Long-Term Outcomes in Adult Patients With Pulmonary Hypertension After Percutaneous Closure of Atrial Septal Defects

2021 ◽  
Author(s):  
Selai Akseer ◽  
Lusine Abrahamyan ◽  
Douglas S. Lee ◽  
Ella Huszti ◽  
Lukas M. Meier ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Long Term Outcomes ◽  
Septal Defects ◽  
Mean Pulmonary Arterial Pressure ◽  
Cerebrovascular Events ◽  
Pulmonary Arterial ◽  
Asd Closure

Background: Pulmonary hypertension (PH), recently redefined as mean pulmonary arterial pressure >20 mm Hg (PH 20 ), may be observed in patients with atrial septal defects (ASD). We aimed to determine the effect of preprocedural PH 20 status on outcomes among patients undergoing ASD closure. Methods: Study population was selected from a retrospective registry of adult patients who underwent percutaneous ASD closure from 1998 to 2016 from a single center and had right heart catheterizations during the procedure. The clinical registry was linked to administrative databases to capture short- and long-term outcomes. Results: We included a total of 632 ASD closure patients of whom 359 (56.8%) had PH 20 . The mean follow-up length was 7.6±4.6 years. Patients with PH 20 were older (mean age 56.5 versus 43.1 years, P <0.001) and a higher prevalence of comorbidities including hypertension (54.3% versus 21.6%, P <0.001) and diabetes (18.1% versus 5.9%, P <0.001) than those without PH. In a Cox proportional hazards model after covariate adjustment, patients with PH had a significantly higher risk of developing major adverse cardiac and cerebrovascular events (heart failure, stroke, myocardial infarction, or cardiovascular mortality), with hazards ratio 2.45 (95% CI, 1.4–4.4). When applying the prior, mean pulmonary arterial pressure ≥25 mm Hg (PH 25 ) cutoff, a significantly higher hazard of developing major adverse cardiac and cerebrovascular events was observed in PH versus non-PH patients. Conclusions: ASD patients with PH undergoing closure suffer from more comorbidities and worse long-term major adverse cardiac and cerebrovascular events outcomes, compared with patients without PH. The use of the new PH 20 definition potentially dilutes the effect of this serious condition on outcomes in this population.

scholarly journals Mean pulmonary arterial pressure after percutaneous mitral valvuloplasty predicts long-term adverse outcomes

2012 ◽  
Vol 31 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Elisabete Jorge ◽  
Rui Baptista ◽  
Henrique Faria ◽  
João Calisto ◽  
Vítor Matos ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Adverse Outcomes ◽  
Mitral Valvuloplasty ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Correlation of acute with chronic hypoxic pulmonary hypertension in cattle

1975 ◽  
Vol 38 (3) ◽  
pp. 495-498 ◽  
Author(s):  
D. H. Will ◽  
J. L. Hicks ◽  
C. S. Card ◽  
J. T. Reeves ◽  
A. F. Alexander
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Acute Hypoxia ◽  
Common Mechanism ◽  
Mean Pulmonary Arterial Pressure ◽  
Pressor Responses ◽  
Pulmonary Arterial ◽  
Highly Correlated

We investigated acute and chronic hypoxic pulmonary pressor responses in two groups of calves, one bred to be susceptible, the other resistant to high-altitude pulmonary hypertension. Twelve 5-mo-old susceptible calves residing at 1,524 m increased their mean pulmonary arterial pressure from 26 +/- 2 (SE) to 55 +/- 4 mmHg during 2 h at a simulated altitude of 4,572 m. In 10 resistant calves pressure increased from 22 +/- 1 to 37 +/- 2 mmHg. Five calves were selected from each group for further study. When 9 mo old, the 5 susceptible calves again showed a greater pressor response to acute hypoxia (27 +/- 1 to 55 +/- 4 mmHg) than did 5 resistant calves (23 +/- 1 to 41 +/- 3 mmHg). When 12 mo old, the 5 susceptible calves also developed a greater increase in pulmonary arterial pressure (21 +/- 2 to 9 +/- 4 mmHg) during 18 days at 4,572 m than did the 5 resistant calves (21 +/- 1 to 64 +/- 4 mmHg). Acute and chronic hypoxic pulmonary pressor responses were highly correlated (r = 0.91; P less than 0.001) indicating that they were probably produced through a common mechanism.

scholarly journals Impact of the updated hemodynamic definitions on diagnosis rates of pulmonary hypertension

2020 ◽  
Vol 10 (3) ◽  
pp. 204589402093129
Author(s):  
Seda Tanyeri ◽  
Ozgur Y. Akbal ◽  
Berhan Keskin ◽  
Aykun Hakgor ◽  
Ali Karagoz ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
European Society ◽  
Pulmonary Arterial Pressure ◽  
Heart Catheterization ◽  
Mean Pulmonary Arterial Pressure ◽  
Pressure Threshold ◽  
Normal Mean ◽  
Pulmonary Arterial ◽  
European Society Of Cardiology

We evaluated whether updated pulmonary hypertension definitive criteria proposed in sixth World Symposium on Pulmonary Hypertension had an impact on diagnosis of overall pulmonary hypertension and pre-capillary and combined pre- and post-capillary phenotypes as compared to those in European Society of Cardiology/European Respiratory Society 2015 pulmonary hypertension Guidelines. Study group comprised the retrospectively evaluated 1300 patients (age 53.1 ± 18.8 years, female 807, 62.1%) who underwent right heart catheterization with different indications between 2006 and 2018. Mean pulmonary arterial pressure ≥25 mmHg (European Society of Cardiology) and PAMP (mean pulmonary arterial pressure) >20 mmHg (World Symposium on Pulmonary Hypertension) right heart catheterization definitions criteria were used, respectively. For pre-capillary pulmonary hypertension, pulmonary artery wedge pressure ≤15 mmHg and pulmonary vascular resistance ≥3 Wood units criteria were included in the both definitions. Normal mean pulmonary arterial pressure (<21 mmHg), borderline mean pulmonary arterial pressure elevation (21–24 mmHg), and overt pulmonary hypertension (≥25 mmHg) were documented in 21.1, 9.8, and 69.1% of the patients, respectively. The pre-capillary and combined pre- and post-capillary pulmonary hypertension were noted in 2.9 and 1.1%, 8.7 and 2.5%, and 34.6 and 36.6% of the patients with normal mean pulmonary arterial pressure, borderline, and overt pulmonary hypertension subgroups, respectively. The World Symposium on Pulmonary Hypertension versus European Society of Cardiology/European Respiratory Society definitions resulted in a net 9.8% increase in the diagnosis of overall pulmonary hypertension whereas increases in the pre-capillary pulmonary hypertension and combined pre- and post-capillary pulmonary hypertension diagnosis were only 0.8 and 0.3%, respectively. The re-definition of mean pulmonary arterial pressure threshold seems to increase the frequency of the overall pulmonary hypertension diagnosis. However, this increase was mainly originated from those in post-capillary pulmonary hypertension subgroup whereas its impact on pre-capillary and combined pre- and post-capillary pulmonary hypertension was negligible. Moreover, criteria of pre-capillary pulmonary vascular disease and combined pre- and post-capillary phenotypes were still detectable even in the presence of normal mean pulmonary arterial pressure. The obligatory criteria of pulmonary vascular resistance ≥3 Wood units seems to keep specificity for discrimination between pre-capillary versus post-C pulmonary hypertension after lowering the definitive mean pulmonary arterial pressure threshold to 20 mmHg.

Operation Everest II: pulmonary gas exchange during a simulated ascent of Mt. Everest

1987 ◽  
Vol 63 (6) ◽  
pp. 2348-2359 ◽  
Author(s):  
P. D. Wagner ◽  
J. R. Sutton ◽  
J. T. Reeves ◽  
A. Cymerman ◽  
B. M. Groves ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Sea Level ◽  
Pulmonary Arterial Pressure ◽  
Flow Distribution ◽  
Barometric Pressure ◽  
Normal Subjects ◽  
O2 Uptake ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Eight normal subjects were decompressed to barometric pressure (PB) = 240 Torr over 40 days. The ventilation-perfusion (VA/Q) distribution was estimated at rest and during exercise [up to 80–90% maximal O2 uptake (VO2 max)] by the multiple inert gas elimination technique at sea level and PB = 428, 347, 282, and 240 Torr. The dispersion of the blood flow distribution increased by 64% from rest to 281 W, at both sea level and at PB = 428 Torr (heaviest exercise 215 W). At PB = 347 Torr, the increase was 79% (rest to 159 W); at PB = 282 Torr, the increase was 112% (108 W); and at PB = 240 Torr, the increase was 9% (60 W). There was no significant correlation between the dispersion and cardiac output, ventilation, or pulmonary arterial wedge pressure, but there was a correlation between the dispersion and mean pulmonary arterial pressure (r = 0.49, P = 0.02). When abnormal, the VA/Q pattern generally had perfusion in lung units of zero or near zero VA/Q combined with units of normal VA/Q. Alveolar-end-capillary diffusion limitation of O2 uptake (VO2) was observed at VO2 greater than 3 l/min at sea level, greater than 1–2 l/min VO2 at PB = 428 and 347 Torr, and at higher altitudes, at VO2 less than or equal to 1 l/min. These results show variable but increasing VA/Q mismatch with long-term exposure to both altitude and exercise. The VA/Q pattern and relationship to pulmonary arterial pressure are both compatible with alveolar interstitial edema as the primary cause of inequality.

scholarly journals Hyperuricemia in patients with pulmonary hypertension: A study in a tertiary care center

2021 ◽  
Vol 6 (3) ◽  
pp. 173-177
Author(s):  
C H Raju ◽  
M Ravindranath
Keyword(s):  
Pulmonary Hypertension ◽  
Uric Acid ◽  
Arterial Pressure ◽  
Serum Uric Acid ◽  
Pulmonary Arterial Pressure ◽  
Nyha Class ◽  
High Serum ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
The Right

Pulmonary Hypertension is one of a life-threatening disease with high rate of patient mortality. Decreased cardiac output and tissue hypoxia is measured using Uric acid as a marker for assessment of pulmonary hypertension. 75 patients who were diagnosed with a mean pulmonary arterial pressure of &#62;22mmHg were categorized as group A and 75 healthy patients were considered to be Group B. Blood was collected for Uric acid, creatinine and total Bilirubin estimation. Pulmonary arterial systolic pressure as well as the ventricular function of the patients was evaluated using Colour Doppler ECG and a value of ≥50 mmHg, or a mean pulmonary arterial pressure (at rest) of ≥25 mmHg was taken and the right arterial pressure was calculated. Using the Simpson’s formula, the right and left ventricular ejaculation factors (RVEF, LVEF) were calculated. The serum uric acid levels among the patients were 8.3±1.4mg/dL, creatinine levels were 2.1 ± 0.5 mg/dL, and the total bilirubin levels were 1.9 ± 0.8 mg/dL all of which was significantly higher than the controls. The uric acid levels were also positively correlated to the NHYA class. The blood pressure and the pulmonary arterial pressure were also higher than that of the controls. The correlation was done between the elevated uric acid and ejection fractions and the correlation coefficients of MPAP, LVEF, RVEF and the NYHA class were all significantly associated and the values were 0.394, -0.513, -0.467 and 0.38 respectively. High serum uric acid levels is significantly associated with higher blood pressure, pulmonary arterial pressure and NYHA class. High serum uric acid levels can be a reliable prognostic marker for the detection of pulmonary hypertension. Early therapy may help in the reduction of mortality rate.

scholarly journals Challenges in the Patient With Pulmonary Hypertension and Atrial Septal Defect: Understanding When and How to Close the Defect

2019 ◽  
Vol 18 (1) ◽  
pp. 10-13 ◽  
Author(s):  
Mary P. Mullen
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Congenital Heart ◽  
Septal Defect ◽  
Heart Defects ◽  
Defect Closure ◽  
Long Term Outcomes ◽  
Septal Defects ◽  
Pulmonary Arterial

Atrial septal defects (ASDs) are common congenital heart defects in children and adults. Pulmonary arterial hypertension (PAH) is found in subsets of both pediatric and adult patients with atrial defects under varied clinical contexts. The pulmonary hypertension specialist is often faced with questions surrounding timing and method of defect closure, which may have significant impact on procedural and long-term morbidity and survival. This review highlights important differences in management between children and adults with ASDs associated with PAH, highlighting indications for closure, operability, types of closure, and long-term outcomes.

scholarly journals Korelasi Forced Expiratory Volume in 1 Second % Prediksi dengan Tekanan Rerata Arteri Pulmonalis Menggunakan Ekokardiografi pada Penderita Penyakit Paru Obstruktif Kronik Stabil

2017 ◽  
Vol 3 (4) ◽  
pp. 177
Author(s):  
Munadi Munadi ◽  
M Yamin ◽  
Anna Ujainah ◽  
Cleopas Martin Rumende
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Forced Expiratory Volume ◽  
Chronic Obstructive ◽  
Right Heart ◽  
Obstructive Pulmonary Disease ◽  
Mean Pulmonary Arterial Pressure ◽  
Copd Patients ◽  
Pulmonary Arterial

Pendahuluan. Hipertensi pulmonal merupakan komplikasi tersering pada penyakit paru obstruktif kronis (PPOK). Angka kematian akan meningkat tajam apabila pasien PPOK sudah mengalami komplikasi ini. Selama ini pengukuran tekanan arteri pulmonalis hanya diukur pada saat pasien PPOK eksaserbasi dirawat di ruang intesif dengan cara invasif menggunakan alat right heart catherization (RHC). Data kelompok PPOK stabil yang mengalami hipertensi pulmonal yang diukur dengan cara non invasif masih relatif sedikit yang dipublikasi. Saat ini sudah ada ekokardiografi yang dapat digunakan sebagai pengganti RHC pada kelompok PPOK stabil. Penelitian ini dilakukan untuk mengetahui apakah ada hubungan antara penurunan forced expiratory volume in 1 second (FEV1) % prediksi dengan peningkatan rerata tekanan arteri pulmonalis (mean pulmonary arterial pressure, mPAP) dan mencari titik potong terbaik secara klinis antara FEV1 % prediksi dan mPAP.Metode. Studi potong lintang pada lima puluh delapan subjek PPOK stabil yang dilakukan spirometri dan pengukuran mPAP dengan menggunakan ekokardiografi doppler pada potongan short axis setinggi aorta.Hasil. Nilai rerata FEV1 % prediksi 26,6 (SB 4,7) dan rerata mPAP 37,61 (18,1-59) mmHg. 74 % subjek mengalami hipertensi pulmonal, dengan karakteristik 24 % ringan, 31 % sedang dan 19 % berat. Terdapat korelasi negatif kuat antara penurunan FEV1 % prediksi dengan peningkatan mPAP. Semakin turun FEV1% prediksi semakin meningkat mPAP. Nilai titik potong terbaik secara klinis 55,3 % dengan sensitivitas 93%.Simpulan. FEV1 % prediksi berkorelasi negatif yang sangat kuat dengan tekanan rerata arteri pulmonalis. FEV1 % prediksi 55,3 % memiliki kemampuan yang cukup baik membedakan PPOK stabil yang sudah mengalami hipertensi pulmonal.Kata Kunci: ekokardiografi, FEV1 %, mPAP, PPOK stabil, spirometri  Correlation of Forced Expiratory Volume in 1 Second Prediction with Mean Pulmonary Arterial Pressure Using Echocardiography in Stable Chronic Obstructive Pulmonary Disease Introduction. Pulmonary hypertension is the most common complication of chronic obstructive pulmonary disease (COPD). Mortality rate will increase when COPD complication with pulmonary hypertension. Right heart catheterization (RHC) is the most common tool to measure mean pulmonary arterial pressure (mPAP) either in COPD patients with exacerbations treated in intensive care unit. Data of pulmonary hypertension in stable COPD group is still relatively rare. Alternatively to RHC, nowadays echocardiography is used to measure mean pulmonary arterial pressure in stable COPD group.Methods. A cross-sectional study was conducted on fifty-eight stable male COPD patients (mean age: 67,6) underwent spirometry. Mean pulmonary arterial pressure was measured using transthoracic echocardiography at short axis view in aortic level. Results. Mean value of forced expiratory volume in 1 second (FEV1)% was 26,6 % (SD 4,7) with median value of mean pulmonary arterial pressure was 37,61 mmHg (range 18,3-59). As many as 74% subjects were pulmonary hypertension; 24 % mild, 31 % moderate and 19% severe respectively. The correlation test showed a significant strong-negative correlation (r = -0,948, p <0,001). The best cut-off point of FEV1% prediction, which had a clinical value correlated with mPAP, was 55,3% with the sensitivity 93 %. Conclusions. Forced expiratory volume in one second (FEV1)% prediction has a significant correlation with mean pulmonary arterial pressure in stable COPD patients. The cut-off point FEV1% prediction 55,3% has a good capability to discriminate pulmonary hypertension in stable COPD patient. Keywords: echocardiography, FEV1% prediction, mean pulmonary arterial pressure, stable COPD

scholarly journals Acute Deterioration of Pulmonary Arterial Hypertension (PAH) in a Patient with Neurofibromatosis Type 1 (NF1)

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Seiya Tanaka ◽  
Fuko Kawahara ◽  
Taro Miyamoto ◽  
Satoshi Tsurusaki ◽  
Yoshihito Sanuki ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Pressure ◽  
Arterial Hypertension ◽  
Neurofibromatosis Type 1 ◽  
Pulmonary Arterial Pressure ◽  
Neurofibromatosis Type ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

A 56-year-old woman was diagnosed as having chronic obstructive pulmonary disease with heavy smoking. Mild pulmonary hypertension (mean pulmonary arterial pressure: 31 mmHg) was detected at the first visit. She was diagnosed with pulmonary hypertension due to pulmonary disease and medicated only with bronchodilators. Simultaneous, multiple freckling in the trunk of her body and café au lait macules in her back with some cutaneous neurofibromas were also detected. A plastic surgeon removed one of the neurofibromas and pathologically diagnosed it as neurofibromatosis type 1 (NF1). We finally rediagnosed her with pulmonary hypertension with unclear and/or multifactorial factors when she deteriorated 1 year after being treated only with bronchodilators. We then administrated upfront combination therapy with macitentan and tadalafil. Mean pulmonary arterial pressure rapidly improved. Learning Objective. Pulmonary arterial hypertension (PAH) in neurofibromatosis type 1 (NF1) can occur due to lung disease or due to certain involvement of pulmonary arteries, or a combination of both. Increased awareness of PAH in NF1 is very important for patients survival. The current therapeutic strategy is almost identical to that of idiopathic PAH; however, there is no clinical evidence. Insights gained from clinical experiences should help identify promising novel therapeutic approaches in NF1-PAH.

Hemodynamic effects of arginine vasopressin in rats adapted to chronic hypoxia

1989 ◽  
Vol 66 (1) ◽  
pp. 151-160 ◽  
Author(s):  
H. K. Jin ◽  
R. H. Yang ◽  
Y. F. Chen ◽  
R. M. Thornton ◽  
R. M. Jackson ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Pulmonary Arterial Pressure ◽  
Systemic Arterial Pressure ◽  
Systemic Hemodynamic ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Air Control

Acute and chronic pulmonary and systemic hemodynamic responses to arginine vasopressin (AVP) were examined in 4-wk hypoxia-adapted and air control rats. AVP, administered intravenously as bolus injections or sustained infusions, produced major dose-dependent V1-receptor-mediated reductions in mean pulmonary arterial pressure in hypoxia-adapted rats. These effects were comparable in pentobarbital-anesthetized, thoracotomized animals and in conscious, intact rats. Chronic infusions of AVP induced a sustained reduction in mean pulmonary arterial pressure and partially prevented the development of pulmonary hypertension without changing systemic arterial pressure. AVP induced significant decreases in cardiac output in both groups; the cardiac output response was not significantly different in hypoxia-adapted and air control animals. AVP induced almost no change in MPAP in air control rats. Furthermore the systemic pressor effects of AVP were significantly blunted in hypoxia-adapted rats compared with air controls. We conclude that the pulmonary depressor and blunted systemic pressor effects of AVP observed in hypoxia-adapted rats may be related to release of a vasodilator, such as endothelium-derived relaxing factor, vasodilator prostaglandins, or atrial natriuretic peptides. Further study is needed to elucidate these mechanisms and assess the usefulness of AVP and/or its analogues in the treatment and prevention of hypoxia-induced pulmonary hypertension.

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