Orthostatic hypertension, which appears to be mediated through excess neurohumoral activation while standing, is a common blood pressure trait among patients with and without arterial hypertension. However, lack of consensus regarding the definition of orthostatic hypertension makes it difficult to assess the true prevalence of this condition. Orthostatic hypertension appears to predict the risk for progression to arterial hypertension in younger and risk of cardiovascular morbidity and mortality in older persons. Yet, the risk may differ between populations. Whether orthostatic hypertension indicates a generally increased risk of death, constitutes an intermediate variable in the causal pathway of cardiovascular risk factors, a simple measure of disease severity, or an independently acting mechanism is not known. Since both orthostatic hypotension and orthostatic hypertension herald increased risk of cardiovascular disease, it appears reasonable to screen the patients for abnormal orthostatic blood pressure responses using simple orthostatic testing. However, how presence of orthostatic hypertension may affect clinical management decisions such as the choice of antihypertensive drugs is currently difficult to ascertain. Clearly, this issue deserves more attention.

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The 4D/3DC-US method provides reliable and accurate stenosis quantification and binary classification with good diagnostic accuracy compared with CA and DUS.

Aims Reduced physical activity increases the risk of heart failure; however, non‐invasive methodologies detecting subclinical changes in myocardial function are not available. We hypothesized that myocardial, left ventricular, systolic strain measurements could capture subtle abnormalities in myocardial function secondary to physical inactivity. Methods and results In the AGBRESA study, which assessed artificial gravity through centrifugation as potential countermeasure for space travel, 24 healthy persons (eight women) were submitted to 60 day strict −6° head‐down‐tilt bed rest. Participants were assigned to three groups of eight subjects: a control group, continuous artificial gravity training on a short‐arm centrifuge (30 min/day), or intermittent centrifugation (6 × 5 min/day). We assessed cardiac morphology, function, strain, and haemodynamics by cardiac magnetic resonance imaging (MRI) and echocardiography. We observed no differences between groups and, therefore, conducted a pooled analysis. Consistent with deconditioning, resting heart rate (∆8.3 ± 6.3 b.p.m., P < 0.0001), orthostatic heart rate responses (∆22.8 ± 19.7 b.p.m., P < 0.0001), and diastolic blood pressure (∆8.8 ± 6.6 mmHg, P < 0.0001) increased, whereas cardiac output (∆−0.56 ± 0.94 L/min, P = 0.0096) decreased during bed rest. Left ventricular mass index obtained by MRI did not change. Echocardiographic left ventricular, systolic, global longitudinal strain (∆1.8 ± 1.83%, P < 0.0001) decreased, whereas left ventricular, systolic, global MRI circumferential strain increased not significantly (∆−0.68 ± 1.85%, P = 0.0843). MRI values rapidly returned to baseline during recovery. Conclusion Prolonged head‐down‐tilt bed rest provokes changes in cardiac function, particularly strain measurements, that appear functional rather than mediated through cardiac remodelling. Thus, strain measurements are of limited utility in assessing influences of physical deconditioning or exercise interventions on cardiac function.

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BackgroundCardiovascular risk may be increased in astronauts after long term space flights based on biomarkers indicating premature vascular aging. We tested the hypothesis that 60 days of strict 6° head down tilt bed rest (HDTBR), an established space analog, promotes vascular stiffening and that artificial gravity training ameliorates the response.MethodsWe studied 24 healthy participants (8 women, 24–55 years, BMI = 24.3 ± 2.1 kg/m2) before and at the end of 60 days HDTBR. 16 subjects were assigned to daily artificial gravity. We applied echocardiography to measure stroke volume and isovolumetric contraction time (ICT), calculated aortic compliance (stroke volume/aortic pulse pressure), and assessed aortic distensibility by MRI. Furthermore, we measured brachial-femoral pulse wave velocity (bfPWV) and pulse wave arrival times (PAT) in different vascular beds by blood pressure cuffs and photoplethysmography. We corrected PAT for ICT (cPAT).ResultsIn the pooled sample, diastolic blood pressure (+8 ± 7 mmHg, p &lt; 0.001), heart rate (+7 ± 9 bpm, p = 0.002) and ICT (+8 ± 13 ms, p = 0.036) increased during HDTBR. Stroke volume decreased by 14 ± 15 ml (p = 0.001). bfPWV, aortic compliance, aortic distensibility and all cPAT remained unchanged. Aortic area tended to increase (p = 0.05). None of the parameters showed significant interaction between HDTBR and artificial gravity training.Conclusion60 days HDTBR, while producing cardiovascular deconditioning and cephalad fluid shifts akin to weightlessness, did not worsen vascular stiffness. Artificial gravity training did not modulate the response.

Background Susceptible individuals experience hypoxia‐induced pulmonary hypertension when ascending to high altitude. Descent is considered the primary intervention to treat this condition. A human feasibility study testing influences of severe sustained normobaric hypoxia corresponding to >7,000 m altitude on the heart allowed us to follow the evolution of pulmonary hypertension using state‐of‐the‐art cardiovascular imaging. Material & Methods Two healthy, professional mountaineers (subject A, male 57 years, subject B, female 50 years) first pre‐acclimatized for one week in the field at 4559 m altitude. Then, they stayed at the :envihab facility of the German Aerospace Center in Cologne where normobaric hypoxia was achieved by nitrogen dilution starting at 13.5% O2 to a minimum of 8% O2 over three weeks. Afterwards, 8.5% O2 during the daytime and 8.8% O2 at night was kept for another 14 days. Velocity encoded single plane phase contrast MRI of the pulmonary artery (PA) and echocardiography were performed 1 month before, during and 1 and 3 months after hypoxia for assessment of right ventricular (RV) function, PA pressure, area, flow and distensibility. Results Systolic PA pressure (PAPsys) was closely related to the decrease in oxygen during acclimatization. In subject B PAPsys peaked at 67 mmHg, 48 mmHg higher than baseline. PAPsys decreased steadily to a minimum of 44 mmHg after two weeks while still at 8.55% oxygen. Peak values occurred with clinical symptoms of acute mountain sickness and a drop in exercise capacity but without signs of cerebral or pulmonary edema. In subject A peak PAPsys was 44 mmHg and remained stable over the entire hypoxia exposure. Conclusion In healthy humans, severe normobaric hypoxia induces pulmonary hypertension with paradoxically preserved right ventricular function. Pulmonary hypertension may improve over time in some individuals, even in the face of sustained hypoxia. The findings attest to the remarkable physiological reserve of healthy human beings allowing for adaptation to massively increased pulmonary pressure. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.