Acute pulmonary hypertension (PH) may arise with or without an increase in vascular smooth muscle (VSM) tone. Our objective was to determine how VSM activation affects both the conduit (CF) and wall buffering (BF) functions of the pulmonary artery (PA) during acute PH states. PA instantaneous flow, pressure, and diameter of six sheep were recorded during normal pressure (CTL) and different states of acute PH: 1) passively induced by PA mechanical occlusion (PPH); 2) actively induced by intravenous administration of phenylephrine (APH); and 3) a combination of both (APPH). To evaluate the direct effect of VSM activation, isobaric (PPH vs. APH) and isometric (CTL vs. APPH) analyses were performed. We calculated the local BF from the elastic (E_PD) and viscous (η_PD) indexes as η_PD/E_PD and the characteristic impedance (Z_C) from pressure and flow to evaluate CF as 1/Z_C. We also calculated the absolute and normalized cross-sectional pulsatility (P_CS and NP_CS, respectively), the dynamic compliance (C_DYN), the cross-sectional distensibility (D_CS), and the pressure-strain elastic modulus (E_P). The isobaric analysis showed increase of CF, BF, and η_PD ( P < 0.01) and decrease of E_PD ( P < 0.05) during APH in respect to PPH (concomitant with isobaric VSM activation-induced vasoconstriction, P < 0.01). The isometric analysis showed increase of E_PD and η_PD ( P < 0.01), nonsignificant difference in BF (even in the presence of a significant mean PA pressure rise, from 14 (SD 6) to 25 (SD 8) mmHg, P < 0.01), and decrease in CF ( P < 0.01) during APPH respect to CTL. Mechanical occlusions (PPH and APPH) reduced BF ( P < 0.01) and increased E_PD ( P < 0.05) with regard to their previous steady states (CTL and APH). Nonsignificant differences were found in E_PD between PPH and APPH. VSM activation (APH and APPH) increased η_PD ( P < 0.01) respect to their previous passive states (CTL and PPH), but no significant differences were found within similar levels of VSM activation. In conclusion, VSM plays a relevant role in main pulmonary artery function during acute pulmonary hypertension, because isobaric vasoconstriction induced by VSM activation improves both BF and CF, mainly due to the increase in η_PD concomitant with the arterial compliance. C_DYN and D_CS were the more pertinent clinical indexes of arterial elasticity. Additionally, the η_PD-mediated preservation of the BF could be evaluated by the geometric related indexes (P_CS and NP_CS), which appear to be qualitative markers of arterial wall viscosity status.

Background: People living with HIV (PLWHIV) have a 2-fold higher risk of having a cardiovascular event than HIV-negative individuals.Objectives: The objective of this article is to estimate the pooled proportion of moderate-high cardiovascular risk in PLWHIV obtained through different scores. In addition, this study also aims to establish the prevalence of dyslipidemia, smoking habits, diabetes and high blood pressure in the included studies.Methods: A bibliographic search was conducted in MEDLINE for studies on cardiovascular risk assessment in PLWHVI that took place during the period of inception to July 2018. The eligibility criteria for inclusion were: cross-sectional or longitudinal studies on HIV-positive adults in which the prevalence of moderate-high cardiovascular risk (or data to calculate it) was reported, and included at least one of the following cardiovascular risk scores: Framingham, ASCVD, D:A:D, Progetto Cuore, PROCAM, SCORE, Regicor, and World Health Organization scores.Results: Bibliographic search identified 278 studies. Finally, thirty-nine peer-reviewed publications were identified for a collective total of 13698 subjects. The pooled prevalence of moderate-high cardiovascular risk in PLWHIV obtained with nine different scores through random-effect modeling was 20.41% (95% CI: 16.77-24.31). The most prevalent concomitant cardiovascular risk factor was dyslipidemia (39.5%), smoking (33.0 %), high blood pressure (19.8%) and diabetes (7.24%).Conclusions: Data obtained in this systematic review indicate that more than 1 in every five subjects with HIV have a moderate-high cardiovascular risk. In consequence, the burden of cardiovascular disease in PLWHIV represents a public health problem. There is an urgent need to develop strategies to prevent and detect cardiovascular risk effectively in PLWHIV.