Reflection as a cause of mid-systolic deceleration of pulmonary flow wave in dogs with acute pulmonary hypertension: comparison of pulmonary artery constriction with pulmonary embolisation

Furuno, Y.; Nagamoto, Yasuo; Fujita, Masasuke; Kaku, Tohru; Sakurai, Shugo; Kuroiwa, Akio

doi:10.1093/cvr/25.2.118

Cited by 71 publications

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“…These changes have been explained by increased pulmonary arterial elastance and wave reflection [14,27]. In fact, pulmonary acceleration time decreases with increasing characteristic impedance, which is a major determinant of right ventricular hydraulic load [27,28]. Therefore, decreased pulmonary acceleration time in the study patients would be a reflection of early remodelling of the pulmonary vasculature.…”

Section: Discussionmentioning

confidence: 95%

“…Pulmonary flow waves in PH typically show a decreased acceleration time and late-or mid-systolic deceleration [14]. These changes have been explained by increased pulmonary arterial elastance and wave reflection [14,27]. In fact, pulmonary acceleration time decreases with increasing characteristic impedance, which is a major determinant of right ventricular hydraulic load [27,28].…”

Section: Discussionmentioning

confidence: 99%

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Isolated right ventricular dysfunction in systemic sclerosis: latent pulmonary hypertension?

Huez¹,

Roufosse²,

Vachiéry³

et al. 2007

European Respiratory Journal

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Right ventricular function is frequently abnormal in patients with systemic sclerosis, but whether this is related to pulmonary vascular complications of the disease is unclear.Standard echocardiography with tissue Doppler imaging was performed at rest and during exercise for the study of right ventricular function and pulmonary circulation in 25 consecutive systemic sclerosis patients and in 13 age-matched healthy controls.When compared with the controls, the patients had no difference in systolic right ventricular pressure gradient, but a decreased pulmonary flow acceleration time, and increased right ventricular free wall thickness and end-diastolic dimensions. At the tricuspid annulus, the E maximal velocity was decreased (8.9¡4 versus 11.7¡2.3 cm?s -1 ) and the isovolumic relaxation time corrected to RR interval was increased (6.5¡2.9 versus 4.5¡2.5%). The tissue Doppler imaging profile at the mitral annulus was similar in both groups. At exercise, 18 patients had a decreased maximum workload and cardiac output, no change in systolic right ventricular pressure gradient, but an increase in the slope of pulmonary artery pressure/flow relationships. These results suggest that patients with systemic sclerosis may present with latent pulmonary hypertension as a likely cause of right ventricular diastolic dysfunction, as revealed by stress echocardiography and tissue Doppler imaging.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Isolated right ventricular dysfunction in systemic sclerosis: latent pulmonary hypertension?

Huez¹,

Roufosse²,

Vachiéry³

et al. 2007

European Respiratory Journal

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“…Several authors found an increase in Z C during acute PH induced by an abrupt proximal obstruction of the pulmonary arterial tree. This effect mainly results from the reflected waves that come back during systole (before closure of the pulmonary valve) and thus directly oppose blood ejection during ventricular contraction (11,15,16,23,26,39). On the other hand, previous studies of acute PH induced by lung injuries, such as the injection of small (150 -200 m) glass spheres (11,16,23,27), injury with oleic acid (11,29), and during autologous blood clot embolism (23), reported an increase in peripheral resistance, with either stable or decreased Z C .…”

Section: Discussionmentioning

confidence: 99%

Pulmonary artery smooth muscle activation attenuates arterial dysfunction during acute pulmonary hypertension

Santana¹,

Barra²,

Grignola³

et al. 2005

Journal of Applied Physiology

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Armentano. Pulmonary artery smooth muscle activation attenuates arterial dysfunction during acute pulmonary hypertension. J Appl Physiol 98: 605-613, 2005. First published October 15, 2004 doi:10.1152/ japplphysiol.00361.2004.-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 (EPD) and viscous ( PD) indexes as PD/EPD and the characteristic impedance (ZC) from pressure and flow to evaluate CF as 1/ZC. We also calculated the absolute and normalized cross-sectional pulsatility (PCS and NPCS, respectively), the dynamic compliance (CDYN), the cross-sectional distensibility (DCS), and the pressure-strain elastic modulus (EP). The isobaric analysis showed increase of CF, BF, and PD (P Ͻ 0.01) and decrease of EPD (P Ͻ 0.05) during APH in respect to PPH (concomitant with isobaric VSM activation-induced vasoconstriction, P Ͻ 0.01). The isometric analysis showed increase of EPD and PD (P Ͻ 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 Ͻ 0.01), and decrease in CF (P Ͻ 0.01) during APPH respect to CTL. Mechanical occlusions (PPH and APPH) reduced BF (P Ͻ 0.01) and increased EPD (P Ͻ 0.05) with regard to their previous steady states (CTL and APH). Nonsignificant differences were found in EPD between PPH and APPH. VSM activation (APH and APPH) increased PD (P Ͻ 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 PD concomitant with the arterial compliance. CDYN and DCS were the more pertinent clinical indexes of arterial elasticity. Additionally, the PDmediated preservation of the BF could be evaluated by the geometric related indexes (PCS and NPCS), which appear to be qualitative markers of arterial wall viscosity status. buffering function; arterial wall viscoelasticity; characteristic impedance AT PRESENT, there is worldwide interest in clinically assessing the local mechanical properties of the pulmonary artery (PA) during pulmonary hypertensive states (7, 10, 34). Although measurements of pressure, mean flow, and/or pulmonary vascul...

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“…Although oscillatory components of the pulmonary arterial load are low, and mean resistance may be a valuable index of the pulmonary vascular load, the pulsatile nature of the load may be prominent in numerous pathological situations. Wave reflections play an important role and should be taken into account in pulmonary hypertension resulting from several pathological conditions, like pulmonary embolism and septic shock (1,2,5,14). In this way, the pulmonary arterial impedance spectrum, which is defined in the frequency domain, provides a more precise and complete description of the pulmonary vascular load (12,17).…”

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confidence: 99%

Effective arterial elastance as an index of pulmonary vascular load

Morimont¹,

Lambermont²,

Ghuysen³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Morimont P, Lambermont B, Ghuysen A, Gerard P, Kolh P, Lancellotti P, Tchana-Sato V, Desaive T, D'Orio V. Effective arterial elastance as an index of pulmonary vascular load. Am J Physiol Heart Circ Physiol 294: H2736-H2742, 2008. First published April 18, 2008 doi:10.1152/ajpheart.00796.2007.-The aim of this study was to test whether the simple ratio of right ventricular (RV) endsystolic pressure (Pes) to stroke volume (SV), known as the effective arterial elastance (E a), provides a valid assessment of pulmonary arterial load in case of pulmonary embolism-or endotoxin-induced pulmonary hypertension. Ventricular pressure-volume (PV) data (obtained with conductance catheters) and invasive pulmonary arterial pressure and flow waveforms were simultaneously recorded in two groups of six pure Pietran pigs, submitted either to pulmonary embolism (group A) or endotoxic shock (group B). Measurements were obtained at baseline and each 30 min after injection of autologous blood clots (0.3 g/kg) in the superior vena cava in group A and after endotoxin infusion in group B. Two methods of calculation of pulmonary arterial load were compared. On one hand, Ea provided by using three-element windkessel model (WK) of the pulmonary arterial system [Ea(WK)] was referred to as standard computation. On the other hand, similar to the systemic circulation, Ea was assessed as the ratio of RV Pes to SV [Ea(PV) ϭ Pes/SV]. In both groups, although the correlation between Ea(PV) and Ea(WK) was excellent over a broad range of altered conditions, Ea(PV) systematically overestimated Ea(WK). This offset disappeared when left atrial pressure (Pla) was incorporated into Ea [Ea ‫ء‬ (PV) ϭ (Pes Ϫ Pla)/SV]. Thus Ea ‫ء‬ (PV), defined as the ratio of RV Pes minus Pla to SV, provides a convenient, useful, and simple method to assess the pulmonary arterial load and its impact on the RV function.hemodynamics; pulmonary hypertension; right ventricle; ventriculoarterial coupling IN CURRENT CLINICAL practice, pulmonary arterial load [or right ventricular (RV) afterload] is usually expressed as the mean pulmonary vascular resistance, computed as the ratio of the pressure drop through the pulmonary circulation [difference between mean pulmonary arterial pressure (PAP mean ) and left atrial pressure (Pla)] to the mean pulmonary blood flow [cardiac output (CO)]. Such an evaluation ignores the pulsatile nature of both pressure and flow. Although oscillatory components of the pulmonary arterial load are low, and mean resistance may be a valuable index of the pulmonary vascular load, the pulsatile nature of the load may be prominent in numerous pathological situations. Wave reflections play an important role and should be taken into account in pulmonary hypertension resulting from several pathological conditions, like pulmonary embolism and septic shock (1,2,5,14). In this way, the pulmonary arterial impedance spectrum, which is defined in the frequency domain, provides a more precise and complete description of the pulmonary vascular load (12, 17). However, be...

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Reflection as a cause of mid-systolic deceleration of pulmonary flow wave in dogs with acute pulmonary hypertension: comparison of pulmonary artery constriction with pulmonary embolisation

Abstract: Mid-systolic deceleration of pulmonary flow wave is likely to be related to reflection.

Cited by 71 publications

References 0 publications

Isolated right ventricular dysfunction in systemic sclerosis: latent pulmonary hypertension?

Isolated right ventricular dysfunction in systemic sclerosis: latent pulmonary hypertension?

Pulmonary artery smooth muscle activation attenuates arterial dysfunction during acute pulmonary hypertension

Effective arterial elastance as an index of pulmonary vascular load

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