Carotid Body Denervation and Pulmonary Vascular Resistance in the Rat

Pulmonary arterial hypertension is a progressive disease of the pulmonary vasculature, ultimately leading to right heart failure and death. Current treatment is aimed at targeting three different pathways: the prostacyclin, endothelin and nitric oxide pathways. These therapies improve functional class, increase exercise capacity and improve haemodynamics. In addition, data from a meta-analysis provide compelling evidence of improved survival. Despite these treatments, the outcome is still grim and the cause of death is inevitable – right ventricular failure. One explanation for this paradox of haemodynamic benefit and still worse outcome is that the right ventricle does not benefit from a modest reduction in pulmonary vascular resistance. This article describes the physiological concepts that might underlie this paradox. Based on these concepts, we argue that not only a significant reduction in pulmonary vascular resistance, but also a significant reduction in pulmonary artery pressure is required to save the right ventricle. Haemodynamic data from clinical trials hold the promise that these haemodynamic requirements might be met if upfront combination therapy is used.

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Pulmonary vascular resistance as a potential marker of reactive pulmonary hypertension reduction following sildenafil therapy in patients disqualified from orthotopic heart transplantation

Journal of Cardiology and Cardiovascular Medicine ◽

10.29328/journal.jccm.1001035 ◽

2019 ◽

Vol 4 (2) ◽

pp. 021-029

Author(s):

Agata Duszańska* ◽

Jaroslaw Wasilewski ◽

Michal Zakliczyński

Keyword(s):

Pulmonary Hypertension ◽

Heart Transplantation ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Orthotopic Heart Transplantation ◽

Potential Marker

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PULMONARY VASCULAR RESISTANCE BY ECHOCARDIOGRAPHY-DOPPLER IN ISCHEMIC HEART DISEASE WITH LEFT VENTRCULAR SYSTOLIC DYSFUNCTION

Journal of Medicine and Pharmacy ◽

10.34071/jmp.2017.5.11 ◽

2017 ◽

pp. 89-94

Author(s):

Ke Toan Tran ◽

Thi Thuy Hang Nguyen

Keyword(s):

Heart Disease ◽

Ischemic Heart Disease ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Tricuspid Valve ◽

Left Ventricular ◽

Ischemic Heart ◽

Left Ventricular Ejection ◽

S Wave ◽

Echocardiography Doppler

Objective: To determine pulmonary vascular resistance (PVR) by echocardiography - Doppler and to find correlation between pulmonary vascular resistance with left ventricular EF, PAPs, TAPSE, tissue S-wave of the tricuspid valve in patients with ischemic heart disease. Subjects and Methods: We studied on 82 patients with ischemic heart disease and EF<40% including 36 females, 46 males. Patients were estimated for pulmonary vascular resistance, EF, PAPs, TAPSE, tissue S-wave of the tricuspid valve by echocardiographyDoppler. Results: 64.6% of patients are increased PVR, average of PVR is 3.91 ± 1.85 Wood units and it is increasing with NYHA severity. There are negative correlations between pulmonary vascular resistance with left ventricular ejection fraction (r = - 0.545; p <0.001), TAPSE index (r= -0.590; p <0.001) and tissue S-wave of the tricuspid valve (r = -0.420; p <0.001); positive correlation with systolic pulmonary artery pressure (r = 0.361, p = 0.001), Conclusions: Increased PVR is the primary mechanism for pulmonary hypertension and right heart failure in patients with left heart disease. Determination of PVR in patients with left ventricular dysfunction by echocardiography is important in clinical practice. Key words: Echocardiography-Doppler; Pulmonary vascular resistance; ischemic heart disease

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Plasticity of cardiovascular chemoreflexes after prolonged unilateral carotid body denervation: implications for its therapeutic use

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00451.2019 ◽

2020 ◽

Vol 318 (5) ◽

pp. H1325-H1336

Author(s):

Jaime Eugenín ◽

Carolina Larraín ◽

Patricio Zapata

Keyword(s):

Carotid Body ◽

Therapeutic Use ◽

Therapeutic Effectiveness ◽

Sympathetic Outflow ◽

Sympathetic Hyperactivity ◽

Functional Changes ◽

Human Disorders ◽

Carotid Body Denervation

Unilateral carotid body denervation has been proposed as treatment for sympathetic hyperactivity-related human disorders. Its therapeutic effectiveness for maintaining a persistent decrease in the sympathetic outflow activity will depend on the absence of compensatory chemoreflex plasticity in the remnant carotid and aortic afferents. Here, we suggest that the integrity of central afferents after carotid body denervation is essential to prevent the emergence of plastic functional changes on the contralateral “intact” carotid nerve.

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Pulmonary Vascular Resistance Predicts Mortality and Graft Failure in Transplanted Portopulmonary Hypertension Patients

Liver Transplantation ◽

10.1002/lt.26091 ◽

2021 ◽

Author(s):

Arun Jose ◽

Shimul A Shah ◽

Nadeem Anwar ◽

Courtney R Jones ◽

Kenneth E Sherman ◽

...

Keyword(s):

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Graft Failure ◽

Portopulmonary Hypertension

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Sex Dimorphism in Pulmonary Hypertension: The Role of the Sex Chromosomes

Antioxidants ◽

10.3390/antiox10050779 ◽

2021 ◽

Vol 10 (5) ◽

pp. 779

Author(s):

Daria S. Kostyunina ◽

Paul McLoughlin

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Arterial Hypertension ◽

Arterial Hypertension ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Sex Chromosomes ◽

Bone Morphogenetic Protein 2 ◽

Sex Dimorphism ◽

Pulmonary Arterial ◽

The Impact

Pulmonary hypertension (PH) is a condition characterised by an abnormal elevation of pulmonary artery pressure caused by an increased pulmonary vascular resistance, frequently leading to right ventricular failure and reduced survival. Marked sexual dimorphism is observed in patients with pulmonary arterial hypertension, a form of pulmonary hypertension with a particularly severe clinical course. The incidence in females is 2–4 times greater than in males, although the disease is less severe in females. We review the contribution of the sex chromosomes to this sex dimorphism highlighting the impact of proteins, microRNAs and long non-coding RNAs encoded on the X and Y chromosomes. These genes are centrally involved in the cellular pathways that cause increased pulmonary vascular resistance including the production of reactive oxygen species, altered metabolism, apoptosis, inflammation, vasoconstriction and vascular remodelling. The interaction with genetic mutations on autosomal genes that cause heritable pulmonary arterial hypertension such as bone morphogenetic protein 2 (BMPR2) are examined. The mechanisms that can lead to differences in the expression of genes located on the X chromosomes between females and males are also reviewed. A better understanding of the mechanisms of sex dimorphism in this disease will contribute to the development of more effective therapies for both women and men.

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