Haemodynamics and gas exchange before and after coil embolization of pulmonary arteriovenous malformations

Andrivet, Pierre; Lofaso, F.; Carette, M.F.; Allegrini, J; Adnot, Serge

doi:10.1183/09031936.95.08071228

Cited by 18 publications

(19 citation statements)

References 10 publications

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“…In three out of the four reported cases [9,17,32], each selected from larger series, Ppa increased postembolisation, while in the fourth it was unchanged [11]. There is also a report of worsening PH after surgical resection of a pulmonary AVM [43].…”

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confidence: 93%

“…Out of .700 reported pulmonary AVM embolisations [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][34][35][36][37][38][39][40][41][42], data on Ppa measurements pre-and post-embolisation are scarce [9,11,17,32]. In three out of the four reported cases [9,17,32], each selected from larger series, Ppa increased postembolisation, while in the fourth it was unchanged [11].…”

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confidence: 99%

“…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].…”

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confidence: 99%

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

Shovlin¹,

Tighe²,

Davies³

et al. 2008

European Respiratory Journal

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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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confidence: 93%

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confidence: 99%

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confidence: 99%

See 1 more Smart Citation

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

Shovlin¹,

Tighe²,

Davies³

et al. 2008

European Respiratory Journal

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“…Documented positive immediate effects of vaso-occlusion of PAVMs include the decrease in right-to-left shunting, thus improving arterial blood gases and dyspnea [[60, 64, 127]; see ref. [70] for review].…”

Section: Treatment Of Pavmsmentioning

confidence: 99%

Pulmonary Vascular Manifestations of Hereditary Hemorrhagic Telangiectasia (Rendu-Osler Disease)

et al. 2007

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Hereditary hemorrhagic telangiectasia (HHT) or Rendu-Osler-Weber disease is a genetic disorder with autosomal dominance and variable penetrance, characterized by epistaxis, telangiectasia and visceral manifestations of the disease. The estimated minimal prevalence is 1/10,000 inhabitants. The diagnosis is established on clinical criteria, and may be further confirmed by the identification of causative mutations in either the ENG or the ACVRL1 gene coding for endoglin and ALK1, respectively. Pulmonary vascular manifestations of HHT include pulmonary arteriovenous malforma- tions (PAVMs; especially in patients with ENG mutations) and less frequently pulmonary hypertension (especially in patients with ACVRL1 mutations). In 15–33% of patients with HHT, PAVMs consist of abnormal communications between pulmonary arteries and pulmonary veins, causing right-to-left shunting, and thus, frequently hypoxemia and dyspnea on exertion, although PAVMs may remain asymptomatic and frequently undiagnosed unless complications occur. PAVMs result in severe and frequent complications often at a young age, which may reveal the diagnosis, e.g. transient ischemic attack and cerebral stroke (10–19% of patients), systemic severe infections and abscesses (including cerebral abscess in 5–19% of patients), and rarely massive hemoptysis or hemothorax. Infections in HHT are related to the right-to-left shunting that bypasses the pulmonary capillaries and facilitates the passage of septic or aseptic emboli into the systemic and especially cerebral circulation, and potentially to minor defects in innate immunity. Treatment of PAVMs based on transcatheter coil vaso-occlusion of the feeding artery significantly decreases right-to-left shunting, hypoxemia and dyspnea on exertion, and reduces the risk of systemic complications. Long-term follow-up is warranted after transcatheter vaso-occlusion of PAVMs due to frequent recanalization of treated PAVMs and development or growth of untreated PAVMs. Patients with HHT should be informed of the risk of PAVM and potentially severe complications occurring in heretofore asymptomatic subjects. All adult patients with HHT should be proposed systematic screening for PAVM, by contrast echocardiography (preceded by anteroposterior chest radiograph) or computed tomography of the chest. Pulmonary hypertension is rare in HHT, and may be due either to systemic arteriovenous shunting in the liver increasing cardiac output or be clinically and histologically indistinguishable from idiopathic pulmonary arterial hypertension. Pulmonary hypertension is detected by systematic examination of right cardiac cavities and tricuspid regurgitation flow at echocardiography, and the diagnosis is established by right heart catheterization.

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“…Air embolism occurring during the procedure has been suspected and coil migration into the systemic circulation (often due to coils being to small or too large fistula) has been rarely noted in the treatment of large fistulae. Medium term outcome frequently resulted in improvement of dyspnoea, mean shunt fraction, oxygenation and cardiac output [8,9]. Long-term results of this therapy have been variable in individual series.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary arteriovenous malformations: lung transplantation as a therapeutic option

Reynaud‐Gaubert

Thomas²,

Gaubert³

et al. 1999

Eur Respir J

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Multiple pulmonary arteriovenous malformations (PAVM) constitute an uncommon cause of respiratory disability. They may lead to severe hypoxaemia via right-to-left shunts and are sources of substantial mortality and morbidity. Conservative surgical resection has been proposed as the treatment of choice. More recently, percutaneous balloon or coil embolization of the feeding vessels offered an efficacious and safe alternative therapy for patients whose fistulas are too numerous to excise.This study reports an unusual case of respiratory disability in a patient with multiple and microscopic pulmonary arteriovenous malformations who failed to respond to embolotherapy and who received a double lung transplantation with good initial outcome.

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Haemodynamics and gas exchange before and after coil embolization of pulmonary arteriovenous malformations

Cited by 18 publications

References 10 publications

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

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

Pulmonary Vascular Manifestations of Hereditary Hemorrhagic Telangiectasia (Rendu-Osler Disease)

Pulmonary arteriovenous malformations: lung transplantation as a therapeutic option

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