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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 -
American Family Physician Sep 2017Pleuritic chest pain is characterized by sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling. Pulmonary embolism is the most...
Pleuritic chest pain is characterized by sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling. Pulmonary embolism is the most common serious cause, found in 5% to 21% of patients who present to an emergency department with pleuritic chest pain. A validated clinical decision rule for pulmonary embolism should be employed to guide the use of additional tests such as d-dimer assays, ventilation-perfusion scans, or computed tomography angiography. Myocardial infarction, pericarditis, aortic dissection, pneumonia, and pneumothorax are other serious causes that should be ruled out using history and physical examination, electrocardiography, troponin assays, and chest radiography before another diagnosis is made. Validated clinical decision rules are available to help exclude coronary artery disease. Viruses are common causative agents of pleuritic chest pain. Coxsackieviruses, respiratory syncytial virus, influenza, parainfluenza, mumps, adenovirus, cytomegalovirus, and Epstein-Barr virus are likely pathogens. Treatment is guided by the underlying diagnosis. Nonsteroidal anti-inflammatory drugs are appropriate for pain management in those with virally triggered or nonspecific pleuritic chest pain. In patients with persistent symptoms, persons who smoke, and those older than 50 years with pneumonia, it is important to document radiographic resolution with repeat chest radiography six weeks after initial treatment.
Topics: Algorithms; Aorta; Chest Pain; Coronary Artery Disease; Decision Support Techniques; Diagnosis, Differential; Diagnostic Imaging; Humans; Medical History Taking; Myocardial Infarction; Pericarditis; Physical Examination; Pleural Effusion, Malignant; Pneumonia; Pneumothorax; Pulmonary Embolism
PubMed: 28925655
DOI: No ID Found -
CASE (Philadelphia, Pa.) Feb 2024Two-dimensional transthoracic echocardiogram, short axis view of the main pulmonary artery (MPA, ) demonstrates a saddle pulmonary embolism (PE) with the highly...
Two-dimensional transthoracic echocardiogram, short axis view of the main pulmonary artery (MPA, ) demonstrates a saddle pulmonary embolism (PE) with the highly correlative axial display from the contrast-enhanced computed tomography scan (). , aorta; , pulmonary artery (From Graphical Abstract, , Eugene Yuriditsky, MD )Graphical abstractTwo-dimensional transthoracic echocardiogram, short axis view of the main pulmonary artery (MPA, ) demonstrates a saddle pulmonary embolism (PE) with the highly correlative axial display from the contrast-enhanced computed tomography scan (). , aorta; , pulmonary artery (From Graphical Abstract, , Eugene Yuriditsky, MD ).
PubMed: 38425572
DOI: 10.1016/j.case.2023.12.024 -
Open Access Emergency Medicine : OAEM 2019Shock index (SI) is defined as the heart rate (HR) divided by systolic blood pressure (SBP). It has been studied in patients either at risk of or experiencing shock from...
Shock index (SI) is defined as the heart rate (HR) divided by systolic blood pressure (SBP). It has been studied in patients either at risk of or experiencing shock from a variety of causes: trauma, hemorrhage, myocardial infarction, pulmonary embolism, sepsis, and ruptured ectopic pregnancy. While HR and SBP have traditionally been used to characterize shock in these patients, they often appear normal in the compensatory phase of shock and can be confounded by factors such as medications (eg, antihypertensives, beta-agonists). SI >1.0 has been widely found to predict increased risk of mortality and other markers of morbidity, such as need for massive transfusion protocol activation and admission to intensive care units. Recent research has aimed to study the use of SI in patients immediately on arrival to the emergency department (ED). In this review, we summarize the literature pertaining to use of SI across a variety of settings in the management of ED patients, in order to provide context for use of this measure in the triage and management of critically ill patients.
PubMed: 31616192
DOI: 10.2147/OAEM.S178358 -
Journal of the American College of... Jul 2014Paradoxical embolism is an important clinical entity among patients with venous thromboembolism in the presence of intracardiac or pulmonary shunts. The clinical... (Review)
Review
Paradoxical embolism is an important clinical entity among patients with venous thromboembolism in the presence of intracardiac or pulmonary shunts. The clinical presentation is diverse and potentially life-threatening. Although the serious nature and complications of paradoxical embolism are recognized, the disease entity is still rarely considered and remains under-reported. This paper provides an overview on the different clinical manifestations of paradoxical embolism, describes the diagnostic tools for the detection of intracardiac and pulmonary shunts, reviews therapeutic options, and summarizes guideline recommendations for the secondary prevention of paradoxical embolism.
Topics: Brain Ischemia; Diagnostic Imaging; Embolism, Paradoxical; Global Health; Heart Defects, Congenital; Humans; Morbidity; Myocardial Infarction; Risk Factors
PubMed: 25060377
DOI: 10.1016/j.jacc.2014.04.063 -
Journal of the American College of... Nov 2020
Topics: Betacoronavirus; COVID-19; Coronavirus Infections; Humans; Pandemics; Pneumonia, Viral; Pulmonary Embolism; Registries; SARS-CoV-2; Thromboembolism
PubMed: 33121713
DOI: 10.1016/j.jacc.2020.09.543 -
Frontiers in Molecular Biosciences 2018Cardiovascular diseases (CVD) are the leading cause of death worldwide. CVD comprise a range of diseases affecting the functionality of the heart and blood vessels,... (Review)
Review
Cardiovascular diseases (CVD) are the leading cause of death worldwide. CVD comprise a range of diseases affecting the functionality of the heart and blood vessels, including acute myocardial infarction (AMI) and pulmonary hypertension (PH). Despite their different causative mechanisms, both AMI and PH involve narrowed or blocked blood vessels, hypoxia, and tissue infarction. The endothelium plays a pivotal role in the development of CVD. Disruption of the normal homeostasis of endothelia, alterations in the blood vessel structure, and abnormal functionality are essential factors in the onset and progression of both AMI and PH. An emerging theory proposes that pathological blood vessel responses and endothelial dysfunction develop as a result of an abnormal endothelial metabolism. It has been suggested that, in CVD, endothelial cell metabolism switches to higher glycolysis, rather than oxidative phosphorylation, as the main source of ATP, a process designated as the Warburg effect. The evidence of these alterations suggests that understanding endothelial metabolism and mitochondrial function may be central to unveiling fundamental mechanisms underlying cardiovascular pathogenesis and to identifying novel critical metabolic biomarkers and therapeutic targets. Here, we review the role of the endothelium in the regulation of vascular homeostasis and we detail key aspects of endothelial cell metabolism. We also describe recent findings concerning metabolic endothelial cell alterations in acute myocardial infarction and pulmonary hypertension, their relationship with disease pathogenesis and we discuss the future potential of pharmacological modulation of cellular metabolism in the treatment of cardiopulmonary vascular dysfunction. Although targeting endothelial cell metabolism is still in its infancy, it is a promising strategy to restore normal endothelial functions and thus forestall or revert the development of CVD in personalized multi-hit interventions at the metabolic level.
PubMed: 30723719
DOI: 10.3389/fmolb.2018.00120 -
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