Clinical cases in chronic thromboembolic pulmonary hypertension, 1st ed , william r auger, deepa gopalan, 2020 1349

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Clinical Cases in Cardiology Series Editors: Ravi V Shah · Siddique A Abbasi · James L Januzzi William R Auger Deepa Gopalan Editors Clinical Cases in Chronic Thromboembolic Pulmonary Hypertension Clinical Cases in Cardiology Series Editors: Ravi V. Shah Boston, MA, USA Siddique A. Abbasi Providence, Rhode Island, USA James L. Januzzi Boston, MA, USA Clinical cases are a key component in modern medical education, assisting the trainee or recertifying clinician to work through unusual cases using best practice techniques Cardiology is a key discipline in this regard and is a highly visual subject requiring the reader to describe often very subtle differences in the presentation of patients and define accurately the diagnostic and management criteria on which to base their clinical decision-making This series of concise practical guides is designed to facilitate the clinical decision-making process by reviewing a number of cases and defining the various diagnostic and management decisions open to clinicians Each title will be illustrated and diverse in scope, enabling the reader to obtain relevant clinical information regarding both standard and unusual cases in a rapid, easy to digest format More information about this series at http://www.springer.com/series/14348 William R Auger  •  Deepa Gopalan Editors Clinical Cases in Chronic Thromboembolic Pulmonary Hypertension Editors William R Auger Lewis Katz School of Medicine Temple University Philadelphia, PA USA Deepa Gopalan Department of Radiology Imperial College Hospitals London UK ISSN 2523-3009    ISSN 2523-3017 (electronic) Clinical Cases in Cardiology ISBN 978-3-030-17365-4    ISBN 978-3-030-17366-1 (eBook) https://doi.org/10.1007/978-3-030-17366-1 © Springer Nature Switzerland AG 2020 This work is subject to copyright All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed The use of general descriptive names, registered names, trademarks, service marks, etc in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland Preface It might be best to first acknowledge the origins of Clinical Cases in Chronic Thromboembolic Pulmonary Hypertension Having seen thousands of chronic thromboembolic disease cases over the years, it has always been instructive as to the diagnostic challenges presented by these patients The questions that remain in our understanding of the natural history of this disease, the non-specific nature of the clinical presentation, and the often indistinguishable exam findings between CTEPH and other forms of pulmonary hypertension make an understanding of the evaluation algorithm and the reliance on diagnostic studies a critically important element in ultimately establishing the diagnosis of chronic thromboembolic disease or CTEPH. Consequently, this book focuses not on an overall review of CTEPH as a discipline but rather provides a number of case vignettes, each illustrating an important teaching point that a clinician might find helpful when evaluating a patient suspected of having CTEPH.  Each case is an actual patient presentation referred for endarterectomy surgery; the book is proportioned to present patients who actually exhibited “typical” cases of chronic thromboembolic disease, those with clinically challenging cases, as well as several examples of CTEPH mimics It is our hope that this book will provide a helpful diagnostic road map for the clinician Chronic thromboembolic pulmonary hypertension (CTEPH) is a form of pulmonary hypertension that results from incomplete or non-resolution of a pulmonary embolic burden within the proximal pulmonary arterial bed Though the initial embolic event can be relatively “silent” in some v vi Preface patients who will ultimately develop CTEPH, many patients progress to established disease despite the acute event being recognized and despite an appropriate course of antithrombotic therapy having been prescribed The mechanism of transition between acute and chronic thrombosis is incompletely understood, as are the risk factors in any one individual [1] Complicating matters is that the “obstructive” component due to organized thrombus is but a piece of the entire clinical picture The development of a precapillary vasculopathy and the establishment of systemic collateral circulation “feeding” the pulmonary vasculature are also considered operative in the establishment of the pulmonary hypertension one sees in this disease [2, 3] This complex interplay contributes not only to the variability in clinical presentation but also to a range of radiographic presentations dependent on where any individual is in the course of their chronic thromboembolic disease The “pathology drives the radiology,” and an understanding of this is critically important to the diagnostician Considered to be a rare disease, the actual prevalence of CTEPH worldwide has been difficult to determine [4] Even less is known when considering chronic thromboembolic disease (CTED), which is the presence of persistent, unresolved thrombus in the absence of pulmonary hypertension or right heart compromise [5] The non-specificity of presenting cardiopulmonary complaints, the variability in time course for disease development, and the wide range of patient populations that can be affected account for some of the gaps in our understanding of the epidemiology But equally as important, if not more so, are the difficulties with disease recognition radiographically Confusion as to the utility of ventilation-­­ perfusion scintigraphy, unappreciated pulmonary vascular and parenchymal perfusion findings by CT, and poorly understood pulmonary angiographic patterns in patients with established CTEPH contribute to the underdiagnosis of this disease Difficulties with the distinction between acute, acute-­­ on-­­ chronic, and chronic thromboembolic disease and the misinformation about CTEPH “mimics” further lend to the confusion Preface vii CTEPH is unique among other causes of pulmonary hypertension as it is potentially possible to obtain a complete cure in selected patients, particularly with early intervention Imaging is pivotal for ensuring that the appropriate diagnosis is made at an opportune time [6] The primary goal of imaging is to confirm the presence of CTEPH and evaluate right heart function, while the secondary goal is to delineate the distribution of the disease as a means to determine the most appropriate therapeutic option A single imaging technique is unlikely to provide all the requisite information, and therefore, multimodality imaging is widely used in clinical practice Transthoracic echocardiography is a simple but indispensable noninvasive tool that is routinely employed as the first step in the diagnostic pathway There are several publications detailing the various echocardiographic parameters that are useful in PH evaluation However, it is well recognized that echocardiography relying predominantly on Doppler pressure estimates can miss PH in as many as 10–30%, particularly in the early stages of the disease Technical advances such as three-dimensional (3D) echocardiography can overcome the challenges presented by the complex RV geometry, while RV strain imaging can potentially detect subclinical pulmonary hypertension In a patient with known or suspected pulmonary hypertension, it is necessary to confirm or exclude CTEPH earlier on in the diagnostic pathway Ventilation-perfusion (VQ) scintigraphy is the most sensitive test in the diagnostic algorithm for excluding CTEPH.  A normal perfusion scan carries a high negative predictive valve, and hence, VQ is invaluable as a simple but effective screening tool However, its high sensitivity is unfortunately not matched by high specificity, and there are various conditions in addition to CTEPH that are associated with mismatched perfusion defects Examples of these CTEPH mimics are illustrated in this atlas Any patient with a mismatched perfusion defect will require downstream anatomical testing The vascular abnormalities of CTEPH have been extensively described in the viii Preface literature and include eccentric thrombus that may or may not be calcified, intravascular webs, and stenosis with or without post-stenotic dilatation and pouch defects The vessel may be completely occluded or show abrupt truncation with attenuated segmental branches Systemic collateral vessels (bronchial and non-bronchial) are a feature of chronicity All these features can be delineated using noninvasive techniques such as computed tomography pulmonary angiography (CTPA) and magnetic resonance pulmonary angiography (MRPA) or by the more conventional catheter pulmonary angiography While CTPA is now considered as the standard of care for acute PE, its role in the diagnosis of CTEPH is tinged with controversy There is a well-recognized variability in the diagnostic performance of CTPA in CTEPH that can be partially attributed to relative rarity of the disease and the lack of awareness among the imaging community The lower CT temporal resolution compared to catheter angiography contributes to the suboptimal delineation of the distal pulmonary vasculature This can be circumvented by employing contemporary techniques such as dual-energy CT (DECT) that allow for simultaneous evaluation of pulmonary vascular morphology and lung perfusion abnormalities, but as of now, this lacks prospective validation and hence cannot be mandated for incorporation into routine clinical practice Although CT, MR, and catheter angiography are often considered to be complementary, corroborative information such as mosaic attenuation, another useful discriminator for chronicity in patients with suspected acute or acute-on-­ chronic disease, can be depicted using CTPA, while the bronchopulmonary shunt fraction can be calculated using MR. Cardiac MR is also the reference standard for evaluation of ventricular function There is a growing body of evidence demonstrating the value of multiparametric MR techniques for characterization of RV structure and ­physiology, but their clinical utility in CTEPH is yet to be proven Multidirectional 4D phase-contrast MR is a compelling evolving tool for evaluation of the complex flow patterns within the RV and pulmonary circula- Preface ix tion and could potentially be useful as a screening tool in identifying subclinical PH in the future A few high-volume clinical centers with experience in noninvasive imaging routinely use the road maps of the pulmonary vasculature obtained from CT and MR for operability assessment, but most institutions still resort to catheter angiography for this evaluation Conventional angiography can be tagged to a right heart catheter examination, eliminating the need for a separate puncture While proven to be a safe technique in accomplished hands, it is not without complications Considerable technical expertise is required to ensure that appropriate views are undertaken without excessive exposure to radiation and iodinated contrast medium This involves a fine balance between acquiring orthogonal views following selective or super selective engagement of the catheter into the vessel under consideration and observing the capillary phase for perfusion defects The advent of balloon pulmonary angioplasty has led to further refinement of this technique Rotational angiography and cone-beam CT are used in conjunction with the catheter angiography to get exquisite images of the pulmonary arterial tree to the subsegmental level That multimodality imaging contributes vital information for CTEPH diagnosis as well as to the decision-making process for disease management is incontrovertible Some physicians and surgeons are accustomed to interpreting the imaging data without active input from radiologists While there is no doubt that some clinicians are seasoned veterans with years of experience in dealing with CTEPH, they may still fail to understand the nuances of the different imaging modalities and miss subtle but crucial findings It is best to involve a pulmonary vascular imaging specialist who is conversant with the contemporary techniques and understands the subtleties involved Most international guidelines and scientific statements emphasize the need for suspected or confirmed CTEPH cases to be referred to an expert center for discussion by a multidisciplinary team in which a radiologist performs an essential role 180 L Brown et al Figure 19.3  Lung scintigraphy showing both ventilation and perfusion abnormalities Figure 19.4 Follow up CT angiogram of the chest reveals lining thrombus involving the central pulmonary arteries Given the previous history of pulmonary embolism, a ventilation-perfusion scan was obtained The study showed multiple moderate or large segmental perfusion defects throughout both lungs Ventilation images showed xenon retention (Fig. 19.3) Further assessment was obtained via CT pulmonary angiogram (Figs. 19.4 and 19.5) Due to concern for chronic thromboembolic pulmonary hypertension, a right heart catheterization was ultimately performed The hemodynamic measurements showed a right Chapter 19.  Case 19: Parenchymal Lung Disease… 181 Figure 19.5 Lung windows of the same CT image displayed in Figure 19.4 atrial pressure of 9  mmHg, pulmonary artery pressure of 84/28 mmHg with a mean of 47 mmHg, pulmonary capillary wedge pressure of 12  mmHg, cardiac output of 5.52  L/min and pulmonary vascular resistance of 6.3 Woods unit Expert opinion regarding the patient was subsequently pursued Radiographic Interpretation The series of images in the case exhibit a number of interesting findings Figure 19.1 is a single image from a CT pulmonary angiography demonstrating a lobar filling defect in the lingula (block arrow) in keeping with acute pulmonary embolism There is evidence for a pneumomediastinum and subcutaneous air (arrow heads) and a collapsed lung (thin arrow) with a chest drain that has been inserted for a large pneumothorax (not visible on this mediastinal window) The chest radiograph obtained during a subsequent evaluation reveals severe emphysema on the frontal and lateral chest radiograph (Fig. 19.2) as evidenced by hyperexpanded lungs and flattened hemi-diaphragms with disorganization of bronchovascular markings The heart is not enlarged, though there is dilatation of the proximal pulmonary arteries 182 L Brown et al Accompanying VQ scintigraphy appears abnormal in both the ventilation and perfusion components There are multiple segmental and subsegmental mismatched perfusion defects, but in a pattern atypical for that seen in pulmonary embolic disease Ventilation is diffusely abnormal on both sides The follow up CTPA (Figs. 19.4 and 19.5) shows eccentric clot lining the right main pulmonary artery and “straddling” across the main and left pulmonary artery No clot was present in the segmental and subsegmental vasculature There is mild dilatation of the main pulmonary artery compared to the adjacent ascending aorta Lung windows show severe centrilobular emphysema involving both lungs with large areas of lung destruction, this worse in the right lung These proximal vessel findings are most likely secondary to in-situ thrombus that has developed as a result of altered blood flow in areas of destroyed lung as a consequence of gross emphysema The presence of central of central clot with normal or even large segmental vessels should raise the suspicion of in-situ thrombus Clinical Comments The possibility that this patient’s pulmonary hypertension was secondary to chronic thromboembolic disease was rooted in his initial presentation of acute dyspnea Though his symptoms to a large extent were attributable to his infiltrates and pneumothorax—there was also a documented DVT and radiographic evidence for acute pulmonary emboli And despite appropriate treatment of these entities, including a 12 month course of anticoagulants, he failed to return to his prior clinical status The discovery of pulmonary hypertension by echo, and confirmed by right heart catheterization to be beyond what might be expected from COPD alone, raised concerns that another problem might be contributing to his clinical decline And with unmatched perfusion defects by lung scintigraphy, and the finding of eccentric lining thrombus on CT, considering chronic thromboembolic disease as a factor in his ongoing difficulties was reasonable Chapter 19.  Case 19: Parenchymal Lung Disease… 183 But despite what might be interpreted as a significant thrombus burden in the proximal pulmonary vessels, the assessment as to whether or not thromboendarterectomy surgery is appropriate should follow consideration of two observations—that the lining thrombus may not be the principal problem, and there may be no clinical value in attempting to re-perfuse severely damaged lung parenchyma As has been discussed with other cases in this book (see Chaps 19 and 23), the presence of central lining thrombus is not the reason for pulmonary hypertension in most cases As Dr Gopalan has suggested, the mechanism behind the development of lining thrombus is not entirely understood, but is likely a result of an aberrant flow pattern along the vessel wall In particular, this is the probable mechanism in extremely dilated proximal pulmonary arteries And not only can it occur in the context of chronic lung destruction as in this case, but can also be seen in dilated central vessels associated with congenital heart disease such as atrial or ventricular defects Most notable is the concept that attempted re-perfusion of damage lung parenchyma—be it emphysema or fibrosis—is never a clinically sound decision Though some of the CT and VQ abnormalities in this case might have been on the basis of segmental level chronic thromboembolic disease, an endarterectomy of the vessels supplying lung regions with extensive emphysema would not have provided clinical benefit and would have only added risk to an already risky operation Having said this, however, on occasion there are patients with primarily upper lobe emphysema who present with chronic thromboembolic disease involving vessels supplying r­ elatively “preserved” lung parenchyma An endarterectomy of these vessels can restore perfusion-ventilation “matching” and prove to be clinically beneficial Points of Emphasis Thrombendarterectomy in a patient with extensive parenchymal lung disease requires careful assessment of the limited pulmonary hemodynamic and clinical benefits that can be 184 L Brown et al achieved with this approach Lining thrombus in the central pulmonary arteries can be observed in such patients Diagnoses Emphysema Lining thrombus involving the proximal pulmonary arteries Further Reading Moser KM, Fedullo PF, Finkbeiner WE, Golden J. Do patients with primary pulmonary hypertension develop extensive central thrombi? Circulation 1995;91:741–5 Perloff JK, Hart EM, Greaves SM, et al Proximal pulmonary arterial and intrapulmonary radiologic features of Eisenmenger syndrome and primary pulmonary hypertension Am J Cardiol 2003;92:182–7 Index A Acute respiratory failure, 122 Atrial septal defect cardiac magnetic resonance imaging, 171, 172 chest radiograph, 168, 170 CTA, 168, 169, 172 diagnosis, 175 historical and radiographic aspects, 174 lung scintigraphy, 168, 171 multiplanar CT reconstructions, 174 perfusion scintigram, 175 pulmonary hypertension development, 174 SV-ASD, 173 VQ scintigraphy, 172 B Balloon pulmonary angioplasty diagnosis, 39 guidelines and clinical practice, 39 lung scintigraphy, 38 post-angioplasty, 37 pulmonary angiogram, 37 pulmonary digital subtraction pulmonary arteriogram, 36 Raynaud’s phenomenon, 34 © Springer Nature Switzerland AG 2020 W R Auger, D Gopalan (eds.), Clinical Cases in Chronic Thromboembolic Pulmonary Hypertension, Clinical Cases in Cardiology, https://doi.org/10.1007/978-3-030-17366-1 185 186 Index Balloon pulmonary angioplasty (cont.) ventilation perfusion imaging, 35 vessel density, 38 Bilateral unmatched perfusion defects, 136 C Catheter pulmonary angiography, 48, 138 acute versus chronic thromboembolic disease, 154 CTED, 68 CTEPH, 5, 7, 15 Central pulmonary arteries, 42 Chest CT angiogram, 103, 104 Chest radiograph, 12 atrial septal defect, 168, 170 CTED, 63, 67 CTEPH, 2, 47 distal vessel thromboendarterectomy, 52, 53, 56 parenchymal lung disease and chronic thromboemboli, 179, 181 pulmonary arteritis, 125 pulmonary veins, 100, 104 sarcoidosis and large vessel pulmonary vascular disease, 134, 138 Chest x-ray pulmonary arterial pulmonary hypertension mimic CTEPH, 158, 159 pulmonary artery sarcoma, 84, 87 Chronic obstructive pulmonary disease (COPD), 43, 101, 182 Chronic pulmonary embolism, 142 Chronic thromboembolic disease (CTED) acute vs catheter pulmonary angiography, 154 clinical history, 148 CT angiogram, 149, 150 CTPA, 153 diagnoses, 156 duplex venous ultrasound, 149 echocardiogram, 148 family history, 148 intraluminal filling defects, 151, 152 lung ventilation-perfusion scan, 150, 151 perfusion pattern, return of, 152, 153 physical examination, 148 pulmonary hemodynamic profile, 155 transthoracic echocardiogram, 148, 149 cardiovascular exam, 179 catheter pulmonary angiography, 68 chest radiograph, 63, 67, 179, 181 clinic evaluation, vital signs, 72 Index 187 computed tomography pulmonary angiography, 72 CT angiogram, 73, 75, 178, 180, 181 CT pulmonary angiography, 78 diagnosis, 69, 80, 184 digital subtraction pulmonary arteriogram, 64, 65 distal vessel thromboendarterectomy, 57 family history, 62 laboratory assessment, 179 laboratory data, 63 lung scintigraphy, 64, 180 medical history, 61, 62, 71 minute ventilation, 65 organized thrombus endarterectomized at surgery, 77 pulmonary thromboendarterectomy, 77 residual perfusion defects, 68 surgery, 69 surgical outcomes, 79 ventilation perfusion scintigraphy, 73, 74, 78 VQ scintigraphy, 67, 78 Chronic thromboembolic pulmonary hypertension (CTEPH) calcified thrombus lining, central pulmonary vessels, 45 catheter pulmonary angiography, 5, 7, 48 calcified thrombus lining, central pulmonary vessels, 45 chest radiograph, 2, 42, 47 chronic thromboembolic disease, radiographic evidence for, 145 clot specimen removing, 5, COPD, 43 CT angiography, 3, 7, 142 CT scan, 49 CTPA, 7, 47 diagnosis, 10, 49, 146 diagnostic algorithm, 7, diagnostic guidelines, disease distribution, 48 dyspnea, 41 echocardiogram, 2, 142 exertional dyspnea and functional disability, 141 extensive parenchymal lung disease, 44, 46 features of, 143 lining clot, 144 lining thrombus within enlarged central pulmonary vessels, 146 lung perfusion scan, 143, 144 lung scintigraphy, 145–146 medical history, 43 negative study, oral prostacyclin therapy, 47 PAH with IST, 144 188 Index Chronic thromboembolic pulmonary hypertension (CTEPH) (cont.) physical exam, 42 preoperative lung perfusion scintigraphy, pulmonary arteriogram, 46 pulmonary embolism, 43 transplant evaluation, 47 TTE, 2, unusual presentation for catheter based pulmonary angiogram, 15 computerized tomography pulmonary angiogram, 13 CT angiography, 14, 17 diagnosis, 19 distal arteriopathy, 18 frontal and lateral chest radiographs, 12 lung scintigraphy, 14, 16 organized thrombus removing, 16 pulmonary angiography, 15 ventilation perfusion scan, 44 VQ scintigraphy, Chronic thrombus and metastatic cancer CT scan, 92 diagnosis, 96 endarterectomy specimen, 93, 94 islands of malignancy cells, 94, 95 medical history, 92 PET-CT, 94 pulmonary function testing, 93 pulmonary tumor emboli, 96 ventilation-perfusion scan, 93 Computerized tomography (CT), 92 Computerized tomography angiogram acute versus chronic thromboembolic disease, 149, 150 atrial septal defect, 168, 169, 172 CTED, 73, 75 CTEPH, 14, 17, 142 parenchymal lung disease and chronic thromboemboli, 178, 180, 181 pulmonary artery sarcoma, 82, 86, 87 pulmonary veins, 105 pulmonary veno-occlusive disease, 110, 111, 113, 114 Computerized tomography pulmonary angiogram (CTPA), 47 CTED, 72 CTEPH, pulmonary arterial pulmonary hypertension mimic CTEPH, 164 pulmonary veno-occlusive disease, 117 Congenital heart disease, 145 Index 189 D Deep venous thrombi (DVT), Distal arteriopathy, 18 Digital subtraction pulmonary angiogram CTED, 64, 65 distal chronic thromboembolic disease, 27, 28 pulmonary arteritis, 129 Distal chronic thromboembolic disease chronic thrombotic material removing, 26 diagnosis, 31 ECG, 22 echocardiogram, 23, 27 PA and lateral digital subtraction pulmonary angiogram, 27, 28 perfusion scan, 29 prognostic factor, 30 pulmonary angiogram, 24, 25 risk factor, 30 transthoracic echocardiogram, 23 VQ scan, 23, 24, 29 Distal vessel thromboendarterectomy chest radiograph, 52, 53, 56 chronic thromboembolic disease, 57 diagnosis, 59 endarterectomy, organized thrombus removed at, 56 pulmonary angiogram, 54 pulmonary artery, 55, 56 right heart catheterization, 54 subclavian venogram, 52 surgery evaluation, 58 ventilation perfusion scan, 52, 53 VQ scintigraphy, 56 E Echocardiogram acute versus chronic thromboembolic disease, 148 distal chronic thromboembolic disease, 23, 27 Eisenmenger’s syndrome, 145 Emphysema, 179, 182 Endarterectomy, organized thrombus removed at, 56 Extensive parenchymal lung disease, 44, 46 H Hypoxemia, 99 190 Index I Intraluminal filling defects, 151, 152 L Large vessel pulmonary vascular disease bilateral unmatched perfusion defects, 136 cardiopulmonary exercise testing, 136 catheter angiography, 138 chest radiograph, 134, 138 chronic thromboembolic disease catheter-based pulmonary angiography, 136 mimics of, 139 compressive adenopathy and perfusion defects, 137, 138 CT angiogram, 135 CTPA, 138 diagnosis, 140 echocardiogram, 134 extensive soft tissue, 135, 138 nultifactorial causes, 138 perfusion abnormalities, 139 Lung perfusion scan, 143, 144 Lung scintigraphy atrial septal defect, 168, 171 balloon pulmonary angioplasty, 38 CTED, 64 CTEPH, 14, 16, 146 parenchymal lung disease and chronic thromboemboli, 179, 180 pulmonary arteritis, 122, 123 pulmonary veins, 102 Lung ventilation-perfusion scan, 150, 151 M MR angiogram (MRA), 125, 127 N Nonsteroidal therapy, 101 O Oral prostacyclin therapy, 47 Index 191 P Paget-Schroetter syndrome, 52 Parenchymal lung disease cardiovascular exam, 179 chest radiograph, 179, 181 CT angiogram, 178, 180, 181 diagnoses, 184 laboratory assessment, 179 lung scintigraphy, 180 re-perfusion of, 183 PET CT chronic thrombus and metastatic cancer, 94 pulmonary artery sarcoma, 85–87 Post PE syndrome, 68 Pulmonary angiogram distal chronic thromboembolic disease, 24, 25 distal vessel thromboendarterectomy, 54 pulmonary veins, 104 Pulmonary arterial pulmonary hypertension mimic CTEPH chest x-ray, 158, 159, 163 CT chest with pulmonary angiography, 161 CTPA, 160, 164 diagnosis, 165 echocardiogram, 158, 164 laboratory and routine testing, 158 medical history, 158 pulmonary angiography, 163 pulmonary function test, 158, 159 PVOD, 164 right heart catheterization hemodynamics, 162 ventilation perfusion scanning, 161, 165 xenon ventilation scanning, 160 Pulmonary arteriogram pulmonary veins, 102, 103 pulmonary veno-occlusive disease, 113 Pulmonary arteritis acute respiratory failure, 122 chest radiograph, 125 diagnoses, 130 digital subtraction pulmonary arteriogram, 129 echocardiogram, 121 initial evaluation, 122 lung scintigraphy, 122, 123 192 Index Pulmonary arteritis (cont.) MRA, 125, 127 physical exam, 123 pulmonary artery stenosis, 129 pulmonary vessel anatomy and digital subtraction pulmonary angiography, 125, 126 right main pulmonary artery, 122, 124 subsequent assessment, 128 VQ scan, 122 Pulmonary artery sarcoma chest x-ray, 84, 87 chronic and progressive symptoms, 83 CT pulmonary angiography, 82, 86, 87 diagnosis, 88 fusion PET CT, 85–87 PTE surgery, 83 pulmonary intra-arterial filling defects, 87 pulmonary vascular tumors, 88 social history, 83 surgical specimen removing, 85, 86 ventilation perfusion lung scintigraphy scan, 84 VQ scintigraphy, 87 Pulmonary artery stenosis, 129 Pulmonary digital subtraction pulmonary arteriogram, 36 Pulmonary emboli (PE), Pulmonary veins chest CT angiogram, 103, 104 chest radiograph, 100, 104 computerized tomography, 102 CT angiogram, 105 diagnoses, 106 heart catheterization with pulmonary angiography, 102 hypoxemia, 99 lung scintigraphy, 102 medical history, 101 nonsteroidal therapy, 101 outflow impedance, 105 pulmonary angiogram, 104 pulmonary arteriogram, 102, 103 social history, 101 V/Q scintigraphy, 104 Pulmonary veno-occlusive disease, 109 2D echocardiography, 110 abnormal in, 118 catheter pulmonary angiography, 117 CT angiography, 110, 111, 113, 114 Index 193 CTPA, 117 diagnosis, 118 H and E stain, 116 histopathology, 115 mismatched perfusion defects, 118 multi-disciplinary meeting, 112 pulmonary arteriogram, 113 right cardiac catheterization, 111 ventilation perfusion, 111, 112 ventilation-perfusion scintigraphy, 117 Verhoff stain, 115 Pulmonary veno-occlusive disease (PVOD), 164 R Right heart catheterization, 54 Rivaroxaban, 34 S Sarcoidosis bilateral unmatched perfusion defects, 136 cardiopulmonary exercise testing, 136 catheter angiography, 138 chest radiograph, 134, 138 chronic thromboembolic disease, catheter-based pulmonary angiography, 136 chronic thromboembolic disease, mimics of, 139 compressive adenopathy and perfusion defects, 137, 138 CT angiogram, 135 CTPA, 138 diagnosis, 140 echocardiogram, 134 extensive soft tissue, 135, 138 nultifactorial causes, 138 perfusion abnormalities, 139 Sinus venosus atrial septal defect (SV-ASD), 173 Subclavian venogram, 52 Systemic hypertension, 179 T Takayasu arteritis, 128 Transthoracic echocardiogram (TTE) acute versus chronic thromboembolic disease, 148, 149 CTEPH, 2, 194 Index Thromboembolic disease, acute vs chronic catheter pulmonary angiography, 154 clinical history, 148 CT angiogram, 149, 150 CTPA, 153 diagnoses, 156 duplex venous ultrasound, 149 echocardiogram, 148 family history, 148 intraluminal filling defects, 151, 152 lung ventilation-perfusion scan, 150, 151 perfusion pattern, return of, 152, 153 physical examination, 148 pulmonary hemodynamic profile, 155 transthoracic echocardiogram, 148, 149 V Ventilation perfusion imaging balloon pulmonary angioplasty, 35 chronic thrombus and metastatic cancer, 93 CTPEH, 44 distal vessel thromboendarterectomy, 52, 53 pulmonary arterial pulmonary hypertension mimic CTEPH, 161 pulmonary veno-occlusive disease, 111, 112 Ventilation perfusion scintigraphy, 73, 74, 78, 84, 117 VQ scintigraphy, 104 atrial septal defect, 172 CTED, 67, 78 CTEPH, distal chronic thromboembolic disease, 23, 24 distal vessel thromboendarterectomy, 56 parenchymal lung disease and chronic thromboemboli, 182 pulmonary arteritis, 122 pulmonary artery sarcoma, 87 W Williams syndrome, 129 X Xenon ventilation scanning, 160 ... USA e-mail: Bill.Auger@tuhs.temple.edu © Springer Nature Switzerland AG 2020 W R Auger, D Gopalan (eds.), Clinical Cases in Chronic Thromboembolic Pulmonary Hypertension, Clinical Cases in Cardiology,... USA e-mail: Bill.Auger@tuhs.temple.edu © Springer Nature Switzerland AG 2020 W R Auger, D Gopalan (eds.), Clinical Cases in Chronic Thromboembolic Pulmonary Hypertension, Clinical Cases in Cardiology,... Clinical Cases in Cardiology ISBN 97 8-3 -0 3 0-1 736 5-4     ISBN 97 8-3 -0 3 0-1 736 6-1  (eBook) https://doi.org/10.1007/97 8-3 -0 3 0-1 736 6-1 © Springer Nature Switzerland AG 2020 This work is subject to copyright
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