Chronic lung disease, also known as bronchopulmonary dysplasia, affects thousands of infants worldwide each year. The impact on resources is second only to bronchial asthma, with lung function affected well into adolescence. Diagnostic and therapeutic constructs have almost exclusively focused on pulmonary architecture (alveoli/airways) and pulmonary hypertension. Information on systemic hemodynamics indicates major artery thickness/stiffness, elevated systemic afterload, and/or primary left ventricular dysfunction may play a part in a subset of infants with severe neonatal-pediatric lung disease. Understanding the underlying principles with attendant effectors would aid in identifying the pathophysiological course where systemic afterload reduction with angiotensin-converting enzyme inhibitors could become the preferred treatment strategy over conventional pulmonary artery vasodilatation.NEW & NOTEWORTHY Extremely preterm infants are at a higher risk of developing severe bronchopulmonary dysplasia. In a subset of infants, diuretic and pulmonary vasodilator therapy is ineffective. Recent information points toward systemic hemodynamic disease (systemic arterial stiffness and left ventricular dysfunction) as a contributor via back-pressure changes. Mechanistic links include heightened renin angiotensin aldosterone system activity, inflammation, and oxygen toxicity. Angiotensin-converting enzyme inhibition may be operationally more suited compared with induced pulmonary artery vasodilatation.

OBJECTIVE: This study aimed to clarify whether habitual lower-limb stretching intervention reduces regional arterial stiffness at the stretched site in middle-aged and older women.
METHODS: In this study, the effects of 4 weeks of lower-limb static stretching (of the hip extensor and flexor, knee extensor and flexor, and plantar flexor muscles) were investigated on systemic, central, and peripheral arterial stiffness using pulse wave velocity in 14 healthy middle-aged and older women randomly assigned to either a sedentary control group (67.3 ± 5.6 years; n = 7) or a stretching intervention group (63.4 ± 6.4 years; n = 7).
RESULTS: The femoral-ankle pulse wave velocity (an index of peripheral arterial stiffness) significantly decreased in the intervention group (pre, 1222.4 ± 167.5 cm/s; post, 1122.0 ± 141.1 cm/s) but did not change in the control group (pre, 1122.7 ± 107.7 cm/s; post, 1139.9 ± 77.5 cm/s). However, the brachial-ankle pulse wave velocity as an index of systemic arterial stiffness (control: pre, 1655.7 ± 296.8 cm/s, post, 1646.4 ± 232.1 cm/s; intervention: pre, 1637.6 ± 259.9 cm/s, post, 1560.8 ± 254.7 cm/s) and the carotid-femoral pulse wave velocity as an index of central arterial stiffness (control: pre, 1253.6 ± 346.4 cm/s, post, 1223.6 ± 263.4 cm/s; intervention: pre, 1125.4 ± 204.7 cm/s, post, 1024.9 ± 164.5 cm/s) did not change in either group.
CONCLUSIONS: These findings suggest that lower-limb stretching interventions may reduce regional arterial stiffness at the stretched site.

Background: Resistance training-induced changes in the muscle function is essential for the health promotion of the young and older, but the discrepancies of the effect of resistance training on arterial stiffness leads to the divergence regarding to the effect of resistance training on cardiovascular health. What confuses our understanding in this field may be the following factors: external load (higher intensity vs. lighter intensity), participants\' cardiovascular health, and arterial stiffness assessment measurement. The purpose of the present study was to investigate the effects of the whole-body traditional high-intensity vs. functional low-intensity resistance training protocol on systemic arterial stiffness, and their association with muscular fitness components in untrained young men. Methods: In this randomized controlled trial, twenty-nine untrained young men (mean age about 22.5 years old) were randomized into a 6-weeks (three sessions per week) supervised whole-body traditional high-intensity resistance group (TRT, n = 15) consisting of 4-5 sets of 12 repetitions (70%1RM, lower-repetitions) or a whole-body functional low-intensity resistance group (FRT, n = 14) with 4-5 sets of 20 repetitions (40%1RM, higher-repetitions) to volitional failure. The systemic arterial stiffness (cardio-ankle vascular index, CAVI) and muscular fitness components were assessed before and after the 6-weeks training program. Results: There was a significant decrease (pre-post) for CAVI only in FRT group (p < 0.05), but no significant difference was observed between two groups. In addition, the TRT and FRT groups showed equally significantly increased in maximal strength, muscular endurance and power (within group: both p < 0.01); however, the independent t test exhibited that the difference between two groups in terms of change in maximal strength, muscular endurance and power were no significant (p > 0.05). Furthermore, the reduction in CAVI was negatively correlated with the increase in 1RM of bench press for all participants (r = -0.490, p < 0.01). Conclusion:Using present criterion-standard assessments measurements demonstrates that CAVI was significantly reduced after 6-weeks functional resistance training with beneficial effect on muscular fitness. Negative and significant association between CAVI and 1RM bench press indicated the cardiovascular health may be involved in the regulation of resistance training.

BACKGROUND: In a previous study, the cardio-ankle vascular index (CAVI) was increased significantly in idiopathic pulmonary arterial hypertension (IPAH) patients compared to the healthy group and did not much differ from one in systemic hypertensives. In this study the relations between survival and CAVI was evaluated in patients with IPAH.
METHODS: We included 89 patients with new-diagnosed IPAH without concomitant diseases. Standard examinations, including right heart catheterization (RHC) and systemic arterial stiffness evaluation, were performed. All patients were divided according to CAVI value: the group with CAVI ≥ 8 (n = 18) and the group with CAVI < 8 (n = 71). The mean follow-up was 33.8 ± 23.7 months. Kaplan-Meier and Cox regression analysis were performed for the evaluation of our cohort survival and the predictors of death.
RESULTS: The group with CAVI≥8 was older and more severe compared to the group with CAVI< 8. Patients with CAVI≥8 had significantly reduced end-diastolic (73.79±18.94 vs 87.35±16.69 mL, P<0.009) and end-systolic (25.71±9.56 vs 33.55±10.33 mL, P<0.01) volumes of the left ventricle, the higher right ventricle thickness (0.77±0.12 vs 0.62±0.20 mm, P < 0.006), and the lower TAPSE (13.38±2.15 vs 15.98±4.4 mm, P<0.018). RHC data did not differ significantly between groups, except the higher level of the right atrial pressure in patients with CAVI≥ 8-11.38±7.1 vs 8.76±4.7 mmHg, P<0.08. The estimated overall survival rate was 61.2%. The CAVI≥8 increased the risk of mortality 2.34 times (CI 1.04-5.28, P = 0.041). The estimated Kaplan-Meier survival in the patients with CAVI ≥ 8 was only 46.7 ± 7.18% compared to patients with CAVI < 8 - 65.6 ± 4.2%, P = 0.035. At multifactorial regression analysis, the CAVI reduced but saved its relevance as death predictor - OR = 1.13, CI 1.001-1.871.
CONCLUSIONS: We suggested the CAVI could be a new independent predictor of death in the IPAH population and could be used to better risk stratify this patient population if CAVI is validated as a marker in a larger multicenter trial.

OBJECTIVE: We suggested: 1) patients with idiopathic pulmonary hypertension (IPAH) have active factors which could damage not only the pulmonary but systemic arteries too as in arterial hypertensive patients; 2) if these changes were present, they might correlate with other parameters influencing on the prognosis. This study is the first attempt to use cardio-ankle vascular index (CAVI) for the evaluation of systemic arterial stiffness in patients with IPAH.
METHODS: A total of 112 patients were included in the study: group 1 consisted of 45 patients with new diagnosed IPAH, group 2 included 32 patients with arterial hypertension, and in the control group were 35 healthy persons adjusted by age. Right heart catheterization, ECG, a 6-minute walk test (6MWT), echocardiography, blood pressure (BP) measurement and ambulatory BP monitoring, pulse wave elastic artery stiffness (PWVe; segment carotid-femoral arteries) and muscular artery stiffness (PWVm; segment carotid-radial arteries), CAVI, and N-terminal pro-B-type natriuretic peptide (NT-proBNP) level were provided. The Spearman correlation, a linear regression and multivariable binary logistic analysis were performed to indicate the predictors associated with PWV and CAVI.
RESULTS: The groups were adjusted for principal characteristics influenced on arterial stiffness. IPAH patients had significantly (P<0.001 for all) shorter 6MWT distance and higher Borg dyspnea score than the patients with arterial hypertension (systolic/diastolic BP = 146.1±10.7/94.2±9.8 mmHg) and the control group = 330.2±14.6 vs 523.8±35.3 and 560.9±30.2 m respectively and 6.2±1.8 vs 1.2±2.1 and 0.9±2.8 points. The PWVm and PWVe were the highest in hypertensive patients (10.3±1.5 and 11.42±1.70 m/s). The control group and IPAH did not have significant differences in aorta BP, but PWVm/PWVe values were significantly (P<0.003/0.008) higher in IPAH patients than in the control group (8.1±1.9/8.49±1.92 vs 6.63±1.34/7.29±0.87 m/s). The CAVIs on both sides were significantly lower in the healthy subjects (5.91±0.99/5.98±0.87 right/left side). Patients with IPAH did not differ from the arterial hypertension patients by CAVIs in comparison with the control group (7.40±1.32/7.22±1.32 vs 7.19±0.78/7.2±1.1 PWVe) did not correlate with any parameters except uric acid. PWVm correlated with uric acid (r=0.58, P<0.001), NT-proBNP (r=0.33, P=0.03) and male gender (r=0.37, P=0.013) at Spearman analysis, but not at multifactorial linear regression analysis. The CAVI correlated with age and parameters characterized functional capacity (6MWT distance) and right ventricle function (NT-proBNP, TAPSE) at Spearman analysis and with age and TAPSE at multifactorial linear regression analysis. At binary logistic regression analysis CAVI > 8.0 at right and/or left side had a correlation with age, 6MWT distance, TAPSE, but an independent correlation was only with age (β=1.104, P=0.008, CI 1.026-1.189) and TAPSE (β=0.66, P=0.016, CI 0.474-0.925).
CONCLUSIONS: In spite of equal and at normal range BP level, the age-adjusted patients with IPAH had significantly stiffer arteries than the healthy persons and they were comparable with the arterial hypertensive patients. Arterial stiffness evaluated by CAVI correlated with age and TAPSE in IPAH patients. Based on our results it is impossible to conclude the pathogenesis of arterial stiffening in IPAH patients, but the discovered changes and correlations suggest new directions for further studies, including pathogenesis and prognosis researches.