Functional and haemodynamic assessment of mild-to-moderate pulmonary valve stenosis at rest and during exercise

Meester, Pieter De; Buys, Roselien; Bruaene, Alexander Van De; Gabriels, Charlien; Voigt, Jens‐Uwe; Vanhees, Luc; Herijgers, Paul; Troost, Els; Budts, Werner

doi:10.1136/heartjnl-2014-305627

Cited by 16 publications

(6 citation statements)

References 17 publications

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“…Moreover, crying was also determined to increase pulmonary resistance to the blood flow (11). In a recent study performed in 19 adults with mild-tomoderate pulmonary valve stenosis, a linear increase in gradient with increasing flow was demonstrated (12). Similarly, we also determined a significant increase in heart rate during crying.…”

Section: Discussionsupporting

confidence: 68%

The influence of loud crying on pulmonary gradients obtained by transthoracic echocardiography in children with pulmonary valve stenosis

Çetin¹

2020

Eastern J Med

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Section: Discussionsupporting

confidence: 68%

The influence of loud crying on pulmonary gradients obtained by transthoracic echocardiography in children with pulmonary valve stenosis

Çetin¹

2020

Eastern J Med

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“…32 In contrast, patients with right ventricular pressure overload caused through purely mechanical causes (such as pulmonic stenosis) exhibit prolonged concentric hypertrophy without significant contractile depression. 33,31 Animal models recapitulate this heterogeneity, as development of right ventricular dysfunction is dependent not only on the severity of pressure overload but also on the underlying pathophysiological basis. 34 In models of PH due to administration of endothelial toxins (such as monocrotaline), right ventricular failure is more prominent than in models of mechanical pressure overload induced through pulmonary artery banding.…”

Section: The Extracellular Matrix In Chronic Pressure Overloadmentioning

confidence: 99%

Fibroblasts and the extracellular matrix in right ventricular disease

Frangogiannis

2017

Cardiovascular Research

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Right ventricular failure predicts adverse outcome in patients with pulmonary hypertension (PH), and in subjects with left ventricular heart failure and is associated with interstitial fibrosis. This review manuscript discusses the cellular effectors and molecular mechanisms implicated in right ventricular fibrosis. The right ventricular interstitium contains vascular cells, fibroblasts, and immune cells, enmeshed in a collagen-based matrix. Right ventricular pressure overload in PH is associated with the expansion of the fibroblast population, myofibroblast activation, and secretion of extracellular matrix proteins. Mechanosensitive transduction of adrenergic signalling and stimulation of the renin-angiotensin-aldosterone cascade trigger the activation of right ventricular fibroblasts. Inflammatory cytokines and chemokines may contribute to expansion and activation of macrophages that may serve as a source of fibrogenic growth factors, such as transforming growth factor (TGF)-β. Endothelin-1, TGF-βs, and matricellular proteins co-operate to activate cardiac myofibroblasts, and promote synthesis of matrix proteins. In comparison with the left ventricle, the RV tolerates well volume overload and ischemia; whether the right ventricular interstitial cells and matrix are implicated in these favourable responses remains unknown. Expansion of fibroblasts and extracellular matrix protein deposition are prominent features of arrhythmogenic right ventricular cardiomyopathies and may be implicated in the pathogenesis of arrhythmic events. Prevailing conceptual paradigms on right ventricular remodelling are based on extrapolation of findings in models of left ventricular injury. Considering the unique embryologic, morphological, and physiologic properties of the RV and the clinical significance of right ventricular failure, there is a need further to dissect RV-specific mechanisms of fibrosis and interstitial remodelling.

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“…Supravalvular stenosis is extremely rare and often seen in patients with a specific syndrome such as Williams’ syndrome or in patients with congenital Rubella syndrome. Mild RVOT obstruction is usually well-tolerated during exercise and is not a contraindication for diving [ 48 ]. In patients with moderate or severe RVOT obstruction (mean PG > 20 mmHg or peak PG > 36 mmHg), the additional increase in pulmonary vascular resistance during diving will lead to an increase in pressure loading of the right ventricle; these patients should be advised against diving [ 7 , 8 ].…”

Section: Specific Conditionsmentioning

confidence: 99%

SCUBA Diving in Adult Congenital Heart Disease

Kauling

Rienks

Cuypers

et al. 2023

JCDD

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Conventionally, scuba diving has been discouraged for adult patients with congenital heart disease (ACHD). This restrictive sports advice is based on expert opinion in the absence of high-quality diving-specific studies. However, as survival and quality of life in congenital heart disease (CHD) patients have dramatically improved in the last decades, a critical appraisal whether such restrictive sports advice is still applicable is warranted. In this review, the cardiovascular effects of diving are described and a framework for the work-up for ACHD patients wishing to engage in scuba diving is provided. In addition, diving recommendations for specific CHD diagnostic groups are proposed.

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Functional and haemodynamic assessment of mild-to-moderate pulmonary valve stenosis at rest and during exercise

Abstract: NCT01444222.

Cited by 16 publications

References 17 publications

The influence of loud crying on pulmonary gradients obtained by transthoracic echocardiography in children with pulmonary valve stenosis

The influence of loud crying on pulmonary gradients obtained by transthoracic echocardiography in children with pulmonary valve stenosis

Fibroblasts and the extracellular matrix in right ventricular disease

SCUBA Diving in Adult Congenital Heart Disease

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