Pulmonary Artery Proportional Pulse Pressure Predicts Adverse Clinical Outcomes in Group 1 Pulmonary Hypertension (Analysis of the NIH Pulmonary Hypertension Registry)

2015 ◽  
Vol 21 (8) ◽  
pp. S80
Author(s):  
Sula Mazimba ◽  
James Bergin ◽  
Jamie L.W. Kennedy ◽  
Jose A. Tallaj ◽  
Elizabeth Gay ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Clinical Outcomes ◽  
Pulse Pressure ◽  
Group 1

scholarly journals AGE–RAGE Stress in the Pathophysiology of Pulmonary Hypertension and its Treatment

2019 ◽  
Vol 28 (02) ◽  
pp. 071-079 ◽  
Author(s):  
Kailash Prasad
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Heart Diseases ◽  
Therapeutic Targets ◽  
Vascular Hypertrophy ◽  
Soluble Rage ◽  
Glycation End Products ◽  
Rage Expression ◽  
Pathophysiologic Mechanisms ◽  
Group 1

AbstractPulmonary hypertension (PH) is a rare and fatal disease characterized by elevation of pulmonary artery pressure ≥ 25 mm Hg. There are five groups of PH: (1) pulmonary artery (PA) hypertension (PAH), (2) PH due to heart diseases, (3) PH associated with lung diseases/hypoxia, (4) PH associated with chronic obstruction of PA, and (5) PH due to unclear and/or multifactorial mechanisms. The pathophysiologic mechanisms of group 1 have been studied in detail; however, those for groups 2 to 5 are not that well known. PH pathology is characterized by smooth muscle cells (SMC) proliferation, muscularization of peripheral PA, accumulation of extracellular matrix (ECM), plexiform lesions, thromboembolism, and recanalization of thrombi. Advanced glycation end products (AGE) and its receptor (RAGE) and soluble RAGE (sRAGE) appear to be involved in the pathogenesis of PH. AGE and its interaction with RAGE induce vascular hypertrophy through proliferation of vascular SMC, accumulation of ECM, and suppression of apoptosis. Reactive oxygen species (ROS) generated by interaction of AGE and RAGE modulates SMC proliferation, attenuate apoptosis, and constricts PA. Increased stiffness in the artery due to vascular hypertrophy, and vasoconstriction due to ROS resulted in PH. The data also suggest that reduction in consumption and formation of AGE, suppression of RAGE expression, blockage of RAGE ligand binding, elevation of sRAGE levels, and antioxidants may be novel therapeutic targets for prevention, regression, and slowing of progression of PH. In conclusion, AGE–RAGE stress may be involved in the pathogenesis of PH and the therapeutic targets should be the AGE–RAGE axis.

Increased Pulmonary-Systemic Pulse Pressure Ratio Is Associated With Increased Mortality in Group 1 Pulmonary Hypertension

2019 ◽  
Vol 28 (7) ◽  
pp. 1059-1066 ◽  
Author(s):  
Benjamin K. Ruth ◽  
Kenneth C. Bilchick ◽  
Manu M. Mysore ◽  
Hunter Mwansa ◽  
William C. Harding ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulse Pressure ◽  
Pressure Ratio ◽  
Group 1

scholarly journals PULMONARY-SYSTEMIC PULSE PRESSURE RATIO IS ASSOCIATED WITH ADVERSE CLINICAL OUTCOMES IN GROUP 1 PULMNONARY HYPERTENSION

2017 ◽  
Vol 69 (11) ◽  
pp. 1920
Author(s):  
Sula Mazimba ◽  
Jamie Kennedy ◽  
Manu Mysore ◽  
Jeremy Mazurek ◽  
Andrew Mihalek ◽  
...  
Keyword(s):  
Clinical Outcomes ◽  
Pulse Pressure ◽  
Pressure Ratio ◽  
Group 1

scholarly journals Pulmonary artery pulse pressure and wave reflection in chronic pulmonary thromboembolism and primary pulmonary hypertension

2001 ◽  
Vol 37 (4) ◽  
pp. 1085-1092 ◽  
Author(s):  
Vincent Castelain ◽  
Philippe Hervé ◽  
Yves Lecarpentier ◽  
Pierre Duroux ◽  
Gerald Simonneau ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulse Pressure ◽  
Wave Reflection ◽  
Primary Pulmonary Hypertension ◽  
Pulmonary Thromboembolism

scholarly journals Decreased pulmonary arterial proportional pulse pressure is associated with increased mortality in group 1 pulmonary hypertension

2017 ◽  
Vol 40 (11) ◽  
pp. 988-992
Author(s):  
Hunter Mwansa ◽  
Kenneth C. Bilchick ◽  
Alex M. Parker ◽  
William Harding ◽  
Benjamin Ruth ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulse Pressure ◽  
Pulmonary Arterial ◽  
Group 1

P4690Effects of pulmonary artery wedge pressure on right ventricular pulsatile loading in pulmonary hypertension: a reappraisal based on pulmonary arterial isobaric stiffness

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
D Chemla ◽  
E Berthelot ◽  
J Weatherald ◽  
E Lau ◽  
P Attal ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Stroke Volume ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Pulmonary Artery Wedge Pressure ◽  
Pulmonary Arterial ◽  
Wedge Pressure

Abstract Background Pulmonary hypertension (PH) is associated with stiffening of pulmonary arteries. Previous studies have suggested that high pulmonary artery wedge pressure (PAWP) in postcapillary PH (Pc-PH) further augments PA stiffness at a given level of pulmonary vascular resistance as compared to pulmonary arterial hypertension (PAH). However, these studies do not take into account differences in distending pressure (mean PA pressure, mPAP), which has an effect on stiffness due to non-linear stress-strain behavior of arteries. Purpose To compare total PA stiffness between Pc-PH and idiopathic PAH (iPAH) studied at similar mPAP (isobaric stiffness). Methods This was an analysis of right heart catheterization results obtained in 112 Pc-PH and 112 iPAH patients extracted from the French PAH network registry and matched for mPAP (median 38 vs 39 mmHg, P=NS), age (70.5 years each) and sex (64% female each). Total PA stiffness was calculated as the ratio of PA pulse pressure to indexed stroke volume. Results Total PA stiffness (n=224) increased with mPAP (Spearman's rho = 0.66) and decreased with PAWP (rho = - 0.17) (each P<0.01). The isobaric stiffness was lower in Pc-PH (median (IQR) = 0.91 (0.64–1.39) mmHg/mL/m2) than in iPAH (1.18 (0.83–1.62) mmHg/mL/m2, P<0.01). The patients were then stratified according to their mPAP (25–35 mmHg, n=74 (37/37); 36–43 mmHg, n=75 (34/41); and 44–66 mmHg, n=75 (41/34)). The isobaric stiffness was lower in Pc-PH than iPAH in the 1st mPAP tertile (0.62 vs 0.83 mmHg/mL/m2, P=0.06), in the 2nd mPAP tertile (0.76 vs 1.22 mmHg/mL/m2, P<0.01) and in the 3rd mPAP tertile (1.41 vs 1.77 mmHg/mL/m2, P<0.01). The pulmonary vascular resistance was lower in Pc-PH than iPAH in every mPAP tertile (each P<0.01). Finally, Pc-PH had a higher indexed stroke volume than iPAH (37 (29–48) vs 32 (27–40) mL/m2, P<0.01) while systolic PA pressure and PA pulse pressure were similar. Conclusion Unexpectedly, the isobaric pulmonary arterial stiffness was lower in Pc-PH than iPAH patients. It is proposed that PAWP attenuates the increase in RV pulsatile loading in PH when the natural high-strain-induced stiffening was accounted for. This may contribute to a less impaired right ventricular-PA coupling leading to higher indexed stroke volume in Pc-PH than iPAH despite similar PA pressure. At every mPAP level, both the lower PA stiffness and lower pulmonary vascular resistance in Pc-PH than in iPAH may contribute to explain differences in the pressure overload-induced right ventricular adaptation between the two diseased groups, a point that deserves to be confirmed by further studies. Acknowledgement/Funding University regular funds

scholarly journals Predictors of Chronic Thromboembolic Pulmonary Hypertension

Kardiologiia ◽  
2018 ◽  
Vol 58 (12) ◽  
pp. 60-65
Author(s):  
M. R. Kuznetsov ◽  
I. V. Reshetov ◽  
B. B. Orlov ◽  
A. A. Khotinsky ◽  
A. A. Atayan ◽  
...  
Keyword(s):  
Risk Factors ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Anticoagulant Therapy ◽  
Vena Cava ◽  
Significant Risk ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Thromboembolic Pulmonary Hypertension ◽  
Group 2 ◽  
Group 1

Purpose:to elucidate predictors of development of chronic thromboembolic pulmonary hypertension (CTEPH) after acute pulmonary artery thromboembolism (PTE).Material and methods. We included in this study 210 patients hospitalized with diagnosis of submassive and massive PTE from 2013 to 2017. In 1 to 3 years after initial hospitalization these patients were invited for control examination. According to results of this examination patients were divided into two groups: with (group 1, n=45) and without (group 2, n=165) signs of CTEPH. Severity of pulmonary artery vascular bed involvement was assessed by multislice computed tomography (MSCT) angiography and lung scintigraphy. For detection of thrombosis in the inferior vena cava system we used ultrasound angioscanning.   Examination also included echocardiography.Results.In the process of mathematical analysis, the following risk factors for the development of CTEPH embolism were determined: duration of thrombotic history (group 1 – 13.70±2.05 days, group 2– 16.16±1.13 days, p=0.015), localization of venous thrombosis in the lower extremities (the most favorable – shin veins, popliteal, and common femoral veins, unfavorable – superficial femoral vein). The choice of the drug for thrombolytic and anticoagulant therapy: streptokinase and urokinase were significantly more effective than alteplase, rivaroxaban was superior to the combination of unfractionated or low molecular weight heparins with warfarin. Also, risk factors for the development of CTEPH were the initial degree of pulmonary hypertension and tricuspid insufficiency, as well as the positive dynamics of these indicators at the background of thrombolytic or anticoagulant therapy. Of concomitant diseases, significant risk factors for development of CTEPH were grade 3 hypertensive disease, diabetes mellitus, post­infarction cardiosclerosis. On the other hand, age, gender, degree of severity at the time of admission, presence of infarction pneumonia, surgical prevention of recurrent pulmonary embolism, number of pregnancies and deliveries, history of trauma and malignancies, cardiac arrhythmias produced no significant impact on the development of CTEPH.

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