Effects of chronically elevated pulmonary arterial pressure and flow on right ventricular afterload

Ha, Belinda; Lucas, Carol L.; Henry, George W.; Frantz, Elman G.; Ferreiro, José I.; Wilcox, Benson R.

doi:10.1152/ajpheart.1994.267.1.h155

Cited by 27 publications

(38 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The absence of change suggests a balance between some Z c decrease due to proximal vessels distension and some Z c increase due to proximal vessel stiffness. Chronic pulmonary hypertension, when associated with higher pressure values, is generally associated with an increased Z c due to increased elastance and with increased wave reflection, due to arterial remodeling (11,14,20). Many previous studies reported RV hypertrophy in response to pulmonary hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…From impedance, spectra were derived from the 0-Hz impedance modulus or total resistance (Z 0), and the characteristic impedance (Z c) was computed as the average of moduli between 2 and 15 Hz (4). The pressure wave was separated into forward and backward components, and wave reflection was quantified as the amplitude of the reflected pressure wave (Ampl) (14,21,37). Figure 2 summarizes how RV-arterial coupling was analyzed from RV pressure-volume curves using a single-beat method (5).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Right ventricular adaptation to pulmonary hypertension: an interspecies comparison

Wauthy

Pagnamenta

Vassalli

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Wauthy, Pierre, Alberto Pagnamenta, Fabio Vassalli, Robert Naeije, and Serge Brimioulle. Right ventricular adaptation to pulmonary hypertension: an interspecies comparison. Am J Physiol Heart Circ Physiol 286: H1441-H1447, 2004. First published December 18, 2003 10.1152/ajpheart.00640.2003 adaptation is an important prognostic factor in acute and chronic pulmonary hypertension. Pulmonary vascular basal tone and hypoxic reactivity are known to vary widely between species. We investigated how RV adaptation to acute pulmonary hypertension is preserved in species with low, intermediate, and high pulmonary vascular resistance and reactivity. Acute pulmonary hypertension was induced by hypoxia, distal embolism, and proximal constriction in anesthetized dogs (n ϭ 10), goats (n ϭ 8), and pigs (n ϭ 8). Pulmonary vessels were assessed by flow-pressure curves and by impedance to quantify distal resistance, proximal elastance, and wave reflections. RV function was assessed by pressure-volume curves to quantify afterload, contractility, and ventricular-arterial coupling efficiency. First, hypoxia was associated with a progressive increase of resistance, elastance, and wave reflection from dogs to goats and from goats to pigs. RV contractility increased proportionally to RV afterload, and optimal coupling was preserved in all species. Second, embolism increased resistance and wave reflection but not elastance. The increase in RV contractility matched the increase in RV afterload and optimal coupling was preserved. Finally, proximal pulmonary artery constriction increased resistance, increased and accelerated wave reflection, and markedly increased elastance. RV contractility increased markedly and coupling showed a nonsignificant trend to decrease. We conclude that optimal or near-optimal ventricular-arterial coupling is maintained in acute pulmonary hypertension, whether in absence or presence of chronic species-induced pulmonary hypertension. heart failure; contractility; ventricular-arterial coupling IN CLINICAL PRACTICE, the diagnosis of pulmonary arterial hypertension relies on measurements of pulmonary vascular pressures and cardiac output and calculations of pulmonary vascular resistance (31). These hemodynamic measurements are of prognostic value, with survival being related to cardiac output rather than to pulmonary artery pressure (P PA ) (8,24,33). The clinical state of patients with pulmonary arterial hypertension also appears to be more related to cardiac output than to P PA (25,34). Clinical signs of right heart failure often are not clearly related to progression of pulmonary hypertension as assessed by pulmonary arterial pressure and resistance (34). These observations may be explained by the fact that heart failure in pulmonary hypertension is the consequence of uncoupling of the right ventricle (RV) to the hypertensive pulmonary circulation, which is not actually measured by routine hemodynamic evaluations (30, 34).Sagawa and co-workers (17, 32) previously developed a concept of ventriculoarterial coupling ...

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Right ventricular adaptation to pulmonary hypertension: an interspecies comparison

Wauthy

Pagnamenta

Vassalli

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…Moreover, pressure waveform analysis performed in the time domain makes it possible to calculate the timing and extent of wave reflection in systemic and pulmonary circulation with measures such as augmentation index (as shown in Figure 3D), which roughly represents reflected wave summation (⌬P) in the pulmonary circuit and normalizes for the PA pulse pressure. [32][33][34][35][36][37][38][39][40] These values can be obtained easily at the time of right heart catheterization, and future studies will compare both analyses as potential prognostic indicators in patients with pulmonary hypertension and correlate with the previously described concept of capacitance. 41 …”

Section: Time-domain Analysis Of Pa Pressure Waveformsmentioning

confidence: 99%

“…This can be assessed in much the same way as the LV with E/A and EЈ/AЈ analysis. 35,83 Moreover, diastolic forward flow in the RV outflow tract may serve as a marker of RV diastolic function. [83][84][85] More recently, the improvement of PAH therapy on RV diastolic function has been noted.…”

Section: Champion Et Al Approach To the Rv-pulmonary Circulation Unitmentioning

confidence: 99%

Comprehensive Invasive and Noninvasive Approach to the Right Ventricle–Pulmonary Circulation Unit

2009

View full text Add to dashboard Cite

T here is still no answer to William Harvey's rhetorical question. He included the right ventricle (RV), its "pulse," the large pulmonary arteries (PAs), and the lungs in the same sentence, emphasizing the concept of a "unit." Although Harvey realized the importance of the RV and its interactions with the pulmonary circulation, 4 centuries later, the RV is largely understudied. At the same time, there has been significant progress in our understanding of the pathology of pulmonary vascular disease and, over the past few years, an explosion of clinical therapeutic trials for PA hypertension (PAH). 1 This unbalanced approach has generated a number of problems and controversies. For example, it is now becoming apparent that even if experimental therapies improve or reverse PAH pathology, this does not necessarily lead to clinical improvement and prolonged survival unless accompanied by a parallel improvement in RV function. The degree of pulmonary hypertension (ie, PA pressure [PAP]) does not strongly correlate with symptoms or survival, whereas RV mass and size and right atrial pressure reflect functional status and are strong predictors of survival. 2 The 6-minute walk test, used as the primary end point in most PAH clinical trials, correlates better with RV function (ie, cardiac output) than with the degree of pulmonary pressure elevation. However, this test is being heavily criticized because of multiple inherent problems and the fact that it does not provide information on specific components of RV-pulmonary vascular function. 3 Although therapies aiming at reversing pulmonary vascular remodeling might also have a positive effect on the RV (eg, sildenafil, which has been shown to increase RV inotropy 4 and decrease RV hypertrophy, 5 in addition to its effects on the pulmonary circulation), others might have untoward effects on the RV. For example, imatinib, an antiproliferative/proapoptotic agent that shows preliminary promise in reversing pulmonary vascular remodeling, 6 is potentially associated with primary negative (ie, proapoptotic) effects on the myocardium. 7 As our knowledge of RV physiology and biology increases, it is becoming apparent that a comprehensive approach to the RV, the pulmonary circulation, and their interactions will be beneficial in both clinical management of PAH patients and clinical research. The evolution of RV pathology from the normal to a compensated (hypertrophied) and then decompensated state parallels the evolution of pulmonary vascular pathology from a vasodilated highcapacitance state to vasoconstricted arteries and early loss of endothelial cells/capillaries to an end-stage proliferative and obliterative vascular remodeling (Figure 1). Therefore, it is important to study the RV and the PAs comprehensively and simultaneously as a unit. Here, we discuss standard clinical tests (eg, right heart catheterization and echocardiography) and evolving technologies (eg, magnetic resonance [MR] imaging [MRI] and positron emission tomography [PET]) that have the ability to study the ...

show abstract

“…Right ventricular adaptation is an important prognostic factor in acute [4] and chronic [5] pulmonary hypertension (PH). Regarding the right ventricular mechanical properties or adaptive response to PH, it is important to consider not only PH duration and severity, but also the arterial wall smooth muscle bulk and tone (active versus passive PH) [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Improved right ventricular–vascular coupling during active pulmonary hypertension

Grignola

Ginés

Bia

et al. 2007

International Journal of Cardiology

View full text Add to dashboard Cite

Effects of chronically elevated pulmonary arterial pressure and flow on right ventricular afterload

Cited by 27 publications

References 0 publications

Right ventricular adaptation to pulmonary hypertension: an interspecies comparison

Right ventricular adaptation to pulmonary hypertension: an interspecies comparison

Comprehensive Invasive and Noninvasive Approach to the Right Ventricle–Pulmonary Circulation Unit

Improved right ventricular–vascular coupling during active pulmonary hypertension

Contact Info

Product

Resources

About