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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 -
Journal of Clinical Medicine Aug 2022Pulmonary infarction (PI) is a possible consequence of pulmonary embolism (PE). The real incidence of PI could be underestimated considering only non-fatal PE... (Review)
Review
Pulmonary infarction (PI) is a possible consequence of pulmonary embolism (PE). The real incidence of PI could be underestimated considering only non-fatal PE presentation. However, following postmortem examination, the prevalence of PI is considerably higher. This evidence suggests the necessity of proper diagnostic protocol for identifying PI. Unfortunately, PI diagnosis can sometimes be challenging, due to the overlapping of symptoms with other diseases. Nowadays, the diagnosis is mainly based on radiological evaluation, although the combination with emerging imaging techniques such as ultrasound and nuclear scanning might improve the diagnostic algorithm for PI. This review aims to summarize the available data on the prevalence of PI, the main predisposing factors for the development of PI among patients with PE, to resume the possible diagnostic tools, and finally the clinical and prognostic implications.
PubMed: 36013155
DOI: 10.3390/jcm11164916 -
Cureus Jan 2017The pulmonary veins (PVs) are the most proximal source of arterial thromboembolism. Pulmonary vein thrombosis (PVT) is a rare but potentially lethal disease; its... (Review)
Review
The pulmonary veins (PVs) are the most proximal source of arterial thromboembolism. Pulmonary vein thrombosis (PVT) is a rare but potentially lethal disease; its incidence is unclear, as most of the literature includes case reports. It most commonly occurs as a complica-tion of malignancy, post lung surgery, or atrial fibrillation and can be idiopathic in some cases. Most patients with PVT are commonly asymptomatic or have nonspecific symptoms such as cough, hemoptysis, and dyspnea from pulmonary edema or infarction. The thrombi are typically detected using a variety of imaging modalities including transesophageal echocardiogram (TEE), computed tomography (CT) scanning, magnetic resonance imaging (MRI), or pulmonary angiog-raphy. Treatment should be determined by the obstructing pathological finding and can include antibiotic therapy, anticoagulation, thrombectomy, and/or pulmonary resection. The delay in diagnosing this medical entity can lead to complications including pulmonary infarction, pulmonary edema, right ventricular failure, allograft failure, and peripheral embolism resulting in limb ischemia, stroke, and renal infarction (RI).
PubMed: 28265529
DOI: 10.7759/cureus.993 -
The European Respiratory Journal Sep 2016The combined effects on the heart of smoking and hypoxaemia may contribute to an increased cardiovascular burden in chronic obstructive pulmonary disease (COPD). The use... (Review)
Review
The combined effects on the heart of smoking and hypoxaemia may contribute to an increased cardiovascular burden in chronic obstructive pulmonary disease (COPD). The use of beta-blockers in COPD has been proposed because of their known cardioprotective effects as well as reducing heart rate and improving systolic function. Despite the proven cardiac benefits of beta-blockers post-myocardial infarction and in heart failure they remain underused due to concerns regarding potential bronchoconstriction, even with cardioselective drugs. Initiating treatment with beta-blockers requires dose titration and monitoring over a period of weeks, and beta-blockers may be less well tolerated in older patients with COPD who have other comorbidities. Medium-term prospective placebo-controlled safety studies in COPD are warranted to reassure prescribers regarding the pulmonary and cardiac tolerability of beta-blockers as well as evaluating their potential interaction with concomitant inhaled long-acting bronchodilator therapy. Several retrospective observational studies have shown impressive reductions in mortality and exacerbations conferred by beta-blockers in COPD. However, this requires confirmation from long-term prospective placebo-controlled randomised controlled trials. The real challenge is to establish whether beta-blockers confer benefits on mortality and exacerbations in all patients with COPD, including those with silent cardiovascular disease where the situation is less clear.
Topics: Administration, Inhalation; Adrenergic beta-Antagonists; Bronchodilator Agents; Comorbidity; Forced Expiratory Volume; Heart; Heart Failure; Humans; Myocardial Infarction; Pulmonary Disease, Chronic Obstructive; Respiratory Function Tests
PubMed: 27390282
DOI: 10.1183/13993003.01847-2015 -
Insights Into Imaging Nov 2020Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly spread worldwide since December 2019. Although... (Review)
Review
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly spread worldwide since December 2019. Although the reference diagnostic test is a real-time reverse transcription-polymerase chain reaction (RT-PCR), chest-computed tomography (CT) has been frequently used in diagnosis because of the low sensitivity rates of RT-PCR. CT findings of COVID-19 are well described in the literature and include predominantly peripheral, bilateral ground-glass opacities (GGOs), combination of GGOs with consolidations, and/or septal thickening creating a "crazy-paving" pattern. Longitudinal changes of typical CT findings and less reported findings (air bronchograms, CT halo sign, and reverse halo sign) may mimic a wide range of lung pathologies radiologically. Moreover, accompanying and underlying lung abnormalities may interfere with the CT findings of COVID-19 pneumonia. The diseases that COVID-19 pneumonia may mimic can be broadly classified as infectious or non-infectious diseases (pulmonary edema, hemorrhage, neoplasms, organizing pneumonia, pulmonary alveolar proteinosis, sarcoidosis, pulmonary infarction, interstitial lung diseases, and aspiration pneumonia). We summarize the imaging findings of COVID-19 and the aforementioned lung pathologies that COVID-19 pneumonia may mimic. We also discuss the features that may aid in the differential diagnosis, as the disease continues to spread and will be one of our main differential diagnoses some time more.
PubMed: 33226521
DOI: 10.1186/s13244-020-00933-z -
The New England Journal of Medicine Apr 2023
Topics: Humans; Cardiovascular Diseases; COVID-19; COVID-19 Vaccines; Immunization, Secondary; Myocardial Infarction; Pulmonary Embolism; Stroke; Vaccines, Combined
PubMed: 36988584
DOI: 10.1056/NEJMc2302134 -
Medicine Oct 2015In the setting of acute pulmonary embolism (PE), pulmonary infarction is deemed to occur primarily in individuals with compromised cardiac function.The current study was... (Observational Study)
Observational Study
In the setting of acute pulmonary embolism (PE), pulmonary infarction is deemed to occur primarily in individuals with compromised cardiac function.The current study was undertaken to establish the prevalence of pulmonary infarction in patients with acute PE, and the relationship between infarction and: age, body height, body mass index (BMI), smoking habits, clot burden, and comorbidities.The authors studied prospectively 335 patients with acute PE diagnosed by computed tomographic angiography (CT) in 18 hospitals throughout central Italy. The diagnosis of pulmonary infarction on CT was based on Hampton and Castleman's criteria (cushion-like or hemispherical consolidation lying along the visceral pleura). Multivariable logistic regression was used to model the relationship between covariates and the probability of pulmonary infarction.The prevalence of pulmonary infarction was 31%. Patients with infarction were significantly younger and with significantly lower prevalence of cardiovascular disease than those without (P < 0.001). The frequency of infarction increased linearly with increasing height, and decreased with increasing BMI. In logistic regression, the covariates significantly associated with the probability of infarction were age, body height, BMI, and current smoking. The risk of infarction grew with age, peaked at approximately age 40, and decreased afterwards. Increasing body height and current smoking were significant amplifiers of the risk of infarction, whereas increasing BMI appeared to confer some protection.Our data indicate that pulmonary infarction occurs in nearly one-third of the patients with acute PE. Those with infarction are often young and otherwise healthy. Increasing body height and active smoking are predisposing risk factors.
Topics: Acute Disease; Adult; Age Factors; Aged; Aged, 80 and over; Body Height; Body Mass Index; Cardiovascular Diseases; Female; Humans; Italy; Male; Middle Aged; Prevalence; Pulmonary Embolism; Pulmonary Infarction; Risk Factors; Smoking; Tomography, X-Ray Computed
PubMed: 26469892
DOI: 10.1097/MD.0000000000001488 -
Pulmonary Circulation Oct 2023Patients with pulmonary embolism (PE) commonly manifest concomitant "pneumonia," which is generally believed to be either a cause (infection) or a consequence...
Patients with pulmonary embolism (PE) commonly manifest concomitant "pneumonia," which is generally believed to be either a cause (infection) or a consequence (infarction) of PE. This study aimed to clarify the relationship between PE and "pneumonia-like" lesions beyond pulmonary infection and infarction. Chest computed tomography (CT) images of patients with PE and deep vein thrombosis (DVT) were retrospectively analyzed to compare the incidence of pneumonia lesions. The pathological damage and wet/dry ratio of lung tissues were observed in PE rats and PE plasma-injected rats. In total, 793 and 914 inpatients were enrolled in the PE and DVT groups, respectively. Pneumonia lesions were observed in 36.9% and 26.3% of patients in the PE and DVT groups, respectively ( < 0.0001). Among PE rats, 33.3% exhibited focal severe lung injury, which closely resembled the pathological damage of community-acquired pneumonia. The wet/dry ratio was significantly higher in the PE group than in the PE-control group (4.98 ± 0.08 vs. 4.39 ± 0.06, < 0.0001). Among PE plasma-injected rats, individuals with focal proven lung injury were found at all experimental points, with an incidence of 27.6%. The lung wet/dry ratio was significantly higher in the PE plasma group than in the PE-control plasma group at 1 and 2 h postinjection (5.02 ± 0.12 vs. 4.61 ± 0.06 and 4.76 ± 0.16 vs. 4.34 ± 0.09, respectively; < 0.05). In conclusion, the manifestation of pneumonia lesions in chest CT images was higher among PE patients than among DVT patients. Plasma of PE rats could induce focal pneumonia-like lung injury in healthy rats.
PubMed: 38111797
DOI: 10.1002/pul2.12322 -
Journal of Korean Medical Science Mar 2022In acute pulmonary embolism (PE), circulatory failure and systemic hypotension are important clinically for predicting poor prognosis. While pulmonary artery (PA) clot... (Review)
Review
In acute pulmonary embolism (PE), circulatory failure and systemic hypotension are important clinically for predicting poor prognosis. While pulmonary artery (PA) clot loads can be an indicator of the severity of current episode of PE or treatment effectiveness, they may not be used directly as an indicator of right ventricular (RV) failure or patient death. In other words, pulmonary vascular resistance or patient prognosis may not be determined only with mechanical obstruction of PAs and their branches by intravascular clot loads on computed tomography pulmonary angiography (CTPA), but determined also with vasoactive amines, reflex PA vasoconstriction, and systemic arterial hypoxemia occurring during acute PE. Large RV diameter with RV/left ventricle (LV) ratio > 1.0 and/or the presence of occlusive clot and pulmonary infarction on initial CTPA, and clinically determined high baseline PA pressure and RV dysfunction are independent predictors of oncoming chronic thromboembolic pulmonary hypertension (CTEPH). In this pictorial review, authors aimed to demonstrate clinical and serial CTPA features in patients with acute massive and submassive PE and to disclose acute CTPA and clinical features that are related to the prediction of oncoming CTEPH.
Topics: Angiography; Humans; Hypertension, Pulmonary; Pulmonary Artery; Pulmonary Embolism; Tomography, X-Ray Computed
PubMed: 35289137
DOI: 10.3346/jkms.2022.37.e76 -
Methodist DeBakey Cardiovascular Journal 2021SARS-CoV-2, the virus that causes coronavirus disease 19 (COVID-19), is associated with a bewildering array of cardiovascular manifestations, including myocardial... (Review)
Review
SARS-CoV-2, the virus that causes coronavirus disease 19 (COVID-19), is associated with a bewildering array of cardiovascular manifestations, including myocardial infarction and stroke, myocarditis and heart failure, atrial and ventricular arrhythmias, venous thromboembolism, and microvascular disease. Accumulating evidence indicates that a profound disturbance of endothelial homeostasis contributes to these conditions. Furthermore, the pulmonary infiltration and edema, and later pulmonary fibrosis, in patients with COVID-19 is promoted by endothelial alterations including the expression of endothelial adhesion molecules and chemokines, increased intercellular permeability, and endothelial-to-mesenchyme transitions. The cognitive disturbance occurring in this disease may also be due in part to an impairment of the blood-brain barrier. Venous thrombosis and pulmonary thromboembolism are most likely associated with an endothelial defect caused by circulating inflammatory cytokines and/or direct endothelial invasion by the virus. Endothelial-targeted therapies such as statins, nitric oxide donors, and antioxidants may be useful therapeutic adjuncts in COVID-19 by restoring endothelial homeostasis.
Topics: COVID-19; Humans; Myocarditis; Pulmonary Embolism; SARS-CoV-2; Venous Thromboembolism
PubMed: 34992723
DOI: 10.14797/mdcvj.1044