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Healthcare (Basel, Switzerland) Feb 2024Superficial venous thrombosis (SVT), an inflammatory-thrombotic process of a superficial vein, is a relatively common event that may have several different underlying... (Review)
Review
Superficial venous thrombosis (SVT), an inflammatory-thrombotic process of a superficial vein, is a relatively common event that may have several different underlying causes. This phenomenon has been generally considered benign, and its prevalence has been historically underestimated; the estimated incidence ranges from about 0.3 to 1.5 event per 1000 person-years, while the prevalence is approximately 3 to 11%, with different reports depending on the population studied. However, such pathology is not free of complications; indeed, it could extend to the deep circulation and embolize to pulmonary circulation. For this reason, an ultrasound examination is recommended to evaluate the extension of SVT and to exclude the involvement of deep circulation. Also, SVT may be costly, especially in the case of recurrence. Therefore, accurate management is necessary to prevent sequelae and costs related to the disease. This review aims to analyse the epidemiology of SVT, its complications, optimal medical treatment, and open questions with future perspectives.
PubMed: 38391875
DOI: 10.3390/healthcare12040500 -
American Journal of Physiology. Lung... Aug 2020In the last few months, the number of cases of a new coronavirus-related disease (COVID-19) rose exponentially, reaching the status of a pandemic. Interestingly, early... (Review)
Review
In the last few months, the number of cases of a new coronavirus-related disease (COVID-19) rose exponentially, reaching the status of a pandemic. Interestingly, early imaging studies documented that pulmonary vascular thickening was specifically associated with COVID-19 pneumonia, implying a potential tropism of the virus for the pulmonary vasculature. Moreover, SARS-CoV-2 infection is associated with inflammation, hypoxia, oxidative stress, mitochondrial dysfunction, DNA damage, and lung coagulopathy promoting endothelial dysfunction and microthrombosis. These features are strikingly similar to what is seen in pulmonary vascular diseases. Although the consequences of COVID-19 on the pulmonary circulation remain to be explored, several viruses have been previously thought to be involved in the development of pulmonary vascular diseases. Patients with preexisting pulmonary vascular diseases also appear at increased risk of morbidity and mortality. The present article reviews the molecular factors shared by coronavirus infection and pulmonary vasculature defects, and the clinical relevance of pulmonary vascular alterations in the context of COVID-19.
Topics: Angiotensin-Converting Enzyme 2; Betacoronavirus; COVID-19; Coronavirus Infections; Cytokines; DNA Damage; Heart Injuries; Host Microbial Interactions; Humans; Hypoxia; Inflammation Mediators; Lung; Lung Diseases; Mitochondria; Myocardium; Oxidative Stress; Pandemics; Peptidyl-Dipeptidase A; Pneumonia, Viral; Pulmonary Circulation; Pulmonary Embolism; Receptors, Virus; Risk Factors; SARS-CoV-2; Vasculitis
PubMed: 32551862
DOI: 10.1152/ajplung.00195.2020 -
Journal of Biomechanical Engineering Feb 2022Pulmonary hypertension (PH) is a progressive disease that is characterized by a gradual increase in both resistive and reactive pulmonary arterial (PA) impedance....
Pulmonary hypertension (PH) is a progressive disease that is characterized by a gradual increase in both resistive and reactive pulmonary arterial (PA) impedance. Previous studies in a rodent model of PH have shown that reducing the hemodynamic load in the left lung (by banding the left PA) reverses this remodeling phenomenon. However, banding a single side of the pulmonary circulation is not a viable clinical option, so-using in silico modeling-we evaluated if the banding effect can be recreated by replacing the proximal vasculature with a compliant synthetic PA. We developed a computational model of the pulmonary circulation by combining a one-dimensional model of the proximal vasculature with a zero-dimensional line transmission model to the 12th generation. Using this model, we performed four simulations: (1) Control; (2) PH; (3) PH with a stenosis in the left PA; and (4) PH with proximal vessel compliance returned to Control levels. Simulations revealed that vascular changes associated with PH result in an increase in pulse pressure (PP), maximum pressure (Pmax), maximum wall shear stress (WSS), and maximum circumferential stress (σθθ) relative to controls, in the distal circulation. Banding the left PA reduced these measurements of hemodynamic stress in the left lung, but increases them in the right lung. Furthermore, left PA banding increased reactive PA impedance. However, returning the proximal PA compliance to Control levels simultaneously decreased all measures of hemodynamic stress in both lungs, and returned reactive PA impedance to normal levels. In conclusion, if future in vivo studies support the idea of hemodynamic unloading as an effective therapy for PH, this can be surgically achieved by replacing the proximal PA with a compliant prosthesis, and it will have the added benefit of reducing reactive right ventricular afterload.
Topics: Hemodynamics; Humans; Hypertension, Pulmonary; Pulmonary Artery; Pulmonary Circulation; Vascular Resistance
PubMed: 34251418
DOI: 10.1115/1.4051719 -
The Journal of Physiology Jan 2021The distribution of pulmonary perfusion is affected by gravity, vascular branching structure and active regulatory mechanisms, which may be disrupted by cardiopulmonary...
KEY POINTS
The distribution of pulmonary perfusion is affected by gravity, vascular branching structure and active regulatory mechanisms, which may be disrupted by cardiopulmonary disease, but this is not well studied, particularly in rare conditions. We evaluated pulmonary perfusion in patients who had undergone Fontan procedure, patients with pulmonary arterial hypertension (PAH) and two groups of controls using a proton magnetic resonance imaging technique, arterial spin labelling to measure perfusion. Heterogeneity was assessed by the relative dispersion (SD/mean) and gravitational gradients. Gravitational gradients were similar between all groups, but heterogeneity was significantly increased in both patient groups compared to controls and persisted after removing contributions from large blood vessels and gravitational gradients. Patients with Fontan physiology and patients with PAH have increased pulmonary perfusion heterogeneity that is not explainable by differences in mean perfusion, gravitational gradients, or large vessel anatomy. This probably reflects vascular remodelling in PAH and possibly in Fontan physiology.
ABSTRACT
Many factors affect the distribution of pulmonary perfusion, which may be disrupted by cardiopulmonary disease, but this is not well studied, particularly in rare conditions. An example is following the Fontan procedure, where pulmonary perfusion is passive, and heterogeneity may be increased because of the underlying pathophysiology leading to Fontan palliation, remodelling, or increased gravitational gradients from low flow. Another is pulmonary arterial hypertension (PAH), where gravitational gradients may be reduced secondary to high pressures, but remodelling may increase perfusion heterogeneity. We evaluated regional pulmonary perfusion in Fontan patients (n = 5), healthy young controls (Fontan control, n = 5), patients with PAH (n = 6) and healthy older controls (PAH control) using proton magnetic resonance imaging. Regional perfusion was measured using arterial spin labelling. Heterogeneity was assessed by the relative dispersion (SD/mean) and gravitational gradients. Mean perfusion was similar (Fontan = 2.50 ± 1.02 ml min ml ; Fontan control = 3.09 ± 0.58, PAH = 3.63 ± 1.95; PAH control = 3.98 ± 0.91, P = 0.26), and the slopes of gravitational gradients were not different (Fontan = -0.23 ± 0.09 ml min ml cm ; Fontan control = -0.29 ± 0.23, PAH = -0.27 ± 0.09, PAH control = -0.25 ± 0.18, P = 0.91) between groups. Perfusion relative dispersion was greater in both Fontan and PAH than controls (Fontan = 1.46 ± 0.18; Fontan control = 0.99 ± 0.21, P = 0.005; PAH = 1.22 ± 0.27, PAH control = 0.91 ± 0.12, P = 0.02) but similar between patient groups (P = 0.13). These findings persisted after removing contributions from large blood vessels and gravitational gradients (all P < 0.05). We conclude that patients with Fontan physiology and PAH have increased pulmonary perfusion heterogeneity that is not explained by differences in mean perfusion, gravitational gradients, or large vessel anatomy. This probably reflects the effects of remodelling in PAH and possibly in Fontan physiology.
Topics: Fontan Procedure; Humans; Lung; Perfusion; Pulmonary Arterial Hypertension; Pulmonary Circulation
PubMed: 33026102
DOI: 10.1113/JP280348 -
Journal of Cardiothoracic Surgery Oct 2021Pulmonary arterial hypertension is a type of malignant pulmonary vascular disease, which is mainly caused by the increase of pulmonary vascular resistance due to the... (Review)
Review
Pulmonary arterial hypertension is a type of malignant pulmonary vascular disease, which is mainly caused by the increase of pulmonary vascular resistance due to the pathological changes of the pulmonary arteriole itself, which eventually leads to right heart failure and death. As one of the diagnostic indicators of hemodynamics, pulmonary vascular resistance plays an irreplaceable role in the pathophysiology, diagnosis and treatment of pulmonary arterial hypertension. It provides more references for the evaluation of pulmonary arterial hypertension patients. This article summarizes the clinical application of pulmonary vascular resistance in patients with pulmonary arterial hypertension.
Topics: Familial Primary Pulmonary Hypertension; Hemodynamics; Humans; Hypertension, Pulmonary; Pulmonary Arterial Hypertension; Vascular Resistance
PubMed: 34670595
DOI: 10.1186/s13019-021-01696-4 -
International Journal of Environmental... Aug 2019Obstructive sleep apnea (OSA) causes many systemic disorders via mechanisms related to sympathetic nerve activation, systemic inflammation, and oxidative stress. OSA... (Review)
Review
Obstructive sleep apnea (OSA) causes many systemic disorders via mechanisms related to sympathetic nerve activation, systemic inflammation, and oxidative stress. OSA typically shows repeated sleep apnea followed by hyperventilation, which results in intermittent hypoxia (IH). IH is associated with an increase in sympathetic activity, which is a well-known pathophysiological mechanism in hypertension and insulin resistance. In this review, we show the basic and clinical significance of IH from the viewpoint of not only systemic regulatory mechanisms focusing on pulmonary circulation, but also cellular mechanisms causing lifestyle-related diseases. First, we demonstrate how IH influences pulmonary circulation to cause pulmonary hypertension during sleep in association with sleep state-specific change in OSA. We also clarify how nocturnal IH activates circulating monocytes to accelerate the infiltration ability to vascular wall in OSA. Finally, the effects of IH on insulin secretion and insulin resistance are elucidated by using an in vitro chamber system that can mimic and manipulate IH. The obtained data implies that glucose-induced insulin secretion (GIS) in pancreatic β cells is significantly attenuated by IH, and that IH increases selenoprotein P, which is one of the hepatokines, as well as TNF-α, CCL-2, and resistin, members of adipokines, to induce insulin resistance via direct cellular mechanisms. Clinical and experimental findings concerning IH give us productive new knowledge of how lifestyle-related diseases and pulmonary hypertension develop during sleep.
Topics: Adult; Aged; Aged, 80 and over; Animals; Autonomic Nervous System Diseases; Cohort Studies; Cross-Sectional Studies; Female; Humans; Hypoxia; Male; Middle Aged; Sleep Apnea, Obstructive; Vascular Diseases
PubMed: 31455007
DOI: 10.3390/ijerph16173101 -
Respiratory Medicine Oct 2023As an important place of material exchange, the homeostasis of the pulmonary circulation environment and function lays an essential foundation for the normal execution...
BACKGROUND
As an important place of material exchange, the homeostasis of the pulmonary circulation environment and function lays an essential foundation for the normal execution of various physiological functions of the body. Small metabolic molecules in the circulation can reflect the corresponding state of the pulmonary circulation.
METHODS
We enrolled patients with Patent Foramen Ovale and obtained blood from the pulmonary arteries and veins through heart catheterization. UPLC-MS based untargeted metabolomics was used to compare the changes and metabolic differences of plasma between pulmonary vein and pulmonary artery.
RESULTS
The plasma metabolomics revealed that pulmonary artery had a different metabolomic profile compared to venous. 1060 metabolites were identified, and 61 metabolites were differential metabolites. Purine, Amino acids, Nicotinamide, Tetradecanedioic acid and Bile acid were the most markedly.
CONCLUSION
The differential metabolites are mostly related to immune inflammation and damage repaired. It is suggested that the pulmonary circulation is always in a steady state of injury and repair while pathological changes may be triggered when the homeostasis is broken. These changes play an important role in revealing the development process and etiology of lung homeostasis and related diseases. Relevant metabolites can be used as potential targets for further study of pulmonary circulation homeostasis.
PubMed: 37494975
DOI: 10.1016/j.rmed.2023.107369 -
Pediatric Cardiology Oct 2023The fetal pulmonary circulation represents less than 25% of the fetal cardiac output. In comparison with the pulmonary arteries, studies on pulmonary veins are few and... (Review)
Review
The fetal pulmonary circulation represents less than 25% of the fetal cardiac output. In comparison with the pulmonary arteries, studies on pulmonary veins are few and limited, and many questions remain to be answered. The literature reports that pulmonary veins play an important role in regulating vascular flow, forming an active segment of the pulmonary circulation. The development of more sophisticated ultrasonography technology has allowed the investigation of the extraparenchymal pulmonary veins and their waveform. The recognition of the pulmonary vein anatomy in echocardiography is important for the diagnosis of anomalous pulmonary venous connections, with a significant impact on prognosis. On the other hand, the identification of the normal pulmonary vein waveform seems to be a reliable way to study left heart function, with potential applicability in fetal and maternal pathology. Thus, the goal of this narrative review was to provide a clinically oriented perspective of the available literature on this topic.
Topics: Pregnancy; Female; Humans; Pulmonary Veins; Ultrasonography, Prenatal; Fetus; Echocardiography; Ultrasonography, Doppler
PubMed: 37505268
DOI: 10.1007/s00246-023-03244-4 -
Respiratory Research Feb 2021Chronic obstructive pulmonary disease (COPD) is one of the most common chronic respiratory diseases with high morbidity and mortality. It has become the fifth most... (Review)
Review
Chronic obstructive pulmonary disease (COPD) is one of the most common chronic respiratory diseases with high morbidity and mortality. It has become the fifth most burdened and the third most deadly disease in the global economy and increases year by year. The prevention and treatment of COPD are urgent. Smoking is the main and most common risk factor for COPD. Cigarette smoke (CS) contains a large number of toxic substances, can cause a series of changes in the trachea, lung tissue, pulmonary blood vessels, and promotes the occurrence and development of COPD. In recent years, the development of epigenetics and molecular biology have provided new guidance for revealing the pathogenesis, diagnosis, and treatment of diseases. The latest research indicates that pulmonary vascular endothelial cell apoptosis initiates and participates in the pathogenesis of COPD. In this review, we summarize the current research on the epigenetic mechanisms and molecular biology of CS-induced pulmonary vascular endothelial cell apoptosis in COPD, providing a new research direction for pathogenesis of COPD and a new target for the diagnosis, treatment, and prevention of COPD.
Topics: Animals; Apoptosis; Cigarette Smoking; DNA Methylation; Endothelium, Vascular; Epigenesis, Genetic; Humans; Pulmonary Circulation; Pulmonary Disease, Chronic Obstructive; Tobacco Smoke Pollution
PubMed: 33546691
DOI: 10.1186/s12931-021-01630-1 -
Diagnostics (Basel, Switzerland) Jul 2020The Coronavirus Disease of 2019 (COVID-19) has supposed a global health emergency affecting millions of people, with particular severity in the elderly and patients with... (Review)
Review
The Coronavirus Disease of 2019 (COVID-19) has supposed a global health emergency affecting millions of people, with particular severity in the elderly and patients with previous comorbidities, especially those with cardiovascular disease. Patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) could represent an especially vulnerable population because of the high mortality rates reported for respiratory infections. However, the number of COVID-19 cases reported among PAH and CTEPH patients is surprisingly low. Furthermore, the clinical picture that has been described in these patients is far from the severity that experts would expect. Endothelial dysfunction is a common feature between patients with PAH/CTEPH and COVID-19, leading to ventilation/perfusion mismatch, vasoconstriction, thrombosis and inflammation. In this picture, the angiotensin-converting enzyme 2 plays an essential role, being directly involved in the pathophysiology of both clinical entities. Some of these common characteristics could explain the good adaptation of PAH and CTEPH patients to COVID-19, who could also have obtained a benefit from the disease's specific treatments (anticoagulant and pulmonary vasodilators), probably due to its protective effect on the endothelium. Additionally, these common features could also lead to PAH/CTEPH as a potential sequelae of COVID-19. Throughout this comprehensive review, we describe the similarities and differences between both conditions and the possible pathophysiological and therapeutic-based mechanisms leading to the low incidence and severity of COVID-19 reported in PAH/CTEPH patients to date. Nevertheless, international registries should look carefully into this population for better understanding and management.
PubMed: 32752129
DOI: 10.3390/diagnostics10080548