Libman-Sacks endocarditis: Difference between revisions

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{{Infobox_Disease |
__NOTOC__
  Name          = {{PAGENAME}} |
{{Libman-Sacks endocarditis}}
  Image          = |
{{CMG}} {{AE}} {{S.M.}}
  Caption        = |
  DiseasesDB    = 29254 |
  ICD10          = {{ICD10|I|39||i|30}}, {{ICD10|M|32|1|m|30}} |
  ICD9          = {{ICD9|710.0}} |
  ICDO          = |
  OMIM          = |
  MedlinePlus    = |
  eMedicineSubj  = med |
  eMedicineTopic = 1295 |
  MeshID        = D008180 |
}}
{{Search infobox}}
{{CMG}} {{AE}}{{S.M.}}


{{SK}} Nonbacterial thrombotic endocarditis (NBTE), Marantic endocarditis, Verrucous endocarditis
{{SK}}: Nonbacterial thrombotic endocarditis (NBTE), Marantic endocarditis, Verrucous endocarditis


==Overview==
==Overview==
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* Consists of [[dense]], [[fibrous]], and [[Vascularity|vascularized]] [[tissue]].
* Consists of [[dense]], [[fibrous]], and [[Vascularity|vascularized]] [[tissue]].
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[[File:Cr534e-g004.jpg|thumb|200px|none|Pathology slide of mitral valve vegetation. Lots of necrosis: 10 cm circumference vegetation. Mitral valve tissue shows focal necrosis. No bacterial or fungal organisms were present. [https://cardiologyres.org/index.php/Cardiologyres/article/view/551/592 Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA]]]
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[[File:Cr534e-g005.jpg|thumb|200px|none|R lung, high power: emboli and large necrotic infarcted tissue. [https://cardiologyres.org/index.php/Cardiologyres/article/view/551/592 Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA]]]
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[[File:Cr534e-g006.jpg|thumb|200px|none|Low power of the liver: lots of steatosis and congestion, necrosis. [https://cardiologyres.org/index.php/Cardiologyres/article/view/551/592 Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA]]]
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[[File:Cr534e-g007.jpg|thumb|200px|none|High power pathology slide of the liver showing lots of steatosis, congestion, and necrosis. [https://cardiologyres.org/index.php/Cardiologyres/article/view/551/592 Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA]]]
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[[File:Cr534e-g008.jpg|thumb|200px|none|Low power pathology slide of the lung showing emboli and necrotic tissue.[https://cardiologyres.org/index.php/Cardiologyres/article/view/551/592 Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA]]]
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*It is difficult to [[Prediction|predict]] the [[Underlying representation|underlying]] [[etiology]] in case of a [[stroke]] occurrence in LSE, whether it is due to [[Systemic embolization|systemic emboli]] or the [[Underlying representation|underlying]] [[pathology]] of [[SLE]] or [[Antiphospholipid syndrome|APS]].
*It is difficult to [[Prediction|predict]] the [[Underlying representation|underlying]] [[etiology]] in case of a [[stroke]] occurrence in LSE, whether it is due to [[Systemic embolization|systemic emboli]] or the [[Underlying representation|underlying]] [[pathology]] of [[SLE]] or [[Antiphospholipid syndrome|APS]].
*[[Valvular disease]] in LSE can [[lead]] to the [[heart failure]].
*[[Valvular disease]] in LSE can [[lead]] to the [[heart failure]].
*Double-[[Valvular heart disease|valve]] Libman-Sacks [[endocarditis]] involving both [[Mitral valve|mitral]] and [[aortic valves]] can [[lead]] to [[ventricular fibrillation]] and [[cardiac arrest]].<ref name="pmid21720477">{{cite journal| author=Tanawuttiwat T, Dia M, Hanif T, Mihailescu M| title=Double-valve Libman-Sacks endocarditis causing ventricular fibrillation cardiac arrest. | journal=Tex Heart Inst J | year= 2011 | volume= 38 | issue= 3 | pages= 295-7 | pmid=21720477 | doi= | pmc=3113142 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21720477  }} </ref>
*There's 1% to 2% [[chance]] of [[congenital heart block]] (usually [[Complete heart block|complete]],or [[First degree heart block|1st]] or [[2nd degree heart block|2nd degree]]) in a [[baby]] of mother with [[SLE]] [[Association (statistics)|associated]] with anti-Ro/SS-A ([[Sjögren's syndrome]] [[antigen]] A) [[autoantibodies]] with a 16% [[Recurrence plot|recurrence]] [[rate]]. [[Fluorinated]] [[steroids]] that do not cross the [[placenta]] may be beneficial in [[Prevention|preventing]] the [[congenital heart block]].
*There's 1% to 2% [[chance]] of [[congenital heart block]] (usually [[Complete heart block|complete]],or [[First degree heart block|1st]] or [[2nd degree heart block|2nd degree]]) in a [[baby]] of mother with [[SLE]] [[Association (statistics)|associated]] with anti-Ro/SS-A ([[Sjögren's syndrome]] [[antigen]] A) [[autoantibodies]] with a 16% [[Recurrence plot|recurrence]] [[rate]]. [[Fluorinated]] [[steroids]] that do not cross the [[placenta]] may be beneficial in [[Prevention|preventing]] the [[congenital heart block]].


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==History and symptoms==
==History and Symptoms==
*Mostly [[patients]] with Libman-Sacks [[endocarditis]] are [[asymptomatic]].
*Mostly [[patients]] with Libman-Sacks [[endocarditis]] are [[asymptomatic]].
*There may be the [[Features (pattern recognition)|features]] of [[valvular disease]] if [[valves]] are severely [[Affect|affected]] with the [[mitral valve disease]] being more common than the [[aortic valve disease]].
*There may be the [[Features (pattern recognition)|features]] of [[valvular disease]] if [[valves]] are severely [[Affect|affected]] with the [[mitral valve disease]] being more common than the [[aortic valve disease]].
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==Laboratory findings==
==Laboratory Findings==
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==Imaging findings==
==Imaging Findings==
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!style="background: #4479BA; width: 200px;" | {{fontcolor|#FFF|Imagining Findings}}
!style="background: #4479BA; width: 200px;" | {{fontcolor|#FFF|Imagining Findings}}
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|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Echocardiography]]<ref name="pmid25807885">{{cite journal| author=Roldan CA, Tolstrup K, Macias L, Qualls CR, Maynard D, Charlton G | display-authors=etal| title=Libman-Sacks Endocarditis: Detection, Characterization, and Clinical Correlates by Three-Dimensional Transesophageal Echocardiography. | journal=J Am Soc Echocardiogr | year= 2015 | volume= 28 | issue= 7 | pages= 770-9 | pmid=25807885 | doi=10.1016/j.echo.2015.02.011 | pmc=4592775 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25807885  }} </ref>
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Echocardiography]]<ref name="pmid25807885">{{cite journal| author=Roldan CA, Tolstrup K, Macias L, Qualls CR, Maynard D, Charlton G | display-authors=etal| title=Libman-Sacks Endocarditis: Detection, Characterization, and Clinical Correlates by Three-Dimensional Transesophageal Echocardiography. | journal=J Am Soc Echocardiogr | year= 2015 | volume= 28 | issue= 7 | pages= 770-9 | pmid=25807885 | doi=10.1016/j.echo.2015.02.011 | pmc=4592775 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25807885 }} </ref><ref name="pmid18085739">{{cite journal| author=Roldan CA, Qualls CR, Sopko KS, Sibbitt WL| title=Transthoracic versus transesophageal echocardiography for detection of Libman-Sacks endocarditis: a randomized controlled study. | journal=J Rheumatol | year= 2008 | volume= 35 | issue= 2 | pages= 224-9 | pmid=18085739 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18085739  }} </ref><ref name="pmid19763069">{{cite journal| author=Roldan CA| title=Diagnostic value of transesophageal echocardiography in Libman-Sacks endocarditis. | journal=Minerva Cardioangiol | year= 2009 | volume= 57 | issue= 4 | pages= 467-81 | pmid=19763069 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19763069 }} </ref>
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*[[Echocardiography]] is the key [[diagnostic test]] for Libman-Sacks [[endocarditis]] (although it doesn't [[Detection theory|detect]] all the [[lesions]]).
*[[Echocardiography]] is the key [[diagnostic test]] for Libman-Sacks [[endocarditis]] (although it doesn't [[Detection theory|detect]] all the [[lesions]]).
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*Although the [[Two-dimensional echocardiography|two-dimensional]] [[Transesophageal echocardiography (TEE)|transesophageal echocardiography]] ([[2D echocardiography|2D-TEE]]) has a higher [[diagnostic]] [[Value (mathematics)|value]] for the [[Detection theory|detection]] of Libman-Sacks [[Vegetation (pathology)|vegetations]], but the three-[[Dimensional analysis|dimensional]] [[Transesophageal echocardiography (TEE)|TEE]] (3D-[[Transesophageal echocardiography (TEE)|TEE]]) has the following benefits over [[Two dimensional echocardiography|2D-TEE]]:
*Although the [[Two-dimensional echocardiography|two-dimensional]] [[Transesophageal echocardiography (TEE)|transesophageal echocardiography]] ([[2D echocardiography|2D-TEE]]) has a higher [[diagnostic]] [[Value (mathematics)|value]] for the [[Detection theory|detection]] of Libman-Sacks [[Vegetation (pathology)|vegetations]], but the three-[[Dimensional analysis|dimensional]] [[Transesophageal echocardiography (TEE)|TEE]] (3D-[[Transesophageal echocardiography (TEE)|TEE]]) has the following benefits over [[Two dimensional echocardiography|2D-TEE]]:
**Improved [[Detection theory|detection]]
**Improved [[Detection theory|detection]]
**Improved [[Characterization (mathematics)|characterization]] &
**Improved [[Characterization (mathematics)|characterization]]
**Improved [[clinical]] [[Correlation|correlations]] of Libman-Sacks [[Vegetation (pathology)|vegetations]]
**Improved [[clinical]] [[Correlation|correlations]] of Libman-Sacks [[Vegetation (pathology)|vegetations]]
**Provides [[Clinical|clinically]] [[Relevance|relevant]] [[Addition reaction|additive]] [[Information science|information]] [[Complement|complementing]] the [[Two dimensional echocardiography|2D-TEE]] for the [[Characterization (mathematics)|characterization]], [[Detection theory|detection]], and [[Association (statistics)|association]] with the [[cerebrovascular disease]] of Libman-Sacks [[endocarditis]].
**Provides [[Clinical|clinically]] [[Relevance|relevant]] [[Addition reaction|additive]] [[Information science|information]] [[Complement|complementing]] the [[Two dimensional echocardiography|2D-TEE]] for the [[Characterization (mathematics)|characterization]], [[Detection theory|detection]], and [[Association (statistics)|association]] with the [[cerebrovascular disease]] of Libman-Sacks [[endocarditis]].
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[[File:Cr534e-g002.jpg|thumb|400px|none|2D transesophageal ultrasound. Image on the left shows a thickened mitral valve with a 1 cm vegetation that can be seen on the anterior mitral leaflet. Image on the right is a four-chamber color flow Doppler view showing biventricular dilatation, severe left ventricular dysfunction. For orientation purposes, left ventricle is the bottom right chamber. Video of both views is attached as a supplementary file. [https://cardiologyres.org/index.php/Cardiologyres/article/view/551/592 Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA]]]
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|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Chest X-ray|Chest X-Ray]]
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Chest X-ray|Chest X-Ray]]
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**[[Calcification]] of the [[lesions]] (uncommon)
**[[Calcification]] of the [[lesions]] (uncommon)
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|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |MRI<ref>https://radiopaedia.org/articles/libman-sacks-endocarditis-1?lang=us</ref>
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[MRI]]<ref>https://radiopaedia.org/articles/libman-sacks-endocarditis-1?lang=us</ref>
|Currently, the role of 4D-flow MRI imaging as useful noninvasive tool for evaluating abnormal flow patterns, ventricular dimensions, stroke volume, and regional myocardial function, is being investigated. Some early studies have shown promising results as they have been able to more accurately demonstrate the above parameters compared to traditional TOE 8.
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* According to the ongoing [[current]] [[Study arms|studies]], [[4D]]-[[flow]] [[Magnetic resonance imaging|MRI]] [[imaging]] is considered as a promising useful [[Noninvasive test|noninvasive tool]] [[Comparability|compared]] to the [[Traditional medicine|traditional]] [[Transesophageal echocardiography (TEE)|TEE]] for evaluating the following:
**[[Abnormal]] [[flow]] [[Pattern|patterns]]
**[[Ventricular]] [[Dimension|dimensions]]
**[[Stroke volume]]
**[[Region of interest|Regional]] [[myocardial]] [[Function (biology)|function]]
 
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[[File:Cr534e-g003.jpg|thumb|400px|none|MRI of the brain. Images on the top show increased signal on diffusion weighted imaging (DWI) throughout the bilateral frontal, parietal, and occipital lobes. Images on the bottom show a corresponding decreased signal intensity on apparent diffusion coefficient that is consistent with acute abnormal restricted diffusion. These findings suggest new/ongoing acute infarcts.[https://cardiologyres.org/index.php/Cardiologyres/article/view/551/592 Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA]]]
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|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[CT scan]] ([[Head]])
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* In [[patients]] with [[Cerebrovascular disease|cerebrovascular]] [[emboli]], [[CT scan]] of the [[head]] without [[contrast]] may show extensive multifocal hypoattenuating [[Area|areas]] in the involved [[Region of interest|region]] as shown in the [[image]] below:
 
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[[File:Cr534e-g001.jpg|thumb|250px|none|CT of head without contrast showing extensive multifocal areas of hypoattentuation throughout the bilateral frontal, parietal, occipital, and right > left temporal lobes. No mass effect or midline shift or hemorrhage was seen.[https://cardiologyres.org/index.php/Cardiologyres/article/view/551/592 Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA]]]
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==Other Diagnostic studies==
==Other Diagnostic Studies==
===Cardiac Catheterization===
===Cardiac Catheterization===
*In case of severe [[valvular disease]], [[cardiac catheterization]] may be required with a view to [[valve replacement]].
*In case of severe [[valvular disease]], [[cardiac catheterization]] may be required with a view to [[valve replacement]].
==Treatment==
==Treatment==
*There is no [[Specific activity|specific]] [[Treatment Planning|treatment]] for Libman-Sacks [[endocarditis]].
*There is no [[Specific activity|specific]] [[Treatment Planning|treatment]] for Libman-Sacks [[endocarditis]].
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*[[Digoxin]]
*[[Digoxin]]
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|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Valve replacement surgery|Valve replacement]]
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Valve replacement surgery|Valve replacement]]<ref name="pmid20331896">{{cite journal| author=Bouma W, Klinkenberg TJ, van der Horst IC, Wijdh-den Hamer IJ, Erasmus ME, Bijl M | display-authors=etal| title=Mitral valve surgery for mitral regurgitation caused by Libman-Sacks endocarditis: a report of four cases and a systematic review of the literature. | journal=J Cardiothorac Surg | year= 2010 | volume= 5 | issue=  | pages= 13 | pmid=20331896 | doi=10.1186/1749-8090-5-13 | pmc=2859362 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20331896  }} </ref><ref name="pmid28734427">{{cite journal| author=Samura T, Toda K, Yoshioka D, Nakamura T, Miyagawa S, Yoshikawa Y | display-authors=etal| title=Libman-Sacks Endocarditis Due to Systemic Lupus Erythematosus Activation After Mitral Valve Plasty. | journal=Ann Thorac Surg | year= 2017 | volume= 104 | issue= 2 | pages= e109-e111 | pmid=28734427 | doi=10.1016/j.athoracsur.2017.01.073 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28734427  }} </ref><ref name="pmid21404907">{{cite journal| author=Perier P, Jeserich M, Vieth M, Pohle K, Hohenberger W, Diegeler A| title=Mitral valve reconstruction in a patient with Libman-Sacks endocarditis: a case report. | journal=J Heart Valve Dis | year= 2011 | volume= 20 | issue= 1 | pages= 103-6 | pmid=21404907 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21404907  }} </ref>
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*[[Valve replacement surgery]] is [[done]] in case of severe [[valvular disease]].
*[[Valve replacement surgery]] is [[done]] in case of severe [[valvular disease]].
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==Differential Diagnosis==
==Differentiating Libman-Sacks Endocarditis from other Diseases==


Libman-Sacks [[endocarditis]] should be [[Differentiate|differentiated]] from other [[diseases]] [[Presenting symptom|presenting]] with [[fever]], [[chest pain]] and [[anorexia]]. The [[Difference (philosophy)|differentials]] include the following:<ref name="pmid24550636">{{cite journal |vauthors=Brenes-Salazar JA |title=Westermark's and Palla's signs in acute and chronic pulmonary embolism: Still valid in the current computed tomography era |journal=J Emerg Trauma Shock |volume=7 |issue=1 |pages=57–8 |year=2014 |pmid=24550636 |pmc=3912657 |doi=10.4103/0974-2700.125645 |url=}}</ref><ref name="urlCT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis | RadioGraphics">{{cite web |url=http://pubs.rsna.org/doi/full/10.1148/rg.245045008 |title=CT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis &#124; RadioGraphics |format= |work= |accessdate=}}</ref><ref name="pmid23940438">{{cite journal |vauthors=Bĕlohlávek J, Dytrych V, Linhart A |title=Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism |journal=Exp Clin Cardiol |volume=18 |issue=2 |pages=129–38 |year=2013 |pmid=23940438 |pmc=3718593 |doi= |url=}}</ref><ref name="urlPulmonary Embolism: Symptoms - National Library of Medicine - PubMed Health">{{cite web |url=https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0022657/ |title=Pulmonary Embolism: Symptoms - National Library of Medicine - PubMed Health |format= |work= |accessdate=}}</ref><ref name="pmid20118395">{{cite journal |vauthors=Ramani GV, Uber PA, Mehra MR |title=Chronic heart failure: contemporary diagnosis and management |journal=Mayo Clin. Proc. |volume=85 |issue=2 |pages=180–95 |year=2010 |pmid=20118395 |pmc=2813829 |doi=10.4065/mcp.2009.0494 |url=}}</ref><ref name="pmid18215495">{{cite journal |vauthors=Blinderman CD, Homel P, Billings JA, Portenoy RK, Tennstedt SL |title=Symptom distress and quality of life in patients with advanced congestive heart failure |journal=J Pain Symptom Manage |volume=35 |issue=6 |pages=594–603 |year=2008 |pmid=18215495 |pmc=2662445 |doi=10.1016/j.jpainsymman.2007.06.007 |url=}}</ref><ref name="pmid19168510">{{cite journal |vauthors=Hawkins NM, Petrie MC, Jhund PS, Chalmers GW, Dunn FG, McMurray JJ |title=Heart failure and chronic obstructive pulmonary disease: diagnostic pitfalls and epidemiology |journal=Eur. J. Heart Fail. |volume=11 |issue=2 |pages=130–9 |year=2009 |pmid=19168510 |pmc=2639415 |doi=10.1093/eurjhf/hfn013 |url=}}</ref><ref name="pmid9465867">{{cite journal |vauthors=Takasugi JE, Godwin JD |title=Radiology of chronic obstructive pulmonary disease |journal=Radiol. Clin. North Am. |volume=36 |issue=1 |pages=29–55 |year=1998 |pmid=9465867 |doi= |url=}}</ref><ref name="pmid14651761">{{cite journal |vauthors=Wedzicha JA, Donaldson GC |title=Exacerbations of chronic obstructive pulmonary disease |journal=Respir Care |volume=48 |issue=12 |pages=1204–13; discussion 1213–5 |year=2003 |pmid=14651761 |doi= |url=}}</ref><ref name="pmid23833163">{{cite journal |vauthors=Nakawah MO, Hawkins C, Barbandi F |title=Asthma, chronic obstructive pulmonary disease (COPD), and the overlap syndrome |journal=J Am Board Fam Med |volume=26 |issue=4 |pages=470–7 |year=2013 |pmid=23833163 |doi=10.3122/jabfm.2013.04.120256 |url=}}</ref><ref name="pmid20511488">{{cite journal |vauthors=Khandaker MH, Espinosa RE, Nishimura RA, Sinak LJ, Hayes SN, Melduni RM, Oh JK |title=Pericardial disease: diagnosis and management |journal=Mayo Clin. Proc. |volume=85 |issue=6 |pages=572–93 |year=2010 |pmid=20511488 |pmc=2878263 |doi=10.4065/mcp.2010.0046 |url=}}</ref><ref name="pmid23610095">{{cite journal |vauthors=Bogaert J, Francone M |title=Pericardial disease: value of CT and MR imaging |journal=Radiology |volume=267 |issue=2 |pages=340–56 |year=2013 |pmid=23610095 |doi=10.1148/radiol.13121059 |url=}}</ref><ref name="pmid11680112">{{cite journal |vauthors=Gharib AM, Stern EJ |title=Radiology of pneumonia |journal=Med. Clin. North Am. |volume=85 |issue=6 |pages=1461–91, x |year=2001 |pmid=11680112 |doi= |url=}}</ref><ref name="pmid23507061">{{cite journal |vauthors=Schmidt WA |title=Imaging in vasculitis |journal=Best Pract Res Clin Rheumatol |volume=27 |issue=1 |pages=107–18 |year=2013 |pmid=23507061 |doi=10.1016/j.berh.2013.01.001 |url=}}</ref><ref name="pmid16891436">{{cite journal |vauthors=Suresh E |title=Diagnostic approach to patients with suspected vasculitis |journal=Postgrad Med J |volume=82 |issue=970 |pages=483–8 |year=2006 |pmid=16891436 |pmc=2585712 |doi=10.1136/pgmj.2005.042648 |url=}}</ref><ref name="pmid123074">{{cite journal |vauthors=Stein PD, Dalen JE, McIntyre KM, Sasahara AA, Wenger NK, Willis PW |title=The electrocardiogram in acute pulmonary embolism |journal=Prog Cardiovasc Dis |volume=17 |issue=4 |pages=247–57 |year=1975 |pmid=123074 |doi= |url=}}</ref><ref name="pmid23413894">{{cite journal |vauthors=Warnier MJ, Rutten FH, Numans ME, Kors JA, Tan HL, de Boer A, Hoes AW, De Bruin ML |title=Electrocardiographic characteristics of patients with chronic obstructive pulmonary disease |journal=COPD |volume=10 |issue=1 |pages=62–71 |year=2013 |pmid=23413894 |doi=10.3109/15412555.2012.727918 |url=}}</ref><ref name="pmid23000104">{{cite journal |vauthors=Stein PD, Matta F, Ekkah M, Saleh T, Janjua M, Patel YR, Khadra H |title=Electrocardiogram in pneumonia |journal=Am. J. Cardiol. |volume=110 |issue=12 |pages=1836–40 |year=2012 |pmid=23000104 |doi=10.1016/j.amjcard.2012.08.019 |url=}}</ref><ref name="pmid26209947">{{cite journal |vauthors=Hazebroek MR, Kemna MJ, Schalla S, Sanders-van Wijk S, Gerretsen SC, Dennert R, Merken J, Kuznetsova T, Staessen JA, Brunner-La Rocca HP, van Paassen P, Cohen Tervaert JW, Heymans S |title=Prevalence and prognostic relevance of cardiac involvement in ANCA-associated vasculitis: eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis |journal=Int. J. Cardiol. |volume=199 |issue= |pages=170–9 |year=2015 |pmid=26209947 |doi=10.1016/j.ijcard.2015.06.087 |url=}}</ref><ref name="pmid20112390">{{cite journal |vauthors=Dennert RM, van Paassen P, Schalla S, Kuznetsova T, Alzand BS, Staessen JA, Velthuis S, Crijns HJ, Tervaert JW, Heymans S |title=Cardiac involvement in Churg-Strauss syndrome |journal=Arthritis Rheum. |volume=62 |issue=2 |pages=627–34 |year=2010 |pmid=20112390 |doi=10.1002/art.27263 |url=}}</ref>
Libman-Sacks [[endocarditis]] should be [[Differentiate|differentiated]] from other [[diseases]] [[Presenting symptom|presenting]] with [[fever]], [[chest pain]] and [[anorexia]]. The [[Difference (philosophy)|differentials]] include the following:<ref name="pmid24550636">{{cite journal |vauthors=Brenes-Salazar JA |title=Westermark's and Palla's signs in acute and chronic pulmonary embolism: Still valid in the current computed tomography era |journal=J Emerg Trauma Shock |volume=7 |issue=1 |pages=57–8 |year=2014 |pmid=24550636 |pmc=3912657 |doi=10.4103/0974-2700.125645 |url=}}</ref><ref name="urlCT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis | RadioGraphics">{{cite web |url=http://pubs.rsna.org/doi/full/10.1148/rg.245045008 |title=CT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis &#124; RadioGraphics |format= |work= |accessdate=}}</ref><ref name="pmid23940438">{{cite journal |vauthors=Bĕlohlávek J, Dytrych V, Linhart A |title=Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism |journal=Exp Clin Cardiol |volume=18 |issue=2 |pages=129–38 |year=2013 |pmid=23940438 |pmc=3718593 |doi= |url=}}</ref><ref name="urlPulmonary Embolism: Symptoms - National Library of Medicine - PubMed Health">{{cite web |url=https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0022657/ |title=Pulmonary Embolism: Symptoms - National Library of Medicine - PubMed Health |format= |work= |accessdate=}}</ref><ref name="pmid20118395">{{cite journal |vauthors=Ramani GV, Uber PA, Mehra MR |title=Chronic heart failure: contemporary diagnosis and management |journal=Mayo Clin. Proc. |volume=85 |issue=2 |pages=180–95 |year=2010 |pmid=20118395 |pmc=2813829 |doi=10.4065/mcp.2009.0494 |url=}}</ref><ref name="pmid18215495">{{cite journal |vauthors=Blinderman CD, Homel P, Billings JA, Portenoy RK, Tennstedt SL |title=Symptom distress and quality of life in patients with advanced congestive heart failure |journal=J Pain Symptom Manage |volume=35 |issue=6 |pages=594–603 |year=2008 |pmid=18215495 |pmc=2662445 |doi=10.1016/j.jpainsymman.2007.06.007 |url=}}</ref><ref name="pmid19168510">{{cite journal |vauthors=Hawkins NM, Petrie MC, Jhund PS, Chalmers GW, Dunn FG, McMurray JJ |title=Heart failure and chronic obstructive pulmonary disease: diagnostic pitfalls and epidemiology |journal=Eur. J. Heart Fail. |volume=11 |issue=2 |pages=130–9 |year=2009 |pmid=19168510 |pmc=2639415 |doi=10.1093/eurjhf/hfn013 |url=}}</ref><ref name="pmid9465867">{{cite journal |vauthors=Takasugi JE, Godwin JD |title=Radiology of chronic obstructive pulmonary disease |journal=Radiol. Clin. North Am. |volume=36 |issue=1 |pages=29–55 |year=1998 |pmid=9465867 |doi= |url=}}</ref><ref name="pmid14651761">{{cite journal |vauthors=Wedzicha JA, Donaldson GC |title=Exacerbations of chronic obstructive pulmonary disease |journal=Respir Care |volume=48 |issue=12 |pages=1204–13; discussion 1213–5 |year=2003 |pmid=14651761 |doi= |url=}}</ref><ref name="pmid23833163">{{cite journal |vauthors=Nakawah MO, Hawkins C, Barbandi F |title=Asthma, chronic obstructive pulmonary disease (COPD), and the overlap syndrome |journal=J Am Board Fam Med |volume=26 |issue=4 |pages=470–7 |year=2013 |pmid=23833163 |doi=10.3122/jabfm.2013.04.120256 |url=}}</ref><ref name="pmid20511488">{{cite journal |vauthors=Khandaker MH, Espinosa RE, Nishimura RA, Sinak LJ, Hayes SN, Melduni RM, Oh JK |title=Pericardial disease: diagnosis and management |journal=Mayo Clin. Proc. |volume=85 |issue=6 |pages=572–93 |year=2010 |pmid=20511488 |pmc=2878263 |doi=10.4065/mcp.2010.0046 |url=}}</ref><ref name="pmid23610095">{{cite journal |vauthors=Bogaert J, Francone M |title=Pericardial disease: value of CT and MR imaging |journal=Radiology |volume=267 |issue=2 |pages=340–56 |year=2013 |pmid=23610095 |doi=10.1148/radiol.13121059 |url=}}</ref><ref name="pmid11680112">{{cite journal |vauthors=Gharib AM, Stern EJ |title=Radiology of pneumonia |journal=Med. Clin. North Am. |volume=85 |issue=6 |pages=1461–91, x |year=2001 |pmid=11680112 |doi= |url=}}</ref><ref name="pmid23507061">{{cite journal |vauthors=Schmidt WA |title=Imaging in vasculitis |journal=Best Pract Res Clin Rheumatol |volume=27 |issue=1 |pages=107–18 |year=2013 |pmid=23507061 |doi=10.1016/j.berh.2013.01.001 |url=}}</ref><ref name="pmid16891436">{{cite journal |vauthors=Suresh E |title=Diagnostic approach to patients with suspected vasculitis |journal=Postgrad Med J |volume=82 |issue=970 |pages=483–8 |year=2006 |pmid=16891436 |pmc=2585712 |doi=10.1136/pgmj.2005.042648 |url=}}</ref><ref name="pmid123074">{{cite journal |vauthors=Stein PD, Dalen JE, McIntyre KM, Sasahara AA, Wenger NK, Willis PW |title=The electrocardiogram in acute pulmonary embolism |journal=Prog Cardiovasc Dis |volume=17 |issue=4 |pages=247–57 |year=1975 |pmid=123074 |doi= |url=}}</ref><ref name="pmid23413894">{{cite journal |vauthors=Warnier MJ, Rutten FH, Numans ME, Kors JA, Tan HL, de Boer A, Hoes AW, De Bruin ML |title=Electrocardiographic characteristics of patients with chronic obstructive pulmonary disease |journal=COPD |volume=10 |issue=1 |pages=62–71 |year=2013 |pmid=23413894 |doi=10.3109/15412555.2012.727918 |url=}}</ref><ref name="pmid23000104">{{cite journal |vauthors=Stein PD, Matta F, Ekkah M, Saleh T, Janjua M, Patel YR, Khadra H |title=Electrocardiogram in pneumonia |journal=Am. J. Cardiol. |volume=110 |issue=12 |pages=1836–40 |year=2012 |pmid=23000104 |doi=10.1016/j.amjcard.2012.08.019 |url=}}</ref><ref name="pmid26209947">{{cite journal |vauthors=Hazebroek MR, Kemna MJ, Schalla S, Sanders-van Wijk S, Gerretsen SC, Dennert R, Merken J, Kuznetsova T, Staessen JA, Brunner-La Rocca HP, van Paassen P, Cohen Tervaert JW, Heymans S |title=Prevalence and prognostic relevance of cardiac involvement in ANCA-associated vasculitis: eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis |journal=Int. J. Cardiol. |volume=199 |issue= |pages=170–9 |year=2015 |pmid=26209947 |doi=10.1016/j.ijcard.2015.06.087 |url=}}</ref><ref name="pmid20112390">{{cite journal |vauthors=Dennert RM, van Paassen P, Schalla S, Kuznetsova T, Alzand BS, Staessen JA, Velthuis S, Crijns HJ, Tervaert JW, Heymans S |title=Cardiac involvement in Churg-Strauss syndrome |journal=Arthritis Rheum. |volume=62 |issue=2 |pages=627–34 |year=2010 |pmid=20112390 |doi=10.1002/art.27263 |url=}}</ref>
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**Eventual [[right heart failure]]
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Latest revision as of 20:57, 19 August 2020

Libman-Sacks endocarditis Microchapters

Overview

Historical Perspective

Pathophysiology

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Imaging Findings

Other Diagnostic Studies

Treatment

Differentiating Libman-Sacks Endocarditis from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Mohsin, M.D.[2]

Synonyms and keywords:: Nonbacterial thrombotic endocarditis (NBTE), Marantic endocarditis, Verrucous endocarditis

Overview

Libman-Sacks endocarditis (LSE) is a form of nonbacterial thrombotic endocarditis (NBTE) that is considered to be the most common cardiac manifestation seen in patients with systemic lupus erythematosus. LSE is a term used for sterile and verrucous vegetations around the heart valves mostly affecting the mitral and aortic heart valves but other valves may also be involved. Valvular involvement in LSE may lead to valvular regurgitation, aortic insufficiency, thromboembolic cerebrovascular events, and increased risk of infective endocarditis. It is also usually associated with the other autoimmune diseases such as antiphospholipid syndrome (APS) and some malignancies. Secondary APS has a higher rate of cardiac involvement as compared to primary APS, mostly due to the autoimmune causes related to the SLE. LSE can be complicated by embolic cerebrovascular disease, superimposed infective endocarditis, and peripheral arterial embolism. It is also associated with increased mortality, hence, early recognition of LSE and appropriate treatment are of significant importance in preventing any further complications.

Historical Perspective

Pathophysiology

Pathology

Factors responsible for the initiation of Libman-Sacks endocarditis
Initiation factor Description
Immune complexes
Hypoxia
Hypercoagulability
Carcinomatosis Following carcinomas are commonly associated with NBTE and Libman-Sacks endocarditis:

Gross pathology

Allen and Sirota macroscopic classification of NBTE
Type of NBTE Features
Type 1
  • Small
  • < 3 mm
  • Univerrucal
  • Firmly attached to the valve
Type 2
Type 3
  • Small
  • 1 - 3 mm
  • Multiverrucal
  • Friable
Libman Sacks Endocarditis. The presence of vegetations predisposes patients to bacterial endocarditis. Source: Brigden et al,1960.
Libman-Sacks endocarditis. Source: Kumar et al, 2010/Courtesy Dr. Fred Schoen, Department of Pathology, Brigham and Women's Hospital

Microscopic Pathology

Stages of evolution of vegetations in Libman-Sacks endocarditis
Stage Description
Stage 1 (active verrucae)
Stage 2 (Combined active and healed lesions)
Stage 3 (Healed lesions)
Pathology slide of mitral valve vegetation. Lots of necrosis: 10 cm circumference vegetation. Mitral valve tissue shows focal necrosis. No bacterial or fungal organisms were present. Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA
R lung, high power: emboli and large necrotic infarcted tissue. Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA
Low power of the liver: lots of steatosis and congestion, necrosis. Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA
High power pathology slide of the liver showing lots of steatosis, congestion, and necrosis. Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA
Low power pathology slide of the lung showing emboli and necrotic tissue.Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA

Epidemiology and Demographics

Risk Factors

Risk factors for the development of Libman-Sacks endocarditis
Risk factor Details
Advanced stage malignancy Advanced stage malignancies such as:
Chronic diseases Chronic diseases such as:
Connective tissue disorders with hypercoagulable state
Trauma Trauma due to:

Natural History, Complications and Prognosis

Complications

Prognosis

Diagnosis

Mckay and Wahler triad for diagnosis of NBTE
1:
2:
3:

History and Symptoms

Common manifestations of patients with Libman-Sacks endocarditis
Manifestation Description
Heart failure Heart failure can occur secondary to the valvular dysfunction (most commonly mitral regurgitation), leading to the following signs and symptoms:
Cerebrovascular embolism[29] Cerebrovascular embolism can present as any of the following:
Systemic thromboembolism Systemic thromboembolism can cause any of the following:
Secondary infective endocarditis Secondary infective endocarditis can present as:

Physical Examination

Physical examination findings in a patient of Libman-Sacks endocarditis
Pathology Physical examination finding
Left ventricular hypertrophy[30][31][32][33][34][35] LVH can present as any of the following:
Congestive heart failure Physical examination findings of CHF include:
Infective endocarditis (IE)[36][37][38][39] IE can present as:
Mitral valve disease[40]
Aortic valve disease
Tricuspid valve disease

Laboratory Findings

Laboratory Investigations in Libman-Sacks Endocarditis Laboratory test findings
Blood culture
SLE investigations

(Immunological assays)

CBC
Studies to rule out DIC
Polymerase chain reaction (PCR)


Imaging Findings

Imaging tests in Libman-Sacks Endocarditis Imagining Findings
Echocardiography[41][26][42]
2D transesophageal ultrasound. Image on the left shows a thickened mitral valve with a 1 cm vegetation that can be seen on the anterior mitral leaflet. Image on the right is a four-chamber color flow Doppler view showing biventricular dilatation, severe left ventricular dysfunction. For orientation purposes, left ventricle is the bottom right chamber. Video of both views is attached as a supplementary file. Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA
Chest X-Ray
MRI[43]
MRI of the brain. Images on the top show increased signal on diffusion weighted imaging (DWI) throughout the bilateral frontal, parietal, and occipital lobes. Images on the bottom show a corresponding decreased signal intensity on apparent diffusion coefficient that is consistent with acute abnormal restricted diffusion. These findings suggest new/ongoing acute infarcts.Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA
CT scan (Head)
CT of head without contrast showing extensive multifocal areas of hypoattentuation throughout the bilateral frontal, parietal, occipital, and right > left temporal lobes. No mass effect or midline shift or hemorrhage was seen.Source: Ghulam Murtaza. et al, Department of Internal Medicine, Advocate Christ Medical Center, Oak Lawn, IL, USA

Other Diagnostic Studies

Cardiac Catheterization

Treatment

Common treatment options for Libman-Sacks endocarditis depending on the underlying cause
Treatment option Details
Steroids and immunosuppressive agents They are useful in the treatment of underlying disease but they have a controversial role in the pathogenesis of vegetations:
Anticoagulants
Other medications
Valve replacement[7][44][11]

Differentiating Libman-Sacks Endocarditis from other Diseases

Libman-Sacks endocarditis should be differentiated from other diseases presenting with fever, chest pain and anorexia. The differentials include the following:[45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61][62][63][64]

Diseases Diagnostic tests Physical Examination Symptoms Past medical history Other Findings
CT scan and MRI EKG Chest X-ray Tachypnea Tachycardia Fever Chest Pain Hemoptysis Dyspnea on Exertion Wheezing Chest Tenderness Nasalopharyngeal Ulceration Carotid Bruit
Pulmonary embolism
  • On CT angiography:
    • Intra-luminal filling defect
  • On MRI:
    • Narrowing of involved vessel
    • No contrast seen distal to obstruction
    • Polo-mint sign (partial filling defect surrounded by contrast)
✔ (Low grade) ✔ (In case of massive PE) - - - -
Infective Endocarditis
  • Goldberg's criteria may aid in diagnosis of left ventricular dysfunction: (High specificity)
    • SV1 or SV2 + RV5 or RV6 ≥3.5 mV
    • Total QRS amplitude in each of the limb leads ≤0.8 mV
    • R/S ratio <1 in lead V4
- - - - - -
Non-bacterial thrombotic endocarditis
  • ST elevation
  • PR depression
✔ (Low grade) ✔ (Relieved by sitting up and leaning forward) - - - - -
  • May be clinically classified into:
    • Acute (< 6 weeks)
    • Sub-acute (6 weeks - 6 months)
    • Chronic (> 6 months)
Libman Sack Endocarditis - - - -
Vasculitis

Homogeneous, circumferential vessel wall swelling

-
Fever of unknown origin (FUO) - - - - - -

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