Pulmonary vascular changes induced by congenital obstruction of pulmonary venous return

Endo, Masato; Yamaki, Shohei; Ohmi, M; Tabayashi, Koichi

doi:10.1016/s0003-4975(99)01079-6

Cited by 54 publications

(39 citation statements)

References 18 publications

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“…436,437 The histopathology of pulmonary venous hypertension includes medial thickening of pulmonary arteries and veins and, less commonly, intimal fibrosis of veins and arteries in children. 438,439 …”

Section: Left-sided Heart Diseasementioning

confidence: 99%

Pediatric Pulmonary Hypertension

Abman¹,

Hansmann²,

Archer³

et al. 2015

Circulation

949

405

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Abstract-Pulmonary hypertension is associated with diverse cardiac, pulmonary, and systemic diseases in neonates, infants, and older children and contributes to significant morbidity and mortality. However, current approaches to caring for pediatric patients with pulmonary hypertension have been limited by the lack of consensus guidelines from experts in the field. In a joint effort from the American Heart Association and American Thoracic Society, a panel of experienced clinicians and clinician-scientists was assembled to review the current literature and to make recommendations on the diagnosis, evaluation, and treatment of pediatric pulmonary hypertension. This publication presents the results of extensive literature reviews, discussions, and formal scoring of recommendations for the care of children with pulmonary hypertension. Key Words: AHA Scientific Statements ◼ bronchopulmonary dysplasia ◼ congenital diaphragmatic hernia ◼ congenital heart disease ◼ genetics ◼ persistent pulmonary hypertension of the newborn ◼ sickle cell disease © 2015 by the American Heart Association, Inc., and the American Thoracic Society.Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIR.0000000000000329 †Deceased. The American Heart Association and the American Thoracic Society make every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.This document was approved by the American Heart Association Science Advisory and Coordinating Committee on May 12, 2015, the American Heart Association Executive Committee on July 22, 2015, and the American Thoracic Society on July 24, 2015.The online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000329/-/DC1. The American Heart Association requests that this document be cited as follows: Abman SH, Hansmann G, Archer SL, Ivy DD, Adatia I, Chung WK, Hanna BD, Rosenzweig EB, Raj JU, Cornfield D, Stenmark KR, Steinhorn R, Thébaud B, Fineman JR, Kuehne T, Feinstein JA, Friedberg MK, Earing M, Barst RJ, Keller RL, Kinsella JP, Mullen M, Deterding R, Kulik T, Mallory G, Humpl T, Wessel DL; on behalf of the American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation, Council on Clinical Cardiology, Council on Cardiovascular Disease in the Young, Council on Cardiovascular Radiology and Intervention, Council on Cardiovascular Surgery and Anesthesia, and the American Thoracic Society. Pediatric pulmonary hypertension: guidelines from the American Heart Association and American Thoracic Society. Circulation. 2015;132:2037-2099 Copies: This document is available on the World Wide Web site of the American Heart Associat...

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Section: Left-sided Heart Diseasementioning

confidence: 99%

Pediatric Pulmonary Hypertension

Abman¹,

Hansmann²,

Archer³

et al. 2015

Circulation

949

405

View full text Add to dashboard Cite

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“…However, data from other studies of pulmonary artery hypertension caused by pulmonary venous hypertension have found that pulmonary vascular changes may be reversible after relief of pulmonary venous hypertension, even after protracted elevation of left atrial pressure. [17][18][19] Conclusions and Implications for the Future HLHS with intact or severely restrictive atrial septum continues to have a high mortality rate before and after stage I palliation, despite prenatal diagnosis and recent advances in interventional catheterization, surgical technique, and critical care management strategies. Beyond the high-risk neonatal perioperative period, early childhood survival may not differ from that of other HLHS patients, but the long-term outlook is unknown.…”

Section: Discussionmentioning

confidence: 99%

Hypoplastic Left Heart Syndrome With Intact or Highly Restrictive Atrial Septum

et al. 2004

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Background-Hypoplastic left heart syndrome (HLHS) with intact or very restrictive atrial septum is a highly lethal combination. We review our 13-year institutional experience treating this high-risk subgroup of patients with emergent catheter therapy. Methods and Results-Infants with HLHS requiring catheter septostomy within the first 2 days of life were compared with a matched control group with adequate interatrial communication. Preoperative, early postoperative, and medium-term survival were evaluated. Earlier experience was compared with recent results to assess the effect of changes in catheterization and surgical and intensive care unit management strategies over the study period. From 1990 to 2002, 33 newborns with HLHS (11% of newborns with HLHS managed during this period) underwent urgent/semiurgent catheterization to create or enlarge an interatrial communication before surgical palliation. Preoperative and early postoperative mortality were high (48%) compared with control HLHS patients, regardless of prenatal diagnosis and despite successful catheter-based atrial septostomy with clinical stabilization. Mortality trended down during the later part of the study period. Those who survived the neonatal period had late survival, pulmonary artery pressure, and resistance similar to those of control subjects. Conclusions-Neonatal mortality in the subgroup of HLHS patients with intact or highly restrictive atrial septum remains high despite successful urgent septostomy. Persistently poor outcomes for these patients have prompted efforts at our center to develop techniques for fetal intervention for this condition, in the hope that prenatal relief of left atrial and pulmonary venous hypertension may promote normal pulmonary vascular and parenchymal development and improve both short-and long-term outcomes.

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“…As previously noted, despite having PH for many years, adults and older children 52,54,56,64 with mitral valve dis- Figure 2. Change in pulmonary vascular resistance (PVR) after mitral valve intervention to effect relief of mitral stenosis/regurgitation (circles; n = 61 patients) or closure of ventricular septal defect (VSD; dots, n = 110 patients).…”

Section: Evolution and Resolution Of Phmentioning

confidence: 72%

“…What happens to the intimal proliferation is unclear. Intimal proliferation and fibrosis do not imply a fixed increase in PVR with mitral stenosis, [50][51][52]54 even though such lesions often portend an unfavorable outcome with shunting lesions. 68 This may be mostly a matter of degree: perhaps the fraction of the vascular bed occluded by intima is smaller with PVH than other forms of PH; the observation by Wagenvoort and Wagenvoort 50 that intimal lesions are rarely occlusive with PVH is consistent with this.…”

Section: Evolution and Resolution Of Phmentioning

confidence: 99%

“…28,63,65,66 Most available hemodynamic data are for ≤1 year of follow-up, but one large series demonstrated that the reduction in PVR lasts at least several years. 67 Reliable reduction of PVR with mitral valve replacement or repair probably also occurs in the first few years of life, 31,54,56 although the available data are limited and far from definitive. (Published long-term follow-up data for patients with significant and isolated [i.e., without left-to-right shunting] PVH and PH at birth are scant, which is surely a reflection of the tendency of these patients to die early absent relief of the PVH.)…”

Section: Evolution and Resolution Of 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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Pulmonary vascular changes induced by congenital obstruction of pulmonary venous return

Cited by 54 publications

References 18 publications

Pediatric Pulmonary Hypertension

Pediatric Pulmonary Hypertension

Hypoplastic Left Heart Syndrome With Intact or Highly Restrictive Atrial Septum

Pulmonary Hypertension Caused by Pulmonary Venous Hypertension

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