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Background Inflammatory joint diseases (IJD) are accompanied by an increased risk of cardiovascular disease (CVD). Cardiorespiratory fitness (CRF) is a modifiable CVD risk factor and low levels of CRF associate with an elevated CVD risk. This study aimed to investigate the associations between CVD risk factors, disease activity and CRF in patients with IJD and to explore differences between patients with normal versus low levels of CRF. Methods CRF was measured as peak oxygen uptake (VO2peak) with a cardiopulmonary exercise test. Participants were also evaluated for: Body composition, blood pressure, blood lipids, inflammatory markers and disease activity. Patient-reported use of cigarettes/snuff, medication, disease duration, pain, fatigue, CVD history, habitual physical activity and exercise beliefs and self-efficacy were collected by questionnaire. Cross-sectional associations between CVD risk factors, disease-related factors and CRF were analyzed by multiple linear regression. CRF was categorized to normal CRF (VO2peak ≥ 80%) or low CRF (VO2peak Results In 60 Norwegian patients with IJD [34 females, age 59 years (IQR: 52–63)], mean VO2peak was 30.2 (± 6.9) mL/kg/min, corresponding to 83% (± 18) of normative reference values. Age (coefficient: − 0.18 years, p = 0.01) and fat mass (coefficient: − 0.67 %, p p = 0.05) was positively associated with CRF (R2 = 0.66). There were no significant associations between CRF, classical CVD risk factors and disease-related variables. Compared to patients with low CRF (n = 30), patients with normal CRF (n = 30) had higher peak oxygen uptake (+ 9.4 mL/kg/min, p −1, p p p p −1, p Conclusions In this sample of IJD-patients, age, fatmass and physical activity level were associated with CRF. CRF was lower than reference values and patients with normal CRF presented with a more favorable health profile. There is a continued need for exercise interventions to improve CRF in patients with IJD. Trial registration: NCT04922840.

Inflammatory joint diseases (IJD), including rheumatoid arthritis (RA), spondyloarthropathy (SpA) and psoriatic arthritis (PsA) are inflammatory autoimmune diseases with common symptoms of joint inflammation, pain, stiffness and fatigue. Compared to the general population, this large patient-group has an increased risk of cardiovascular disease (CVD) and CVD-related mortality. The elevated CVD risk in IJD is only partly attributed to a higher prevalence and burden of traditional risk factors, and the systemic, chronic inflammation is recognized as an independent CVD risk factor. Physical activity is inversely associated with risk of metabolic disease, but cardiorespiratory fitness (CRF) has emerged as an even stronger mediator of health outcomes. National and international data show a strong correlation between high levels of CRF and lower risk of CVD and all-cause mortality. In patients with IJD, disease-related factors and uncertainty regarding the dosage of exercise programs are consistent barriers to physical activity. Less time spent at spent at activities with moderate and vigorous intensity may negatively affect CRF and low levels of CRF are reported in patients with IJD. Collectively, the burden of disease and consequent inactivity may be a catalyst for reduced CRF and thus a component of the elevated CVD risk in IJD. A common notion that intensive exercise can increase disease activity and result in joint destruction and physical discomfort in patients with IJD has previously prevailed, but recent studies demonstrate that vigorous exercise is safe and well-tolerated. High-intensity training (HIIT) is proven superior to exercise at lower intensities in eliciting physiological adaptations. The evidence of HIIT is largely based on supervised clinical trial settings and application of HIIT to real world contexts requires more investigation. Common reservations regarding feasibility, adherence and safety need to be addressed. Although CRF is identified as a robust physiological marker and a prominent/major risk factor for CVD, assessment of CRF is not included in CVD risk models. A routine measure of CRF as a key vital sign is strongly recommended, though seldom performed in health care settings. CRF is often quantified as peak or maximal oxygen uptake (VO2peak) and the gold standard for measurement of VO2peak is a CardioPulmonary Exercise Test (CPET). In absence of CPET, non-exercise algorithms that predict VO2peak are viable options. These models use commonly measured clinical variables to estimate CRF and are thereby feasible for use in both primary and specialized clinical care. Notably, the ability of non-exercise algorithms to detect longitudinal change in VO2peak is unclear and presents an important knowledge need.

High-doses of anabolic–androgenic steroids (AAS) is efficient for building muscle mass, but pose a risk of cardiovascular side effects. Little is known of the effect of AAS on vasculature, but previous findings suggest unfavorable alterations in vessel walls and vasoreactivity. Here, long-term effect of AAS on vascular function and morphology were examined in male weightlifters, and in a mimicking animal model. Arterial elasticity and morphology were tested with ultrasound, pulse wave velocity (PWV) and carotid intima media thickness (cIMT) in 56 current male AAS users, and 67 non-exposed weightlifting controls (WLC). Female mice were treated with testosterone for 14 days and echocardiography were applied to evaluate vascular function and morphology. Male AAS users had higher PWV (p = 0.044), reduced carotid artery compliance (p = 0.0005), and increased cIMT (p = 0.041) compared to WLC. Similar functional changes were found in the ascending aorta of mice after 7- (p = 0.043) and 14 days (p = 0.001) of testosterone treatment. This animal model can be used to map molecular mechanisms responsible for complications related to AAS misuse. Considering the age-independent stiffening of major arteries and the predictive power of an increase in PWV and cIMT, the long-term users of AAS are at increased risk of severe cardiovascular events.

Supplemental material, sj-docx-1-JVA-10.1177_11297298211060960 for Validation of a novel ultrasound Doppler monitoring device (earlybird) for measurements of volume flow rate in arteriovenous fistulas for hemodialysis by Erik Mulder Pettersen, J��rgen Avdal, Stefano Fiorentini, ��yvind Salvesen, Jonny Hisdal, Hans Torp and Arne Seternes in The Journal of Vascular Access

Whilst both cardiac output (CO) and total peripheral resistance (TPR) determine mean arterial blood pressure (MAP), their relative importance in the pressor response to isometric exercise remains unclear. This study aimed to elucidate the relative importance of these two different factors by examining pressor responses during cardiopulmonary unloading leading to step-wise reductions in CO. Hemodynamics were investigated in 11 healthy individuals before, during and after two-minute isometric exercise during lower body negative pressure (LBNP; -20mmHg and -40mmHg). The blood pressure response to isometric exercise was similar during normal and reduced preload, despite a step-wise reduction in CO during LBNP (-20mmHg and -40mmHg). During -20mmHg LBNP, the decreased stroke volume, and consequently CO, was counteracted by an increased TPR, while heart rate (HR) was unaffected. HR was increased during -40 mmHg LBNP, although insufficient to maintain CO; the drop in CO was perfectly compensated by an increased TPR to maintain MAP. Likewise, transient application of LBNP (-20mmHg and -40mmHg) resulted in a short transient drop in MAP, caused by a decrease in CO, which was compensated by an increase in TPR. This study suggests that, in case of reductions of CO, changes in TPR are primarily responsible for maintaining the pressor response during isometric exercise. This highlights the relative importance of TPR compared to CO in mediating the pressor response during isometric exercise.

Reductions in cerebral oxygen saturation (ScO2) measured by near infra-red spectroscopy have been found during compensated hypovolemia in the lower body negative pressure (LBNP)-model, which may reflect reduced cerebral blood flow. However, ScO2 may also be contaminated from extracranial (scalp) tissues, mainly supplied by the external carotid artery (ECA), and it is possible that a ScO2 reduction during hypovolemia is caused by reduced scalp, and not cerebral, blood flow. The aim of the present study was to explore the associations between blood flow in precerebral arteries and ScO2 during LBNP-induced hypovolemia. Twenty healthy volunteers were exposed to LBNP 20, 40, 60 and 80 mmHg. Blood flow in the internal carotid artery (ICA), ECA and vertebral artery (VA) was measured by Doppler ultrasound. Stroke volume for calculating cardiac output was measured by suprasternal Doppler. Associations of changes within subjects were examined using linear mixed-effects regression models. LBNP reduced cardiac output, ScO2 and ICA and ECA blood flow. Changes in flow in both ICA and ECA were associated with changes in ScO2 and cardiac output. Flow in the VA did not change during LBNP and changes in VA flow were not associated with changes in ScO2 or cardiac output. During experimental compensated hypovolemia in healthy, conscious subjects, a reduced ScO2 may thus reflect a reduction in both cerebral and extracranial blood flow.

Changes in lipid levels and carotid plaque height in the RORA-AS study. Description of data: Additional file 1 shows carotid plaque height, carotid intima-media thickness, LDL cholesterol, HDL cholesterol, triglycerides and total cholesterol at baseline and at study end. It also shows the mean change and corresponding p values for these parameters during the course of the study. (PDF 185Â kb)