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Aims: To investigate the left ventricular response to exercise in young adults with hypertension, and identify whether this response can be predicted from changes in left atrial function at rest. Methods: A total of 127 adults aged 18–40 years who completed clinical blood pressure assessment and echocardiography phenotyping at rest and during cardiopulmonary exercise testing, were included. Measurements were compared between participants with suboptimal blood pressure ≥120/80mm Hg (n = 68) and optimal blood pressure <120/80mm Hg (n = 59). Left ventricular systolic function during exercise was obtained from an apical four chamber view, while resting left atrial function was assessed from apical four and two chamber views. Results: Participants with suboptimal blood pressure had higher left ventricular mass (p = 0.031) and reduced mitral E velocity (p = 0.02) at rest but no other cardiac differences. During exercise, their rise in left ventricular ejection fraction was reduced (p = 0.001) and they had higher left ventricular end diastolic and systolic volumes (p = 0.001 and p = 0.001, respectively). Resting cardiac size predicted left ventricular volumes during exercise but only left atrial booster pump function predicted the left ventricular ejection fraction response (β=.29, p = 0.011). This association persisted after adjustment for age, sex, body mass index, and mean arterial pressure. Conclusion: Young adults with suboptimal blood pressure have a reduced left ventricular systolic response to exercise, which can be predicted by their left atrial booster pump function at rest. Echocardiographic measures of left atrial function may provide an early marker of functionally relevant, subclinical, cardiac remodelling in young adults with hypertension. [ABSTRACT FROM AUTHOR]

Introduction: Experimental and clinical studies show that prematurity leads to altered right ventricular (RV) performance with potentially clinically significant impairments in RV systolic function in young adulthood. Hypothesis: We hypothesized that reductions in RV function would be out of proportion to changes in pulmonary physiology. Methods: We recruited 101 normotensive young adults born preterm (n=47, mean gestational age 32.8±3.2 weeks) and term (n=54, mean gestational age 39.5±1.4 weeks) for detailed cardiovascular phenotyping. The gestational age range for the preterm cohort was 23 to 36 weeks, with 80.9% (n=38) born 32-36 weeks; 10.6% (n=5) born 28-31 weeks; and 8.5% (n=4) born <28weeks. Resting echocardiograms were performed to characterize RV morphology, RV function, and pulmonary hemodynamics, and spirometry was performed to assess lung function. Results: Preterm-born individuals had smaller RV end-diastolic (p<0.001) and end-systolic areas (p=0.035) and inferior RV lengths (p=0.001) compared to term-born individuals. Measures of RV function, RV fractional area of change (FAC) and tricuspid annular plane systolic excursion (TAPSE) were lower in preterm compared to term-born young adults (FAC: 38.2±9.75 vs 43.8±7.01%, p=0.009 and TAPSE: 1.77±0.26 vs 2.24±0.37 cm, p<0.001). Pulmonary artery acceleration time (PAAT), a reliable estimate of pulmonary hemodynamics, was lower in the preterm-born young adults (PAAT: 123.4±23.8 vs 159.0±23.2 msec, p<0.001), though there were no differences between groups in estimated RV-pulmonary vascular (PV) coupling (TAPSE/PAAT: 0.15±0.02 vs 0.14±0.03 m/sec, p=0.77). Percentage predicted lung function measures were similar between those born preterm and term: forced expiratory volume in 1 second (FEV1, p=0.41); forced vital capacity (FVC, p=0.88); and FEV1/FVC ratio (p=0.84). Lower RV FAC and TAPSE in preterm-born individuals remained significant when adjusting for pulmonary function parameters (p<0.05). Conclusions: Preterm-born young adults have reduced RV function, independent of lung physiology. RV afterload is increased, but the RV remains hemodynamically coupled to its pulmonary circulation despite worse RV function and altered morphology in young adults born preterm. [ABSTRACT FROM AUTHOR]

Background: Arrested pulmonary development is suspected to lead to reduced exercise capacity in those born preterm. However, severe neonate respiratory distress is uncommon, affecting <10% of preterm infants and premature cohort studies show normal lung capacity is typical by adolescence. Our recent clinical studies in preterm-born individuals have identified altered left ventricular (LV) structure and function including reducing ejection fraction (EF) with increasing exercise intensity. Hypothesis: Preterm-born young adults have reductions in exercise capacity proportional to the degree of systolic impairment in their exercise stress response. Methods: We recruited 101 normotensive young adults born preterm (n=47 mean gestational age 32.8±3.2 weeks) and term (n=54) for cardiovascular phenotyping. Baseline spirometry and echocardiography were performed and subjects completed peak cardiopulmonary exercise testing to measure exercise capacity. Exercise stress echocardiograms were then performed with apical four-chamber views collected while exercising at 40%, 60%, and 80% of peak exercise load. Results: Exercise capacity was lower in preterm participants (94±20% vs 108±25% of predicted peak VO2, P=0.001). Baseline EF was similar between groups. Change in EF from rest to 40% and 60% exercise intensity predicted peak VO2 in the preterm-born group (r2=0.367, P=0.014 and r2=0.373, P=0.007 respectively), but not controls (r2=-0.069, P=0.746 and r2=-0.024, P=0.644 respectively). Resting and dynamic pulmonary measures were similar between groups and did not explain differing exercise capacity. Conclusions: Preterm-born young adults have reduced exercise capacity that relates to their blunted left ventricular systolic response to exercise but not to pulmonary capacity. How prematurity impacts the response to chronic aerobic training and associated alterations in exercise capacity and cardiovascular risk profile requires further investigation. [ABSTRACT FROM AUTHOR]

Background: Individual experience of exercise and willingness to comply with exercise prevention programs varies. We hypothesised early subclinical cardiovascular adaptions in young adults with modest blood pressure (BP) elevation may result in a more adverse response to low intensity exercise. Objectives: To study whether young adults with elevated BP have an altered cardiac stress response and whether this relates to left ventricular structure. Methods: We recruited 146 young adults (age 27±5 years) with a range of blood pressures for resting structural phenotyping with cardiac magnetic resonance. A sub-group (n=71) underwent cardiopulmonary exercise testing and exercise stress echocardiography while exercising at 40%, 60%, and 80% of peak exercise load. Myocardial stress response was assessed by changes in ejection fraction (EF) and post-exercise plasma stress marker (copeptin) release. Results were compared in those with systolic or diastolic BP ≥ 120/80 mm Hg (n=62, mean BP 129/77 mm Hg) vs those with systolic and diastolic BP < 120/80 mm Hg (n=84, mean BP 110/66 mm Hg). Results: Resting EF was similar between groups. However, during physical exercise higher BP was associated with lower EF at 40% and 60% workload (73.9±3.25 vs 80.0±4.54%, p<0.001 and 75.2±6.59 vs 79.4±4.70%, p=0.026 respectively) as well as smaller increases in EF from resting levels (10.4±5.92 vs 19.0±6.90%, p<0.001 and 11.5±8.34 vs 17.5±7.31%, p=0.029 at 40% and 60% respectively). Furthermore, at 40% workload, perceived exertion was greater in those with higher BP (10.7±1.9 vs 9.3±2.4 on Borg scale, p=0.018). Finally, elevated post-exercise plasma copeptin levels were predicted by lower EF at 40% workload (r2=0.188, p=0.043). Higher BP was associated with greater LV mass index (0.68±0.13 vs 0.62±0.12 g/ml, p=0.007) and wall thickness (7.21±1.31 vs 6.62±1.44 mm, p=0.05) but values were within clinically normal ranges and did not predict variation in myocardial stress response. Conclusions: Young adults with modest blood pressure elevation experience greater fatigue and a physiologically significant systolic defect in early response to exercise. Whether intervention can halt functional declines and how perceived exertion may confound exercise prescription needs further study. [ABSTRACT FROM AUTHOR]

Introduction: Microvesicles are elevated in the circulation during cardiac stress; a response that is blunted in those with cardiovascular disease. Microvesicles play both activating and regulatory roles in the pathogenesis of hypertension, and their release is believed to be a protective mechanism during cardiac stress. Hypothesis: We hypothesised that microvesicle release during exercise-induced cardiac stress differs in young adults with and without hypertension. Methods: Microvesicle release was measured in 106 participants (79 normotensive, 27 hypertensive). Blood samples were obtained during maximal exercise testing at three time-points: before, immediately post and following 20 minutes recovery. The level of microvesicle procoagulant activity was determined in all participants. Microvesicles were phenotyped by flow cytometry in a subset of participants. Results: Exercise was associated with a significant elevation in the total procoagulant activity of microvesicles (p<0.001) and this increase was significantly higher in the normotensive group than the hypertensives (median(IQR) +0.7(0.0-2.1) vs -0.1(-0.4-0.4), p=0.001). Circulating procoagulant, platelet, endothelial, leucocyte, granulocyte and monocyte-derived microvesicles were shown to be elevated during exercise (p<0.05). The elevation in endothelial and leucocyte microvesicle levels returned to baseline within 20 minutes recovery. The significant elevation in procoagulant, platelet, granulocyte and monocyte-derived microvesicles was only seen in the normotensive participants, not in those with hypertension. Furthermore, amongst the normotensive participants, those with a blunted release of platelet microvesicles had higher peak diastolic blood pressures (86.8±8.4 vs 73.5±14.5, p=0.028) during exercise and increased global arterial stiffness measured at rest by the cardio-ankle vascular index (CAVI: 6.1±0.6 vs 5.4±0.5, p=0.022). Conclusions: In young adult hypertension there is a blunted release of microvesicles during exercise-induced cardiac stress. Normotensive young adults with a blunted platelet microvesicle release demonstrate early markers of future hypertension risk with greater peripheral resistance and arterial stiffness. [ABSTRACT FROM AUTHOR]