Clinical Correlates and Reference Intervals for Pulmonary Artery Systolic Pressure Among Echocardiographically Normal Subjects

McQuillan, Brendan; Picard, Michael H.; Leavitt, Marcia; Weyman, Arthur E.

doi:10.1161/hc4801.100076

Cited by 599 publications

(420 citation statements)

References 24 publications

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“…The present authors assumed the right atrial pressure to be 5 mmHg, since all subjects had normal vena cava diameters and respiratory variability. The current upper limit of normal values (PASP 41 mmHg) agrees well with a study establishing normal values in a large number of subjects when one considers that these investigators assumed the right atrial pressure to be 10 mmHg [20]. Furthermore, the current measurements are in agreement with other studies assessing PASP at rest and during exercise [20][21][22][23][24].…”

Section: Pulmonary Vascular Responsesupporting

confidence: 87%

Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

Dehnert

Grünig²,

Mereles³

et al. 2005

Eur Respir J

106

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Individuals susceptible to high-altitude pulmonary oedema (HAPE) are characterised by an abnormal increase of pulmonary artery systolic pressure (PASP) in hypoxia and during normoxic exercise, reduced hypoxic ventilatory response, and smaller lung volume.In 37 mountaineers with well-documented altitude tolerance, it was investigated whether any combination of these noninvasive measurements, including exercise in hypoxia, could improve the identification of HAPE-susceptible subjects at low altitude.HAPE-susceptible subjects showed a significant higher increase of PASP during hypoxia at rest (48¡10 mmHg) compared with controls (38¡3 mmHg), as well as during normoxic exercise (57¡14 versus 38¡7 mmHg) and hypoxic exercise (69¡13 versus 49¡8 mmHg). PASP could not be assessed in three and eight subjects during normoxic or hypoxic exercise, respectively, due to insufficient Doppler profiles or systemic arterial hypertension. Sensitivity (77-94%) and specificity (76-93%) were not significantly different between the various testing conditions. Additional assessment of hypoxic ventilatory response and lung function parameters did not improve identification of HAPE-susceptible subjects in a multivariate analysis.Due to the greater number of missing values in pulmonary artery systolic pressure measurements during hypoxic exercise, it was concluded that pulmonary artery systolic pressure measurements at rest during hypoxia or exercise in normoxia are most feasible for the identification of high-altitude pulmonary oedema-susceptible subjects.KEYWORDS: Doppler echocardiography, exercise, hypoxia, hypoxic ventilatory response, lung volumes, pulmonary artery pressure H igh-altitude pulmonary oedema (HAPE) is a noncardiogenic pulmonary oedema that occurs at an altitude of 4,559 m in up to 6% of otherwise healthy unselected subjects [1]. Altitude, speed of ascent, pre-acclimatisation and, above all, individual susceptibility are determinants for its occurrence. The combination of fast ascent and susceptibility to HAPE increases the incidence of HAPE at 4,559 m to ,60% [1]. Since HAPE is a life-threatening condition, it would be helpful to identify HAPE-susceptible subjects at low altitude, particularly in those with no previous altitude exposure.It has been widely demonstrated that increased hypoxic pulmonary vasoconstriction leading to abnormally high pulmonary artery pressure is the major contributor in the development of HAPE. The crucial role of high pulmonary artery pressure is confirmed by elevated pulmonary artery pressures in patients with HAPE [2-4], enhanced pulmonary vasoconstrictive response in HAPE-susceptible subjects to acute hypoxia [5][6][7][8] or exercise in normoxia [6,7,9]. It is also confirmed by the fact that interventions decreasing pulmonary artery pressure are effective in the treatment [10, 11] and prevention [4] of HAPE. A previous study suggested that pulmonary artery systolic pressure (PASP) does not exceed 40 mmHg in healthy subjects during acute hypoxic exposure (inspiratory oxygen fractio...

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Section: Pulmonary Vascular Responsesupporting

confidence: 87%

Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

Dehnert

Grünig²,

Mereles³

et al. 2005

Eur Respir J

106

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“…Age was expected to influence Ppa, since catheterisation data at rest in two groups of healthy individuals (17 aged [48]. In the present patient series, associations of Ppa measurements with age were performed using Spearman rank analyses and linear regression.…”

Section: Statisticsmentioning

confidence: 99%

Embolisation of pulmonary arteriovenous malformations: no consistent effect on pulmonary artery pressure

Shovlin¹,

Tighe²,

Davies³

et al. 2008

Eur Respir J

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Increasing evidence supports the use of embolisation to treat pulmonary arteriovenous malformations (AVMs). Most pulmonary AVM patients have hereditary haemorrhagic telangiectasia (HHT), a condition that may be associated with pulmonary hypertension.The current authors tested whether pulmonary AVM embolisation increases pulmonary artery pressure (Ppa) in patients without baseline severe pulmonary hypertension. Ppa was measured at the time of pulmonary AVM embolisation in 143 individuals, 131 (92%) of whom had underlying HHT. Angiography/embolisation was not performed in four individuals with severe pulmonary hypertension, whose systemic arterial oxygen saturation exceeded levels usually associated with dyspnoea in pulmonary AVM patients.In 143 patients undergoing pulmonary AVM embolisation, Ppa was significantly correlated with age, with the most significant increase occurring in the upper quartile (aged .58 yrs). In 43 patients with repeated measurements, there was no significant increase in Ppa as a result of embolisation. In half, embolisation led to a fall in Ppa. The maximum rise in mean Ppa was 8 mmHg: balloon test occlusion was performed in one of these individuals, and did not predict the subsequent rise in Ppa following definitive embolisation of the pulmonary AVMs.In the present series of patients, which excluded those with severe pulmonary hypertension, pulmonary artery pressure was not increased significantly by pulmonary arteriovenous malformation embolisation.KEYWORDS: Brain abscess, hypoxaemia, nosebleeds, oxygen saturation, right-to-left shunt, stroke D oes embolisation of pulmonary arteriovenous malformations (AVMs) precipitate pulmonary hypertension (PH)? The reason this question is important is that for individuals with pulmonary AVMs, embolisation is an effective means of reducing lifetime risks of paradoxical embolic stroke and brain abscess [1,2], improving oxygenation [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] and treating pulmonary AVM-related haemoptysis [18,19]. Conversely, embolisation may be expected to elevate pulmonary artery pressure (Ppa), since pulmonary AVMs are abnormal dilated vessels between pulmonary arteries and veins that provide low resistance pathways for pulmonary blood flow [20].The question of whether pulmonary AVM embolisation increases Ppa is particularly pertinent, since most individuals with pulmonary AVMs have underlying hereditary haemorrhagic telangiectasia (HHT). Typically recognised by nosebleeds, mucocutaneous telangiectasia and visceral AVMs [21], HHT may be associated with PH [9,[22][23][24][25][26][27][28][29][30]. The secondary causes of PH in HHT are diverse, as they are in the normal population [31], but PH particularly occurs either as a true pulmonary arterial hypertension (PAH) phenotype [9,22,[28][29][30] or in the context of high output cardiac failure secondary to hepatic AVMs, when PH may be reversible after hepatic AVM treatment [32]. The frequencies of PAH and hepatic AVMs differ with HHT genotype: HHT is caused by mutatio...

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“…At birth, pressure within the pulmonary artery falls (mean pressure ~15 mm Hg), and it receives all of the right ventricular output after closure of the ductus arteriosus (20). This change from high pressure/low flow to low pressure/high flow, when it occurs prematurely, may result in abnormal changes to the walls of the pulmonary artery.…”

mentioning

confidence: 99%

Preterm birth with antenatal corticosteroid administration has injurious and persistent effects on the structure and composition of the aorta and pulmonary artery

et al. 2011

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INTRODUCTION:Preterm birth affects 8-12% of live births and is associated with the development of elevated arterial blood pressure and aortic narrowing in later life; this suggests that preterm birth may alter the development of arteries. Our objective was to determine the effects of preterm birth, accompanied by antenatal corticosteroid administration, on the structure of the aorta and pulmonary artery, which experience different alterations in pressure flow at birth. RESULTS: at 11 wk, preterm lambs had significantly thicker aortic walls and a smaller lumen, whereas the morphometry of the pulmonary artery was unaffected. elastin deposition was markedly increased in the aorta and pulmonary artery and smooth muscle content was reduced in the aorta only. In preterm lambs we found injury in the aorta only; controls were unaffected. DISCUSSION: We conclude that moderate preterm birth after antenatal betamethasone can cause injury and persistent alterations in the structure and composition of the aorta, with lesser effects in the pulmonary artery. Our findings suggest that preterm birth may increase the risk of atherosclerosis and aortic aneurysms in later life. METHODS:Using an established ovine model of preterm birth, lambs were born at 0.9 of gestation and underwent necropsy at 11 wk after birth; controls were born at term.

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Clinical Correlates and Reference Intervals for Pulmonary Artery Systolic Pressure Among Echocardiographically Normal Subjects

Cited by 599 publications

References 24 publications

Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

Embolisation of pulmonary arteriovenous malformations: no consistent effect on pulmonary artery pressure

Preterm birth with antenatal corticosteroid administration has injurious and persistent effects on the structure and composition of the aorta and pulmonary artery

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