Improved right ventricular–vascular coupling during active pulmonary hypertension

Grignola, Juan C.; Ginés, Fernando; Bia, Daniel; Armentano, Ricardo L.

doi:10.1016/j.ijcard.2006.03.007

Cited by 33 publications

(29 citation statements)

References 41 publications

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“…The effect of wave reflection on pulmonary hemodynamics was quantified using two indices 9 : ΔSP defined as the difference between the systolic pressure of measured and forward pressure waves, and ΔPP defined as the difference between the PP of measured and forward pressure waves. To quantify the effect of PAH and estrogen on the timing of wave reflection, we defined the normalized time between the beginning of systolic to the peak of the reflected pressure wave (t peak = Δt/T), where T is the period of cardiac cycle.…”

Section: Methodsmentioning

confidence: 99%

“…The total hydraulic power (W t ) was calculated as the time-average of the product of the instantaneous pulmonary PA pressure (P(t)) and flow (Q(t)) over the cardiac cycle, ignoring the small kinetics terms 9 . The steady power (W s ) was calculated as the product of mPAP and CO, and the oscillatory power (W o ) was the difference between W t and W s .…”

Section: Methodsmentioning

confidence: 99%

“…Right ventricular-vascular coupling was assessed by two indices 9 , i.e., the oscillatory power fraction ratio, defined as W o /W t and transpulmonary vascular efficiency defined as CO/W t (energy cost of maintaining or increasing CO).…”

Section: Methodsmentioning

confidence: 99%

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Estrogen Preserves Pulsatile Pulmonary Arterial Hemodynamics in Pulmonary Arterial Hypertension

Liu¹,

Hacker

Eickhoff

et al. 2016

Ann Biomed Eng

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Pulmonary arterial hypertension (PAH) is caused by extensive pulmonary vascular remodeling that increases right ventricular (RV) afterload and leads to RV failure. PAH predominantly affects women; paradoxically, female PAH patients have better outcomes than men. The roles of estrogen in PAH remain controversial, which is referred to as “the estrogen paradox”. Here, we sought to determine the role of estrogen in pulsatile pulmonary arterial hemodynamic changes and its impact on RV functional adaption to PAH. Female mice were ovariectomized and replenished with estrogen or placebo. PAH was induced with SU5416 and chronic hypoxia (SuHx). In vivo hemodynamic measurements showed that (1) estrogen prevented loss of pulmonary vascular compliance with limited effects on the increase of pulmonary vascular resistance in PAH; (2) estrogen attenuated increases in wave reflections in PAH and limited its adverse effects on PA systolic and pulse pressures; and (3) estrogen maintained the total hydraulic power and preserved transpulmonary vascular efficiency in PAH. This study demonstrates that estrogen preserves pulmonary vascular compliance independent of pulmonary vascular resistance, which provides a mechanical mechanism for ability of estrogen to delay disease progression without preventing onset. The estrogenic protection of pulsatile pulmonary hemodynamics underscores the therapeutic potential of estrogen in PAH.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Estrogen Preserves Pulsatile Pulmonary Arterial Hemodynamics in Pulmonary Arterial Hypertension

Liu¹,

Hacker

Eickhoff

et al. 2016

Ann Biomed Eng

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“…Because the right ventricle contributes to the effi ciency of the cardiovascular system through right V-A coupling, the assessment of the Ea/Ees of the right side of the circulation can play a role in the management of critically ill patients [48]. RV V-A coupling expresses the optimal interaction between RV performance and fun ction of the pulmonary vascular system.…”

Section: Right Ventricular Dysfunction and V-a Couplingmentioning

confidence: 99%

Ventriculo-arterial Decoupling in Acutely Altered Hemodynamic States

Guarracino¹,

Baldassarri²,

Pinsky³

2013

Annual Update in Intensive Care and Emergency Medicine 2013

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Th e dynamic interaction between the heart and the systemic circulation allows the cardiovascular system to be effi cient in providing adequate cardiac output and arterial pressures necessary for suffi cient organ perfusion [1]. Th e cardiovascular system provides adequate pressure and fl ow to the peripheral organs in diff erent physiological (rest and exercise) and pathological conditions because of the continuous modulation of the arterial system compliance, stiff ness and resistance with respect to left ventricular (LV) systolic performance [2]. Card iac output is the fi nal result of this dynamic modulation. Because LV stroke volume depends on myocardial contractility and loading conditions (preload and afterload), both cardiac and arterial dysfunction can lead to acute hemodynamic decompensation and shock. According to the underlying pathophysiological mechanisms, altered hemodynamic profi les can be classifi ed as primarily refl ecting cardiogenic, hypovolemic, obstructive or distributive shock.Low cardiac output resulting in systemic hypoperfusion requires prompt and adequate treatment to restore cardio vascular function and prevent organ hypo perfusion. Current clinical guidelines recommend resuscitation with intravascular fl uid infusions supplemented with selective use of inotropes and vasopressors to reverse shock in critically ill patients [3,4]. Howe ver, the treatment of acute he modynamic impairment should be tailored based on the etiological mechanism of the cardiovascular dysfunction. Herein lies a major problem with present guidelines: Th ey cannot distinguish the underlying causes of impaired LV stroke volume leading to impaired cardiac output. Ventriculo-arterial couplingTh e concept that the cardiovascular system works better when the heart and the ar terial system are coupled has been well demonstrated [5,6]. When t he h eart pumps blood into the vascular tree at a rate and volume that matches the capability of the arterial system to receive it, both cardiovascular performance and its associated cardiac energetics are optimal [7,8]. A cont ract ility or arterial tone that is too high or too low decouples these processes and can lead to cardiac failure independent of myocardial ischemia or the toxic eff ects of sepsis and related systemic disease processes. Th is optimization means that the LV workload and the arterial system optimally match when the left ventricle ejects the blood into the arterial system and is quantifi ed by ventriculo-arterial (V-A) coupling analysis. Th is process is optimized without excessive changes in LV pressure, and the mechanical energy of LV ejection is completely transferred from the ventricle to the arterial system [9,10]. Th e ro le o f V-A coupling in the management of critically ill patients with severe hemodynamic instability and shock is becoming increasingly clear.V-A coupling can be defi ned as the ratio of the arterial elastance (Ea) to the ventricular elastance (Ees). Th is ratio was fi rst proposed by Suga [11] as a method t o evaluate the mechanica...

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“…In a recent series of studies, PA pressure-diameter (PD) measurements were performed directly in “active” and “passive” forms of acute PH in sheep obtained through phenylephrine injection and left PA occlusion, respectively (14, 15, 61, 62, 149). The results from this sheep model suggest that SMC activity strongly contributes to vascular mechanics in response to acute pressure increases, in that SMC activation maintained or slightly reduced the diameter at which vascular buffering function occurred (Fig.…”

Section: Stiffening Modalitiesmentioning

confidence: 99%

Pulmonary Vascular Stiffness: Measurement, Modeling, and Implications in Normal and Hypertensive Pulmonary Circulations

Hunter

Lammers

Shandas

2011

Comprehensive Physiology

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This article introduces the concept of pulmonary vascular stiffness, discusses its increasingly recognized importance as a diagnostic marker in the evaluation of pulmonary vascular disease, and describes methods to measure and model it clinically, experimentally, and computationally. It begins with a description of systems-level methods to evaluate pulmonary vascular compliance and recent clinical efforts in applying such techniques to better predict patient outcomes in pulmonary arterial hypertension. It then progresses from the systems-level to the local level, discusses proposed methods by which upstream pulmonary vessels increase in stiffness, introduces concepts around vascular mechanics, and concludes by describing recent work incorporating advanced numerical methods to more thoroughly evaluate changes in local mechanical properties of pulmonary arteries.

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Improved right ventricular–vascular coupling during active pulmonary hypertension

Cited by 33 publications

References 41 publications

Estrogen Preserves Pulsatile Pulmonary Arterial Hemodynamics in Pulmonary Arterial Hypertension

Estrogen Preserves Pulsatile Pulmonary Arterial Hemodynamics in Pulmonary Arterial Hypertension

Ventriculo-arterial Decoupling in Acutely Altered Hemodynamic States

Pulmonary Vascular Stiffness: Measurement, Modeling, and Implications in Normal and Hypertensive Pulmonary Circulations

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