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Circulation Research May 2019
Topics: Animals; Dissent and Disputes; History, 17th Century; Humans; Italy; Lung; Pathology, Clinical; Pulmonary Circulation
PubMed: 31071004
DOI: 10.1161/CIRCRESAHA.119.314936 -
Archivos de Cardiologia de Mexico 2022
Topics: Heart; History, Medieval; Pulmonary Circulation
PubMed: 34987236
DOI: 10.24875/ACM.M21000080 -
Anesthesiology Clinics Jun 2017Pulmonary hypertension (PH) is a complex disease process of the pulmonary vasculature system characterized by elevated pulmonary arterial pressures. Patients with PH are... (Review)
Review
Pulmonary hypertension (PH) is a complex disease process of the pulmonary vasculature system characterized by elevated pulmonary arterial pressures. Patients with PH are at increased risk for morbidity and mortality, including intraoperatively and postoperatively. Appreciation by the clinical anesthesiologist of the pathophysiology of PH is warranted. Careful and meticulous strategy using appropriate anesthetic medications, pulmonary vasodilator and inotropic agents, and careful fluid management all increase the likelihood of the best possible outcome in this challenging patient population.
Topics: Anesthesia; Humans; Hypertension, Pulmonary; Muscle, Smooth, Vascular; Nitric Oxide; Pulmonary Circulation; Vascular Resistance; Vasodilator Agents
PubMed: 28526144
DOI: 10.1016/j.anclin.2017.01.008 -
American Heart Journal Oct 2016Pulmonary hypertension is usually related to obstruction of pulmonary blood flow at the level of the pulmonary arteries (eg, pulmonary embolus), pulmonary arterioles... (Review)
Review
Pulmonary hypertension is usually related to obstruction of pulmonary blood flow at the level of the pulmonary arteries (eg, pulmonary embolus), pulmonary arterioles (idiopathic pulmonary hypertension), pulmonary veins (pulmonary venoocclusive disease) or mitral valve (mitral stenosis and regurgitation). Pulmonary hypertension is also observed in heart failure due to left ventricle myocardial diseases regardless of the ejection fraction. Pulmonary hypertension is often regarded as a passive response to the obstruction to pulmonary flow. We review established fluid dynamics and physiology and discuss the mechanisms underlying pulmonary hypertension. The important role that the right ventricle plays in the development and maintenance of pulmonary hypertension is discussed. We use principles of thermodynamics and discuss a potential common mechanism for a number of disease states, including pulmonary edema, through adding pressure energy to the pulmonary circulation.
Topics: Humans; Hydrodynamics; Hypertension, Pulmonary; Pulmonary Circulation; Thermodynamics
PubMed: 27659877
DOI: 10.1016/j.ahj.2016.07.003 -
Current Opinion in Pulmonary Medicine Sep 2021While there has been a longstanding interest in metabolic disease in pulmonary hypertension, publications in the last several years have translated basic science... (Review)
Review
PURPOSE OF REVIEW
While there has been a longstanding interest in metabolic disease in pulmonary hypertension, publications in the last several years have translated basic science findings to human disease and even led to recently published studies of metabolic therapy in pulmonary arterial hypertension that are discussed here.
RECENT FINDINGS
Progress has been made in four key areas including mechanisms of insulin resistance in pulmonary arterial hypertension, the role of obesity in pulmonary vascular disease, novel clinical trials targeting metabolism in pulmonary hypertension, and the role of metabolism in chronic thromboembolic pulmonary hypertension.
SUMMARY
: Insulin resistance in pulmonary arterial hypertension is primarily in the lipid axis. There are systemic manifestations of insulin resistance including right ventricular lipotoxicity. Obesity is associated with elevation of right ventricular systolic pressure even in a healthy population and therapies in pulmonary arterial hypertension that target metabolism hold promise for improving exercise, right ventricular function, and visceral adiposity. Finally, there are emerging data that chronic thromboembolic pulmonary hypertension is similarly characterized by metabolic alterations, though the specific metabolites may be different from pulmonary arterial hypertension.
Topics: Heart Ventricles; Humans; Hypertension, Pulmonary; Pulmonary Arterial Hypertension; Pulmonary Artery; Pulmonary Circulation; Ventricular Function, Right
PubMed: 34127621
DOI: 10.1097/MCP.0000000000000794 -
Seminars in Respiratory and Critical... Dec 2023The right ventricle plays a pivotal role in patients with pulmonary hypertension (PH). Its adaptation to pressure overload determines a patient's functional status as... (Review)
Review
The right ventricle plays a pivotal role in patients with pulmonary hypertension (PH). Its adaptation to pressure overload determines a patient's functional status as well as survival. In a healthy situation, the right ventricle is part of a low pressure, high compliance system. It is built to accommodate changes in preload, but not very well suited for dealing with pressure overload. In PH, right ventricular (RV) contractility must increase to maintain cardiac output. In other words, the balance between the degree of RV contractility and afterload determines stroke volume. Hypertrophy is one of the major hallmarks of RV adaptation, but it may cause stiffening of the ventricle in addition to intrinsic changes to the RV myocardium. Ventricular filling becomes more difficult for which the right atrium tries to compensate through increased stroke work. Interaction of RV diastolic stiffness and right atrial (RA) function determines RV filling, but also causes vena cava backflow. Assessment of RV and RA function is critical in the evaluation of patient status. In recent guidelines, this is acknowledged by incorporating additional RV parameters in the risk stratification in PH. Several conventional parameters of RV and RA function have been part of risk stratification for many years. Understanding the pathophysiology of RV failure and the interactions with the pulmonary circulation and right atrium requires consideration of the unique RV anatomy. This review will therefore describe normal RV structure and function and changes that occur during adaptation to increased afterload. Consequences of a failing right ventricle and its implications for RA function will be discussed. Subsequently, we will describe RV and RA assessment in clinical practice.
Topics: Humans; Hypertension, Pulmonary; Heart Ventricles; Pulmonary Circulation; Heart Failure; Stroke Volume; Ventricular Function, Right; Ventricular Dysfunction, Right
PubMed: 37487527
DOI: 10.1055/s-0043-1770117 -
The Canadian Journal of Cardiology Apr 2015Pulmonary arterial hypertension (PAH) is characterized by remodelling of pulmonary arteries caused by a proliferation/apoptosis imbalance within the vascular wall. This... (Review)
Review
Pulmonary arterial hypertension (PAH) is characterized by remodelling of pulmonary arteries caused by a proliferation/apoptosis imbalance within the vascular wall. This pathological phenotype seems to be triggered by different environmental stress and injury events such as increased inflammation, DNA damage, and epigenetic deregulation. It appears that one of the first hit to occur is endothelial cells (ECs) injury and apoptosis, which leads to paracrine signalling to other ECs, pulmonary artery smooth muscle cells (PASMCs), and fibroblasts. These signals promote a phenotypic change of surviving ECs by disturbing different signalling pathways leading to sustained vasoconstriction, proproliferative and antiapoptotic phenotype, deregulated angiogenesis, and formation of plexiform lesions. EC signalling also recruits proinflammatory cells, leading to pulmonary infiltration of lymphocytes, macrophages, and dendritic cells, sustaining the inflammatory environment and autoimmune response. Finally, EC signalling promotes proliferative and antiapoptotic PAH-PASMC phenotypes, which acquire migratory capacities, resulting in increased vascular wall thickness and muscularization of small pulmonary arterioles. Adaptation and remodelling of pulmonary circulation also involves epigenetic components, such as microRNA deregulation, DNA methylation, and histone modification. This review will focus on the different cellular and epigenetic aspects including EC stress response, molecular mechanisms contributing to PAH-PASMC and PAEC proliferation and resistance to apoptosis, as well as epigenetic control involved in adaptation and remodelling of the pulmonary circulation in PAH.
Topics: Adaptation, Physiological; Humans; Hypertension, Pulmonary; Pulmonary Artery; Pulmonary Circulation; Pulmonary Wedge Pressure; Vascular Remodeling
PubMed: 25630876
DOI: 10.1016/j.cjca.2014.10.023 -
Heart Failure Clinics Jul 2018The most common cause of right heart failure is increased afterload caused by pulmonary hypertension. Right ventricular function adaptation to increased afterload is... (Review)
Review
The most common cause of right heart failure is increased afterload caused by pulmonary hypertension. Right ventricular function adaptation to increased afterload is basically systolic, with secondary increase in dimensions and systemic congestion. Increased right ventricular dimensions and decreased ejection fraction are associated with a decreased survival in severe pulmonary hypertension. Targeted therapies titrated to reverse the right ventricular remodeling dimensions improve survival in severe pulmonary hypertension.
Topics: Adaptation, Physiological; Heart Failure; Heart Ventricles; Humans; Hypertension, Pulmonary; Pulmonary Circulation; Ventricular Function, Right; Ventricular Remodeling
PubMed: 29966623
DOI: 10.1016/j.hfc.2018.02.001 -
The Journal of Pediatrics Jul 2023
Topics: Humans; Pulmonary Circulation; Oxygen; Heart Septal Defects, Atrial
PubMed: 37028753
DOI: 10.1016/j.jpeds.2023.113413 -
Swiss Medical Weekly 2015Elevation of the mean pulmonary arterial pressure to ≥25 mm Hg within the low-pressure system of the pulmonary circulation is defined as pulmonary hypertension.... (Review)
Review
Elevation of the mean pulmonary arterial pressure to ≥25 mm Hg within the low-pressure system of the pulmonary circulation is defined as pulmonary hypertension. Pulmonary hypertension may be the consequence of various clinical and pathophysiological entities. Many of these conditions, however, result in a final common pathway of pathogenesis. This pathway is characterised by the triad of excessive vasoconstriction, microthrombosis and remodelling of pulmonary arteries. Remodelling is arguably the most important factor: its complex pathogenesis is not completely understood and no specific treatment directly targets vascular remodelling. This article aims to review the current understanding of the pathogenesis of pulmonary hypertension and to give insights in future developments in this evolving field.
Topics: Humans; Hypertension, Pulmonary; Pulmonary Artery; Pulmonary Circulation; Vascular Remodeling; Vasoconstriction
PubMed: 26479975
DOI: 10.4414/smw.2015.14202