Although obesity is clearly associated with an increased prevalence of hypertension, many obese individuals may not develop hypertension. Protecting factors may exist and it is important to understand why obesity is not always related to hypertension. The aim of this review is to highlight the knowledge gap for the association between obesity, hypertension, and potential genetic and racial differences or environmental factors that may protect obese patients against the development of hypertension and other co-morbidities. Specific mutations in the leptin and the melaninocortin receptor genes in animal models of obesity without hypertension, the actions of α-melanocyte stimulating hormone, and SNS activity in obesity-related hypertension may promote recognition of protective and promoting factors for hypertension in obesity. Furthermore, gene-environment interactions may have the potential to modify gene expression and epigenetic mechanisms could also contribute to the heritability of obesity-induced hypertension. Finally, differences in nutrition, gut microbiota, exposure to sun light and exercise may play an important role in the presence or absence of hypertension in obesity.
    Journal of Hypertension 06/2015; 33(8). DOI:10.1097/HJH.0000000000000645 · 4.72 Impact Factor
  • Peter M Nilsson
    Hypertension 06/2015; 66(2). DOI:10.1161/HYPERTENSIONAHA.115.05621 · 6.48 Impact Factor
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    ABSTRACT: Background: The observational relationship between obesity and periodontitis is widely known, yet causal evidence is lacking. Our objective was to investigate causal associations between periodontitis and body mass index (BMI). Methods: We performed Mendelian randomization analyses with BMI-associated loci combined in a genetic risk score (GRS) as the instrument for BMI. All analyses were conducted within the Gene-Lifestyle Interactions and Dental Endpoints (GLIDE) Consortium in 13 studies from Europe and the USA, including 49,066 participants with clinically assessed (seven studies, 42.1% of participants) and self-reported (six studies, 57.9% of participants) periodontitis and genotype data (17,672/31,394 with/without periodontitis); 68,761 participants with BMI and genotype data; and 57,871 participants (18,881/38,990 with/without periodontitis) with data on BMI and periodontitis. Results: In the observational meta-analysis of all participants, the pooled crude observational odds ratio (OR) for periodontitis was 1.13 [95% confidence interval (CI): 1.03, 1.24] per standard deviation increase of BMI. Controlling for potential confounders attenuated this estimate (OR = 1.08; 95% CI:1.03, 1.12). For clinically assessed periodontitis, corresponding ORs were 1.25 (95% CI: 1.10, 1.42) and 1.13 (95% CI: 1.10, 1.17), respectively. In the genetic association meta-analysis, the OR for periodontitis was 1.01 (95% CI: 0.99, 1.03) per GRS unit (per one effect allele) in all participants and 1.00 (95% CI: 0.97, 1.03) in participants with clinically assessed periodontitis. The instrumental variable meta-analysis of all participants yielded an OR of 1.05 (95% CI: 0.80, 1.38) per BMI standard deviation, and 0.90 (95% CI: 0.56, 1.46) in participants with clinical data. Conclusions: Our study does not support total adiposity as a causal risk factor for periodontitis, as the point estimate is very close to the null in the causal inference analysis, with wide confidence intervals.
    International Journal of Epidemiology 06/2015; 44(2). DOI:10.1093/ije/dyv075 · 9.18 Impact Factor
  • P M Nilsson · E Nilsson · M Gottsäter · G Östling
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    ABSTRACT: Arterial stiffness (AS) in the aorta is a well-documented and independent risk marker of cardiovascular disease risk and total mortality according to meta-analyses. Aortic AS can be measured by carotid-femoral pulse wave velocity (c-f PWV) as the "golden standard" method. A surrogate marker is pulse pressure (PP) during resting conditions, reflecting isolated systolic hypertension. During ageing the amplification of central blood pressure (cBP) in relation to brachial BP (bBP) is reduced. Our aim was to investigate cross-sectional associations between c-f PWV and cPP as well as bPP in an elderly population. We examined a total of 3001 subjects (mean age 72 years, 38% men) from MDCS by use of Sphygmocor® for determination of c-f PWV and pulse wave analysis (PWA) in arteria radialis after an additional mean 30 minutes (range: 15-40 min) of supine rest in a quiet room and well standardized procedures. PWA derived data were used for estimation of central hemodynamics by a transfer function in the device after addition of data on resting brachial BP. Finally, the difference (delta) in bBP during 30 minutes of rest between PWV and PWA measurements was calculated. Adjustment was made for age and sex. Mean values (SD) were for bBP: 131.0/73.4 (17.1/8.8) mmHg and for cBP: 122.3/74.4 (16.8/9.0) mmHg, with corresponding bPP: 57.5 (12.9) mmHg and cPP: 48.0 (12.3) mmHg, respectively. The pulse pressure amplification (bPP/cPP) was 21.2 (10.5) percentage. The mean c-f PWV was 10.5 (2.5) m/s. In multiple regression analysis after adjustment for age and sex, c-f PWV correlated significantly (p<0.001) and separately with both bPP (r= 0.37) and cPP (r= 0.29).: Mean c-f PWV levels in cPP quartiles ranged from 9.4 to 11.7 m/s, and in bPP quartiles from 9.2 to 12.1 m/s. c-f PWV was inversely correlated with delta bBP (r= -0.09; p<0.001) after full adjustment. In elderly subjects c-f PWV (as a marker of AS) is modestly associated with both central and brachial PP, but not more closely with central PP as was expected. Selective survival bias may have influenced the findings.
    Journal of Hypertension 06/2015; 33 Suppl 1 - ESH 2015 Abstract Book:e63. DOI:10.1097/ · 4.72 Impact Factor
  • A Fawad · C Schultz · P M Nilsson · M Orho-Melander · O Melander
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    ABSTRACT: Neurotensin is released from the gut after fat intake and has a role in appetite regulations. Proneurotensin is a stable fragment of the neurotensin precursor hormone and fasting plasma proneurotensin levels have shown to be significantly associated with the development of cardiovascular disease in middle aged participants of the Malmö Diet and Cancer Study. Here, we aimed at replicating the initial findings in an independent second cohort and to extend its validity to an older population. Malmö Preventive Project (MPP) is a Swedish population based prospective study which comprised 18240 subjects for reexamination in 2002-2006. Fasting proneurotensin was measured in plasma from a random sample of 4804 participants (Age 69 SD (6,2), 68% Male). Multivariate Cox proportional hazard models adjusted for age, sex, use of antihypertensive medications, systolic blood pressure, BMI, current smoking, high density lipoprotein cholesterol (HDL-C), LDL-C, history of diabetes were used to relate the log transformed levels of fasting proneurotensin to the risk of first fatal or non-fatal cardiovascular event (myocardial infarction or stroke) in the mean follow up time of up to 6.5 years. There were 456 cardiovascular events observed in the study. Hazard ratios (HR) for CVD were expressed per 1 (SD) increment of log transformed proneurotensin for cardiovascular disease as HR 1,102; 95% CI; 1,006-1,088; P = 0,037. In addition, proneurotensin was divided in to quartiles where quartile 1 defined as (Ref = 1). The risk of CVD was 1,107(0,848-1,444), 1,349 (1,040-1,749), 1,336 (1,016-1,757) in quartile 2-4 when compared with the reference quartile (P for trend = 0.013). Fasting proneurotensin levels are independently associated with the risk of developing cardiovascular disease which replicates the findings in MDC study.
    Journal of Hypertension 06/2015; 33 Suppl 1 - ESH 2015 Abstract Book:e11. DOI:10.1097/01.hjh.0000467381.67485.4c · 4.72 Impact Factor
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    ABSTRACT: High dietary salt is a leading risk for death and disability largely by causing increased blood pressure. Other associated health risks include gastric and renal cell cancers, osteoporosis, renal stones, and increased disease activity in multiple sclerosis, headache, increased body fat and Meniere's disease. The World Hypertension League (WHL) has prioritized advocacy for salt reduction. WHL resources and actions include a non-governmental organization policy statement, dietary salt fact sheet, development of standardized nomenclature, call for quality research, collaboration in a weekly salt science update, development of a process to set recommended dietary salt research standards and regular literature reviews, development of adoptable power point slide sets to support WHL positions and resources, and critic of weak research studies on dietary salt. The WHL plans to continue to work with multiple governmental and non-governmental organizations to promote dietary salt reduction towards the World Health Organization (WHO) recommendations.
    06/2015; 5(3):238-42. DOI:10.3978/j.issn.2223-3652.2015.04.08
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    ABSTRACT: To explore possible hemodynamic and glucometabolic determinants of left ventricular filling pressures as assessed by the non-invasive surrogate marker, averaged E/é, in otherwise healthy, middle-aged male survivors from a random population sample. Prospective population-based cohort study examining associations between hemodynamic factors [systolic blood pressure (SBP), heart rate (HR)), glucometabolic factors (fasting blood glucose, fasting plasma insulin, Homeostatic Model Assessment (HOMA) derived indices of beta-cell function (HOMA-2B) and insulin sensitivity (HOMA-2S)], other traditional cardiovascular risk factors [age, smoking status, body mass index (BMI), total serum cholesterol, serum creatinine] assessed at baseline, and values of E/é assessed at follow-up examination, using multivariable linear regression analysis (significance level 0.05, p-stay 0.20 on multivariable analysis). Subjects with prevalent cardiovascular disease and/or diabetes mellitus were excluded. E/é was positively skewed and, therefore, naturally log-transformed, as was fasting plasma insulin. HOMA-indices were assessed as continuous variables, both non-transformed and after natural log-transformation, as well as categorically, using quartiles. Study subjects were included 1974-1992, whilst the follow-up with echocardiography was performed 2002-2006. The final study population comprised 246 men with a median (IQR) age of 47 (47-48) years. Median (IQR) follow-up time was 28 (27-28) years, and median (IQR) E/é was 10 (8-12). In univariable analyses, E/é was associated positively with higher age, BMI, and serum creatinine, and negatively with shorter follow-up time. The multivariable model (adjusted r = 0.15) included all of these variables, i.e. age (beta = 0.016 per year [95% confidence interval (CI), 0.006 to 0.027]; p = 0.002), BMI (beta = 0.03 per kg/m [95% CI, 0.02 to 0.04]; p < 0.0001), serum creatinine (beta = 0.002 per micromole/l [95% CI, -0.001 to 0.005]; p = 0.18), and time elapsed between baseline examination and echocardiography (beta = -0.03 per year [-0.06 to -0.01]; p = 0.01). We did not find any significant interactions in the prediction of E/é. In a prospective population-based cohort study including apparently healthy, middle-aged male subjects, higher age, BMI, and creatinine, but not SBP or HR, were significantly associated with higher left ventricular filling pressures as assessed by averaged E/é.
    Journal of Hypertension 06/2015; 33 Suppl 1 - ESH 2015 Abstract Book:e67. DOI:10.1097/01.hjh.0000467530.97498.73 · 4.72 Impact Factor
  • M Pareek · M L Nielsen · M Leósdóttir · P M Nilsson · M H Olsen
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    ABSTRACT: Cardiac troponins are biomarkers of myocardial injury and serve both diagnostic and prognostic purposes. Even mild elevations represent subclinical myocardial damage in the general population. The objective of this study was to investigate the relationship between glucometabolic status and cardiac troponin T in middle-aged or older apparently healthy subjects. We examined cross-sectional associations between high-sensitivity cardiac troponin T (hsTnT) and FPG categorized as normal fasting glucose (NFG: FPG</=6.0mmol/L), impaired fasting glucose (IFG: FPG 6.1-6.9mmol/L), and diabetes mellitus (DM: FPG>/=7.0mmol/L), in 535 men and 226 women aged 56-79 years without overt cardiovascular disease who received no cardiovascular, antidiabetic or lipid lowering drugs, using multiple linear regression analysis. FPG category (r = 0.159; p < 0.001) was positively correlated with hsTnT. Mean hsTnT levels increased significantly with worsening glucometabolic status (NFG: 7.55 ng/L +/- standard deviation 3.99 ng/L; IFG: 8.09 ng/L +/- 6.81 ng/L; DM: 10.28 ng/L +/- 7.55 ng/L; p < 0.001). Levels were significantly higher in subjects with DM compared to NFG (p < 0.001) and IFG (p = 0.005), but there was no significant difference between subjects with NFG and IFG (p = 0.26). After adjusting for age and sex, FPG category remained significantly predictive of hsTnT (B = 1.08 [95% confidence interval (CI), 0.56-1.59]; p < 0.001). After further adjusting for traditional cardiovascular risk factors, cystatin C levels, and electrocardiographic left ventricular hypertrophy (LVH) defined by the Sokolow-Lyon index and/or Cornell voltage-duration product, FPG category remained significantly associated with hsTnT (B = 0.87 [95% CI, 0.35-1.39]; p = 0.001), independently of age (B = 0.29 [95% CI, 0.22-0.36]; p < 0.001), sex (B = 2.08 [95% CI, 1.20-2.95]; p < 0.001), systolic blood pressure (B = 0.032 [95% CI, 0.012-0.051]; p = 0.001), and cystatin C (B = 3.69 [95% CI, 1.60-5.79]; p = 0.001). There was a significant interaction between FPG category and age (NFG: B = 0.22 [95% CI, 0.16-0.29]; IFG: B = 0.33 [95% CI, 0.18-0.48]; DM: B = 0.41 [95% CI, 0.20-0.62]; p = 0.03). In middle-aged or older apparently healthy subjects, untreated DM was associated with higher levels of hsTnT, independently of traditional cardiovascular risk factors. The importance of age increased with worsening glucometabolic status.
    Journal of Hypertension 06/2015; 33 Suppl 1 - ESH 2015 Abstract Book:e54-e55. DOI:10.1097/01.hjh.0000467491.14601.38 · 4.72 Impact Factor
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    ABSTRACT: A high intake of omega-3 polyunsaturated fatty acids (ω-3 PUFAs), has been associated with reduced levels of blood pressure (BP). Their antihypertensive action may be due to the reduction of the ω-6/ω-3 ratio and the resulting competitive effect of ω-3 as compared to arachidonic acid (an ω-6 PUFA) as a substrate of cytochrome P450 (CYP450) enzymes involved in the production of vasoactive mediators. Some functional polymorphisms (SNPs), in genes which encode for the same enzymes, were associated with hypertension and ischemic stroke in the Malmö Diet and Cancer (MDC), a Swedish urban-based longitudinal study. The aim of this study was to evaluate the effect of the intake of different types of PUFAs on BP change over time (Δ-BP; mean follow-up 16.6±1.5 years; n=3,550 with complete phenotypic data), also considering the interaction with SNPs in genes involved in their metabolism via CYP450. PUFA intakes were collected by a modified diet history method, and functional SNPs in CYP4F2, CYP4A11, CYP2J2 and EPHX2 were genotyped by Taqman. We did not find any overall association between ω-6 or ω-3 PUFA intakes, or their ratio, with Δ-BP but observed an interaction between CYP4F2 V433M genotype and total omega-3, α-linolenic acid and linoleic/α-linolenic ratio, so that a higher ω-3 PUFA intake was significantly associated with a more pronounced BP decrease over time in subjects with the 433VV genotype (-0.041±0.018mmHg/year; p=0.024; p-interaction=0.031) CONCLUSIONS: Our data do not support a major role of ω-6 or ω-3 PUFA intakes on BP change over time, but suggest a possible interaction of ω-3 PUFA with the CYP4F2 V433M. Copyright © 2015. Published by Elsevier Inc.
    Prostaglandins & other lipid mediators 05/2015; DOI:10.1016/j.prostaglandins.2015.05.003 · 2.38 Impact Factor
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    ABSTRACT: Atrial fibrillation (AF) episodes are thought to be started by an electrical trigger reaching a susceptible atria. Such a trigger could be present long before the occurrence of sustained symptomatic arrhythmia. We sought to determine if supraventricular extrasystoles (SVES) and supraventricular tachycardias (SVT) measured at 24 h Holter ECG were associated with increased incidence of AF. In 1998-2000, 389 individuals (44% men, mean age 65 years) were examined using 24 h Holter ECG. Six individuals with known prevalent AF were excluded. After a mean follow-up of 10.3 years there were 45 cases of incident AF. Hazard ratios (HR) were computed using multivariable Cox regression adjusting for age, gender, systolic blood pressure, height, weight, smoking and HOMA-IR (homeostatic model assessment of insulin resistance). Frequency of SVES as well as SVT episodes per hour were independent predictors of incident AF, HR per log unit 1.38, 95% confidence interval (CI) 1.14-1.68, p= 0.001; and HR 1.95, 95% CI 1.21-3.13, p=0.006, respectively. Further adjustment for education level, alcohol use, use of medication and physical activity did not substantially alter the results, nor did analysis using competing risks regression accounting for a competing risk of death. The maximum duration of SVT or the heart rate at SVT was not significantly associated with incidence of AF. SVES and SVT independently predict AF. The prognostic significance was similar for SVES, SVT and a combination of the two. Repeated efforts to detect AF could be of merit in individuals with frequent supraventricular activity. Copyright © 2015. Published by Elsevier Inc.
    Heart rhythm: the official journal of the Heart Rhythm Society 05/2015; 12(9). DOI:10.1016/j.hrthm.2015.04.042 · 5.08 Impact Factor
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    ABSTRACT: Arterial stiffness reflects the ageing processes in the vascular system, and studies have shown an association between reduced cognitive function and cerebral small vessel disease. Small vessel disease can be visualized as white matter hyperintensities (WMH) and lacunar infarcts but also as cerebral microbleeds on brain magnetic resonance imaging (MRI). We aimed to investigate if arterial stiffness influences the presence of microbleeds, WMH and cognitive function in a population of cognitively healthy elderly. The study population is part of the Swedish BioFinder study and consisted of 208 individuals without any symptoms of cognitive impairment, who scored >27 points on the Mini-Mental State Examination. The participants (mean age, 72 years; 59% women) underwent MRI of the brain with visual rating of microbleeds and WMH. Arterial stiffness was measured with carotid-femoral pulse wave velocity (cfPWV). Eight cognitive tests covering different cognitive domains were performed. Microbleeds were detected in 12% and WMH in 31% of the participants. Mean (±standard deviation, SD) cfPWV was 10.0 (±2.0) m/s. There was no association between the presence of microbleeds and arterial stiffness. There was a positive association between arterial stiffness and WMH independent of age or sex (odds ratio, 1.58; 95% confidence interval, 1.04-2.40, p < 0.05), but the effect was attenuated when further adjustments for several cardiovascular risk factors were performed (p > 0.05). Cognitive performance was not associated with microbleeds, but individuals with WMH performed slightly worse than those without WMH on the Symbol Digit Modalities Test (mean ± SD, 35 ± 7.8 vs. 39 ± 8.1, p < 0.05). Linear regression revealed no direct associations between arterial stiffness and the results of the cognitive tests. Arterial stiffness was not associated with the presence of cerebral microbleeds or cognitive function in cognitively healthy elderly. However, arterial stiffness was related to the presence of WMH, but the association was attenuated when multiple adjustments were made. There was a weak negative association between WMH and performance in one specific test of attention. Longitudinal follow-up studies are needed to further assess the associations.
    05/2015; 5(2):41-51. DOI:10.1159/000377710
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    ABSTRACT: Blood pressure (BP) in patients with sickle cell disease (SCD) has been reported to be lower than in persons in the general population. Data on arterial stiffness, which is an important risk factor for the progression of BP, are inconclusive for this patient population. Forty-five adult patients with SCD and 40 controls matched for sex, age, and body mass index were studied. Brachial systolic BP (SBP) and diastolic BP (DBP) were significantly lower in the patient group (SBP 115.1±13.8 mm Hg vs 121.9±11.3 mm Hg and DBP 68.5±8.0 mm Hg vs 80.6±9.1 mm Hg, P<.05, respectively). Augmentation index (AIx), however, was significantly higher in SCD patients compared with healthy controls (24.9±9.6 for patients vs 12.4±10.8 for controls, P<.001), while carotid femoral pulse wave velocity was comparable between the two groups. The study shows that mechanisms other than arterial elasticity are involved in the low BP phenotype of patients with SCD. ©2015 Wiley Periodicals, Inc.
    Journal of Clinical Hypertension 05/2015; 17(9). DOI:10.1111/jch.12572 · 2.85 Impact Factor

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  • 2012–2015
    • Skåne University Hospital
      Malmö, Skåne, Sweden
    • University Medical Center Utrecht
      Utrecht, Utrecht, Netherlands
  • 1987–2015
    • Lund University
      • • Department of Clinical Sciences, Malmö
      • • Department of Community Health Sciences
      • • Department of Health Sciences
      Lund, Skåne, Sweden
  • 2014
    • Örebro universitet
      Örebro, Örebro, Sweden
    • Danderyds Sjukhus AB
      Tukholma, Stockholm, Sweden
  • 2001–2014
    • Malmö University
      • Faculty of Health and Society (HS)
      Malmö, Skåne, Sweden
  • 2010
    • Örebro University Hospital
      Örebro, Örebro, Sweden
  • 2003–2010
    • Uppsala University
      • • Department of Medical Sciences
      • • Department of Public Health and Caring Sciences
      Uppsala, Uppsala, Sweden
  • 2005–2009
    • Akademiska Sjukhuset
      Uppsala, Uppsala, Sweden
    • Uppsala University Hospital
      Uppsala, Uppsala, Sweden
    • Sahlgrenska University Hospital
      • Department of Cardiology
      Goeteborg, Västra Götaland, Sweden
  • 2008
    • Karolinska University Hospital
      • Department of Cardiology
      Tukholma, Stockholm, Sweden
  • 2007
    • Justus-Liebig-Universität Gießen
      Gieben, Hesse, Germany
    • Università degli Studi di Milano-Bicocca
      Milano, Lombardy, Italy
  • 2005–2006
    • AHEPA University Hospital
      Saloníki, Central Macedonia, Greece
  • 1997–2005
    • University of Gothenburg
      • • Occupational Therapy Unit (OT)
      • • Unit of Social Medicine
      Göteborg, Vaestra Goetaland, Sweden
  • 2002
    • Region Skåne
      Malmö, Skåne, Sweden