April 2023 Medical Image of the Month: Atrial Myxoma in the setting of Raynaud’s Phenomenon: Early Echocardiography and Management of Thrombotic Disease

Figure 1. ECG demonstrating sinus bradycardia and T-wave inversion in lead III and aVF.

Figure 2.  Transthoracic echo apical four-chamber view (zoomed) demonstrating 2.3 x 2.6 cm echogenic mass of the left atrium. LV = left ventricle. RA = right atrium. LA = left atrium.

Figure 3.  Transesophageal echo, midesophageal long axis view demonstrating 2.5 x 1.71 cm echogenic left atrial mass attached to upper dome of the left atrium. LA = left atrium. LV = left ventricle.

A 43-year-old woman presents to the Emergency Department (ED) with right-sided weakness and numbness for several hours. Medical history is significant for Raynaud’s Phenomenon (RP), initially presenting six months prior to presentation, manifesting as intermittent episodes of painless discoloration of multiple fingers.  Cardiac exam was unremarkable with regular rhythm and no discernable murmur. Neurological exam demonstrated right arm pronator drift. Other examination findings were unremarkable. Labs demonstrated a troponin of 0.00 ng/mL, C-reactive protein of 2.28 mg/dL, and an erythrocyte sedimentation rate of 40 mm/hr. The electrocardiogram (ECG) demonstrated sinus bradycardia and notable for T-wave inversion in lead III and aVF, but without any ST-segment deviations (Figure 1).  Magnetic Resonance Imagining (MRI) of the brain demonstrated acute ischemic left frontal, left parietal, and right parietal infarcts along with mild subcortical left parietal infarct, concerning for venous or watershed distal embolic arterial infarct. MRI Angiogram of the brain showing diminutive bilateral, lateral transverse dural venous sinuses, consistent with thrombus. The patient’s neurological deficits resolved within five hours of ED arrival. Given the background diagnoses of RP and new thrombosis, a complete autoimmune and hypercoagulability workup was pursued and was otherwise negative.

As part of acute stroke work-up, the patient also underwent transthoracic echocardiogram (TTE) with a bubble study, which was significant for left atrial (LA) echogenic intracardiac structure attached to the superior part of the LA (Figure 2). Transesophageal Echocardiogram (TEE) was performed which demonstrated a large, 2.5 x 1.71 cm mass, consistent with an atrial myxoma, not appearing to involve the interatrial septum but instead thought to originate from the upper dome of the atrium immediately adjacent to the pulmonary veins (Figure 3). Patient was also evaluated by neurology and started on anticoagulation with parental continuous unfractionated heparin infusion given the dural venous sinus thrombosis and a possible hypercoagulable state due to the underlying myxoma. Patient underwent surgical resection of the atrial mass Histopathological examination of the resected mass was consistent with the diagnosis of atrial myxoma.

Although atrial myxomas are the most common primary cardiac tumor, clinical presentation ranges from incidental imaging findings to profound life-threading cardiovascular manifestations (1). This range of presentation is closely associated with size, mobility, and location (2). Pinede et al. studied 112 cases of atrial myxomas and reported that signs of cardiac obstruction were the primary manifestation of LA myxoma. Approximately, 67% of patients presented with signs of cardiac obstruction, such as heart failure, syncope, or myocardial infarction, while embolic signs were only present in 29% of patients. Systemic signs including fever and weight loss were only reported in 34% of patients with only 5% of patients having associated connective tissue disease (3). Rarely, RP has been described as the primary presenting symptom of atrial myxoma (4,5), underscoring the utility of maintaining a high degree of suspicion when symptomatology coexists.

RP is a vascular response to stress or cold temperature that appears as color changes in the digits (6). Although primary RP has no known underlying etiology, it is more commonly seen in female patients with a history of smoking, migraine headaches, and cardiovascular disease (6). This is in contrast to secondary RP, which presents in patient with an underlying autoimmune rheumatic disease including, but not limited, to Systemic Sclerosis, Mixed Connective Tissue Disease, Systemic Lupus Erythematosus, Sjogren’s Syndrome, and hematologic disorders such as Cryoglobulinemia, Cold Agglutinins Disease, and Paraproteinemia (7).

Atrial myxoma may rarely make its initial appearance under the guise of RP (4). This phenomenon is likely attributable to overproduction of IL-6 by the myxoma (9-11). Our patient presented with RP six months prior to her presentation to the ED with right-sided weakness and numbness and a complete autoimmune and hypercoagulability workup was negative; this may suggest that the underlying pathophysiology of her RP is the associated overproduction of IL-6 by the atrial myxoma.

TTE may be considered in the initial diagnostic evaluation of a patient presenting with RP without additional findings suggestive of secondary etiologies. Given that myxomas are typically localized within the atrial lumen, transthoracic echocardiography is a highly sensitive modality for diagnosis, whereas CT and MRI may also help in diagnostics in uncertain cases. Once suspicion of a cardiac myxoma has been supported by imaging modalities, surgical removal of the tumor should be performed as soon as possible due to the risk of myxoma associated embolic episodes (5).  Post intervention, long term prognosis is excellent with an approximated 5% rate of recurrence (3). Long-term follow-up with serial TTE are recommended, particularly in younger patients (3) but there is no specific guideline regarding the frequency of TTE surveillance post atrial myxoma resection.

Ali A. Mahdi MD, Chris Allahverdian MD, Vishal Patel MD, Serap Sobnosky MD

Dignity Health, St. Mary Medical Center, Department of Internal Medicine, Long Beach, CA

References

1. Roberts WC. Primary and secondary neoplasms of the heart. Am J Cardiol. 1997 Sep 1;80(5):671-82. [CrossRef] [PubMed]
2. Zaher MF, Bajaj S, Habib M, Doss E, Habib M, Bikkina M, Shamoon F, Hoyek WN. A giant left atrial myxoma. Case Rep Med. 2014;2014:819052. [CrossRef]
3. Pinede L, Duhaut P, Loire R. Clinical presentation of left atrial cardiac myxoma. A series of 112 consecutive cases. Medicine (Baltimore). 2001 May;80(3):159-72. [CrossRef] [PubMed]
4. Skanse B, Berg No, Westfelt L. Atrial myxoma with Raynaud's phenomenon as the initial symptom. Acta Med Scand. 1959 Jul 25;164:321-4. [CrossRef] [PubMed]
5. Reynen K. Frequency of primary tumors of the heart. Am J Cardiol. 1996 Jan 1;77(1):107. [CrossRef] [PubMed]
6. Abdulla, M. C., & Alungal, J. (2015). Atrial myxoma in a primigravida presenting as Raynaud’s phenomenon. Rheumatology Reports, 7(1). [CrossRef]
7. Prete M, Favoino E, Giacomelli R, et al. Evaluation of the influence of social, demographic, environmental, work-related factors and/or lifestyle habits on Raynaud's phenomenon: a case-control study. Clin Exp Med. 2020 Feb;20(1):31-37. [CrossRef] [PubMed]
8. Khouri C, Blaise S, Carpentier P, Villier C, Cracowski JL, Roustit M. Drug-induced Raynaud's phenomenon: beyond β-adrenoceptor blockers. Br J Clin Pharmacol. 2016 Jul;82(1):6-16. [CrossRef] [PubMed]
9. Jourdan M, Bataille R, Seguin J, Zhang XG, Chaptal PA, Klein B. Constitutive production of interleukin-6 and immunologic features in cardiac myxomas. Arthritis Rheum. 1990 Mar;33(3):398-402. [CrossRef] [PubMed]
10. Saji T, Yanagawa E, Matsuura H, Yamamoto S, Ishikita T, Matsuo N, Yoshirwara K, Takanashi Y. Increased serum interleukin-6 in cardiac myxoma. Am Heart J. 1991 Aug;122(2):579-80. [CrossRef] [PubMed]
11. Parissis JT, Mentzikof D, Georgopoulou M, Gikopoulos M, Kanapitsas A, Merkouris K, Kefalas C. Correlation of interleukin-6 gene expression to immunologic features in patients with cardiac myxomas. J Interferon Cytokine Res. 1996 Aug;16(8):589-93. [CrossRef] [PubMed]

Cite as: Mahdi AA, Allahverdian C, Patel V, Sobnosky S. April 2023 Medical Image of the Month: Atrial Myxoma in the setting of Raynaud’s Phenomenon: Early Echocardiography and Management of Thrombotic Disease. Southwest J Pulm Crit Care Sleep. 2023;26(4):56-58. doi:https://doi.org/10.13175/swjpccs006-23 PDF

Medical Image of the Month: Bilateral Atrial Enlargement

Figure 1. Portable chest radiograph showing elevation of the left mainstem bronchus (red arrow).

Figure 2. Thoracic CT scan showing right atrial enlargement (blue circle) and left atrium (red circle).

Figure 3. Upper Image: Static image from echocardiogram showing right atrial enlargement (white circle). Lower image: video of echocardiogram.

A 97-year-old woman was repeatedly admitted for dyspnea, hypoxemia and treated with antibiotics for presumed left lower lobe pneumonia. She has a past medical history of atrial fibrillation, congestive heart failure and sick sinus syndrome with placement of a cardiac pacemaker. Notably on physical examination, she had heart rate of 110 beats/minute, temperature of 98.8°F, blood pressure of 122/72 mm Hg, and a respiratory rate of 27 breaths/minute. She had a sternal heave, a grade 4/6 "blowing" holosystolic murmur, a loud S2, jugular venous distension and an enlarged liver. Chest x-ray showed obscuration of the left lower lobe - the left heart border cannot be seen, and the L mainstem bronchus is straightened and lifted superiorly (Figure 1). An image of the heart is shown from a CT abdomen obtained 6 months previously, showing cardiomegaly, particularly massive atrial enlargement (Figure 2). An ultrasound showed bilateral atrial enlargement with moderate mitral regurgitation and severe tricuspid regurgitation (Figure 3). The left ventricular ejection fraction was 55%, but with abnormal septal motion. She was treated with gentle diuresis to help relieve volume overload, and isosorbide dinitrate for preload and afterload reduction. Pulmonary hypertension was attributed to chronic mitral regurgitation. The cause was unclear - the patient remembered that her brother had rheumatic fever as a young recruit in WWII, but didn't know whether she had ever experienced it.

Atrial enlargement can be of prognostic significance. Left atrium size has been found to be a predictor of mortality due to both cardiovascular issues as well as all-cause mortality (1). Larger right atrium than left atrium has been associated with all-cause mortality in elderly patients with heart failure (2).

Robert A. Raschke, MD

University of Arizona College of Medicine-Phoenix

Phoenix, AZ USA

References

1. Patel DA, Lavie CJ, Milani RV, Shah S, Gilliland Y. Clinical implications of left atrial enlargement: a review. Ochsner J. 2009 Winter;9(4):191-6. [PubMed]
2. Almodares Q, Wallentin Guron C, Thurin A, Fu M, Kontogeorgos S, Thunstrom E, Johansson MC. Larger right atrium than left atrium is associated with all-cause mortality in elderly patients with heart failure. Echocardiography. 2017 May;34(5):662-7. [CrossRef] [PubMed]

Cite as: Raschke RA. Medical image of the month: bilateral atrial enlargement. Southwest J Pulm Crit Care. 2019;19(1):10-1. doi: https://doi.org/10.13175/swjpcc023-19 PDF

Medical Image of the Month: Massive Right Atrial Dilation After Mitral Valve Replacement

Figure 1. Chest radiograph demonstrating massive cardiomegaly with pulmonary congestion and markedly dilated right atrium.

Figure 2. Transthoracic echocardiogram demonstrating marked dilation of the right atrium to 9.6 cm in its greatest dimension.

A 92-year-old woman with a history of mechanical mitral valve replacement (+25 years prior to presentation), coronary artery bypass grafting, pacemaker placement and heart failure (EF 25%) presented from a nursing facility for dyspnea of 1 day’s duration. Recently, the patient had experienced a bowel perforation s/p surgical repair 3 weeks prior.

Admission chest radiograph was significant for massive cardiomegaly with pulmonary congestion and markedly dilated right atrium (Figure 1). Formal echocardiography was ordered, which re-demonstrated the patient’s known heart failure with reduced ejection fraction. Additionally, all 4 chambers of the heart were noted to be dilated, but the right atrium was revealed to be severely enlarged to >9 cm (Figure 2). On review of outside records, the patient’s cardiac history was notable for chronic dilation of the RA, RV and LA for several years with low, but stable, LV ejection fraction. Ultimately, the patient was noted to have worsening abdominal distension concerning for acute abdomen. However rather than pursue additional aggressive work up after her recent surgery, comfort measures were preferred.

This case illustrates some of the possible long-term effects of mitral valve replacement. In recent years mitral valve repair has become the preferred method over replacement for degenerative valve disease in western countries (1). While there are documented short term benefits to both mitral valve replacement and mitral valve repair long term data is less available (2). Long-term survival in most studies is reported in 5,10, and 15-year intervals. As was the case with our patient, patients with mitral valve replacement greater than 20 years in age have significantly less information associated with them. Although at this time longitudinal studies suggest benefits for both mitral valve replacement and repair, further investigation into long term complications is warranted (3). As our society continues to age, understanding the risks and complications associated with previous valve repair will help guide therapeutic interventions in the geriatric patient.

Richard Young, MD* and Alexander Ravajy, BS**

*University of Arizona Department of Internal Medicine

**University of Oklahoma Department of Microbiology

Banner University Medical Center

Tucson, AZ USA

References

1. Gammie JS, Sheng S, Griffith BP, Peterson ED, Rankin JS, O'Brien SM, Brown JM. Trends in mitral valve surgery in the United States: results from the Society of Thoracic Surgeons Adult Cardiac Surgery Database. Ann Thorac Surg. 2009 May;87(5):1431-7. [CrossRef] [PubMed]
2. McNeely CA, Vassileva CM. Long-term outcomes of mitral valve repair versus replacement for degenerative disease: a systematic review. Curr Cardiol Rev. 2015;11(2):157-62. [CrossRef] [PubMed]
3. Christina MV, Gregory M, Christian M, Theresa B, Stephen M, Steven S, Stephen H. Long term survival of patients undergoing mitral valve repair and replacement a longitudinal analysis of Medicare fee-for-service beneficiaries. Circulation. 2013;127(18):1870–6. [CrossRef] [PubMed]

Cite as: Young R, Ravajy A. Medical image of the month: Massive right atrial dilation after mitral valve replacement. Southwest J Pulm Crit Care. 2018;18(1):8-9. doi: https://doi.org/10.13175/swjpcc111-18 PDF 

Medical Image of the Week: Cardiac Magnetic Resonance Imaging Findings of Severe RV Failure

  

Figure 1. Transthoracic echocardiography, short-axis view (1A) and four-chamber view (1B) demonstrating leftward deviation with flattening of interventricular septum (“D-sign”) due to increased right ventricular pressure and volume overload from severe pulmonary arterial hypertension (PAH). RV=right ventricle. RA=right atrium. LV=left ventricle.

Figure 2. Cardiac Magnetic Resonance Imaging, sagittal view (2A), and cross-sectional view (2B) show the same signs of massive right ventricular (RV) pressure and volume overload with severe RV dysfunction. RV ejection fraction of 13%. RV=right ventricle. RA=right atrium. LV=left ventricle. LA=left atrium.

A 56-year-old man with history a of alcohol abuse presents with progressive shortness of breath on exertion, bilateral lower extremity swelling and 12-pound weight gain over two weeks.

His transthoracic echocardiography (Figure 1) demonstrated severely increased global right ventricle (RV) size, severely dilated right atrium (RA), severe pulmonary artery (PA) dilation, moderate tricuspid regurgitation (TR) and right ventricular systolic pressure (RVSP) estimated at 85 + central venous pressure (CVP) in the context of severely reduced RV systolic function.  Right heart catheterization (RHC) showed PA pressure (systolic/diastolic, mean) of 94/28, 51 mmHg with a PA occlusion pressure of 12 mmHg. After extensive evaluation, our patient’s presentation of right heart failure seemed to be a manifestation of idiopathic pulmonary arterial hypertension.

Our patient subsequently had cardiac MRI (cMRI) with findings shown above (Figure 2). CMRI is a valuable, three-dimensional imaging modality that provides detailed morphology of the cardiac chambers along with accurate quantification of chamber volumes, myocardial mass and transvalvular flow (1). Cardiac MRI is an accurate tool to estimate the RV function at baseline and to follow up response to treatment. RV function at presentation and after treatment are very important determinants of prognosis independent of other hemodynamic indices (2).  

Kelly Wickstrom, DO¹, Huthayfa Ateeli, MBBS², Sachin Chaudhary, MD²

¹Internal Medicine Department and ²Pulmonary and Critical Care Division

Banner University Medical Center

Tucson, AZ USA

References

1. Grünig E, Peacock AJ. Imaging the heart in pulmonary hypertension: an update. Eur Respir Rev. 2015 Dec;24(138):653-64. [CrossRef] [PubMed]
2. Swift AJ, Wild JM, Nagle SK, et al. Quantitative magnetic resonance imaging of pulmonary hypertension: a practical approach to the current state of the art. J Thorac Imaging. 2014 Mar;29(2):68-79. [CrossRef] [PubMed]

Cite as: Wickstrom K, Ateeli H, Chaudhary S. Medical image of the week: cardiac magnetic resonance imaging findings of severe RV failure. Southwest J Pulm Crit Care. 2018;16(5):252-3. doi: https://doi.org/10.13175/swjpcc047-18 PDF

The “Hidden Attraction” of Cardiac Magnetic Resonance Imaging for Diagnosing Pulmonary Embolism

Ahmed A. Harhash MD¹

James Cassuto MD PhD²

Ryan J. Avery MD³

Phillip H. Kuo MD PhD³ 

¹Division of Cardiology, Department of Medicine, and the ³Department of Radiology University of Arizona, Tucson, Arizona USA

²Department of Radiology, Jackson Memorial Hospital, Miami, Florida USA

Abstract

While various modalities exist for the diagnosis of pulmonary embolism (PE), CT pulmonary angiography (CTPA) is the most widely used and can establish the diagnosis quickly and reliably. We report a patient who presented with syncope who developed pulseless electrical activity (PEA) arrest in the emergency department. Given the presence of acute renal injury, CTA was felt to be contraindicated. A ventilation-perfusion lung (VQ) scan demonstrated low probability for PE; however, echocardiography revealed evidence for right heart strain. Subsequent cardiac magnetic resonance imaging (CMR) unexpectedly revealed a saddle PE. This case highlights the potential role for MR for the diagnosis of PE when high clinical suspicion is discordant with results of conventional imaging.

Introduction

High-risk acute pulmonary embolism (PE) - generally defined as patients presenting with shock or hypotension- is associated with up to 22% 30-day mortality (1). The role of imaging for diagnosing PE is critical, with CT pulmonary angiography (CTPA) the most widely used and generally accepted as the test of choice. CTPA offers high sensitivity and specificity for PE, short acquisition time, and the ability to diagnose alternative diagnoses in patients presenting with symptoms suggesting acute PE but with negative CTPA results. In the setting of stable chronic renal insufficiency (GFR ≥30 mL/min/1.73m2) the risk of contrast-induced nephropathy from intravenous iodinated contrast media is low, and administration of iodinated intravenous contrast in this setting considered safe for most patients (2). However, few data regarding the safety of CTPA in the setting of worsening acute kidney injury are available. In these circumstances, an understanding of alternative imaging modalities for the assessment of suspected acute PE is critical. 

Case Presentation

A 61-year-old man with no past medical history presented unresponsive to the emergency department after collapsing while shopping. The patient was minimally arousable during initial assessment and reported sudden onset of shortness of breath prior to syncope. In the emergency room, the patient developed pulseless electrical activity- cardiac arrest. Return of spontaneous circulation was achieved after 2-cycles of CPR and endotracheal intubation. The patient then developed ventricular fibrillation with return of spontaneous circulation following defibrillation. The ECG demonstrated supraventricular arrhythmia with right bundle branch block. Emergent cardiac catheterization was performed for possible acute coronary syndrome but revealed no obstructive lesions. CT pulmonary angiography was then considered to evaluate for PE, however alternative examinations were pursued secondary to acute kidney injury (creatinine 2.3 mg/dL vs. baseline 1.1 mg/dL). Transthoracic echocardiography revealed right ventricular enlargement and hypokinesis (Figure 1).

Figure 1. Apical four chamber view (transthoracic echocardiogram after intravenous administration of DEFINITY® perflutren lipid microsphere) demonstrated septal flattening consistent with right ventricular pressure/volume overload (black arrows).

Immediate anticoagulation with intravenous heparin infusion was started as clinical suspicion for PE was high, particularly given the presence of right heart strain. The patient regained hemodynamic stability and was extubated by hospital day three. To assess for the presence of PE, a VQ scan was performed, which showed low probability for PE (Figure 2). 

Figure 2. Nuclear ventilation-perfusion scan was performed first with 50 millicuries of technetium-99m diethylenetriaminepentaacetic acid aerosol administered via inhalation with multi-view planar imaging of the lungs, followed by intravenous administration of 6 millicuries of technetium-99m macroaggregated albumin with repeat multi-view planar imaging. Matched ventilation-perfusion defects are seen involving the anterior and apical right upper lobe and basal posterior left lower lobe (black arrows), no segmental mismatched perfusion defects were detected. The final impression was low probability for acute pulmonary embolism.

As the RV dysfunction remained unexplained, cardiac magnetic resonance (CMR) was performed to evaluate right ventricular function and revealed no intrinsic RV disease, but did reveal a central, “saddle” PE (Figure 3).  

Figure 3. Axial black blood cardiac MRI sequence (free breathing HASTE, TR 700 ms, TE 46 ms, slice thickness 8mm, slice gap 2mm) was performed prior to intravenous contrast injection and revealed a non-obstructive saddle embolus at the bifurcation of the pulmonary trunk (white arrows).

Discussion

The incidence of symptomatic venous thromboembolism in adults is 1-2:1000, with one-third of patients presenting with PE. Early diagnosis is the cornerstone for improving outcomes due to acute PE - mortality decreases from 25% to 2-8% with prompt management (3). As the array of imaging modalities expands, the role and value of radiologists as consultants for guiding clinicians for the evaluation of PE also increases, particularly for complicated patients. This case highlights both a pitfall in the use of VQ scanning and a role for MR for evaluating PE. For PE patients with non-occlusive thrombus and balanced oligemia, as in the patient presented, lungs may show no mismatched defects. This situation may lead to a falsely low probability VQ scan result as the test relies upon the relative perfusion (or lack thereof) of lung segments compared to others. Prior to the VQ scan, the patient had been anticoagulated for three days with marked clinical improvement. Accordingly, the VQ scan might have been high probability had it been performed prior to anticoagulation. As reported in the PIOPED I study, which integrated both clinical and imaging findings, a low probability VQ scan in the context of high clinical suspicion was associated with 21% probability of PE at catheter pulmonary angiography (4).

This case demonstrates that CMR can incidentally diagnose central PE, although CMR protocols are optimized for cardiac evaluation and not for PE detection, and therefore should never be used in place of dedicated exams for PE.

Magnetic resonance pulmonary angiography offers several advantages for PE evaluation compared with CTPA, including utilization of non-ionizing radiation and not requiring the use of iodinated contrast agents. However, historically, pulmonary MR imaging has been hampered by long acquisition times, limited spatial resolution, and inadequate volumes of coverage compared with CTPA (5). The largest efficacy study of the use of MR pulmonary angiography for the diagnosis of acute PE was the PIOPED III study, in which 371 patients underwent contrast-enhanced pulmonary MRA for the assessment of suspected PE. Pulmonary MR examinations were compared with references standards to establish or exclude the diagnosis of PE. In the PIOPED III study, pulmonary MRA was found to be technically inadequate in 25% of patients, typically the result of poor pulmonary arterial opacification or motion artifacts, with the sensitivity of pulmonary MRA only 57% when including the patients with technically inadequate examinations (6). While specificity for PE diagnosis was high (99%), the sensitivity of pulmonary MRA only rose to 78% when technically limited examinations were excluded. The PIOPED III study has frequently been cited as a cautionary note regarding the use of pulmonary MR to diagnose PE, but it should be noted that this study only employed one technique for the evaluation of possible PE- pulmonary MRA- and the technical aspects of the MR acquisition are now over a decade old (5). Recent improvements in scanner technology, including shorter echo times, time-resolved imaging, improved receiver coils and gradients, more optimized bolus injection techniques, and the implementation of parallel imaging, have reduced acquisition times and decreased artifacts, allowing for more robust MR pulmonary imaging (5). Furthermore, a multiparametric approach to venous thromboembolism imaging using MR, including unenhanced imaging employing balanced steady state free precession sequences combined with enhanced imaging, first using time-resolved contrast-enhanced perfusion imaging, followed by pulmonary MRA using a rapid 3D spoiled gradient echo sequence (typically several vascular phase acquisitions are obtained to optimize pulmonary arterial enhancement), and completed with an additional post-contrast T1-weighted spoiled gradient recalled acquisition, provide complete pulmonary vascular assessment and offer multiple methods for PE detection should one particular sequence be suboptimal (5). A more recent single center study of 190 patients undergoing magnetic resonance pulmonary angiography using a multiparametric approach as the primary study to evaluate for PE showed the negative predictive value of the test to be 97% at 3-months and 96% at 12-months follow-up, similar to CTPA (7). Furthermore, while magnetic resonance pulmonary angiography may show somewhat reduced sensitivity for the detection of distal segmental and sub-segmental PE compared with CTPA, the clinical relevance of such small emboli remains in doubt and many patients with such small emboli may not require anticoagulation.         

Conclusion

We report the somewhat unusual finding of central, “saddle” PE diagnosed using cardiac MR in a patient with clinical suspicion for PE but a low probability VQ scan. Our study highlights the important and growing role of MR for the diagnosis of acute PE and serves as a reminder to evaluate all structures within the field of view, not just the heart, when interpreting CMR examinations. Even with the amazing advances in imaging, no imaging modality is perfect and clinical acumen should never be replaced or discounted, especially for a diagnosis as critical as PE.

References

1. Becattini C, Agnelli G, Lankeit M, et al. Acute pulmonary embolism: mortality prediction by the 2014 European Society of Cardiology risk stratification model. Eur Respir J. 2016 Sep;48(3):780-6. [CrossRef] [PubMed]
2. Davenport MS, Khalatbari S, Cohan RH, Dillman JR, Myles JD, Ellis JH. Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material: risk strati cation by using estimated glomerular ltration rate. Radiology. 2013;268(3):719-728. [CrossRef] [PubMed]
3. Lavorini F, Di Bello V, De Rimini ML, et al. Diagnosis and treatment of pulmonary embolism: a multidisciplinary approach. Multidiscip Respir Med. 2013 Dec 19;8(1):75. [CrossRef] [PubMed]
4. Worsley DF, Alavi A. Comprehensive analysis of the results of the PIOPED Study. Prospective Investigation of Pulmonary Embolism Diagnosis Study. J Nucl Med. 1995 Dec;36(12):2380-7. [PubMed]
5. Schiebler ML, Nagle SK, François CJ. Effectiveness of MR angiography for the primary diagnosis of acute pulmonary embolism: clinical outcomes at 3 months and 1 year. J Magn Reson Imaging. 2013 Oct;38(4):914-25. [CrossRef] [PubMed]
6. Stein PD, Chenevert TL, Fowler SE, Goodman LR, Gottschalk A, Hales CA, et al. Gadolinium-enhanced magnetic resonance angiography for pulmonary embolism: amulticenter prospective study (PIOPED III). Ann Intern Med 2010;152(7):434-43, . [CrossRef] [PubMed]
7. Schiebler ML, Nagle SK, François CJ. Effectiveness of MR angiography for the primary diagnosis of acute pulmonary embolism: clinical outcomes at 3 months and 1 year. J Magn Reson Imaging. 2013;38(4):914-25. [CrossRef] [PubMed]

Cite as: Harhash AA, Cassuto J, Avery RJ, Kuo PH. The “hidden attraction” of cardiac magnetic resonance imaging for diagnosing pulmonary embolism. Southwest J Pulm Crit Care. 2017;14(5):230-5. doi: https://doi.org/10.13175/swjpcc057-17 PDF 

Medical Image of the Week: Mediastinal Metastases Causing Right Ventricular Outflow Obstruction

Figure 1. Computed tomography (CT) of chest showed large right mediastinal mass (arrow) causing mass effect on the heart.

Figure 2.  Echocardiography showing large extra-cardiac mass (white arrow) compressing on right ventricle and its outflow tract (black arrow).

A 36-year-old man with a history of testicular choriocarcinoma with metastases to the lung presented with a 2-days history of hemoptysis. Initial diagnosis of the malignancy was made about 5 months earlier and he was treated with platinum based chemotherapy with a partial response.

He reported two days of significant hemoptysis, associated with shortness of breath and pleuritic chest pain and rapidly developed acute hypoxic respiratory failure requiring emergent intubation and mechanical ventilation. Computed tomography (CT) of chest showed large right mediastinal mass with diffuse reticular and nodular opacities predominantly in the left lung (Figure 1).

A pulmonary angiogram was performed that showed multiple active bleeding sites in the bronchial arterial system. These were treated with embolization. He developed shock and during investigations the echocardiogram showed a significant compression of the superior vena cava, right atrium and right ventricle by the malignant mass (Figure 2). Despite aggressive therapy and resuscitative therapies he continued to deteriorate and did not survive the hospital stay.

Mediastinal tumors are a rare cause of extrinsic right ventricular outflow tract (RVOT) obstruction. Echocardiography is an important tool in the assessment of hemodynamic effects caused due to such pathology including degree of compression and pressure gradients.

Kai Rou Tey MD¹, Bhupinder Natt MD²

¹Department of Internal Medicine, University of Arizona College of Medicine- South Campus, Tucson, AZ USA

²Division of Pulmonary, Critical Care, Allergy and Sleep, University of Arizona Medical Center, Tucson, AZ USA

Cite as: Tey KR, Natt B. Medical image of the week: mediastinal metastases causing right ventricular outflow obstruction. Southwest J Pulm Crit Care. 2016:12(1):22-3. doi: http://dx.doi.org/10.13175/swjpcc145-15 PDF

February 2015 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ

Clinical History: A 37-year-old man, a former smoker (quit 10 years ago) presented to his physician as an outpatient with complaints of intermittent chest pain, malaise, and intermittent fever. Stress ECG and upper endoscopy were negative. His previous medical history was otherwise unremarkable. Various physicians told the patient his symptoms were due to “stress”; presumptive antibiotic treatment had no effect.

Frontal chest radiography (Figure 1) was performed.

Figure 1. Frontal chest radiography.

Which of the following statements regarding the chest radiograph is most accurate? (Click on the correct answer to proceed to the second of five panels)

1. The chest radiograph shows a circumscribed pulmonary mass
2. The chest radiograph shows asymmetric pulmonary vascularity
3. The chest radiograph shows bilateral linear and reticular opacities and diminished lung volumes suggesting fibrotic lung disease
4. The chest radiograph shows cardiomegaly and small pleural effusions
5. The chest radiograph shows numerous small nodules

Reference as: Gotway MB. February 2015 imaging case of the month. Soutwest J Pulm Crit Care. 2015:10(2):70-6. doi: http://dx.doi.org/10.13175/swjpcc018-15 PDF

Medical Image of the Week: Pulmonary Arteriovenous Fistula

Figure 1. Panel A: Micro-bubbles appear in the right atrium (RA) and right ventricle (RV) with delayed appearance in the left atrium (LA) and left ventricle (LV). Panels B and C: The density of the micro-bubbles were same in the left and the right cardiac chambers even after 10 cardiac cycles. Panel D: When the injection was stopped, there were micro-bubbles in the left cardiac chambers, but none in the right cardiac chambers.

A 60 year-old man with hepatic cirrhosis, was referred for chest pain, shortness of breath, and progressive cyanosis and an echocardiographic evaluation. PaO2 was 64 mm Hg on room air, but only 74 mm Hg on 100% oxygen.  Chest X-ray and pulmonary function testing were normal. A contrast echocardiography using agitated saline (bubble study) was performed. A delayed appearance of a substantial amount of micro-bubbles in the left atrium greater than three cardiac cycles after appearance in the right atrium and ventricle was suggestive of pulmonary arteriovenous fistula (Figure 1A). The delayed appearance and a large amount of micro-bubbles in the left atrium preclude the intracardiac shunting result of a patent foramen ovale (PFO) or atrial septal defect (ASD). Interestingly, the density of micro-bubbles were same in the left and the right cardiac chambers even after 10 cardiac cycles (Figure 1B and 1C). When the injection was stopped, there were micro-bubbles in the left cardiac chambers, but none in the right cardiac chambers (Figure 1D). Although pulmonary angiography remains the gold standard method for definitive diagnosis of the pulmonary arteriovenous malformations, contrast echocardiography can suggest arteriovenous fistula in the setting of unexplained hypoxemia before angiography, especially in hospitals without on-site angiography facilities.

Manisha Bajracharya MD, Madhu Gupta MD, Liping Chen MD PhD

Department of Gynecology and the Cardiovascular Disease Center, Norman Bethune College of Medicine, Jilin University, Changchun, China

Reference

Nanthakumar K, Graham AT, Robinson TI, Grande P, Pugash RA, Clarke JA, Hutchison SJ, Mandzia JL, Hyland RH, Faughnan ME. Contrast echocardiography for detection of pulmonary arteriovenous malformations. Am Heart J. 2001;141(2):243-6. [CrossRef] [PubMed]

Reference as: Bajracharya M, Gupta M, Chen L. Medical image of the week: pulmonary arteriovenous fistula. Southwest J Pulm Crit Care. 2014;8(4): . doi: http://dx.doi.org/10.13175/swjpcc035-14 PDF

Medical Image of the Week: Extensive Small Cell Lung Cancer with Cardiac Invasion

A 73 year old woman was seen with a lung mass and acute onset of ataxia. MRI of the brain was notable for multifocal infarcts (Figure 1). Echocardiography (ECHO) was obtained to identify cardiac source of emboli and was notable for freely mobile mass tethered to the lateral left atrial wall, crossing the mitral valve into the left atrium (Figure 2). A contrast enhanced CT scan of the chest was obtained which confirmed the presence of a large right upper lobe mass with extension to the right pulmonary vein, left atrium and into the left ventricle (Figures 3 and 4). The biopsy confirmed small cell lung cancer.

Figure 1. Axial MRI brain showing multifocal embolic infarcts.

Figure 2. Transthoracic ECHO 4-chamber view showing a mobile mass originating within the left atrium, across the mitral valve, and into the left ventricle.

Figure 3. Axial CT of the chest showing tumor extension into the right pulmonary vein (arrow).

Figure 4. Coronal CT of the chest showing large right apical mass extending into the left atrium and across the mitral valve into the left ventricle (arrow).

Ryan Nahapetian MD, MPH.

Internal Medicine Residency.

University of Arizona at South Campus.

Carmen Luraschi-Monjagatta MD.

Division of Pulmonary, Allergy, Critical Care and Sleep Medicine.

Arizona Respiratory Center

University of Arizona

Tucson, Arizona.

Reference as: Nahapetian R, Luraschi-Monjagatta C. Medical image of the week: extensive small cell lung cancer with cardiac invasion. Southwest J Pulm Crit Care. 2013;6(3):143-4. PDF