Comparison Between Two Drugs on the Hemodynamic Evaluation of Pulmonary Hypertension Prior to Heart Transplantation

Jimenez, Maria; Ortega, A.M. Escoresca; Pérez, Rosalía Martínez; Gallé, E. Lage; Avilés, Á. Herruzo; Marquez, Misael; López, Medina; Rodriguez, Nancy R.; Yglesia, Rocío Pérez de la; Martı́nez, Ángel

doi:10.1016/j.transproceed.2008.08.123

Cited by 5 publications

(3 citation statements)

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“…For example, PH of variable magnitude and some tendency for pulmonary vasodilators to provoke pulmonary edema are seen with both LA hypertension and pulmonary veno-occlusive disease. [8][9][10][11] On the other hand, the biology of pathological vascular remodeling originating within the lung (rather than in response to increased LA or proximal pulmonary venous pressure) 12 must be in some ways different from that seen with category 1 PVH. Discussion in this review refers to observations made in and pertinent to category 1 PVH.…”

Section: Causes Of Pvhmentioning

confidence: 99%

“…34 Reducing precapillary constriction with vasodilators can indeed provoke pulmonary edema in some patients with PVH. [8][9][10][11] On the other hand, at least one clinician, practicing early in the days of mitral valve palliation, concluded that those with mitral valve disease and high PAP had increased risk of dyspnea attacks relative to those with lower pressure, 60 and it is certainly plausible that, for some patients, limitation of right ventricular output due to PH, not lung water, is what causes most symptoms. Pharmacologic modulation of the body's (apparently excessive) response to myocardial dysfunction (diuretics, angiotensin converting enzyme inhibitors, and beta blockers) is foundation therapy for congestive LV failure, and one could argue analogously that carefully monitored use of agents aimed at reducing excessively increased PVR could be useful for some patients with PVH.…”

Section: Treating Pvh-phmentioning

confidence: 99%

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Pulmonary Hypertension Caused by Pulmonary Venous Hypertension

Kulik

2014

Pulm. circ.

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The effect of pulmonary venous hypertension (PVH) on the pulmonary circulation is extraordinarily variable, ranging from no impact on pulmonary vascular resistance (PVR) to a marked increase. The reasons for this are unknown. Both acutely reversible pulmonary vasoconstriction and pathological remodeling (especially medial hypertrophy and intimal hyperplasia) account for increased PVR when present. The mechanisms involved in vasoconstriction and remodeling are not clearly defined, but increased wall stress, especially in small pulmonary arteries, presumably plays an important role. Myogenic contraction may account for increased vascular tone and also indirectly stimulate remodeling of the vessel wall. Increased wall stress may also directly cause smooth muscle growth, migration, and intimal hyperplasia. Even long-standing and severe pulmonary hypertension (PH) usually abates with elimination of PVH, but PVH-PH is an important clinical problem, especially because PVH due to left ventricular noncompliance lacks definitive therapy. The role of targeted PH therapy in patients with PVH-PH is unclear at this time. Most prospective studies indicate that these medications are not helpful or worse, but there is ample reason to think that a subset of patients with PVH-PH may benefit from phosphodiesterase inhibitors or other agents. A different approach to evaluating possible pharmacologic therapy for PVH-PH may be required to better define its possible utility.Keywords: pulmonary hypertension, pulmonary venous hypertension. As a perfect example of how clinical imperative can drive basic physiological investigation, studies of the effect of pulmonary venous hypertension (PVH) on the lung's circulation were in full swing by the very early 1950s, 1 close on the heels of the development of surgical relief of mitral valve stenosis. Cardiac catheterization of patients with mitral valve disease has characterized the physiology of PVH, and histological investigations demonstrated the microvascular changes provoked by PVH. Just as important, the effect of relief of left atrial (LA) hypertension on the circulation has been extensively reported, usually for patients who have had mitral valve intervention. We have learned that the circulatory alterations provoked by PVH share some characteristics with other forms of pulmonary hypertension (PH), such as the idiopathic variety, PH due to chronic alveolar hypoxia, and PH secondary to congenital cardiac shunting lesions. For example, acute "reactivity" to vasodilators may be observed, and there is overlap in the microarchitectural abnormalities seen. On the other hand, the "natural history" of PVH-PH is very different than that of the idiopathic variety or that seen with shunting defects: in the former (as demonstrated with mitral valve disease), PH is likely to largely or completely resolve if PVH is relieved, even with long-standing and severely increased pulmonary vascular resistance (PVR), 2,3 while in the latter two, PH is more likely to inexorably increase. PVH-PH is ther...

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Section: Causes Of Pvhmentioning

confidence: 99%

Section: Treating Pvh-phmentioning

confidence: 99%

Pulmonary Hypertension Caused by Pulmonary Venous Hypertension

Kulik

2014

Pulm. circ.

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“…,b, Mogollon Jimenez et al . ) (Tables and ). All of these studies demonstrated improvement in pulmonary haemodynamics together with an increase in cardiac output or cardiac index, depending on the parameter observed.…”

Section: The Treatment Of Ph Due To Lhfmentioning

confidence: 99%

Pathophysiology and potential treatments of pulmonary hypertension due to systolic left heart failure

Lundgren

Rådegran

2014

Acta Physiologica

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Pulmonary hypertension (PH) due to left heart failure is becoming increasingly prevalent and is associated with poor outcome. The precise pathophysiological mechanisms behind PH due to left heart failure are, however, still unclear. In its early course, PH is caused by increased left ventricular filling pressures, without pulmonary vessel abnormalities. Conventional treatment for heart failure may partly reverse such passive PH by optimizing left ventricular function. However, if increased pulmonary pressures persist, endothelial damage, excessive vasoconstriction and structural changes in the pulmonary vasculature may occur. There is, at present, no recommended medical treatment for this active component of PH due to left heart failure. However, as the vascular changes in PH due to left heart failure may be similar to those in pulmonary arterial hypertension (PAH), a selected group of these patients may benefit from PAH treatment targeting the endothelin, nitric oxide or prostacyclin pathways. Such potent pulmonary vasodilators could, however, be detrimental in patients with left heart failure without pulmonary vascular pathology, as selective pulmonary vasodilatation may lead to further congestion in the pulmonary circuit, resulting in pulmonary oedema. The use of PAH therapies is therefore currently not recommended and would require the selection of suitable patients based on the underlying causes of the disease and careful monitoring of their progress. The present review focuses on the following: (i) the pathophysiology behind PH resulting from systolic left heart failure, and (ii) the current evidence for medical treatment of this condition, especially the role of PAH-targeted therapies in systolic left heart failure.

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Diagnosis and Management of Right-Sided Heart Failure in Subjects Supported With Left Ventricular Assist Devices

Romano

Cowger

Aaronson

et al. 2010

Curr Treat Options Cardio Med

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Right ventricular failure (RVF) is a cause of major morbidity and mortality in the left ventricular assist device (LVAD) population. Many LVAD candidates have clinical or subclinical right ventricular (RV) dysfunction, and the perioperative period is fraught with insults that may provoke reactive pulmonary vascular hypertension and acute or chronic development of RVF. Thus, preoperative patient optimization using diuretics, pulmonary vasodilators, and inotropes to reduce RV wall stress and improve contractility is critical. An assessment of the LVAD candidate's risk for developing postoperative RVF is also key, especially in the destination therapy population for whom good options for long-term RV support currently are lacking. Intraoperatively, various pharmacologic and surgical interventions are available to reduce RVF risk. This review discusses RVF diagnosis and management strategies in subjects undergoing LVAD implantation.

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Comparison Between Two Drugs on the Hemodynamic Evaluation of Pulmonary Hypertension Prior to Heart Transplantation

Cited by 5 publications

References 10 publications

Pulmonary Hypertension Caused by Pulmonary Venous Hypertension

Pulmonary Hypertension Caused by Pulmonary Venous Hypertension

Pathophysiology and potential treatments of pulmonary hypertension due to systolic left heart failure

Diagnosis and Management of Right-Sided Heart Failure in Subjects Supported With Left Ventricular Assist Devices

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