Complication Of Pulmonary Embolism Research Articles

Chronic thromboembolic pulmonary disease.

Chronic thromboembolic pulmonary hypertension is a complication of pulmonary embolism and a treatable cause of pulmonary hypertension. The pathology is a unique combination of mechanical obstruction due to failure of clot resolution, and a variable degree of microvascular disease, that both contribute to pulmonary vascular resistance. Accordingly, multiple treatments have been developed to target the disease components. However, accurate diagnosis is often delayed. Evaluation includes high-quality imaging modalities, necessary for disease confirmation and for appropriate treatment planning. All patients with chronic thromboembolic pulmonary disease, and especially those with pulmonary hypertension, should be referred to expert centres for multidisciplinary team decision on treatment. The first decision remains assessment of operability, and the best improvement in symptoms and survival is achieved by the mechanical therapies, pulmonary endarterectomy and balloon pulmonary angioplasty. With the advances in multimodal therapies, excellent outcomes can be achieved with 3-year survival of >90%.

Real-world Safety and Effectiveness of Edoxaban in Patients with Venous Thromboembolism with or without Preceding Parenteral Anticoagulants: A Single-center Retrospective Study.

Objective Edoxaban is an anticoagulant used for venous thromboembolism (VTE) treatment and requires pretreatment with parenteral anticoagulants. However, pretreatment is not always performed in the clinical setting. In this study, we investigated the safety and effectiveness of edoxaban treatment in patients with VTE with or without pretreatment. Methods We retrospectively enrolled 364 patients who received edoxaban for VTE treatment between September 2014 and March 2020 and investigated patient demographics, VTE recurrence, and major bleeding as clinical outcomes in patients with or without pretreatment. Furthermore, the factors contributing to pretreatment decisions were assessed. Results Patients without pretreatment (n=208) had more active cancer cases and fewer pulmonary embolism complications than those with pretreatment (n=156). Lower levels of hemoglobin and higher levels of white blood cell counts, C-reactive protein, and D-dimer at the diagnosis were found in patients who received pretreatment than in those without pretreatment. No symptomatic VTE recurrence was observed. After propensity score matching, the cumulative incidence of major bleeding was not significantly higher in patients with pretreatment than in those without it (log-rank test, p=0.136). The incidence of deteriorated VTE on imaging did not significantly differ between patients with and without pretreatment, even after propensity matching (log-rank test, p=0.414). Conclusion In a real-world clinical setting, where physicians determined the use of parenteral anticoagulant lead-in according to their experience, patient demographics, and VTE characteristics, no significant differences were found regarding safety and effectiveness in edoxaban-treated VTE patients with or without pretreatment with parenteral anticoagulants.

Pulmonary Embolism (PE) to Chronic Thromboembolic Pulmonary Disease (CTEPD): Findings from a Survey of UK Physicians.

Chronic thromboembolic pulmonary disease (CTEPD) is a complication of pulmonary embolism (PE). We conducted an online survey of UK PE-treating physicians to understand practices in the follow-up of PE and awareness of CTEPD. The physicians surveyed (N = 175) included 50 each from cardiology, respiratory and internal medicine, plus 25 haematologists. Most (89%) participants had local guidelines for PE management, and 65% reported a PE follow-up clinic, of which 69% were joint clinics. Almost half (47%) had a protocol for the investigation of CTEPD. According to participants, 129 (74%) routinely consider a diagnosis of CTEPD and 97 (55%) routinely investigate for CTEPD, with 76% of those 97 participants investigating in patients who are symptomatic at 3 months and 22% investigating in all patients. This survey demonstrated variability in the follow-up of PE and the awareness of CTEPD and its investigation. The findings support the conduct of a national audit to understand the barriers to the timely detection of CTEPD.

THE DIAGNOSTIC AND TREATMENT CHALLENGES OF CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION IN LOW- AND MIDDLE-INCOME COUNTRIES: CASE SERIES

Chronic thromboembolic pulmonary hypertension (CTEPH), a complication of pulmonary embolism, is one of the major causes of right heart failure and death. It is characterised pathologically by organised thromboembolic material and altered vascular remodelling initiated and potentiated by a combination of defective angiogenesis, impaired fibrinolysis and endothelial dysfunction. One of the challenges in the management of CTEPH is making early and accurate diagnosis as well as instituting prompt and appropriate treatment. We report 4 successfully managed cases of CTEPH occurring in 2 elderly males and 2 young females. All the patients were initially managed for cardiovascular disease, and were referred to the respiratory unit after a period of four to eight months due to worsening dyspnoea. The diagnoses were made using a combination of CT angiogram, Doppler sonogram and 2-D echo; and the patients successfully managed medically. Our aim is to highlight the diagnostic and treatment challenges associated with CTEPH in our environment and the need for a high index of suspicion in dyspnoeic patients.

Validación externa del algoritmo InShape II para la exclusión de la enfermedad tromboembólica crónica en los pacientes con tromboembolismo pulmonar

Background and aimThe most severe long-term complication of pulmonary embolism (PE) is chronic thromboembolic pulmonary hypertension (CTEPH), and its early diagnosis often requires numerous diagnostic tests. The InShape II study proposes an early screening algorithm that aims to reduce the number of echocardiographic studies. The objective of our study is to validate this algorithm in our patient cohort. Materials and methodsWe retrospectively analyzed patients admitted to Hospital Rey Juan Carlos between November 2017 and February 2020, who were diagnosed with PE based on computed tomography angiography (CTA). Patients were followed for at least one year, and clinical, laboratory, and complementary test data were collected at three months and one year. The InShape II algorithm was applied to these patients to validate its results. ResultsDuring the study period, 236 patients were diagnosed with PE, of which 137 were excluded. The algorithm was validated in 99 patients. Applying the InShape II score, 19 echocardiograms would have been performed (three of them with intermediate-high probability of CTEPH), while 80 echocardiograms would have been avoided (two of them with intermediate-high probability). This yielded a sensitivity of 60% and a specificity of 83% for the score, with an area under the curve (AUC) of 0.715 (95% CI: 0.472-0.958). ConclusionsOur results support the notion that the InShape II algorithm could be a useful tool for initial screening of CTEPH in low-incidence settings, as it would avoid unnecessary echocardiograms that do not provide additional value.

External validation of the InShape II study algorithm for exclusion of chronic thromboembolic pulmonary hypertension in patients with pulmonary thromboembolism

Background and aimThe most severe long-term complication of pulmonary embolism (PE) is chronic thromboembolic pulmonary hypertension (CTEPH), and its early diagnosis often requires numerous diagnostic tests. The InShape II study proposes an early screening algorithm that aims to reduce the number of echocardiographic studies. The objective of our study is to validate this algorithm in our patient cohort. Materials and methodsWe retrospectively analyzed patients admitted to Hospital Rey Juan Carlos between November 2017 and February 2020, who were diagnosed with PE based on computed tomography angiography (CTA). Patients were followed for at least one year, and clinical, laboratory, and complementary test data were collected at three months and one year. The InShape II algorithm was applied to these patients to validate its results. ResultsDuring the study period, 236 patients were diagnosed with PE, of which 137 were excluded. The algorithm was validated in 99 patients. Applying the InShape II score, 19 echocardiograms would have been performed (three of them with intermediate-high probability of CTEPH), while 80 echocardiograms would have been avoided (two of them with intermediate-high probability). This yielded a sensitivity of 60% and a specificity of 83% for the score, with an area under the curve (AUC) of 0.715 (95% CI: 0.472–0.958). ConclusionsOur results support the notion that the InShape II algorithm could be a useful tool for initial screening of CTEPH in low-incidence settings, as it would avoid unnecessary echocardiograms that do not provide additional value.

Chronic pulmonary thromboembolic disease

Chronic Thromboembolic Pulmonary Hypertension (CTEPH), defined as precapillary pulmonary hypertension (PH) with right heart catheterization and imaging consistent with chronic thromboembolism, is a long-term complication of Pulmonary Embolism (PE). CTEPH defines symptomatic patients with maladaptive perfusion disorders after at least 3 months of therapeutic anticoagulation. In this setting, pulmonary hypertension results from extensive Pulmonary Artery (PA) obstruction by only organized fibrotic clots and may also be present as micro vasculopathy. Echocardiographic (ECHO) examination to determine a pulmonary surgical operation if the patient complains of anticipation and/or the risk for CTEPH is widely demonstrated (prior PE episodes, existing imaging size as index event suggestive of CTEPH, key features such as hypothyroidism and cancer), It is the preferred recognition method because of its availability and the high data value and amount of data. Patients diagnosed with CTEPH or with a strong suspicion of CTEPH should be referred to a specialist pulmonary cardiovascular clinic for further multidisciplinary diagnosis and treatment, such as Pulmonary Endarterectomy (PEA), balloon Pulmonary Angioplasty (BPA), and/or Targeted pulmonary medical therapy. In recent years, significant progress has been made in evaluating patients with sequelae after a pulmonary embolism, confirming clinical, biochemical, and hemodynamic criteria. Further work is needed to elucidate and develop appropriate standing protocols to support limited purposes and ongoing archives to ensure physical care capacity and life security.

Abstract 220: Post-gwas Functional Genomics Analysis Of Abo Locus To Identify Novel Pathogenic Mechanisms For Chronic Thromboembolic Pulmonary Hypertension

Background: Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare and mysterious complication of pulmonary embolism, characterized by chronic pulmonary arterial thrombosis, occlusions and vasculopathy. Emerging evidence has suggested genetic relevance of CTEPH, particularly to ABO blood type. Genome-wide association study (GWAS) has identified ABO gene as the most significant genetic locus associated with CTEPH. This locus, however, consists only intronic SNPs and there is no mechanistic explanation on how these non-coding SNPs control the risk of CTEPH. Methods: GWAS-identified CTEPH-associated ABO locus was analyzed, and haplotype SNPs were identified based on linkage disequilibrium (LD). Electrophoretic mobility shift assay (EMSA) was applied to screen functional SNPs (fSNPs) based on allele-imbalanced nuclear protein binding. SNP-binding nuclear transcription factors (TFs) were identified by proteomics. Hi-C chromatin-interaction analysis was utilized to determine potential target genes affected by fSNPs. Knockdown of fSNP-associated TFs in human pulmonary artery endothelial cells (hPAECs) was applied to validate the regulation of TFs on target genes. Results: Based on GWAS, the minor allele of tag SNP rs2519093 is associated with higher risk of CTEPH (Odds ratio 2.22). It defines 11 haplotype SNPs in a LD with R 2 > 0.8. Screened by EMSA with hPAEC nuclear proteins, intronic SNPs rs579459 and rs550057 were identified functional given their allele-specific protein binding. Proteomics analysis identified 3 candidate TFs that allele-specifically bind to fSNP rs579459: PBX1, CTCF and SAFB2. Candidate target gene ADAMTS13 is chosen based on its prominent interaction with fSNP revealed by Hi-C analysis, and the potential role in thromboembolism through vWF cleavage. TF knockdown by siRNA downregulates ADAMTS13 in hPAECs, suggesting their regulatory function as activators. Conclusion: Leveraging our post-GWAS functional genomics approach, we identified fSNPs in ABO locus that define a genetic architecture controlling the susceptibility of CTEPH. This genetic architecture, along with the newly identified fSNP-associated TFs and target gene ADAMTS13, provides a biological explanation for the pathogenesis of CTEPH.

Post-pulmonary embolism syndrome: long-term complications of pulmonary embolism

Background: People who survive an episode of pulmonary embolism (PE) have an increased risk of developing chronic complications even despite curative anticoagulant treatment. The association of dyspnea, low functional capacity, right heart failure, chronic thromboembolic pulmonary hypertension or chronic thromboembolic pulmonary disease is part of the notion of post-pulmonary embolic syndrome (PPES). Due to the fact that this syndrome is still not clearly described and mainly underdiagnosed, a poor awareness of the disease by patients and physicians leads to delaying specific treatment with unlikely improvement of quality of life for these patients. Chronic thromboembolic pulmonary hypertension is the most severe complication, which, if not diagnosed and not treated in time, can lead to fatal consequences. To improve the overall health outcomes of patients with acute PE, adequate measures to diagnose it and strategies to prevent long-term outcomes of pulmonary embolism are essential. Conclusions: In this article, the data from the latest publications have been summarized to clarify the notion of PPES and its diagnostic algorithm.

Post-Pulmonary Embolism Impairment Six Months after Acute Pulmonary Embolism: A Prospective Registry.

Little evidence is available on post-pulmonary embolism impairment (PPEI), a recently defined complication of pulmonary embolism (PE) encompassing dysfunctional clinical and imaging parameters. In the present study, we sought to evaluate its frequency with a focus on the main components. In this prospective registry, we included patients with a confirmed diagnosis of acute PE and focused on those with initial right ventricular (RV) dysfunction. Their baseline, pre-discharge, and 6month follow-up clinical and imaging characteristics were recorded. The main study outcomes were incomplete RV functional recovery, exercise capacity limitations (based on the 6minute walk test), and their combination, which defines PPEI, within six months of acute PE. Of 170 consecutive patients with a confirmed diagnosis of acute PE, 123 accepted to participate in the follow-up study, of whom 87 had initial RV dysfunction. The 6month rates of incomplete RV functional recovery, signs of an intermediate-to-high echocardiographic probability of PH, and exercise limitations were observed in 58.6, 32.1, and 45.9%, respectively. A total of 22 (25.2%; 95% CI 15.5-34.4%) patients had PPEI. The RV/LV ratio and the fractional area change on discharge after acute PE were more often impaired among patients with incomplete RV recovery, exercise limitations, and a high probability of PH at 6months. In contrast, an initial impaired RV diastolic function indices appeared to characterize patients with a limited exercise capacity at 6months. PPEI affects one fourth of patients surviving acute PE with half of them presenting with RV dysfunction or exercise limitations.

Inhibition of heterogeneous nuclear ribonucleoproteins A1 and oxidative stress reduces glycolysis via pyruvate kinase M2 in chronic thromboembolic pulmonary hypertension

Abstract Background and Objective Chronic thromboembolic pulmonary hypertension (CTEPH) is a lethal complication of pulmonary embolism involving pulmonary artery occlusion and microvascular disease. The glucose metabolism and reactive oxygen species (ROS) production may be perturbed in CTEPH, but the precise mechanisms are unclear. This study investigated glucose metabolism in CTEPH employing pulmonary endarterectomy (PEA)-derived pulmonary artery smooth muscle cells (PASMCs) and characterized the roles of pyruvate kinase M2 (PKM2) and its regulation by heterogeneous nuclear ribonucleoproteins A1 (hnRNPA1) and ROS in CTEPH. Methods PEA tissues and blood samples of CTEPH patients were collected to study the levels of PKM2. Primary PASMCs were isolated from PEA tissues. We used small interfering RNAs to knock down PKM2 and hnRNPA1, and applied antioxidant N-acetylcysteine (NAC) and mito-TEMPO to reduce ROS production. The expression of glucometabolic genes, ROS production, glycolysis rate and proliferative and migratory activities were analyzed in PEA-derived PASMCs. Results PKM2 levels in serum and PEA tissues of CTEPH patients were higher than that of the healthy controls. Compared to the control PASMCs, PEA-derived PASMCs showed increased PKM2 expression and ROS production. The rates of glycolysis, proliferation and migration were increased in PEA-PASMCs and could be mitigated by PKM2 downregulation through hnRNPA1 or ROS inhibition. Conclusions Increased glycolysis and PKM2 expression were found in PEA-PASMCs. Inhibition of hnRNPA1 or ROS corrected the aberrant glycolysis, cell proliferation and migration by downregulating PKM2. Regulation of the hnRNPA1/PKM2 axis represents a potential therapeutic target for the treatment of CTEPH.

Does age at surgery influence short-term outcomes and readmissions following anatomic total shoulder arthroplasty?

BackgroundIncreasing age has been associated with adverse outcomes in various orthopedic procedures including anatomic total shoulder arthroplasty (aTSA). Moreover, both indications and the ages at which the procedure is done has expanded. For these reasons, it is important to characterize the impact age has on complication and readmission rates following shoulder replacement. MethodsThe National Readmissions Database was used to identify patients who underwent aTSA between the years 2016–2018. Patients were stratified into five cohorts based on age at surgery: 18–49, 50–59, 60–69, 70–79, and 80+ years old. We analyzed and compared data related to patient demographics, length of stay, readmission and complication rates, and healthcare charges. A multivariate analysis was used to identify the independent impact of age on complication rates. Results42,505 patients were included with 1,541, 6,552, 16,364, 14,694, 3,354, patients in the 18–49, 50–59, 60–69, 70–79, and 80+ years old cohorts respectively. Length of stay had a stepwise increase with age increases (p < 0.001), however total charges were comparable between cohorts (p = 0.40). Older patients were more likely to experience intraoperative complications, pulmonary embolism complications, and postoperative infection, but were less likely to experience hardware, surgical site, and prosthetic joint complications. Older patients had higher rates of readmission. Age was an independent predictor for higher 30-/90-day readmission, postoperative/intraoperative complication, and respiratory complication rates. Increasing age provided a protective measure for prosthetic complications surgical site infection. ConclusionThis study identified multiple differences in complication rates following aTSA based on age at surgery. Overall, age had varying effects on intraoperative and postoperative complication rates at short-term follow-up. However, increasing age was associated with longer lengths of stay and increased readmission rates. Surgeons should be aware of the identified complications that are most prevalent in each age group and use this information to avoid adverse outcomes following shoulder replacement surgery.

Acute phase characteristics and long-term complications of pulmonary embolism in COVID-19 compared to non-COVID-19 cohort: a large single-centre study

BackgroundTo compare the severity of pulmonary embolism (PE) and the long-term complications between patients with and without COVID-19, and to investigate whether the tools for risk stratification of death are valid in this population.MethodsWe retrospectively included hospitalized patients with PE from 1 January 2016 to 31 December 2022. Comparisons for acute episode characteristics, risk stratification of the PE, outcomes, and long-term complications were made between COVID and non-COVID patients.ResultsWe analyzed 116 (27.5%) COVID patients and 305 (72.4%) non-COVID patients. In patients with COVID-19, the traditional risk factors for PE were absent, and the incidence of deep vein thrombosis was lower. COVID patients showed significantly higher lymphocyte count, lactate dehydrogenase, lactic acid, and D-dimer levels. COVID patients had PE of smaller size (12.3% vs. 25.5% main pulmonary artery, 29.8% vs. 37.1% lobar, 44.7% vs. 29.5% segmental and 13.2% vs. 7.9% subsegmental, respectively; p < 0.001), less right ventricular dysfunction (7.7% vs. 17.7%; p = 0.007) and higher sPESI score (1.66 vs. 1.11; p < 0.001). The need for mechanical ventilation was significantly higher in COVID patients (8.6% vs. 1.3%; p < 0.001); However, the in-hospital death was less (5.2% vs. 10.8%; p = 0.074). The incidence of long-term complications was lower in COVID cohort (p < 0.001). PE severity assessed by high sPESI and intermediate and high-risk categories were independently associated with in-hospital mortality in COVID patients.ConclusionThe risk of in-hospital mortality and the incidence of long-term complications were lower in COVID-19. The usual tools for risk stratification of PE are valid in COVID patients.

Preexisting Chronic Thromboembolic Pulmonary Hypertension in Acute Pulmonary Embolism

Chronic thromboembolic pulmonary hypertension (CTEPH) is considered a complication of pulmonary embolism (PE). However, signs of CTEPH may exist in patients with a first symptomatic PE. Which radiologic findings on CT pulmonary angiography (CTPA) at the time of acute PE could indicate the presence of preexisting CTEPH? This study included unselected patients with acute PE who were prospectively followed up for 2 years with a structured visit schedule. Two expert radiologists independently assessed patients' baseline CTPAs for preexisting CTEPH; in case of disagreement, a decision was reached by a 2:1 majority with a third expert radiologist. In addition, the radiologists checked for predefined individual parameters suggesting chronic PE and pulmonary hypertension. Signs of chronic PE or CTEPH at baseline were identified in 46 of 303 included patients (15%). Intravascular webs, arterial narrowing or retraction, dilated bronchial arteries, and right ventricular hypertrophy were the main drivers of the assessment. Five (1.7%) patients were diagnosed with CTEPH during follow-up. All four patients diagnosed with CTEPH early (83-108days following acute PE) were found in enriched subgroups based on the experts' overall assessment or fulfilling a minimum number of the predefined radiologic criteria at baseline. The specificity of preexisting CTEPH diagnosis and the level of radiologists' agreement improved as the number of required criteria increased. Searching for predefined radiologic parameters suggesting preexisting CTEPH at the time of acute PE diagnosis may allow for targeted follow-up strategies and risk-adapted CTEPH screening, thus facilitating earlier CTEPH diagnosis.

Balloon Pulmonary Angioplasty in the Management of Chronic Thromboembolic Pulmonary Hypertension.

Chronic thromboembolic pulmonary hypertension (CTEPH), which is classified as group 4 pulmonary hypertension (PH) in the 2015 European Society of Cardiology/European Respiratory Society guidelines for the diagnosis and treatment of PH, is regarded as a complication of pulmonary embolism and is caused by the transformation of incompletely resolved thrombi into fibrous tissue that occludes the pulmonary arteries. The current established reference standard curative therapy for CTEPH is pulmonary endarterectomy (PEA), which provides good long-term outcomes with a low mortality rate. For patients with inoperable disease with inaccessible lesions and risk factors for surgery or patients who are diagnosed with residual or recurrent PH after PEA, medical therapy with riociguat is recommended. Balloon pulmonary angioplasty (BPA) is an emerging alternative treatment option for patients with inoperable disease or those with residual or recurrent PH after PEA. BPA has been reported to improve hemodynamics, cardiac function, exercise capacity, and symptoms, as well as PEA. A detailed assessment of thromboembolic lesions in pulmonary arteries by using multiple imaging techniques and treatment strategies with multiple staged procedures based on the patient's condition is important for safe and effective BPA. However, this new technique may still induce life-threatening complications, such as reperfusion pulmonary edema, wire perforation, vessel dissection, and vessel rupture. Meticulous attention to technique is mandatory to minimize serious complications owing to the nature of the anatomic territory involved. The authors summarize the current roles, goals, and complications of BPA in patients with CTEPH and demonstrate ways to formulate an effective and safe treatment strategy. The future perspective of BPA is also discussed. Online supplemental material is available for this article. ©RSNA, 2022.

RADIOGRAPHIC FINDINGS OF CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION

RADIOGRAPHIC FINDINGS OF CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION

Pulmonary embolism and 529 human blood metabolites: genetic correlation and two-sample Mendelian randomization study

BackgroundThe incidence of pulmonary embolism complications in the literature ranges from 10 to 50%, with a 0.5–10% risk of fatal pulmonary embolism. However, the biological cause of pulmonary embolism is unknown.MethodsThis study used data from the Genome-Wide Association Study (GWAS) of Pulmonary Embolism and Human Blood Metabolites from the UK Biobank, and the data from subjects of European ancestry were analyzed. We explored the relationship between pulmonary embolism and blood metabolites in three ways. We first analyzed the genetic correlation between pulmonary embolism and human blood metabolites using the linkage disequilibrium score regression (LDSC) and then analyzed the causal relationship between pulmonary embolism and meaningful blood metabolites obtained from the LDSC, a procedure for which we used Mendelian randomization analysis. Finally, we obtained transcriptome sequencing data for patients with a pulmonary embolism from the GEO database, analyzed differentially expressed genes (DEGs) in patients with pulmonary embolism versus healthy populations, and compared the DEGs with the resulting blood metabolite genes to further validate the relationship between pulmonary embolism and blood metabolites.ResultWe found six human blood metabolites genetically associated with pulmonary embolism, stearic acid glycerol phosphate ethanolamine (correlation coefficient = 0.2582, P = 0.0493), hydroxytryptophan (correlation coefficient = 0.2894, P = 0.0435), and N1-methyladenosine (correlation coefficient = 0.0439, P = 0.3728), and a significant causal relationship was discovered between hydroxytryptophan and pulmonary embolism. After screening microarray data from the GEO database, we performed differential gene analysis on the GSE19151 dataset and screened a total of 22,216 genes with P values less than 0.05, including 17,361 upregulated genes and 4854 downregulated genes. By comparing the resulting differentially expressed genes with six genes encoding blood metabolites, LIPC and NAT2 were found to be differentially expressed in association with pulmonary embolism.

Imaging Advances in Chronic Thromboembolic Pulmonary Hypertension

Chronic thromboembolic pulmonary hypertension (CTEPH) is an under recognized complication of pulmonary embolism with significant morbidity and mortality when left untreated. There have been ongoing advances in the treatment of CTEPH with potentially excellent outcomes for patients when diagnosed and treated in a timely fashion. Although ventilation-perfusion scintigraphy remains critical in screening for CTEPH, the radiologic diagnosis involves multiple modalities from digital subtraction angiography to high quality computed tomography pulmonary angiography. State of the art imaging in CTEPH now also includes dual energy computed tomography, lung subtraction iodine mapping, and magnetic resonance imaging.

Incidence and Risk Factors of Pulmonary Hypertension After Venous Thromboembolism: An Analysis of a Large Health Care Database.

Background Pulmonary hypertension (PH) is a devastating potential complication of pulmonary embolism, a manifestation of venous thromboembolism (VTE). The incidence of and risk factors for PH in those with prior VTE are poorly characterized. Methods and Results International Classification of Diseases (ICD) codes from inpatient and outpatient medical claims from MarketScan administrative databases for years 2011 to 2018 were used to identify cases of VTE, comorbidities before the VTE event, and PH occurring subsequent to the VTE event. Cumulative incidence and hazard ratios (HR), and their 95% CI, were calculated. The 170021 VTE cases included in the analysis were on average (±SD) 57.5±15.8years old and 50.5% were female. A total of 5943 PH cases accrued over an average follow-up of 1.94years. Two years after incident VTE, the cumulative incidence (95% CI) of PH was 3.5% (3.4%-3.7%) overall. It was higher among older individuals, among women (3.9% [3.8%-4.1%]) than men (3.2% [3.0%-3.3%]), and among patients presenting with pulmonary embolism (6.2% [6.0%-6.5%]) than those presenting with deep vein thrombosis only (1.1% [1.0%-1.2%]). Adjusting for age and sex, risk of PH was higher among patients with VTE with underlying comorbidities. Using the Charlson comorbidity index, there was a dose-response relationship, whereby greater scores were associated with increased PH risk (score ≥5 versus 0: HR, (2.50 [2.30-2.71])). When evaluating individual comorbidities, the strongest associations were observed with concomitant heart failure (HR, 2.17 [2.04-2.31]), chronic pulmonary disease (2.01 [1.90-2.14]), and alcohol abuse (1.66 [1.29-2.13]). Conclusions In this large, real-world population of insured people with VTE, 3.5% developed PH in the 2years following their initial VTE event. Risk was higher among women, with increasing age, and in those with additional comorbidities at the time of the VTE event. These data provide insights into the burden of PH and risk factors for PH among patients with VTE.

Chronic Thromboembolic Pulmonary Hypertension.

Chronic thromboembolic pulmonary hypertension (CTEPH), defined as precapillary pulmonary hypertension (PH) by right heart catheterization and imaging consistent with chronic thromboembolism, is a long-term complication of pulmonary embolism (PE). Pathobiological mechanisms involve pulmonary artery occlusion from organized thromboembolic material despite at least three months of uninterrupted therapeutic anticoagulation followingacute PE and secondary microvasculopathy. Delay in diagnosis and management of CTEPH is associated with poor outcomes. High clinical suspicion,comprehensiveassessment of residual dyspnea or exercise intolerance in the aftermath of PE andaccurate interpretation ofcomputed tomography pulmonary angiography (CTPA) are pivotal steps inthe diagnosis. Ventilation-perfusion (V/Q) scan is the preferred initial radiologicscreening tool as normal V/Q essentiallyrules outCTEPH. Any mismatched perfusion defect on the V/Q scan in the setting of PH or any finding compatible with chronic thromboembolism on CTPA should prompt referral to an expert CTEPH center. Once the diagnosis is verified, all eligible patients should be offered pulmonary thromboendarterectomy (PTE). Pulmonary vasodilators or balloon pulmonary angioplasty are safe and effective in inoperable or post-PTE persistent/recurrent CTEPH. During the course of their disease, a patient may receive a combination of treatments, at times consisting of all three strategies. Lifelong therapeutic anticoagulation is recommended for CTEPH.