Normal Range for Pulmonary Artery Systolic Pressure—Reply

JAMA ◽  
2008 ◽  
Vol 299 (17) ◽  
pp. 2022
Author(s):  
Roberto F. Machado
Keyword(s):  
Pulmonary Artery ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Normal Range

Elevated Estimated Pulmonary Arterial Pressures in Patients with Chuvash Polycythemia.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1634-1634
Author(s):  
Victor R. Gordeuk ◽  
Adelina I. Sergueeva ◽  
Galina Y. Miasnikova ◽  
Lydia A. Polyakova ◽  
Daniel J. Okhotin ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Tricuspid Regurgitation ◽  
Chronic Hypoxia ◽  
Primary Pulmonary Hypertension ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Normal Range ◽  
Pulmonary Arterial ◽  
The Mean

Abstract Chuvash polycythemia is characterized by a homozygous 598C>T mutation in VHL and up regulation of HIF-1α during normoxia. Disorders of chronic hypoxia may be complicated by the development of pulmonary hypertension. Because of the up regulation of the hypoxic response in Chuvash polycythemia, we postulated that there may be a tendency to increased pulmonary artery pressures in this condition as well. To test this hypothesis, we analyzed results for Doppler echocardiography in 15 patients with Chuvash polycythemia and 15 Chuvash individuals without polycythemia. The tricuspid regurgitation velocity (TRV) allows estimation of pulmonary artery systolic pressure. A TRV of 2.5 m/sec or higher corresponds to a pulmonary artery systolic pressure of at least 35 mm Hg (normal up to 32 mm Hg), while a TRV of 3.0 m/sec or higher to a pressure of at least 46 mm Hg. The results are summarized in the Table. Pulmonary artery pressures as estimated by tricuspid regurgitation velocity (TRV) in Chuvash subjects with and without polycythemia Chuvash polycythemia (n = 15) Controls (n = 15) P Age in years; mean (SD) 35 (17) 35 (17) 1.0 Female sex in no. (%) 8 (53%) 8 (53%) 1.0 Hemoglobin in g/dL; mean (SD) 16.7 (2.3) 13.3 (1.2) <0.001 TRV in m/sec; mean (SD) 2.2 (0.6) 1.4 (0.6) 0.001 TRV > 2.4 m/sec in no. (%) 4 (27%) 0 (0%) 0.1 Most of the patients with Chuvash polycythemia were receiving phlebotomy therapy and therefore many had hemoglobin concentrations in the upper normal range. Four of the patients with Chuvash polycythemia and none of the others had TRV ≥ 2.5 m/sec (range of 2.5 to 3.0), and mean TRVs were significantly higher in the patients with Chuvash polycythemia. Interestingly, the mean ± SD TRV in these 15 patients with Chuvash polycythemia was identical to the mean ± SD TRV that was recently reported in 195 American patients with sickle cell disease (Gladwin et al, NEJM2004;350:886), another hematological condition with a tendency to pulmonary hypertension. While the pulmonary arterial pressures detected so far in Chuvash polycythemia patients are lower than those in patients with primary pulmonary hypertension, our results suggest that pulmonary hypertension may be an unrecognized complication of Chuvash polycythemia.

Effect of acute lower respiratory tract infection on pulmonary artery pressure in children with post-tricuspid left-to-right shunt

2021 ◽  
pp. 1-5
Author(s):  
Sakshi Sachdeva ◽  
Shyam S. Kothari ◽  
Saurabh K. Gupta ◽  
Sivasubramanian Ramakrishnan ◽  
Anita Saxena
Keyword(s):  
Tract Infection ◽  
Pulmonary Artery ◽  
Respiratory Tract ◽  
Respiratory Tract Infection ◽  
Lower Respiratory Tract Infection ◽  
Pulmonary Artery Pressure ◽  
Lower Respiratory Tract ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Artery Pressure

Abstract We sought to examine the influence of clinically severe lower respiratory tract infection on pulmonary artery pressure in children having CHD with post-tricuspid left-to-right shunt, as it may have physiological and clinical implications. In a prospective single-centre observational study, 45 children with post-tricuspid left-to-right shunt and clinically severe lower respiratory tract infection were evaluated during the illness and 2 weeks after its resolution. Pulmonary artery systolic pressure was estimated non-invasively using shunt gradient by echocardiography and systolic blood pressure measured non-invasively. Median pulmonary artery systolic pressure during lower respiratory tract infection was only mildly (although statistically significantly) elevated during lower respiratory tract infection [60 (42–74) versus 53 (40–73) mmHg, (p < 0.0001)]. However, clinically significant change in pulmonary artery systolic pressure defined as the increase of >10 mmHg was present in only 9 (20%) patients. In the absence of hypoxia or acidosis, only a small minority (9%, n = 4) showed significant pulmonary artery systolic pressure rise >10 mmHg. In the absence of hypoxia or acidosis, severe lower respiratory tract infection in patients with acyanotic CHD results in only mild elevation of pulmonary artery systolic pressure in most of the patients.

scholarly journals Serum-Free Thyroxine Levels Were Associated with Pulmonary Hypertension and Pulmonary Artery Systolic Pressure in Euthyroid Patients with Coronary Artery Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-8
Author(s):  
Bingjie Wu ◽  
Jingjing Jiang ◽  
Minghui Gui ◽  
Lin Liu ◽  
Qiqige Aleteng ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Pulmonary Hypertension ◽  
Regression Analysis ◽  
Coronary Artery ◽  
Pulmonary Artery ◽  
Systolic Pressure ◽  
Free Thyroxine ◽  
Pulmonary Artery Systolic Pressure ◽  
Serum Free ◽  
Artery Disease

The aim of this study was to evaluate the association between thyroid hormone levels, pulmonary hypertension (PH), and pulmonary artery systolic pressure (PASP) in euthyroid patients with coronary artery disease (CAD). A cross-sectional study was conducted in individuals who underwent coronary angiography and were diagnosed as CAD from March 2013 to November 2013. 811 subjects (185 women and 626 men) were included in this study. PASP was measured by transthoracic Doppler echocardiography. 86 patients were diagnosed as PH and had significantly higher free thyroxine (FT4) levels than those without PH. Multiple logistic regression analysis demonstrated an independent association of FT4 levels with PH after adjustment of gender, age, body mass index, systolic blood pressure, left ventricular ejection fraction, hypertension, and medication use of calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists, and nitrates. Serum-free triiodothyronine (FT3) and thyroid-stimulating hormone (TSH) were not associated with PH. Furthermore, multivariate linear regression analysis showed that FT4 levels emerged as an independent predictor for PASP, while FT3 and TSH levels were not associated with PASP. Our study demonstrated that, in euthyroid patients with CAD, FT4 was an independent risk factor for PH, and FT4 levels were independently associated with PASP.

Abstract 15388: Persistent Pulmonary Hypertension After Transcatheter Aortic Valve Implantation: Impact on Mortality

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Maria Drakopoulou ◽  
Konstantinos Stathogiannis ◽  
Konstantinos Toutouzas ◽  
George Latsios ◽  
Andreas Synetos ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Aortic Stenosis ◽  
Pulmonary Artery ◽  
Severe Aortic Stenosis ◽  
Systolic Pressure ◽  
Right Atrial ◽  
Pulmonary Artery Systolic Pressure ◽  
End Point ◽  
The Right ◽  
The Impact

Objective: Severe aortic stenosis leads to increased pulmonary arterial systolic pressure. A controversy still remains regarding the impact of persistent pulmonary hypertension (PHT) on prognosis of patients undergoing transcatheter aortic valve implantation (TAVI). We sought to investigate the impact of persistent PHT on 2-year all-cause mortality of patients with severe aortic stenosis following TAVI. Methods: Patients with severe and symptomatic aortic stenosis (effective orifice area [EOA]≤1 cm 2 ) who were scheduled for TAVI with a self-expanding valve at our institution were prospectively enrolled. Prospectively collected echocardiographic data before and after TAVI were retrospectively analyzed in all patients. Pulmonary artery systolic pressure was estimated as the sum of the right ventricular to the right atrial gradient during systole and the right atrial pressure. PHT following TAVI was classified as absent if <35 mmHg and persistent if ≥35 mmHg. Primary clinical end-point was 2-year all-cause mortality defined according to the criteria proposed by the Valve Academic Research Consortium-2. Results: Hundred and forty patients (mean age: 82±9 years) were included in the study. The primary clinical end point occurred in 17 patients (12%) during a median follow-up period of 2 years. Mean pulmonary artery systolic pressure was reduced in all patients following TAVI (45±9 versus 41±6 mmHg, p<0.01). Mortality rate was higher in patients with persistent PHT compared to patients with normal pulmonary artery systolic pressure following TAVI (26% versus 14 %, p<0.01). Patients that reached the primary clinical end point had a higher post procedural mean systolic pulmonary pressure (43±9 versus 39±6 mmHg, p=0.02). In multivariate regression analysis, persistence of PHT (OR: 2.51, 95% CI: 1.109-7.224, p=0.01) was an independent predictor of long-term mortality. Conclusions: The persistence of pulmonary hypertension after TAVI is associated with long term mortality. Identifying the population that will clearly benefit from TAVI is still need to be validated by larger trials.

Normal Fluctuations in Pulmonary Artery Pressures and Cardiac Output in Patients with Severe Left Ventricular Dysfunction

2002 ◽  
Vol 1 (2) ◽  
pp. 131-137 ◽  
Author(s):  
Debra K. Moser ◽  
Susan K. Frazier ◽  
Mary A. Woo ◽  
Linda K. Daley
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Capillary Wedge Pressure ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Pulmonary Artery Systolic Pressure ◽  
Pulmonary Capillary ◽  
Normal Fluctuations

Background: One barrier to accurate interpretation of changes in hemodynamic pressures and cardiac output is lack of data about what constitutes a normal fluctuation. Few investigators have examined normal fluctuations in these parameters and none have done so in patients with left ventricular dysfunction. Aims: To describe normal fluctuations in pulmonary artery pressures and cardiac output in patients with left ventricular dysfunction. Methods: Hemodynamically stable advanced heart failure patients ( N=39; 55±6 years old; 62% male) with left ventricular dysfunction (mean ejection fraction 22±5%) were studied. Cardiac output and pulmonary artery pressures were measured every 15 min for 2 h. Results: Mean±standard deviation fluctuations were as follows: pulmonary artery systolic pressure=7±4 mmHg; pulmonary artery diastolic pressure=6±3 mmHg; pulmonary capillary wedge pressure=5±3 mmHg; cardiac output=0.7±0.3 l/min. The coefficient of variation for fluctuations in pulmonary artery systolic pressure was 6.7%, in pulmonary artery diastolic pressure was 9.3%, in pulmonary capillary wedge pressure was 9.2%, and in cardiac output was 7.2%. Conclusions: Values that vary <8% for pulmonary artery systolic pressure, <11% for pulmonary artery diastolic pressure, <12% for pulmonary capillary wedge pressure, and <9% for cardiac output from baseline represent normal fluctuations in these parameters in patients with left ventricular dysfunction.

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