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Thrombosis Research Jun 2021Pulmonary infarction results from occlusion of the distal pulmonary arteries leading to ischemia, hemorrhage and ultimately necrosis of the lung parenchyma. It is most... (Review)
Review
Pulmonary infarction results from occlusion of the distal pulmonary arteries leading to ischemia, hemorrhage and ultimately necrosis of the lung parenchyma. It is most commonly caused by acute pulmonary embolism (PE), with a reported incidence of around 30%. Following an occlusion of the pulmonary artery, the bronchial arteries are recruited as primary source of perfusion of the pulmonary capillaries. The relatively higher blood pressure in the bronchial circulation causes an increase in the capillary blood flow, leading to extravasation of erythrocytes (i.e. alveolar hemorrhage). If this hemorrhage cannot be resorbed, it results in tissue necrosis and infarction. Different definitions of pulmonary infarction are used in literature (clinical, radiological and histological), although the diagnosis is nowadays mostly based on radiological characteristics. Notably, the infarcted area is only replaced by a fibrotic scar over a period of months. Hence and formally, the diagnosis of pulmonary infarction cannot be confirmed upon diagnosis of acute PE. Little is known of the impact and relevance of pulmonary infarction in acute PE, and whether specific management strategies should be applied to prevent and/or treat complications such as pain, pneumonia or post-PE syndrome. In this review we will summarize current knowledge on the pathophysiology, epidemiology, diagnosis and prognosis of pulmonary infarction in the setting of acute PE. We highlight the need for dedicated studies to overcome the current knowledge gaps.
Topics: Acute Disease; Humans; Lung; Pulmonary Artery; Pulmonary Embolism; Pulmonary Infarction
PubMed: 33862471
DOI: 10.1016/j.thromres.2021.03.022 -
Vascular Health and Risk Management 2021The causes and mechanisms of increased cardiac troponin T and I (cTnT and cTnI) concentrations are numerous and are not limited to acute myocardial infarction (AMI)... (Review)
Review
The Main Causes and Mechanisms of Increase in Cardiac Troponin Concentrations Other Than Acute Myocardial Infarction (Part 1): Physical Exertion, Inflammatory Heart Disease, Pulmonary Embolism, Renal Failure, Sepsis.
The causes and mechanisms of increased cardiac troponin T and I (cTnT and cTnI) concentrations are numerous and are not limited to acute myocardial infarction (AMI) (ischemic necrosis of cardiac myocytes). Any type of reversible or irreversible cardiomyocyte injury can result in elevated serum cTnT and cTnI levels. Researchers and practitioners involved in the diagnosis and treatment of cardiovascular disease, including AMI, should know the key causes and mechanisms of elevated serum cTnT and cTnI levels. This will allow to reduce or completely avoid diagnostic errors and help to choose the most correct tactics for further patient management. The purpose of this article is to discuss the main causes and mechanisms of increase in cardiac troponins concentrations in frequently occurring physiological (physical exertion, psycho-emotional stress) and pathological conditions (inflammatory heart disease, pulmonary embolism, chronic renal failure and sepsis (systemic inflammatory response)) not related to myocardial infarction.
Topics: Acute Disease; Biomarkers; Humans; Myocardial Infarction; Physical Exertion; Pulmonary Embolism; Pulmonary Heart Disease; Renal Insufficiency; Sepsis; Troponin; Troponin I; Troponin T
PubMed: 34584417
DOI: 10.2147/VHRM.S327661 -
Comprehensive Physiology Jan 2023Lung transplant is a treatment option for patients with end-stage lung diseases; however, survival outcomes continue to be inferior when compared to other solid organs.... (Review)
Review
Lung transplant is a treatment option for patients with end-stage lung diseases; however, survival outcomes continue to be inferior when compared to other solid organs. We review the several anatomic and physiologic changes that result from lung transplantation surgery, and their role in the pathophysiology of common complications encountered by lung recipients. The loss of bronchial circulation into the allograft after transplant surgery results in ischemia-related changes in the bronchial artery territory of the allograft. We discuss the role of bronchopulmonary anastomosis in blood circulation in the allograft posttransplant. We review commonly encountered complications related to loss of bronchial circulation such as allograft airway ischemia, necrosis, anastomotic dehiscence, mucociliary dysfunction, and bronchial stenosis. Loss of dual circulation to the lung also increases the risk of pulmonary infarction with acute pulmonary embolism. The loss of lymphatic drainage during transplant surgery also impairs the management of allograft interstitial fluid, resulting in pulmonary edema and early pleural effusion. We discuss the role of lymphatic drainage in primary graft dysfunction. Besides, we review the association of late posttransplant pleural effusion with complications such as acute rejection. We then review the impact of loss of afferent and efferent innervation from the allograft on control of breathing, as well as lung protective reflexes. We conclude with discussion about pulmonary function testing, allograft monitoring with spirometry, and classification of chronic lung allograft dysfunction phenotypes based on total lung capacity measurements. We also review factors limiting physical exercise capacity after lung transplantation, especially impairment of muscle metabolism. © 2023 American Physiological Society. Compr Physiol 13:4269-4293, 2023.
Topics: Humans; Lung; Lung Transplantation; Bronchial Arteries; Ischemia; Pleural Effusion
PubMed: 36715279
DOI: 10.1002/cphy.c220008 -
Expert Review of Respiratory Medicine 2023Given the heterogeneity of predisposing factors associated with pulmonary infarction (PI) and the lack of clinically relevant outcomes among patients with acute...
BACKGROUND
Given the heterogeneity of predisposing factors associated with pulmonary infarction (PI) and the lack of clinically relevant outcomes among patients with acute pulmonary embolism (PE) complicated by PI, further investigation is required.
METHODS
Retrospective study of patients with central PE in an 11-year period. Data were stratified according to the diagnosis of PI. Multivariable logistic regression analysis was used to analyze factors associated with PI development and determine if PI was associated with severe hypoxemic respiratory failure and mechanical ventilation use.
RESULTS
Of 645 patients with central PE, 24% ( = 156) had PI. After adjusting for demographics, comorbidities, and clinical features on admission, only age (OR 0.98, CI 0.96-0.99; = 0.008) was independently associated with PI. Regarding outcomes, 35% ( = 55) had severe hypoxemic respiratory failure, and 19% ( = 29) required mechanical ventilation. After adjusting for demographics, PE severity, and right ventricular dysfunction, PI was independently associated with severe hypoxemic respiratory failure (OR 1.78; CI 1.18-2.69, = 0.005) and mechanical ventilation (OR 1.92; CI 1.14-3.22, = 0.013).
CONCLUSIONS
Aging is a protective factor against PI. In acute central PE, subjects with PI had higher odds of developing severe hypoxemic respiratory failure and requiring mechanical ventilation.
Topics: Humans; Retrospective Studies; Pulmonary Infarction; Respiratory Insufficiency; Pulmonary Embolism; Respiration, Artificial; Acute Disease
PubMed: 37750314
DOI: 10.1080/17476348.2023.2263359 -
The New England Journal of Medicine Nov 2021
Topics: Adult; Computed Tomography Angiography; Female; Humans; Lung; Pulmonary Artery; Pulmonary Embolism; Pulmonary Infarction; Radiography; Recurrence
PubMed: 34714611
DOI: 10.1056/NEJMicm2109756 -
European Respiratory Review : An... Jun 2020COPD is strongly associated with cardiovascular disease, in particular acute myocardial infarction (AMI). Besides shared risk factors, COPD-related factors, such as... (Review)
Review
COPD is strongly associated with cardiovascular disease, in particular acute myocardial infarction (AMI). Besides shared risk factors, COPD-related factors, such as systemic inflammation and hypoxia, underlie the pathophysiological interaction between COPD and AMI. The prevalence of COPD amongst AMI populations ranges from 7% to 30%, which is possibly even an underestimation due to underdiagnoses of COPD in general. Following the acute event, patients with COPD have an increased risk of mortality, heart failure and arrhythmias during follow-up. Adequate risk stratification can be performed using various imaging techniques, evaluating cardiac size and function after AMI. Conventional imaging techniques such as echocardiography and cardiac magnetic resonance imaging have already indicated impaired cardiac function in patients with COPD without known cardiovascular disease. Advanced imaging techniques such as speckle-tracking echocardiography and T1 mapping could provide more insight into cardiac structure and function after AMI and have proven to be of prognostic value. Future research is required to better understand the impact of AMI on patients with COPD in order to provide effective secondary prevention. The present article summarises the current knowledge on the pathophysiologic factors involved in the interaction between COPD and AMI, the prevalence and outcomes of AMI in patients with COPD and the role of imaging in the acute phase and risk stratification after AMI in patients with COPD.
Topics: Humans; Myocardial Infarction; Prognosis; Pulmonary Disease, Chronic Obstructive; Risk Assessment; Risk Factors; Secondary Prevention
PubMed: 32581139
DOI: 10.1183/16000617.0139-2019 -
European Journal of Radiology Dec 2014The impact of absent pulmonary arterial and venous flow on the pulmonary parenchyma depends on a host of factors. These include location of the occlusive insult, the... (Review)
Review
The impact of absent pulmonary arterial and venous flow on the pulmonary parenchyma depends on a host of factors. These include location of the occlusive insult, the speed at which the occlusion develops and the ability of the normal dual arterial supply to compensate through increased bronchial arterial flow. Pulmonary infarction occurs when oxygenation is cut off secondary to sudden occlusion with lack of recruitment of the dual supply arterial system. Thromboembolic disease is the commonest cause of such an insult but a whole range of disease processes intrinsic and extrinsic to the pulmonary arterial and venous lumen may also result in infarcts. Recognition of the presence of infarction can be challenging as imaging manifestations often differ from the classically described wedge shaped defect and a number of weighty causes need consideration. This review highlights aetiologies and imaging appearances of pulmonary infarction, utilising cases to illustrate the essential role of a multimodality imaging approach in order to arrive at the appropriate diagnosis.
Topics: Humans; Multimodal Imaging; Pulmonary Infarction
PubMed: 25241050
DOI: 10.1016/j.ejrad.2014.07.016 -
Thrombosis Research Jun 2023Pulmonary infarction (PI) is relatively common in pulmonary embolism (PE). The association between PI and persistent symptoms or adverse events is largely unknown.
BACKGROUND
Pulmonary infarction (PI) is relatively common in pulmonary embolism (PE). The association between PI and persistent symptoms or adverse events is largely unknown.
AIM
To evaluate the predictive value of radiological PI signs at acute PE diagnosis on 3-month outcomes.
METHODS
We studied a convenience cohort with computed tomography pulmonary angiography (CTPA)-confirmed PE for whom extensive 3-month follow-up data were available. The CTPAs were re-evaluated for signs of suspected PI. Associations with presenting symptoms, adverse events (recurrent thrombosis, PE-related readmission and mortality) and self-reported persistent symptoms (dyspnea, pain and post-PE functional impairment) at 3-month follow-up were investigated using univariate Cox regression analysis.
RESULTS
At re-evaluation of the CTPAs, 57 of 99 patients (58 %) had suspected PI, comprising a median of 1 % (IQR 1-3) of total lung parenchyma. Patients with suspected PI more often presented with hemoptysis (11 % vs. 0 %) and pleural pain (OR 2.7, 95%CI 1.2-6.2), and with more proximal PE on CTPA (OR 1.6, 95%CI 1.1-2.4) than patients without suspected PI. There was no association with adverse events, persistent dyspnea or pain at 3-month follow-up, but signs of PI predicted more functional impairment (OR 3.03, 95%CI 1.01-9.13). Sensitivity analysis with the largest infarctions (upper tertile of infarction volume) yielded similar results.
CONCLUSIONS
PE patients radiologically suspected of PI had a different clinical presentation than patients without those signs and reported more functional limitations after 3 months of follow-up, a finding that could guide patient counselling.
Topics: Humans; Pulmonary Infarction; Computed Tomography Angiography; Pulmonary Embolism; Pulmonary Artery; Dyspnea
PubMed: 37121011
DOI: 10.1016/j.thromres.2023.04.005 -
Orvosi Hetilap Mar 2016Brugada phenocopies are clinical entities that are different from the true Brugada syndrome which is a channelopathy. Brugada phenocopy has reversible underlying... (Review)
Review
Brugada phenocopies are clinical entities that are different from the true Brugada syndrome which is a channelopathy. Brugada phenocopy has reversible underlying conditions and, if underlying conditions resolve, the ECG pattern disappears. In this paper the author reviews and illustrates the known Brugada phenocopies. The most important etiologic categories of Brugada phenocopy include metabolic abnormalities (most commonly hyperkalemia), myocardial infarction, pulmonary embolism (massive), right ventricular mechanical compression, and others. The most important clinical issue is the different treatment of the Brugada syndrome and phenocopies in order to prevent cardiac death. In Brugada syndrome the implantable cardioverter defibrillator is the only effective treatment, while in Brugada phenocopies early, etiology-specific treatment can prevent cardiac death.
Topics: Brugada Syndrome; Death; Defibrillators, Implantable; Electrocardiography; Heart Conduction System; Humans; Myocardial Infarction; Phenotype; Pulmonary Embolism; Treatment Outcome
PubMed: 26996896
DOI: 10.1556/650.2016.30385