Search Results

You are looking at 11 - 20 of 186 items for

  • Abstract: Arteries x
  • Abstract: Carotid x
  • Abstract: Circulation x
  • Abstract: Stroke x
  • Abstract: Veins x
  • Abstract: Heart x
  • Abstract: Cardio* x
Clear All Modify Search
Akinori Sairaku Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

Search for other papers by Akinori Sairaku in
Google Scholar
PubMed
Close
,
Yukiko Nakano Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

Search for other papers by Yukiko Nakano in
Google Scholar
PubMed
Close
,
Yuko Uchimura Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

Search for other papers by Yuko Uchimura in
Google Scholar
PubMed
Close
,
Takehito Tokuyama Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

Search for other papers by Takehito Tokuyama in
Google Scholar
PubMed
Close
,
Hiroshi Kawazoe Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

Search for other papers by Hiroshi Kawazoe in
Google Scholar
PubMed
Close
,
Yoshikazu Watanabe Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

Search for other papers by Yoshikazu Watanabe in
Google Scholar
PubMed
Close
,
Hiroya Matsumura Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

Search for other papers by Hiroya Matsumura in
Google Scholar
PubMed
Close
, and
Yasuki Kihara Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

Search for other papers by Yasuki Kihara in
Google Scholar
PubMed
Close

Background

The impact of subclinical hypothyroidism on the cardiovascular risk is still debated. We aimed to measure the relationship between subclinical hypothyroidism and the left atrial (LA) pressure.

Methods

The LA pressures and thyroid function were measured in consecutive patients undergoing atrial fibrillation (AF) ablation, who did not have any known heart failure, structural heart disease, or overt thyroid disease.

Results

Subclinical hypothyroidism (4.5≤ thyroid-stimulating hormone <19.9 mIU/L) was present in 61 (13.0%) of the 471 patients included. More subclinical hypothyroidism patients than euthyroid patients (55.7% vs 40.2%; P=0.04).’euthyroid patients had persistent or long-standing persistent AF (55.7% vs 40.2%; P = 0.04). The mean LA pressure (10.9 ± 4.7 vs 9.1 ± 4.3 mmHg; P = 0.002) and LA V-wave pressure (17.4 ± 6.5 vs 14.3 ± 5.9 mmHg; P < 0.001) were, respectively, higher in the patients with subclinical hypothyroidism than in the euthyroid patients. After an adjustment for potential confounders, the LA pressures remained significantly higher in the subclinical hypothyroidism patients. A multiple logistic regression model showed that subclinical hypothyroidism was independently associated with a mean LA pressure of >18 mmHg (odds ratio 3.94, 95% CI 1.28 11.2; P = 0.02).

Conclusions

Subclinical hypothyroidism may increase the LA pressure in AF patients.

Open access
Jens P Goetze
Search for other papers by Jens P Goetze in
Google Scholar
PubMed
Close
,
Linda M Hilsted
Search for other papers by Linda M Hilsted in
Google Scholar
PubMed
Close
,
Jens F Rehfeld
Search for other papers by Jens F Rehfeld in
Google Scholar
PubMed
Close
, and
Urban Alehagen Department of Clinical Biochemistry, Division of Cardiovascular Medicine, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

Search for other papers by Urban Alehagen in
Google Scholar
PubMed
Close

Cardiovascular risk assessment remains difficult in elderly patients. We examined whether chromogranin A (CgA) measurement in plasma may be valuable in assessing risk of death in elderly patients with symptoms of heart failure in a primary care setting. A total of 470 patients (mean age 73 years) were followed for 10 years. For CgA plasma measurement, we used a two-step method including a screening test and a confirmative test with plasma pre-treatment with trypsin. Cox multivariable proportional regression and receiver-operating curve (ROC) analyses were used to assess mortality risk. Assessment of cardiovascular mortality during the first 3 years of observation showed that CgA measurement contained useful information with a hazard ratio (HR) of 5.4 (95% CI 1.7–16.4) (CgA confirm). In a multivariate setting, the corresponding HR was 5.9 (95% CI 1.8–19.1). When adding N-terminal proBNP (NT-proBNP) to the model, CgA confirm still possessed prognostic information (HR: 6.1; 95% CI 1.8–20.7). The result for predicting all-cause mortality displayed the same pattern. ROC analyses in comparison to NT-proBNP to identify patients on top of clinical variables at risk of cardiovascular death within 5 years of follow-up showed significant additive value of CgA confirm measurements compared with NT-proBNP and clinical variables. CgA measurement in the plasma of elderly patients with symptoms of heart failure can identify those at increased risk of short- and long-term mortality.

Open access
Xiaoyi Qi Departments of Cardiology, Peking University Shenzhen Hospital, Shenzhen, China
Medical College, Shantou University, Shantou, China

Search for other papers by Xiaoyi Qi in
Google Scholar
PubMed
Close
,
Liangxian Qiu Departments of Cardiology, Peking University Shenzhen Hospital, Shenzhen, China

Search for other papers by Liangxian Qiu in
Google Scholar
PubMed
Close
,
Shijia Wang Departments of Cardiology, Peking University Shenzhen Hospital, Shenzhen, China

Search for other papers by Shijia Wang in
Google Scholar
PubMed
Close
,
Xiongbiao Chen Departments of Cardiology, Peking University Shenzhen Hospital, Shenzhen, China

Search for other papers by Xiongbiao Chen in
Google Scholar
PubMed
Close
,
Qianwen Huang Departments of Cardiology, Peking University Shenzhen Hospital, Shenzhen, China

Search for other papers by Qianwen Huang in
Google Scholar
PubMed
Close
,
Yixuan Zhao Departments of Cardiology, Peking University Shenzhen Hospital, Shenzhen, China
Medical College, Shantou University, Shantou, China

Search for other papers by Yixuan Zhao in
Google Scholar
PubMed
Close
,
Kunfu Ouyang Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, School of Chemical Biology and Biotechnology, State Key Laboratory of Chemical Oncogenomics, Peking University Shenzhen Graduate School, Shenzhen, China

Search for other papers by Kunfu Ouyang in
Google Scholar
PubMed
Close
, and
Yanjun Chen Departments of Cardiology, Peking University Shenzhen Hospital, Shenzhen, China

Search for other papers by Yanjun Chen in
Google Scholar
PubMed
Close

Background

Heart failure (HF) is a complex and multifactorial syndrome caused by impaired heart function. The high morbidity and mortality of HF cause a heavy burden of illness worldwide. Non-thyroidal illness syndrome (NTIS) refers to aberrant serum thyroid parameters in patients without past thyroid disease. Observational studies have indicated that NTIS is associated with a higher risk of all-cause mortality in HF. This meta-analysis aimed to investigate the association between NTIS and HF prognosis.

Methods

Medline, Embase, Web of Science, and the Cochrane database were searched for any studies reporting an association between NTIS and HF prognosis from inception to 1 July 2022. A meta-analysis was then performed. The quality of studies was assessed using the Newcastle–Ottawa Scale. The heterogeneity of the results was assessed with I 2 and Cochran's Q statistics. Sensitivity analysis and publication bias analysis were also conducted.

Results

A total of 626 studies were retrieved, and 18 studies were finally included in the meta-analysis. The results showed that NTIS in HF patients was significantly associated with an increased risk of all-cause mortality and major cardiovascular events (MACE), but not with in-hospital mortality. The stability of the data was validated by the sensitivity analysis. There was no indication of a publication bias in the pooled results for all-cause mortality and MACE.

Conclusions

This meta-analysis showed that NTIS was associated with a worse outcome in HF patients. However, the association between NTIS and in-hospital mortality of HF patients requires further investigation.

Open access
Melinda Kertész Department of Medicine and Nephrology-Diabetes Centre, Medical School, University of Pécs, Pécs, Baranya, Hungary

Search for other papers by Melinda Kertész in
Google Scholar
PubMed
Close
,
Szilárd Kun Department of Medicine and Nephrology-Diabetes Centre, Medical School, University of Pécs, Pécs, Baranya, Hungary

Search for other papers by Szilárd Kun in
Google Scholar
PubMed
Close
,
Eszter Sélley Department of Medicine and Nephrology-Diabetes Centre, Medical School, University of Pécs, Pécs, Baranya, Hungary

Search for other papers by Eszter Sélley in
Google Scholar
PubMed
Close
,
Zsuzsanna Nagy Department of Medicine and Nephrology-Diabetes Centre, Medical School, University of Pécs, Pécs, Baranya, Hungary

Search for other papers by Zsuzsanna Nagy in
Google Scholar
PubMed
Close
,
Tamás Kőszegi Department of Laboratory Medicine, Medical School, University of Pécs, Pécs, Baranya, Hungary

Search for other papers by Tamás Kőszegi in
Google Scholar
PubMed
Close
, and
István Wittmann Department of Medicine and Nephrology-Diabetes Centre, Medical School, University of Pécs, Pécs, Baranya, Hungary

Search for other papers by István Wittmann in
Google Scholar
PubMed
Close

Background

Type 2 diabetes is characterized, beyond the insulin resistance, by polyhormonal resistance. Thyroid hormonal resistance has not yet been described in this population of patients. Metformin is used to decrease insulin resistance, and at present, it is assumed to influence the effect of triiodothyronine, as well.

Methods

In this open-label, pilot, hypothesis-generating, follow-up study, 21 patients were included; all of them were euthyroid with drug naïve, newly diagnosed type 2 diabetes. Before and after 4 weeks of metformin therapy, fructosamine, homeostasis model assessment for insulin resistance (HOMA-IR), thyroid hormones, T3/T4 ratio, and TSH, as well as blood pressure and heart rate using ambulatory blood pressure monitor were measured. We also conducted an in vitro study to investigate the possible mechanisms of T3 resistance, assessing T3-induced Akt phosphorylation among normal (5 mM) and high (25 mM) glucose levels with or without metformin treatment in a human embryonal kidney cell line.

Results

Metformin decreased the level of T3 (P < 0.001), the ratio of T3/T4 (P = 0.038), fructosamine (P = 0.008) and HOMA-IR (P = 0.022). All these changes were accompanied by an unchanged TSH, T4, triglyceride, plasma glucose, bodyweight, blood pressure, and heart rate. In our in vitro study, T3-induced Akt phosphorylation decreased in cells grown in 25 mM glucose medium compared to those in 5 mM. Metformin could not reverse this effect.

Conclusion

Metformin seems to improve T3 sensitivity in the cardiovascular system in euthyroid, type 2 diabetic patients, the mechanism of which may be supracellular.

Open access
Lasse Oinonen Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland

Search for other papers by Lasse Oinonen in
Google Scholar
PubMed
Close
,
Antti Tikkakoski Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland
Department of Clinical Physiology, Tampere University Hospital, Tampere, Finland

Search for other papers by Antti Tikkakoski in
Google Scholar
PubMed
Close
,
Jenni Koskela Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland

Search for other papers by Jenni Koskela in
Google Scholar
PubMed
Close
,
Arttu Eräranta Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland

Search for other papers by Arttu Eräranta in
Google Scholar
PubMed
Close
,
Mika Kähönen Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland
Department of Clinical Physiology, Tampere University Hospital, Tampere, Finland

Search for other papers by Mika Kähönen in
Google Scholar
PubMed
Close
,
Onni Niemelä Department of Laboratory Medicine and Medical Research Unit, Seinäjoki Central Hospital, Seinäjoki, Finland

Search for other papers by Onni Niemelä in
Google Scholar
PubMed
Close
,
Jukka Mustonen Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland

Search for other papers by Jukka Mustonen in
Google Scholar
PubMed
Close
, and
Ilkka Pörsti Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland

Search for other papers by Ilkka Pörsti in
Google Scholar
PubMed
Close

Parathyroid hormone has been related with the risk of hypertension, but the matter remains controversial. We examined the association of parathyroid hormone with central blood pressure and its determinants in 622 normotensive or never-treated hypertensive subjects aged 19–72 years without diabetes, cardiovascular or renal disease, or cardiovascular medications. The methods were whole-body impedance cardiography and analyses of pulse wave and heart rate variability. Cardiovascular function was examined in sex-specific tertiles of plasma parathyroid hormone (mean concentrations 3.0, 4.3 and 6.5 pmol/L, respectively) during head-up tilt. Explanatory factors for haemodynamics were further investigated using linear regression analyses. Mean age was 45.0 (s.d. 11.7) years, BMI 26.8 (4.4) kg/m2, seated office blood pressure 141/90 (21/12) mmHg, and 309 subjects (49.7%) were male. Only five participants had elevated plasma parathyroid hormone and calcium concentrations. Highest tertile of parathyroid hormone presented with higher supine and upright aortic diastolic blood pressure (P < 0.01) and augmentation index (P < 0.01), and higher upright systemic vascular resistance (P < 0.05) than the lowest tertile. The tertiles did not present with differences in pulse wave velocity, cardiac output, or measures of heart rate variability. In linear regression analyses, parathyroid hormone was an independent explanatory factor for aortic systolic (P = 0.005) and diastolic (P = 0.002) blood pressure, augmentation index (P = 0.002), and systemic vascular resistance (P = 0.031). To conclude, parathyroid hormone was directly related to central blood pressure, wave reflection, and systemic vascular resistance in subjects without cardiovascular comorbidities and medications. Thus, parathyroid hormone may play a role in the pathophysiology of primary hypertension.

Open access
Ulrik Ø Andersen Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Institute of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

Search for other papers by Ulrik Ø Andersen in
Google Scholar
PubMed
Close
,
Dijana Terzic Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Institute of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

Search for other papers by Dijana Terzic in
Google Scholar
PubMed
Close
,
Nicolai Jacob Wewer Albrechtsen Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Institute of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Novo Nordisk Foundation Centre for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

Search for other papers by Nicolai Jacob Wewer Albrechtsen in
Google Scholar
PubMed
Close
,
Peter Dall Mark Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Institute of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

Search for other papers by Peter Dall Mark in
Google Scholar
PubMed
Close
,
Peter Plomgaard Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

Search for other papers by Peter Plomgaard in
Google Scholar
PubMed
Close
,
Jens F Rehfeld Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark

Search for other papers by Jens F Rehfeld in
Google Scholar
PubMed
Close
,
Finn Gustafsson Department of Cardiology, Rigshospitalet, Copenhagen, Denmark

Search for other papers by Finn Gustafsson in
Google Scholar
PubMed
Close
, and
Jens P Goetze Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Institute of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

Search for other papers by Jens P Goetze in
Google Scholar
PubMed
Close

Aims

Neprilysin degrades natriuretic peptides in circulation and is also suggested to degrade the gut hormones gastrin and cholecystokinin. Neprilysin inhibition has become a therapeutic strategy and thus a regimen in need of further testing in terms of other hormonal axes besides natriuretic peptides. The aim of this study was to examine whether acute inhibition of neprilysin affects meal-induced responses in gastrin and cholecystokinin concentrations in healthy individuals.

Methods and results

Nine healthy young men were included in an open-labelled, randomized cross-over clinical trial. The participants received a standardized meal (25 g fat, 26 g protein, 42 g carbohydrate) on two separate days with or without a one-time dosage of sacubitril ((194 mg)/valsartan (206 mg)). Blood pressure, heart rate and blood samples were measured and collected during the experiment. Statistical differences between groups were assessed using area under the curve together with an ANOVA with a Bonferroni post hoc test. Sacubitril/valsartan increased the postprandial plasma concentrations of both gastrin and cholecystokinin (80% (AUC0-270 min, P = 0.004) and 60% (AUC0-270 min, P = 0.003), respectively) compared with the control meal. No significant hemodynamic effects were noted (blood pressure, AUC0-270 min, P = 0.86, heart rate, AUC0-270 min, P = 0.96).

Conclusion

Our study demonstrates that sacubitril/valsartan increases the postprandial plasma concentrations of gastrin and cholecystokinin in healthy individuals. The results thus suggest that neprilysin-mediated degradation of gastrin and cholecystokinin is physiologically relevant and may have a role in heart failure patients treated with sacubitril/valsartan.

Open access
Julie Smith Department of Clinical Biochemistry (KB3014), Department of Technology, Department of Clinical Biochemistry, Department of Biomedical Sciences, Department of Clinical Medicine, Rigshospitalet, University of Copenhagen, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark

Search for other papers by Julie Smith in
Google Scholar
PubMed
Close
,
Jan Fahrenkrug Department of Clinical Biochemistry (KB3014), Department of Technology, Department of Clinical Biochemistry, Department of Biomedical Sciences, Department of Clinical Medicine, Rigshospitalet, University of Copenhagen, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark

Search for other papers by Jan Fahrenkrug in
Google Scholar
PubMed
Close
,
Henrik L Jørgensen Department of Clinical Biochemistry (KB3014), Department of Technology, Department of Clinical Biochemistry, Department of Biomedical Sciences, Department of Clinical Medicine, Rigshospitalet, University of Copenhagen, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark

Search for other papers by Henrik L Jørgensen in
Google Scholar
PubMed
Close
,
Christina Christoffersen Department of Clinical Biochemistry (KB3014), Department of Technology, Department of Clinical Biochemistry, Department of Biomedical Sciences, Department of Clinical Medicine, Rigshospitalet, University of Copenhagen, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark
Department of Clinical Biochemistry (KB3014), Department of Technology, Department of Clinical Biochemistry, Department of Biomedical Sciences, Department of Clinical Medicine, Rigshospitalet, University of Copenhagen, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark

Search for other papers by Christina Christoffersen in
Google Scholar
PubMed
Close
, and
Jens P Goetze Department of Clinical Biochemistry (KB3014), Department of Technology, Department of Clinical Biochemistry, Department of Biomedical Sciences, Department of Clinical Medicine, Rigshospitalet, University of Copenhagen, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark
Department of Clinical Biochemistry (KB3014), Department of Technology, Department of Clinical Biochemistry, Department of Biomedical Sciences, Department of Clinical Medicine, Rigshospitalet, University of Copenhagen, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark

Search for other papers by Jens P Goetze in
Google Scholar
PubMed
Close

Disruption of the circadian rhythm can lead to obesity and cardiovascular disease. In white adipose tissue, activation of the natriuretic peptide receptors (NPRs) stimulates lipolysis. We have previously shown that natriuretic peptides are expressed in a circadian manner in the heart, but the temporal expression profile of their cognate receptors has not been examined in white adipose tissue. We therefore collected peri-renal white adipose tissue and serum from WT mice. Tissue mRNA contents of NPRs – NPR-A and NPR-C, the clock genes Per1 and Bmal1, and transcripts involved in lipid metabolism were quantified at 4-h intervals: in the diurnal study, mice were exposed to a period of 12 h light followed by 12 h darkness (n=52). In the circadian study, mice were kept in darkness for 24 h (n=47). Concomitant serum concentrations of free fatty acids, glycerol, triglycerides (TGs), and insulin were measured. Per1 and Bmal1 mRNA contents showed reciprocal circadian profiles (P<0.0001). NPR-A mRNA contents followed a temporal pattern (P=0.01), peaking in the dark (active) period. In contrast, NPR-C mRNA was expressed in an antiphase manner with nadir in the active period (P=0.007). TG concentrations in serum peaked in the active dark period (P=0.003). In conclusion, NPR-A and NPR-C gene expression is associated with the expression of clock genes in white adipose tissue. The reciprocal expression may thus contribute to regulate lipolysis and energy homeostasis in a diurnal manner.

Open access
Vito Francic Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Vito Francic in
Google Scholar
PubMed
Close
,
Martin Keppel Department of Laboratory Medicine, Paracelsus Medical University, Salzburg, Austria

Search for other papers by Martin Keppel in
Google Scholar
PubMed
Close
,
Verena Schwetz Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Verena Schwetz in
Google Scholar
PubMed
Close
,
Christian Trummer Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Christian Trummer in
Google Scholar
PubMed
Close
,
Marlene Pandis Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Marlene Pandis in
Google Scholar
PubMed
Close
,
Valentin Borzan Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Valentin Borzan in
Google Scholar
PubMed
Close
,
Martin R Grübler Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Martin R Grübler in
Google Scholar
PubMed
Close
,
Nicolas D Verheyen Division of Cardiology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Nicolas D Verheyen in
Google Scholar
PubMed
Close
,
Marcus E Kleber Vth Department of Medicine (Nephrology, Hypertensiology, Rheumatology, Endocrinology, Diabetology), Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany

Search for other papers by Marcus E Kleber in
Google Scholar
PubMed
Close
,
Graciela Delgado Vth Department of Medicine (Nephrology, Hypertensiology, Rheumatology, Endocrinology, Diabetology), Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany

Search for other papers by Graciela Delgado in
Google Scholar
PubMed
Close
,
Angela P Moissl Vth Department of Medicine (Nephrology, Hypertensiology, Rheumatology, Endocrinology, Diabetology), Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany

Search for other papers by Angela P Moissl in
Google Scholar
PubMed
Close
,
Benjamin Dieplinger Department of Laboratory Medicine, Konventhospital Barmherzige Brueder Linz, Linz, Austria

Search for other papers by Benjamin Dieplinger in
Google Scholar
PubMed
Close
,
Winfried März Vth Department of Medicine (Nephrology, Hypertensiology, Rheumatology, Endocrinology, Diabetology), Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
Synlab Academy, Synlab Holding Germany GmbH, Heidelberg, Germany

Search for other papers by Winfried März in
Google Scholar
PubMed
Close
,
Andreas Tomaschitz Specialist Clinic of Rehabilitation Bad Gleichenberg, Bad Gleichenberg, Austria

Search for other papers by Andreas Tomaschitz in
Google Scholar
PubMed
Close
,
Stefan Pilz Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Stefan Pilz in
Google Scholar
PubMed
Close
, and
Barbara Obermayer-Pietsch Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Barbara Obermayer-Pietsch in
Google Scholar
PubMed
Close

Objective

Cardiovascular disease manifestation and several associated surrogate markers, such as vitamin D, have shown substantial seasonal variation. A promising cardiovascular biomarker, soluble ST2 (sST2), has not been investigated in this regard – we therefore determined if systemic levels of sST2 are affected by seasonality and/or vitamin D in order to investigate their clinical interrelation and usability.

Design

sST2 levels were measured in two cohorts involving hypertensive patients at cardiovascular risk, the Styrian Vitamin D Hypertension Trial (study A; RCT design, 8 weeks 2800 IU cholecalciferol daily) and the Ludwigshafen Risk and Cardiovascular Health Study (LURIC; study B; cross-sectional design).

Methods

The effects of a vitamin D intervention on sST2 levels were determined in study A using ANCOVA, while seasonality of sST2 levels was determined in study B using ANOVA.

Results

The concentrations of sST2 remained unchanged by a vitamin D intervention in study A, with a mean treatment effect (95% confidence interval) of 0.1 (−0.6 to 0.8) ng/mL; P = 0.761), despite a rise in 25(OH)D (11.3 (9.2–13.5) ng/mL; P < 0.001) compared to placebo. In study B, seasonal variations were present in 25(OH)D levels in men and women with or without heart failure (P < 0.001 for all subgroups), while sST2 levels remained unaffected by the seasons in all subgroups.

Conclusions

Our study provides the first evidence that systemic sST2 levels are not interrelated with vitamin D levels or influenced by the seasons in subjects at cardiovascular risk.

Open access
Charlotte Janus Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Danish Diabetes Academy, Odense University Hospital, Odense, Denmark

Search for other papers by Charlotte Janus in
Google Scholar
PubMed
Close
,
Dorte Vistisen Steno Diabetes Center Copenhagen, Gentofte, Denmark

Search for other papers by Dorte Vistisen in
Google Scholar
PubMed
Close
,
Hanan Amadid Steno Diabetes Center Copenhagen, Gentofte, Denmark
Department of Public Health, Research Unit of Epidemiology, Aarhus University, Aarhus, Denmark

Search for other papers by Hanan Amadid in
Google Scholar
PubMed
Close
,
Daniel R Witte Danish Diabetes Academy, Odense University Hospital, Odense, Denmark
Department of Public Health, Research Unit of Epidemiology, Aarhus University, Aarhus, Denmark
Steno Diabetes Center Aarhus, Aarhus, Denmark

Search for other papers by Daniel R Witte in
Google Scholar
PubMed
Close
,
Torsten Lauritzen Department of Public Health, Research Unit of Epidemiology, Aarhus University, Aarhus, Denmark

Search for other papers by Torsten Lauritzen in
Google Scholar
PubMed
Close
,
Søren Brage MRC Epidemiology Unit, University of Cambridge, Cambridge, UK

Search for other papers by Søren Brage in
Google Scholar
PubMed
Close
,
Anne-Louise Bjerregaard Department of Public Health, Research Unit of Epidemiology, Aarhus University, Aarhus, Denmark

Search for other papers by Anne-Louise Bjerregaard in
Google Scholar
PubMed
Close
,
Torben Hansen Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark

Search for other papers by Torben Hansen in
Google Scholar
PubMed
Close
,
Jens J Holst Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark

Search for other papers by Jens J Holst in
Google Scholar
PubMed
Close
,
Marit E Jørgensen Steno Diabetes Center Copenhagen, Gentofte, Denmark
National Institute of Public Health, University of Southern Denmark, Odense, Denmark

Search for other papers by Marit E Jørgensen in
Google Scholar
PubMed
Close
,
Oluf Pedersen Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark

Search for other papers by Oluf Pedersen in
Google Scholar
PubMed
Close
,
Kristine Færch Steno Diabetes Center Copenhagen, Gentofte, Denmark

Search for other papers by Kristine Færch in
Google Scholar
PubMed
Close
, and
Signe S Torekov Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark

Search for other papers by Signe S Torekov in
Google Scholar
PubMed
Close

Rationale

The hormone glucagon-like peptide-1 (GLP-1) decreases blood glucose and appetite. Greater physical activity (PA) is associated with lower incidence of type 2 diabetes. While acute exercise may increase glucose-induced response of GLP-1, it is unknown how habitual PA affects GLP-1 secretion. We hypothesised that habitual PA associates with greater glucose-induced GLP-1 responses in overweight individuals.

Methods

Cross-sectional analysis of habitual PA levels and GLP-1 concentrations in 1326 individuals (mean (s.d.) age 66 (7) years, BMI 27.1 (4.5) kg/m2) from the ADDITION-PRO cohort. Fasting and oral glucose-stimulated GLP-1 responses were measured using validated radioimmunoassay. PA was measured using 7-day combined accelerometry and heart rate monitoring. From this, energy expenditure (PAEE; kJ/kg/day) and fractions of time spent in activity intensities (h/day) were calculated. Cardiorespiratory fitness (CRF; mL O2/kg/min) was calculated using step tests. Age-, BMI- and insulin sensitivity-adjusted associations between PA and GLP-1, stratified by sex, were evaluated by linear regression analysis.

Results

In 703 men, fasting GLP-1 concentrations were 20% lower (95% CI: −33; −3%, P = 0.02) for every hour of moderate-intensity PA performed. Higher CRF and PAEE were associated with 1–2% lower fasting GLP-1 (P = 0.01). For every hour of moderate-intensity PA, the glucose-stimulated GLP-1 response was 16% greater at peak 30 min (1; 33%, P rAUC0-30 = 0.04) and 20% greater at full response (3; 40%, P rAUC0-120 = 0.02). No associations were found in women who performed PA 22 min/day vs 32 min/day for men.

Conclusion

Moderate-intensity PA is associated with lower fasting and greater glucose-induced GLP-1 responses in overweight men, possibly contributing to improved glucose and appetite regulation with increased habitual PA.

Open access
Frans H H Leenen Brain and Heart Research Group, University of Ottawa Heart Institute, Ottawa, Ontario, Canada

Search for other papers by Frans H H Leenen in
Google Scholar
PubMed
Close
,
Mordecai P Blaustein Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA
Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA

Search for other papers by Mordecai P Blaustein in
Google Scholar
PubMed
Close
, and
John M Hamlyn Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA

Search for other papers by John M Hamlyn in
Google Scholar
PubMed
Close

In the brain, angiotensinergic pathways play a major role in chronic regulation of cardiovascular and electrolyte homeostasis. Increases in plasma angiotensin II (Ang II), aldosterone, [Na+] and cytokines can directly activate these pathways. Chronically, these stimuli also activate a slow neuromodulatory pathway involving local aldosterone, mineralocorticoid receptors (MRs), epithelial sodium channels and endogenous ouabain (EO). This pathway increases AT1R and NADPH oxidase subunits and maintains/further increases the activity of angiotensinergic pathways. These brain pathways not only increase the setpoint of sympathetic activity per se, but also enhance its effectiveness by increasing plasma EO and EO-dependent reprogramming of arterial and cardiac function. Blockade of any step in this slow pathway or of AT1R prevents Ang II-, aldosterone- or salt and renal injury-induced forms of hypertension. MR/AT1R activation in the CNS also contributes to the activation of sympathetic activity, the circulatory and cardiac RAAS and increase in circulating cytokines in HF post MI. Chronic central infusion of an aldosterone synthase inhibitor, MR blocker or AT1R blocker prevents a major part of the structural remodeling of the heart and the decrease in LV function post MI, indicating that MR activation in the CNS post MI depends on aldosterone, locally produced in the CNS. Thus, Ang II, aldosterone and EO are not simply circulating hormones that act on the CNS but rather they are also paracrine neurohormones, locally produced in the CNS, that exert powerful effects in key CNS pathways involved in the long-term control of sympathetic and neuro-endocrine function and cardiovascular homeostasis.

Open access