Abstract 1597: Safety and Efficacy of Inhaled Iloprost Via a Disposable Nebulizer in Heart Failure Patients With Elevated Pulmonary Vascular Resistance

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
David Baran ◽  
Luis H Arroyo ◽  
Jill Hebron ◽  
Candace Carr ◽  
Mark J Zucker

Background : Pulmonary vascular resistance (PVR) is routinely measured in patients (pts) being evaluated for a heart transplant. Pts with a high PVR are often treated with a milrinone or intravenous vasodilator “challenge” to establish that the PVR is not “fixed”. However, all current agents have dose-limiting side effects such as arrhythmias and hypotension. Inhaled iloprost would be an option but it is given with a costly adaptive aerosol delivery device. In addition, the efficacy and safety of this drug in left heart failure is poorly studied. Methods : 10 adult heart failure pts who were found to have a PVR of greater than 200 dyne-sec on routine right heart catheterization were enrolled. 50 micrograms (mcg) of iloprost was inhaled while in the catheterization laboratory using a disposable nebulizer and outflow filter, over 10 minutes. Hemodynamics were monitored at baseline, following drug inhalation, and 20 minutes later. Results : The average age of the patients (6 male, 4 female) was 64.8 ± 8.9 years. The mean left ventricular ejection fraction was 20.6 ± 8.6 %. The mean creatinine clearance (Cockroft-Gault) was 48.7 ± 18.9 ml/hr. The mean arterial pressure (MAP), pulmonary artery systolic (PAS), PA diastolic (PAD), PCWP, transpulmonic gradient (TPG), cardiac output (CO), and PVR at baseline, 10 minutes and 20 minutes post-inhalation are detailed below. Iloprost significantly reduced PAS, TPG and PVR without changes in MAP, PAD, PCWP or CO. These effects remained significant at study completion as well. There were no adverse events noted. Conclusion : Iloprost inhalation was well tolerated in heart failure patients undergoing right heart catheterization. Inhalation of 50 mcg of iloprost via a simple hospital nebulizer was associated with safe, rapid, and significant declines in indices of pulmonary vascular tone, without affecting cardiac output or PCWP. Further investigation of this novel use of iloprost is warranted. Results

2020 ◽  
Vol 26 (6) ◽  
pp. 64-76
Author(s):  
Yu. M. Sirenko ◽  
I. O. Zhyvylo ◽  
G. D. Radchenko

The aim – critical review of our own experience, its compliance with current recommendations and data from international registries, as also assessment of pulmonary and systemic hemodynamics obtained in patients with pulmonary arterial hypertension (PAH) in Ukraine. Materials and methods. 220 procedures of the right heart and pulmonary artery catheterization were performed in 195 patients with medium or high probability of PAH according to echocardiography in compliance with current recommendations. All patients were hospitalized at National Scientific Center “M.D. Strazhesko Institute of Cardiology” of NAMS of Ukraine with suspected PAH (primary) or with worsening of the disease course (repeatedly) or in order to confirm the status of vasoreactivity (repeated).Results and discussion. 220 successful catheterization procedures were performed. Primary (diagnostic) right heart catheterization was performed in 195 patients, and repeated – in 25. A diagnosis of pulmonary hypertension was confirmed in 178 patients. In 17 patients, according to the results of catheterization, the diagnosis of PAH was excluded: the mean pressure in the pulmonary artery was less than 20 mm Hg. The structure of nosology in patients who underwent right heart catheterization was as follows: idiopathic PAH was fixed in 68 (38 %) patients, of which 11 (6 %) were vasoreactive; PAH associated with connective tissue diseases – in 21 (12 %) patients; PAH associated with HIV infection in – 4 (2 %) patients; PAH associated with portal hypertension – in 4 (2 %) patients; PAH associated with congenital heart disease – in 26 (15 %) patients; chronic thromboembolic pulmonary hypertension – in 50 (28 %) patients. Vasoreactivity testing was performed in 33 patients with idiopathic PAH. In 11 of them it was positive (33 %). In patients with a positive vasoreactivity testing, the mean pulmonary artery pressure decreased by an average of 21.8 mm Hg to the level of 26.5 mm Hg (p 0.0001), while the cardiac index increased by 31 % and reached 3.8 l · min · m–2 (p<0.1). Pulmonary vascular resistance decreased by 6.4 Wood units to the level of 2.7 Wood units (p<0.0001). In patients with a negative vasoreactivity testing, the decrease in mean pulmonary artery pressure and pulmonary vascular resistance was not statistically significant (p>0.05), and no changes in the cardiac index were detected. Conclusions. Based on the experience of our center, hemodynamic assessment using catheterization is safe and remains the diagnostic standard for PAH. Catheterization is necessary to clarify 4 parameters that are critical for the clinical profile of patients with pulmonary hypertension: right atrium pressure, pulmonary vascular resistance, cardiac output, pulmonary wedge pressure. Patients with idiopathic PAH also need to have vasoreactivity evaluated in order to predict sensitivity to calcium channel blockers therapy, the presence of which is associated with better treatment and survival outcomes.


Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4065-4065
Author(s):  
Jose Maria Segovia ◽  
Emilio Ojeda ◽  
Gomez-Bueno Manuel Francisco ◽  
Rafael Fores ◽  
Jose A Garcia-Marco ◽  
...  

Abstract Background: Pulmonary Hypertension (PH) is a well-known complication of the advanced phase of Myeloproliferative Diseases (MPD) such as Polycythemia Vera (PV), Essential Thrombocytopenia (ET) and Myelofibrosis (MF). Although initially attributed to increased pulmonary vascular resistance (group 1 PH of the WHO classification), this entity was classified in 2009 in group 5 PH (unknown mechanism and miscellaneous PH). Our aim was to describe the prevalence and possible causes of PH in a series of patients with MF. Methods: We studied a series of patients with Primary MF or Secondary MF to other MPD with cardiac ultrasound, right heart catheterization and scintigraphy after intraarterial infusion of Tc99-labeled albumin macroaggregates. Results: We studied 11 consecutive patients with MF (7 male, mean age 58 years, 4 with MF post-PV, 4 post-TE and 3 Primary MF) during the period 2009-2014. All of them had mutations of JAK-2 gene, fibrosis in bone marrow biopsy and visceromegaly (all with intermediate-2 or higher IPSS). Median NTproBNP levels were 4597 pg/ml (range 175-5700). Echocardiogram showed high systolic pulmonary pressure in most cases, with a mean of 54 ± 17 mmHg (range 35-80). Right heart catheterization showed high cardiac output (HCO) in all patients (table 1). After ruling out other causes of HCO, a scintigraphy was performed after administration of Tc99-labeled albumin macroaggregates in descending thoracic aorta. In every case, a percentage of the labeled macroaggregates (6.1 ± 2.0% of the radioactivity) were plugged in the pulmonary capillary bed, what is diagnostic of the presence of microfistulas in infradiaphragmatic territory. In two of these patients, scintigraphies were performed at diagnosis and after been treated with the anti-JAK drug Ruxolitinib (Novartis Pharma). A favourable impact of this drug was obtained in the two cases, probably due to a reduction of spleen volume. Conclusion: Most patients with MF show pulmonary hypertension associated with high cardiac output caused by microfistulas, without significant increase in pulmonary resistance. This finding has important clinical implications, because pulmonary vasodilators (once recommended) should be contraindicated, since they could cause worsening of the clinical picture. Ruxolitinib could resolve PH in MF and a prospective study in this sense could be indicated. Table 1. Patient 1 2 3 4 5 6 7 8 9 10 11 Pulmonary Artery Pres. (S/D/Mean) 58/38/ 42 69/41/ 50 48/29/ 40 84/26/ 45 57/17/ 30 22/17 / 19 51/16 / 28 22/9 / 13 25/8 / 14 71/23 / 39 30/7 / 15 Pulmonary wedge pres. 28 37 27 13 9 7 13 7 8 12 6 Cardiac output (l/min) 12.5 8.0 11 7.1 8 7.3 8.7 6.7 7.45 6 7.8 Cardiac index (l/m/m2) 5.5 4.0 6.6 3.6 5 4 4.8 4.0 4.5 3.9 5.1 Pulmonary vascular resistance (Wood U.) 1.2 1.4 1.2 4.5 2.6 3 1.7 0.9 0.8 4.5 1.1 Disclosures Ojeda: Alexion Pharmaceuticals: Consultancy, Membership on an entity's Board of Directors or advisory committees, Speakers Bureau. Fores:Alexion Pharmaceuticals: Consultancy, Speakers Bureau.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eva Rumiz ◽  
Andrés Cubillos ◽  
Juan Vicente Vilar ◽  
Pilar García ◽  
Alberto Berenguer ◽  
...  

AbstractPulmonary vascular resistance (PVR) is a marker of pulmonary vascular remodeling. A non-invasive model assessed by cardiovascular magnetic resonance (CMR) has been proposed to estimate PVR. However, its accuracy has not yet been evaluated in patients with heart failure. We prospectively included 108 patients admitted with acute heart failure (AHF), in whom a right heart catheterization (RHC) and CMR were performed at the same day. PVR was estimated by CMR applying the model: PVR = 19.38 − [4.62 × Ln pulmonary artery average velocity (in cm/s)] − [0.08 × right ventricle ejection fraction (in %)], and by RHC using standard formulae. The median age of the cohort was 67 years (interquartile range 58–73), and 34% were females. The median of PVR assessed by RHC and CMR were 2.2 WU (1.5–4) and 5 WU (3.4–7), respectively. We found a weak correlation between invasive PVR and PVR assessed by CMR (Spearman r = 0.21, p = 0.02). The area under the ROC curve for PVR assessed by CMR to detect PVR ≥ 3 WU was 0.57, 95% confidence interval (CI): 0.47–0.68. In patients with AHF, the non-invasive estimation of PVR using CMR shows poor accuracy, as well as a limited capacity to discriminate increased PVR values.


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