Reversal of pulmonary hypertension after ligation of a brachiocephalic arteriovenous fistula

Clarkson, Michael R.; Giblin, Louise; Brown, Alasdair; Little, D.; Donohoe, J.

doi:10.1053/ajkd.2002.34932

Cited by 58 publications

(59 citation statements)

References 5 publications

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“…Therefore, in the present study, reduction in PAP following reduction in CO seems to be due not only to the flow dependency of PAP but also to a decrease in pulmonary resistance [19]. Clarkson et al [20] recently reported PHT of 60 mmHg in an ESRD patient receiving chronic HD therapy via an aneurysmal brachicephalic A-V fistula. In line with our finding, surgical ligation of the A-V fistula and insertion of a tunnelled semi-permanent internal jugular dialysis catheter reduced the PAP to 30 mmHg.…”

Section: Discussionsupporting

confidence: 50%

The pathogenesis of pulmonary hypertension in haemodialysis patients via arterio-venous access

Nakhoul¹,

Yigla²,

Gilman³

et al. 2005

Nephrology Dialysis Transplantation

166

161

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Background. We recently have shown a high incidence of unexplained pulmonary hypertension (PHT) in end-stage renal disease (ESRD) patients on chronic haemodialysis (HD) therapy via arterio-venous (A-V) access. This study evaluated the possibility that PHT in these patients is triggered or aggravated by chronic HD via surgical A-V access, and the role of endothelin-1 (ET-1) and nitric oxide (NO) in this syndrome. Methods. Forty-two HD patients underwent clinical evaluation. Pulmonary artery pressure (PAP) was evaluated using Doppler echocardiography. Levels of ET-1 and NO metabolites in plasma were determined before and after the HD procedure and were compared between subgroups of patients with and without PHT. Results. Out of 42 HD patients studied, 20 patients (48%) had PHT (PAP ¼ 46±2; range 36-82 mmHg) while the rest had a normal PAP (29±1 mmHg) (P<0.0001). HD patients with PHT had higher cardiac output compared with those with normal PAP (6.0±1.2 vs 5.2±0.9 l/min, P<0.034). HD patients, with or without PHT, had elevated plasma ET-1 levels compared with controls (1.6±0.7 and 2.4±0.8 fmol/ml vs 1.0±0.2, P<0.05) that remained unchanged after the HD procedure. HD patients without PHT and control subjects showed similar basal plasma levels of NO 2 þ NO 3 (24.2±5.2 vs 19.7±3.1 mM, P>0.05) that was significantly higher compared with HD patients with PHT (14.3±2.3 mM, P<0.05). HD therapy caused a significant increase in plasma NO metabolites that was greater in patients without PHT (from 24.2±5.2 to 77.1±9.6 mM, P<0.0001, and from 14.3±2.3 to 39.9±11.4 mM, P<0.0074, respectively). Significant declines in PAP (from 49.8±2.8 to 38.6±2.2 mmHg, P<0.004) and cardiac output (CO) (from 7.6±0.6 to 6.1±0.3 l/min, P<0.03) were found in 11 HD patients with PHT that underwent successful transplantation. Similarly, temporary closure of the A-V access by a sphygmomanometer in eight patients with PHT resulted in a transient decrease in CO (from 6.4±0.6 to 5.3± 0.5 l/min, P ¼ 0.18) and systolic PAP (from 47.2±3.8 to 34.6±2.8 mmHg, P<0.028).Conclusions. This study demonstrates a high prevalence of PHT among patients with ESRD on chronic HD via a surgical A-V fistula. In view of the vasodilatory and antimitogenic properties of NO, it is possible that the attenuated basal and HD-induced NO production in patients with PHT contributes to the increased pulmonary vascular tone. Furthermore, the partial restoration of normal PAP and CO in HD patients that underwent either temporal A-V shunt closure or successful transplantation indicates that excessive pulmonary blood flow is involved in the pathogenesis of the disease.

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Section: Discussionsupporting

confidence: 50%

The pathogenesis of pulmonary hypertension in haemodialysis patients via arterio-venous access

Nakhoul¹,

Yigla²,

Gilman³

et al. 2005

Nephrology Dialysis Transplantation

166

161

View full text Add to dashboard Cite

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“…An association between AVF creation and symptomatic RHF has been reported twice previously. Clarkson and colleagues 5 described the case of a 52-year-old man whose PH and RHF developed 6 years after AVF creation for hemodialysis and rapidly resolved after surgical ligation of the AVF. That patient had PH, but not ascites.…”

Section: Discussionmentioning

confidence: 99%

Right Ventricular Enlargement within Months of Arteriovenous Fistula Creation in 2 Hemodialysis Patients

Ragupathi¹,

Johnson²,

Marhefka³

2016

Texas Heart Institute Journal

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Surgically created arteriovenous fistulae (AVF) for hemodialysis can contribute to hemodynamic changes. We describe the cases of 2 male patients in whom new right ventricular enlargement developed after an AVF was created for hemodialysis. Patient 1 sustained high-output heart failure solely attributable to the AVF. After AVF banding and subsequent ligation, his heart failure and right ventricular enlargement resolved. In Patient 2, the AVF contributed to new-onset right ventricular enlargement, heart failure, and ascites. His severe pulmonary hypertension was caused by diastolic heart failure, diabetes mellitus, and obstructive sleep apnea. His right ventricular enlargement and heart failure symptoms did not improve after AVF ligation. We think that our report is the first to specifically correlate the echocardiographic finding of right ventricular enlargement with AVF sequelae. Clinicians who treat end-stage renal disease patients should be aware of this potential sequela of AVF creation, particularly in the upper arm. We recommend obtaining preoperative echocardiograms in all patients who will undergo upper-arm AVF creation, so that comparisons can be made postoperatively. Alternative consideration should be given to creating the AVF in the radial artery, because of less shunting and therefore less potential for right-sided heart failure and pulmonary hypertension. A multidisciplinary approach is optimal when selecting patients for AVF banding or ligation.

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“…However, only half of the hemodialysis patients develop PH, and this may imply that non-uremic mechanisms may be involved in the pathogenesis of this disorder. 1,34 This is an additional argument in favor of the excessive pulmonary flow as a pathogenetic factor for PH. 7 Nevertheless, in a recent study by Acarturk et al, there was no direct relationship between blood flow rate of arteriovenous fistula and PAP.…”

Section: Etiologic Factors For Ph-pathophysiology Of Phmentioning

confidence: 99%

Pulmonary Hypertension in Dialysis Patients

et al. 2013

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Pulmonary hypertension in end-stage renal disease patients is associated with significantly increased morbidity and mortality. The prevalence of pulmonary hypertension in dialysis patients is relatively high and varies in different studies from 17% to 49.53% depending on the mode of dialysis and other selection factors, such as the presence of other cardiovascular comorbidities. The etiopathogenic mechanisms that have been studied in relatively small studies mainly include arteriovenous fistula-induced increased cardiac output, which cannot be accomodated by, the spacious under normal conditions pulmonary circulation. Additionally, pulmonary vessels show signs of endothelial dysfunction, dysregulation of vascular tone due to an imbalance in vasoactive substances, and local as well as systemic inflammation. It is also believed that microbubbles escaping from the dialysis circuit can trigger vasoconstriction and vascular sclerosis. The non-specific therapeutic options that proved to be beneficial in pulmonary artery pressure reduction are endothelin inhibitors, phosphodiesterase inhibitor sildenafil, and vasodilatory prostaglandins in various forms. The specific modes of treatment are renal transplantation, size reduction or closure of high-flow arteriovenous fistulas, and transfer from hemodialysis to peritoneal dialysis-a modality that is associated with a lesser prevalence of pulmonary hypertension.

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Reversal of pulmonary hypertension after ligation of a brachiocephalic arteriovenous fistula

Cited by 58 publications

References 5 publications

The pathogenesis of pulmonary hypertension in haemodialysis patients via arterio-venous access

The pathogenesis of pulmonary hypertension in haemodialysis patients via arterio-venous access

Right Ventricular Enlargement within Months of Arteriovenous Fistula Creation in 2 Hemodialysis Patients

Pulmonary Hypertension in Dialysis Patients

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