SO084SILDENAFIL DRUG IN HEMODIALYSIS PATIENTS WITH PULMONARY HYPERTENSION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Maha Abdelmoneim Behairy Said ◽  
Tamer El Said ◽  
Abdelrahman Elbraky ◽  
Hazem Khorshid ◽  
Waleed Anwar ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Pulmonary Hypertension ◽  
Placebo Group ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Hemodialysis Patients ◽  
Artery Pressure ◽  
Daily Dose ◽  
Group 2 ◽  
Group 1

Abstract Background and Aims Pulmonary hypertension (PH) is not an uncommon progressive condition in prevalent hemodialysis (HD) patients, associated with high morbidity and mortality. Sildenafil drug has limited studies about the efficacy of the drug and optimal dose among prevalent HD patients with PH. Aim of the study to assess the effects of sildenafil drug on estimated Pulmonary Artery pressure value (ePAP) mmHg via transthoracic Doppler Echocardiography and 6-minute walk test ( 6MWT) among hemodialysis patients with pulmonary hypertension. Method Randomized, double-blind, placebo-controlled clinical trial, from December 2018 to May 2019, involving 60 eligible patients on regular adequate HD with PH, estimated Pulmonary Artery Pressure (ePAP) ≥35 mmHg via Doppler echocardiography. HD patients with mean age 52.6±10.8 year divided randomly into 3 groups: Group 1 (20 patients) received 25 mg sildenafil, group 2 (20 patients) received 50 mg sildenafil and group 3 (20 patients) who received placebo as daily dose treatment for 3 months duration. Every patient in the study was subjected to full history taking and clinical examination. Exclusion Criteria: Current treatment of pulmonary hypertension, patient with evident history of cardiac diseases or chronic pulmonary diseases or systemic autoimmune diseases, portal hypertension, HIV, patients with uncontrolled hypertension or severe anaemia or hypersensitivity to sildenafil, treatment with any drugs that may interact with sildenafil all were excluded from the study. Transthoracic echocardiography was done at the begging of the study and after three months in mid-week non-dialysis day for assessment of the change in ePAP, pulmonary artery pressure calculated using the modified Bernoulli equation, and assessment of right ventricular functions . Exercise capacity assessment by 6MWT to assess the clinical response to the drug, was done for every patient at the start of the study and after 3 months of treatment. Clinically meaningful change estimate for the 6MWT considered as increase more than 30 meters. Results Significant increase in mean of 6 MWT in both group 1,2 received 25 mg,50 mg sildenafil respectively after 3 m duration of treatment versus non-significant change in placebo group as basal 6 MWT was (171 ±45, 214 ±58, 175 ±39) meters in group 1,2 and placebo group respectively (p>0.05). Means 6 MWT post-treatment were (205 ±57, 258 ±59, 182 ±49) meters (P<0.001) in group 1, 2&3 respectively, as post Hoc test results, showed significant increase in 6MWT2 in group 2 in comparison to group 1 and placebo group (P<0.01), as shown in figure (1).There was a significant decrease in e PAP in each group of studied groups after treatment (P<0.01). As mean basal ePAP1 measures were (48 ±9, 43.5 ±16, 48.5 ±12) mmHg in group 1,2,3 respectively (P>0.05).There were no significant differences between the studied groups regarding means of ePAP2 post-treatment were ( 42 ±9, 39 ±15, 44.5±8) mmHg in group 1,2,3 respectively (P>0.05). However, the degree of severity of PH was more improved after treatment duration with sildenafil as in group 1 there were 5 patients downgraded from moderate to mild and 2 patients downgraded from severe to moderate after treatment. In group 2 there were 4 patients downgraded from moderate to mild PH and 2 patients downgraded from severe to moderate PH. In 3rd group (placebo group) only one patient downgraded from moderate to mild PH. There were 4 patients dropouts from the study two of them from group 2 (receiving 50mg) due to sildenafil related side effects appeared through the study. Conclusion This a clinical trial confirmed the efficiency of both 50mg and 25mg sildenafil daily dose in reducing e PAP and improving functional exercise capacity in chronic haemodialysis patients with pulmonary hypertension disease.

Effects of altered left atrial pressure on pulmonary vascular pressure-flow relationships

1988 ◽  
Vol 255 (1) ◽  
pp. H19-H25 ◽  
Author(s):  
J. Ducas ◽  
U. Schick ◽  
L. Girling ◽  
R. M. Prewitt
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Vasculature ◽  
Pressure Flow ◽  
Artery Pressure ◽  
Time Control ◽  
Pulmonary Capillary ◽  
Anesthetized Dogs ◽  
Group 2 ◽  
Group 1

We studied the effects of changes in pulmonary capillary wedge pressure (PCWP) on the slope (incremental resistance) and the extrapolated pressure intercept (PI) of the mean pulmonary artery pressure (PAP)-cardiac output (CO) relationship. Multipoint plots of PAP against CO were obtained in intact anesthetized dogs. Group 1 consisted of six dogs entirely in West zone 3 and group 2 of four dogs with mixed West zone 2-3. The four conditions studied were the following: 1) fixed low PCWP, 2) fixed high PCWP, 3) variable PCWP, and 4) time-control repeat of condition 1. The PI significantly exceeded PCWP at fixed low PCWP (group 1, 9.3 vs. 11.1 mmHg, group 2, 6.6 vs. 3.9 mmHg). PI became identical to PCWP only at fixed high PCWP in group 1 (19 +/- 2.0 vs. 19 +/- 1.1 mmHg). Thus PCWP reflects the effective vascular outflow pressure when PCWP is fixed and high. For both groups of dogs in condition 3, when PCWP was varied with CO, the slope of the resulting PAP-CO plot was significantly greater than when PCWP was constant. Also in 9 of 10 dogs, PI was less than PCWP when PCWP was varied. These findings demonstrate that when changes in PCWP are allowed to occur during the generation of a pulmonary artery pressure-flow plot, the resulting slope and intercept, as defined by a Starling resistor model, do not accurately represent the incremental resistance and outflow pressure of the pulmonary vasculature.

Abstract 10188: Circulating Levels of MIF, GROα And RANTES Chemokines and Interleukin 17E Correlate With Severity of Pulmonary Hypertension in Young Pediatric Patients With Congenital Heart Disease

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Leína Zorzanelli ◽  
Nair Y Maeda ◽  
Mariana M Clavé ◽  
Ana M Thomaz ◽  
Marlene Rabinovitch ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Congenital Heart ◽  
Young Patients ◽  
Artery Pressure ◽  
Th2 Immune Response ◽  
Group 2 ◽  
Group 1

Introduction: Inflammation and immunity are central in the pathogenesis of pulmonary arterial hypertension (PAH), but have not been fully explored in young patients with congenital heart disease and elevated pulmonary artery pressure (PAH-CHD) undergoing surgical repair. Hypothesis: Cytokines and related proteins may be differentially expressed in PAH-CHD patients with distinct hemodynamic patterns. Methods: Sixteen patients with PAH-CHD were enrolled (Group 1, age 1.13 (0.76-2.48) years, median and interquartile range). Pulmonary artery pressure was 52 (43-66) mmHg, and pulmonary vascular resistance was 5.2 (4.2-8.9) Wood units•m 2 . Patients with pulmonary overcirculation, with no need for cardiac catheterization were included for comparison (Group 2, N=31, age 0.71 (0.43-1.02) years). Pulmonary-to-systemic blood flow ratio (echocardiography) in Group 1 and Group 2 was 1.9 (1.3-2.6) and 2.8 (2.3-3.3) respectively (p=0.008). Thirty-six cytokines were analyzed in serum using a chemiluminescence array. Results: In the whole patient group (N=47), MIF chemokine (macrophage migration inhibitory factor) was significantly increased compared to pediatric controls (respective densities 7510±2755 pixels and 5697±2051 pixels, mean±SD, p=0.027). In patients, GROα chemokine (growth-regulated oncogene alpha) was elevated early in life, but decreased exponentially with the age (R 2 =0.21, p=0.001), while interleukin 17E (also called IL-25) increased progressively (R 2 =0.24, p<0.001). MIF was specifically increased in Group 1 compared to Group 2 and controls (respectively, 8494±619 pixels, 6618±477 pixels and 6548±726 pixels, age-adjusted mean±SEM, p=0.037). In contrast, RANTES chemokine (regulated on activation, normal T cell expressed and secreted) was specifically elevated in Group 2 compared to Group 1 and controls (respectively, 74183±3865 pixels, 60130±6455 pixels and 59332±3970 pixels, mean±SEM, p=0.039). Conclusion: The data indicate a relationship between cytokine levels and severity of the disease (age, groups), with potential pathophysiological implications. Furthermore, involvement of interleukin 17E and MIF emphasize the role of Th2 immune response already described in PAH.

scholarly journals Correlation of Pulse Wave Transit Time with Pulmonary Artery Pressure in a Porcine Model of Pulmonary Hypertension

Biomedicines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1212
Author(s):  
Fabian Mueller-Graf ◽  
Jonas Merz ◽  
Tim Bandorf ◽  
Chiara Albus ◽  
Maike Henkel ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Transit Time ◽  
Pulse Wave ◽  
Correlation Coefficients ◽  
Physiological Basis ◽  
Artery Pressure ◽  
Hypoxic Vasoconstriction ◽  
Pulse Wave Transit Time

For the non-invasive assessment of pulmonary artery pressure (PAP), surrogates like pulse wave transit time (PWTT) have been proposed. The aim of this study was to invasively validate for which kind of PAP (systolic, mean, or diastolic) PWTT is the best surrogate parameter. To assess both PWTT and PAP in six healthy pigs, two pulmonary artery Mikro-Tip™ catheters were inserted into the pulmonary vasculature at a fixed distance: one in the pulmonary artery trunk, and a second one in a distal segment of the pulmonary artery. PAP was raised using the thromboxane A2 analogue U46619 (TXA) and by hypoxic vasoconstriction. There was a negative linear correlation between PWTT and systolic PAP (r = 0.742), mean PAP (r = 0.712) and diastolic PAP (r = 0.609) under TXA. During hypoxic vasoconstriction, the correlation coefficients for systolic, mean, and diastolic PAP were consistently higher than for TXA-induced pulmonary hypertension (r = 0.809, 0.778 and 0.734, respectively). Estimation of sPAP, mPAP, and dPAP using PWTT is feasible, nevertheless slightly better correlation coefficients were detected for sPAP compared to dPAP. In this study we establish the physiological basis for future methods to obtain PAP by non-invasively measured PWTT.

scholarly journals The Relationship between Vitamin D Deficiency and Pulmonary Hypertension

2013 ◽  
Vol 114 (3) ◽  
pp. 154-161 ◽  
Author(s):  
Mehmet Demir ◽  
U. Uyan ◽  
S. Keçeoçlu ◽  
C. Demir
Keyword(s):  
Vitamin D ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Vitamin D Deficiency ◽  
Pulmonary Artery Pressure ◽  
Control Group ◽  
Systolic Pulmonary Artery Pressure ◽  
Control Groups ◽  
Artery Pressure ◽  
Vitamin D Levels

Vitamin D deficiency actives renin-angiotensin-aldosterone system (RAAS) which affects cardiovascular system. Activation of RAAS is associated with pulmonary hypertension (PHT). Relation between vitamin D deficiency and PHT could be therefore suggested. In  our study we compared pulmonary artery pressure between vitamin D deficiency and control groups. 115 consecutive patients (average age: 61.86 ± 5.86) who have detected very low vitamin D (vitamin D levels < 10 ng/ml) were enrolled. 117 age matched persons (average age: 61.74 ± 5.99) were selected as the control group. All groups underwent transthoracic echocardiography. Routine biochemical measurement of 25-OH vitamin D and parathormon (PTH) levels were performed. Baseline characteristics of the study groups were comparable. Systolic pulmonary artery pressure (SPAP) of patients in  the low vitamin D group was higher than the control groups. As a  result our study, a  relation between vitamin D deficiency and pulmonary artery hypertension was revealed.

Importance of Relative Pulmonary Hypertension in Cardiac Surgery: The Mean Systemic-to-Pulmonary Artery Pressure Ratio

2006 ◽  
Vol 20 (3) ◽  
pp. 331-339 ◽  
Author(s):  
Arnaud Robitaille ◽  
André Y. Denault ◽  
Pierre Couture ◽  
Sylvain Bélisle ◽  
Annik Fortier ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Surgery ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pressure Ratio ◽  
Artery Pressure ◽  
The Mean

Pulmonary Hypertension

2013 ◽  
Author(s):  
George K Istaphanous ◽  
Andreas W Loepke
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Pulmonary Artery Pressure ◽  
Disease Process ◽  
Underlying Disease ◽  
Artery Pressure ◽  
Pulmonary Arterial ◽  
Made In

Pediatric pulmonary arterial hypertension (PAH) is characterized by a pathologically elevated pulmonary artery pressure in children. The etiology of PAH is multifactorial, and while its prognosis is closely related to the reversibility of the underlying disease process, much progress has recently been made in its diagnosis and treatment, significantly decreasing the associated morbidity and mortality.

Adrenomedullin activity in chronically hypoxic rat lungs

1996 ◽  
Vol 271 (2) ◽  
pp. H622-H629 ◽  
Author(s):  
L. Zhao ◽  
L. A. Brown ◽  
A. A. Owji ◽  
D. J. Nunez ◽  
D. M. Smith ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Mrna Levels ◽  
Rat Lung ◽  
Artery Pressure ◽  
Isolated Perfused Lung ◽  
Calcitonin Gene ◽  
Perfused Lung ◽  
Hypotensive Response

Adrenomedullin (AM) is a novel vasodilator with structural similarities to calcitonin gene-related peptide (CGRP). This study investigated AM activity in the rat lung during hypoxia-induced pulmonary hypertension. Both rat AM (0.2-10 nmol) and alpha-CGRP (0.2-2 nmol) produced dose-related reductions in pulmonary artery pressure in the isolated perfused lung ventilated with 2% O2. Pretreatment with alpha-CGRP, which demonstrated tachyphylaxis, or its antagonist, CGRP-(8–37), reduced the hypotensive response to AM, suggesting that part of the response to AM is mediated by CGRP receptors. 125I-labeled AM and 125I-labeled CGRP binding was significantly increased in lung membranes from 7-day hypoxic animals (AM from 1.94 +/- 0.3 to 3.36 +/- 0.4 and CGRP from 0.06 +/- 0.01 to 0.12 +/- 0.02 pmol/mg protein), with no change in dissociation constant. Moreover, the hypotensive response to both peptides was increased in the lungs of 7-day hypoxic rats. There was no significant change in lung immunoreactive AM concentrations (hypoxic 5.04 +/- 0.48 vs. control 6.28 +/- 0.76 pmol/g wet wt of tissue) or steady-state AM mRNA levels in 7-day hypoxic rats. Nonetheless, AM may be useful for the acute pharmacological manipulation of pulmonary artery pressure in hypoxia-induced pulmonary hypertension.

Sarcoidosis-Associated Pulmonary Hypertension

2020 ◽  
Vol 41 (05) ◽  
pp. 659-672
Author(s):  
Marloes P. Huitema ◽  
Harold Mathijssen ◽  
Johannes J. Mager ◽  
Repke J. Snijder ◽  
Jan C. Grutters ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Lung Transplant ◽  
Pulmonary Function Tests ◽  
High Morbidity ◽  
Artery Pressure ◽  
Extrinsic Compression ◽  
Tertiary Center ◽  
Parenchymal Disease

AbstractPulmonary hypertension (PH) is a well-known complication of sarcoidosis, defined by a mean pulmonary artery pressure of ≥25 mm Hg. Since both PH and sarcoidosis are rare diseases, data on sarcoidosis-associated PH (SAPH) is retrieved mostly from small retrospective studies. Estimated prevalence of SAPH ranges from 3% in patients referred to a tertiary center up to 79% in patients awaiting lung transplant. Most patients with SAPH show advanced parenchymal disease as the underlying mechanism. However, some patients have disproportional elevated pulmonary artery pressure, and PH can occur in sarcoidosis patients without parenchymal disease. Other mechanisms such as vascular disease, pulmonary embolisms, postcapillary PH, extrinsic compression, and other sarcoidosis-related comorbidities might contribute to SAPH. The diagnosis of PH in sarcoidosis is challenging since symptoms and signs overlap. Suspicion can be raised based on symptoms or tests, such as pulmonary function tests, laboratory findings, electrocardiography, or chest CT. PH screening mainly relies on transthoracic echocardiography. Right heart catheterization should be considered on a case-by-case basis in patients with clinical suspicion of PH, taking into account clinical consequences. Treatment options are considered on patient level in a PH expert center, and might include oxygen therapy, immunosuppressive, or PH-specific therapy. However, qualitative evidence is scarce. Furthermore, in a subset of patients, interventional therapy or eventually lung transplant can be considered. SAPH is associated with high morbidity. Mortality is higher in sarcoidosis patients with PH compared with those without PH, and increases in patients with more advanced stages of sarcoidosis and/or PH.

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