<?xml version="1.0" encoding="UTF-8"?><!DOCTYPE article  PUBLIC "-//NLM//DTD Journal Publishing DTD v3.0 20080202//EN" "http://dtd.nlm.nih.gov/publishing/3.0/journalpublishing3.dtd"><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" dtd-version="3.0" xml:lang="en" article-type="research article"><front><journal-meta><journal-id journal-id-type="publisher-id">WJCD</journal-id><journal-title-group><journal-title>World Journal of Cardiovascular Diseases</journal-title></journal-title-group><issn pub-type="epub">2164-5329</issn><publisher><publisher-name>Scientific Research Publishing</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.4236/wjcd.2019.96037</article-id><article-id pub-id-type="publisher-id">WJCD-93299</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group><subj-group subj-group-type="Discipline-v2"><subject>Medicine&amp;Healthcare</subject></subj-group></article-categories><title-group><article-title>
 
 
  Double Compression of Left Atrium and Pulmonary Artery by a Huge Descending Aortic Aneurysm with Intramural Hematoma Mimicking Pulmonary Embolism: A Case Report
 
</article-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Djibril</surname><given-names>Marie BA</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Aminata</surname><given-names>Diack</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Alain</surname><given-names>Affangla</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Khadidiatou</surname><given-names>Dia</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Mouhamed</surname><given-names>Cherif Mboup</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Mouhamed</surname><given-names>Leye</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Abdoul</surname><given-names>Kane</given-names></name><xref ref-type="aff" rid="aff4"><sup>4</sup></xref></contrib></contrib-group><aff id="aff2"><addr-line>Department of Radiology, Principal Hospital of Dakar, Dakar, Senegal</addr-line></aff><aff id="aff4"><addr-line>Department of Cardiology, Cheikh Anta Diop University, Dakar, Senegal</addr-line></aff><aff id="aff3"><addr-line>Department of Cardiology, Principal Hospital of Dakar, Dakar, Senegal</addr-line></aff><aff id="aff1"><addr-line>Unit of Training and Research in Medical Sciences, University of Thies, Thies, Senegal</addr-line></aff><pub-date pub-type="epub"><day>06</day><month>06</month><year>2019</year></pub-date><volume>09</volume><issue>06</issue><fpage>419</fpage><lpage>424</lpage><history><date date-type="received"><day>21,</day>	<month>January</month>	<year>2019</year></date><date date-type="rev-recd"><day>24,</day>	<month>June</month>	<year>2019</year>	</date><date date-type="accepted"><day>27,</day>	<month>June</month>	<year>2019</year></date></history><permissions><copyright-statement>&#169; Copyright  2014 by authors and Scientific Research Publishing Inc. </copyright-statement><copyright-year>2014</copyright-year><license><license-p>This work is licensed under the Creative Commons Attribution International License (CC BY). http://creativecommons.org/licenses/by/4.0/</license-p></license></permissions><abstract><p>
 
 
  Hemodynamic instability secondary to left atrial (LA) compression by an aortic aneurysm is a rare entity. We report
   
  the case of a 43-year old woman with no previous diagnosis of congestive heart failure who was admitted for an initial diagnosis of pulmonary embolism (PE) based on shortness of breath, hypotension and D
  -
  Dimer
  s
   elevation. The electrocardiogram and blood counts were within normal limits. The chest X-ray revealed widening of the mediastinum. Transthoracic echocardiography demonstrated LA compression by a large descending thoracic aortic aneurysm. Left and right ventricle systolic functions were preserved. Chest angiography showed LA and left pulmonary artery (LPA) compression by a descending aortic aneurysm and an intramural hematoma with no evidence of PE evidence. Emergency surgery could not be done because of her financial status. She was treated medically and was discharged 1
   
  week later with significant improvement. However she remained hypotensive.
 
</p></abstract><kwd-group><kwd>Aortic Aneurysm</kwd><kwd> Left Atrium Compression</kwd><kwd> Pulmonary Artery  Compression</kwd><kwd> Intramural Hematoma</kwd><kwd> Echocardiography</kwd></kwd-group></article-meta></front><body><sec id="s1"><title>1. Introduction</title><p>Thoracic Aortic aneurysm (TAA) may present catastrophically with dissection or rupture or chronically with symptoms from compression of the surrounding structures. Extrinsic compression of the left atrium and the pulmonary vessels is an uncommon cause of hemodynamic compromise and may be secondary to the involvement of mediastinal structures, including TAA. We report a rare case of huge descending aortic aneurysm that caused dyspnea, palpitations and hypotension from compression of left pulmonary artery and left atrium that led to an initial diagnosis of pulmonary embolism.</p></sec><sec id="s2"><title>2. Case Report</title><p>A 43-year-old woman was referred to our institution for initial diagnosis of pulmonary embolism based on shortness of breath, hypotension and D-Dimers elevation. The patient’s electrocardiography (ECG) and blood counts were within normal limits.</p><p>Her medical history revealed a shortness of breath and palpitations that worsened within the past days. She had no previous history of congestive heart failure or cardiovascular risk factors.</p><p>The degree of dyspnea on admission corresponded to New York Heart Association grade II. Her blood pressure was 90/60 mmHg and she had regular pulses of 110 beats/min. No precordial murmurs or bruits were audible. There were inspiratory crackles in the basal segments of left lung.</p><p>The electrocardiogram showed a sinus regular rhythm. The chest X-ray (<xref ref-type="fig" rid="fig1">Figure 1</xref>) revealed widening of the mediastinum. Transthoracic echocardiography (TTE) in the apical four chamber view demonstrated left atrial compression by a large descending TAA (<xref ref-type="fig" rid="fig2">Figure 2</xref>(a)). Left atrium was of 7.2 cm<sup>2</sup> and right atrium of 11.8 cm<sup>2</sup> (<xref ref-type="fig" rid="fig2">Figure 2</xref>(b)). Left and right ventricle systolic functions were preserved with an estimated systolic pulmonary artery pressure of 25 mmHg.</p><p>Chest angiography was performed and revealed a giant 9.3 &#215; 9.8 &#215; 22.9-cm TAA with intramural hematoma (<xref ref-type="fig" rid="fig3">Figure 3</xref>(a) and <xref ref-type="fig" rid="fig3">Figure 3</xref>(b)), which compressed the left pulmonary artery and left atrium without any evidence of pulmonary embolism (<xref ref-type="fig" rid="fig4">Figure 4</xref>(a) and <xref ref-type="fig" rid="fig4">Figure 4</xref>(b)). No intimal flap was seen in any part of the thoracic aorta.</p><p>Surgery was planned, but the patient could not supportsurgery because of financial status.</p><p>She was treated medically by beta blockers and low dose of diuretics and she was discharged after one week. Outcome after 6 months follow-up was favorable with regression of dyspnea but she remained hypotensive.</p></sec><sec id="s3"><title>3. Discussion</title><p>Aortic intramural hematoma was first described by Krukenberg in 1920 as an aortic dissection without intimal tear [<xref ref-type="bibr" rid="scirp.93299-ref1">1</xref>] .</p><p>The natural course of descending aortic intramural hematoma is thought to be less malignant than that of aortic dissections [<xref ref-type="bibr" rid="scirp.93299-ref2">2</xref>] , which may be in part due to the lower frequency of its association with malperfusion syndromes, and there is</p><p>consensus on medical treatment with follow-up for its evolution to aortic dissection or rupture [<xref ref-type="bibr" rid="scirp.93299-ref2">2</xref>] [<xref ref-type="bibr" rid="scirp.93299-ref3">3</xref>] . Although late progression to aneurysm or frank dissection may occur, complete resolution of hematoma has been observed in 50% - 80% of cases [<xref ref-type="bibr" rid="scirp.93299-ref2">2</xref>] [<xref ref-type="bibr" rid="scirp.93299-ref3">3</xref>] .</p><p>Since the descending aorta have parts located very close to the left atrium, occurrence of both dissecting and non dissecting aneurysms compressing left atrium is a well-defined, but uncommon entity with few reports in the literature [<xref ref-type="bibr" rid="scirp.93299-ref4">4</xref>] [<xref ref-type="bibr" rid="scirp.93299-ref5">5</xref>] .</p><p>Left atrium compression is classified into three categories based on the severity of anatomical deformation and its hemodynamic consequences: proximity (a contiguous or adjacent structure without chamber deformation), encroachment (distortion of normal cardiovascular architecture without hemodynamic effect), and compression [<xref ref-type="bibr" rid="scirp.93299-ref6">6</xref>] . Proximity and encroachment are defined as conditions</p><p>that may not lead to symptoms, whereas compression causes severe inflow obstruction resulting in hemodynamic instability and symptoms such as hypotension, hypoxia, tachypnea, and tachycardia, as in our case [<xref ref-type="bibr" rid="scirp.93299-ref6">6</xref>] .</p><p>The possible mechanism of congestive heart failure in our case may be reduced left atrium volume due to compression leading to low cardiac output. In addition, as left atrium pressure rises with subsequently elevated pulmonary venous pressure, this may have eventually led to pulmonary edema.</p><p>Case of aneurysm compressing pulmonary artery are published but these relatively rare cases were reported in the literature more frequently in the period when syphilis was much more common [<xref ref-type="bibr" rid="scirp.93299-ref7">7</xref>] .</p><p>Hemodynamic compromise encountered in patients with pulmonary artery compression is related to right ventricular hypertension and right heart failure.</p><p>Traditionally, the degree of mechanical obstruction of the pulmonary vascular bed was considered to be the only determinant of the Pulmonary Vascular Resistance increase. Over the years, however, a number of observations have challenged this concept. Firstly, several studies have shown that the correlation between the degree of mechanical obstruction and the hemodynamic manifestations of pulmonary embolism is either absent, or poor at best [<xref ref-type="bibr" rid="scirp.93299-ref8">8</xref>] [<xref ref-type="bibr" rid="scirp.93299-ref9">9</xref>] . Furthermore, bringing about a strictly mechanical obstruction by cross-clamping the left or right pulmonary artery during a surgical procedure, or by unilateral balloon occlusion, causes only a modest rise in pulmonary artery pressure, and almost never results in right-sided heart failure [<xref ref-type="bibr" rid="scirp.93299-ref10">10</xref>] [<xref ref-type="bibr" rid="scirp.93299-ref11">11</xref>] [<xref ref-type="bibr" rid="scirp.93299-ref12">12</xref>] , whereas pulmonary embolism with obstruction of 25% of the pulmonary vascular tree can cause marked pulmonary hypertension [<xref ref-type="bibr" rid="scirp.93299-ref13">13</xref>] .</p><p>In our patient, since there was no right ventricular failure or pulmonary hypertension we think that symptoms were more linked to left atrial compression than pulmonary artery compression.</p></sec><sec id="s4"><title>4. Conclusion</title><p>Hemodynamic instability secondary to left atrial compression by an aortic aneurysm is a rare entity. Chest angiography provides an accurate diagnosis. Transthoracic echocardiography is a noninvasive, cheap, and easily applicable method and, thus, should be the first choice in investigating the cause of dyspnea particularly in sub-Saharan countries where most facilities are understaffed.</p></sec><sec id="s5"><title>Conflicts of Interest</title><p>The authors declare no conflicts of interest regarding the publication of this paper.</p></sec><sec id="s6"><title>Cite this paper</title><p>BA, D.M., Diack, A., Affangla, A., Dia, K., Mboup, M.C., Leye, M. and Kane, A. (2019) Double Compression of Left Atrium and Pulmonary Artery by a Huge Descending Aortic Aneurysm with Intramural Hematoma Mimicking Pulmonary Embolism: A Case Report. World Journal of Cardiovascular Diseases, 9, 419-424. https://doi.org/10.4236/wjcd.2019.96037</p></sec></body><back><ref-list><title>References</title><ref id="scirp.93299-ref1"><label>1</label><mixed-citation publication-type="other" xlink:type="simple">Kan, C.B., Chang, R.Y. and Chang, J.P. (2008) Optimal Initial Treatment and Clinical Outcome of Type a Aortic Intramural Hematoma: A Clinical Review. European Journal of Cardio-Thoracic Surgery, 33, 1002-1006. 
https://doi.org/10.1016/j.ejcts.2008.02.016</mixed-citation></ref><ref id="scirp.93299-ref2"><label>2</label><mixed-citation publication-type="other" xlink:type="simple">Sundt, T.M. (2007) Intramural Hematoma and Penetrating Aortic Ulcer. Current Opinion in Cardiology, 22, 504-509.  
https://doi.org/10.1097/HCO.0b013e3282f0fd72</mixed-citation></ref><ref id="scirp.93299-ref3"><label>3</label><mixed-citation publication-type="other" xlink:type="simple">Macura, K.J., Szarf, G., Fishman, E.K. and Bluemke, D.A. (2003) Role of Computed Tomography and Magnetic Resonance Imaging in Assessment of Acute Aortic Syndromes. Seminars in Ultrasound, CT and MRI, 24, 232-254. 
https://doi.org/10.1016/S0887-2171(03)90014-X</mixed-citation></ref><ref id="scirp.93299-ref4"><label>4</label><mixed-citation publication-type="other" xlink:type="simple">Walpot, J., Amsel, B., Pasteuning, W.H. and Olree, M. (2007) Left Atrial Compression by Dissecting Aneurysm of the Ascending Aorta. Journal of the American Society of Echocardiography, 20, 1220.e4-1220.e6. 
https://doi.org/10.1016/j.echo.2007.02.014</mixed-citation></ref><ref id="scirp.93299-ref5"><label>5</label><mixed-citation publication-type="other" xlink:type="simple">Celenk, M.K., Ozeke, O., Selcuk, M.T., Selcuk, H. and Cagli, K. (2005) Left Atrial Compression by Thoracic Aneurysm Mimicking Congestive Heart Failure. Echocardiography, 22, 677-678. https://doi.org/10.1111/j.1540-8175.2005.40083.x</mixed-citation></ref><ref id="scirp.93299-ref6"><label>6</label><mixed-citation publication-type="other" xlink:type="simple">D’Cruz, I.A., Feghali, N. and Gross, C.M. (1994) Echocardiographic Manifestations of Mediastinal Masses Compressing or Encroaching on the Heart. Echocardiography, 11, 523-533. https://doi.org/10.1111/j.1540-8175.1994.tb01093.x</mixed-citation></ref><ref id="scirp.93299-ref7"><label>7</label><mixed-citation publication-type="other" xlink:type="simple">Brill, I.C. and Jones, R.S. (1946) The Syndrome of Compression of the Pulmonary Artery by a Syphilitic Aortic Aneurysm with or without Arterio-Arterial Communication. Annals of Internal Medicine, 24, 111-118. 
https://doi.org/10.7326/0003-4819-24-1-111</mixed-citation></ref><ref id="scirp.93299-ref8"><label>8</label><mixed-citation publication-type="other" xlink:type="simple">McIntyre, K.M. and Sasahara, A.A. (1974) Determinants of Right Ventricular and Hemodynamics after Pulmonary Embolism. Chest, 65, 534-543. 
https://doi.org/10.1378/chest.65.5.534</mixed-citation></ref><ref id="scirp.93299-ref9"><label>9</label><mixed-citation publication-type="other" xlink:type="simple">Miller, R.L., Das, S., Anandarangam, T., et al. (1998) Association between Right Ventricular Function and Perfusion Abnormalities in Hemodynamically Stable Patients with Acute Pulmonary Embolism. Chest, 113, 665-670. 
https://doi.org/10.1378/chest.113.3.665</mixed-citation></ref><ref id="scirp.93299-ref10"><label>10</label><mixed-citation publication-type="other" xlink:type="simple">Sharma, G.V.R.K., McIntyre, K.M., Sharma, S. and Sasahara, A.A. (1984) Clinical and Hemodynamic Correlates in Pulmonary Embolism. Clinics in Chest Medicine, 5, 421-437.</mixed-citation></ref><ref id="scirp.93299-ref11"><label>11</label><mixed-citation publication-type="other" xlink:type="simple">Shield, T.W. (1972) General Thoracic Surgery. Year Book Medical Publishers, Philadelphia, PA.</mixed-citation></ref><ref id="scirp.93299-ref12"><label>12</label><mixed-citation publication-type="other" xlink:type="simple">Boldt, J., Muller, M., Uphus, D., Padberg, W. and Hempelmann, G. (1996) Cardiorespiratory Changes in Patients Undergoing Pulmonary Resection Using Different Anesthetic Management Techniques. Journal of Cardiothoracic and Vascular Anesthesia, 10, 854-859. https://doi.org/10.1016/S1053-0770(96)80045-0</mixed-citation></ref><ref id="scirp.93299-ref13"><label>13</label><mixed-citation publication-type="other" xlink:type="simple">Alpert, J.S., Godtfredsen, J., Ockene, I.S., Anas, J. and Dalen, J.E. (1978) Pulmonary Hypertension Secondary to Minor Pulmonary Embolism. Chest, 73, 795-797. 
https://doi.org/10.1378/chest.73.6.795</mixed-citation></ref></ref-list></back></article>