Cardiovascular Pathology 24 (2015) 244–246
Contents lists available at ScienceDirect
Cardiovascular Pathology
Clinical Case Report
Sudden cardiac death due to coronary artery dissection as a complication of cardiac sarcoidosis Savas Kanaroglou a,1, Vidhya Nair b,c,⁎, John R Fernandes b,c,2 a b c
Hamilton Centre for Kidney Research, St. Joseph's Hospital, Hamilton, Ontario, Canada L8N 4A6 Hamilton General Hospital, Hamilton Health Sciences, Hamilton, Ontario, Canada L8L2X2 Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada L8N3ZS
a r t i c l e
i n f o
Article history: Received 11 November 2014 Received in revised form 31 December 2014 Accepted 1 January 2015 Keywords: Sarcoidosis Vasculitis Spontaneous coronary artery dissection Sudden cardiac death
a b s t r a c t Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome (ACS), cardiac tamponade and sudden cardiac death that typically affects young women in the postpartum period. Rarely, it can be caused by systemic inflammatory conditions such as sarcoidosis. Sarcoidosis is an inflammatory disease most often affecting the lung and lymph nodes that can sometimes affect the heart. The authors report a case of sudden cardiac death caused by SCAD in the context of undiagnosed and subclinical cardiac sarcoidosis. The decedent was a 47-year-old male with a relatively innocuous past medical history. He was found dead in bed. At autopsy, there was a lethal hemopericardium resulting in cardiac tamponade. Gross examination of the heart revealed dissection of the posterior descending coronary branch of the right coronary artery. Histologically, the coronary artery showed acute and organizing dissection with evidence of vasculitis. A chronic inflammatory infiltrate consisting of lymphocytes, histiocytes, eosinophils and giant cells was seen. Sections of the myocardium showed myocarditis with a nonnecrotizing granuloma. The death was attributed to cardiac tamponade secondary to SCAD in the context of systemic sarcoidosis. The presented case demonstrates two concurrent rare pathologies and highlights the importance of considering SCAD in cases of sudden cardiac death at autopsy. © 2015 Elsevier Inc. All rights reserved.
1. Introduction Spontaneous coronary artery dissection (SCAD) refers to cases of coronary artery dissection without a traumatic or iatrogenic cause. SCAD is a rare entity in its own right and has only once been described as a complication of cardiac sarcoidosis. Of particular note is that this is a case of a postpartum female [1]. Nonsarcoid SCAD accounts for 0.1–4% of acute coronary syndromes (ACSs) and has a multifactorial etiology most typically involving an arteriopathy [2]. Examples of arteriopathies that can lead to SCAD include atherosclerosis, the peripartum state, connective tissue disorders, systemic inflammatory conditions and coronary artery spasm [3]. Sarcoidosis is a systemic granulomatous disease that has no known etiology. It is characterized microscopically by noncaseating granulomata and most typically involves the lungs and lymph nodes, though it can affect almost any organ. Cardiac sarcoidosis can manifest as conduction abnormalities, congestive heart failure, ventricular aneurysm, pericardial
Funding: There were no external sources of funding for this case report. The authors report no conflict of interest. The autopsy case was carried out by Dr. John Fernandes at the Hamilton General Hospital. ⁎ Corresponding author. Hamilton General Hospital, 237 Barton Street East, Hamilton, Ontario, Canada L8L 2X2. Tel.: +1-905-527-4322x46170. E-mail addresses: [email protected] (S. Kanaroglou), [email protected] (V. Nair), [email protected] (J.R. Fernandes). 1 Tel.: +1-905-512-8578. 2 Tel.: +1-905-527-4322x46530. http://dx.doi.org/10.1016/j.carpath.2015.01.001 1054-8807/© 2015 Elsevier Inc. All rights reserved.
effusion and pulmonary hypertension [4]. Cardiac manifestations are responsible for up to 50% of deaths associated with sarcoidosis [5]. We describe the case of a man who succumbed to SCAD as a complication of cardiac sarcoidosis. 2. Case description A 47-year-old male was found lifeless in bed. On the previous day, the decedent did gardening for up to 4 h then fell asleep watching television. His past medical history was significant for a previous pulmonary embolism and his medications consisted of tylenol 3 and meloxicam. There was no evidence of trauma or disturbance at the scene. At autopsy, there was a lethal hemopericardium. Cardiac examination revealed a 457-g heart. There was abnormality of the posterior myocardium with possible dissection of the posterior descending branch of the coronary artery (Fig. 1). There was hemorrhage posteriorly involving the posterior right and left ventricles without any grossly evident myocardial infarction (Fig. 1). There were no findings on gross examination indicating a cause for the dissection of the posterior descending coronary branch and hemorrhage of the myocardium. Sections from the myocardium showed variable myocyte hypertrophy and increased interstitial fibrosis. There were multifocal lymphocytic infiltrates with associated myocyte necrosis (Fig. 2A). A nonnecrotizing granuloma composed of giant cells and histiocytes was seen in the posterior wall of the left ventricle (Fig. 2B). Special stains (Gram for bacteria, Grocott methenamine silver for fungus and Ziehl–Neelsen stain for acid fast bacilli) did
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not reveal any microorganisms. The hilar lymph nodes and the lungs showed numerous hyalinized nonnecrotizing granulomata. Special stains were also negative using the same staining panel for microorganisms. Sections from the left anterior descending coronary artery showed atherosclerosis with luminal stenosis of 40%. Sections from the left circumflex coronary artery showed intimal hyperplasia and luminal stenosis of 30%. Sections from the proximal part of the right coronary artery showed atherosclerosis with stenosis of 40%. The posterior descending branch of the right coronary artery showed acute and organizing dissection of the media (Fig. 3A and B). The periadventitial fat showed an infiltrate composed of giant cells, histiocytes and eosinophils (Fig. 4). There was recent hemorrhage into the epicardial fat suggesting external rupture. There was evidence of vasculitis in the distal segment of the posterior descending coronary artery with an organizing thrombus in the lumen and destruction of the media. There was evidence of organization with fibrosis and chronic inflammation involving the media and the periadventitial epicardial fat (Fig. 5).
3. Discussion Fig. 1. Gross photograph showing the hemorrhage along the posterior surface of the heart (white arrow).
The link between SCAD and sarcoidosis has been described previously, yet there is a paucity of case reports in the literature linking the
Fig. 2. (A) Photomicrograph showing lymphocytic infiltration with myocyte necrosis. (Stain: hematoxylin and eosin. Original magnification: ×100.) (B) Photomicrograph showing cardiac myocytes consistent with a nonnecrotizing granuloma composed of giant cells (white arrow) and histiocytes. (Stain: hematoxylin and eosin. Original magnification: ×200.)
Fig. 3. (A) Photomicrograph of the posterior descending coronary artery showing acute and organizing dissection of the tunica media. (B) Photomicrograph showing acute dissection (Stain A and B: hematoxylin and eosin. Original magnification: A is ×40 and B is ×200.)
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S. Kanaroglou et al. / Cardiovascular Pathology 24 (2015) 244–246
Fig. 4. Photomicrograph showing periadventitial fat with an inflammatory infiltrate composed of giant cells (white arrow), histiocytes (black arrow) and eosinophils (black arrow head). (Stain: hematoxylin and eosin. Original magnification: ×200.)
Fig. 5. Photomicrograph of the distal right coronary artery showing dissection of the media with the presence of granulation tissue and chronic inflammation consistent with vasculitis. (Stain: hematoxylin and eosin. Original magnification: ×40.)
two [3]. A solitary case describes SCAD in a 27-year-old postpartum female with systemic sarcoidosis [1]. Our case is thus remarkable as the effects of hormonal fluctuation on connective tissue due to pregnancy are absent and thus it is likely that the patient's SCAD is solely due to vasculitis associated with cardiac sarcoidosis. SCAD is defined as the creation of a false lumen through the coronary arterial wall following the separation of its layers. Generally, this causes a hematoma that then compresses the coronary artery leading to ACS [3]. The oldest known case was reported in 1931 and is that of a 42-yearold woman who succumbed to sudden cardiac death [6]. The most susceptible individuals are thought to be females under the age of 50 years in the postpartum period with up to one third of women who develop SCAD either pregnant or postpartum [7]. In a retrospective case identification study of 11,175 cases of ACS, 17/22 (77%) cases of SCAD were females, all of which had a gravidity of at least one [8]. Of the males identified in this study, only two had no cardiac risk factors [8]. While SCAD is a rare cause of ACS, rarer still is sarcoidosis as a cause of SCAD. Sarcoidosis is a nebulous entity with an obscure etiology. It is known to be a systemic disease characterized by granulomatous inflammation and giant cell formation that is not due to foreign bodies or infection [9]. The most prominent theory on the etiology of sarcoidosis describes it as an aberrant immune response to a heretofore unidentified antigen in the context of genetic predisposition [10]. The epidemiology of sarcoidosis lends itself well to this multifactorial explanation. The incidence is variable based on country: It has an incidence of 1–40 per 100,000 in the United States, 64/10000 in Sweden and 1/100000 in Japan [11]. Prevalence has been increasing steadily, from 164/100000 in 1995 to 330/10000 in 2010 in the United States [12]. It also shows a predilection for the female gender and Afro-American ethnicity. Sarcoidosis remains particularly difficult to diagnose due to its nonspecific presentation, and as such, the stated prevalence is likely to be an underestimation of its true extent in the population. Cardiac involvement is a dreaded manifestation of disease; it is found in up to 30% of systemic sarcoidosis cases at autopsy and can lead to sudden cardiac death [13]. To further complicate matters, diagnosis of cardiac involvement in vivo by biopsy is technically difficult due to patchy distribution and predilection for affecting the left ventricle that is challenging to access [13]. What is clear is that cardiac involvement can remain subclinical in the context of sarcoidosis [14]. Even more concerning is the existence of isolated cardiac involvement in which the nonspecific symptoms of lung involvement fail to manifest to encourage investigation [13]. Further research into the pathogenesis of sarcoidosis may yield an understanding of the context in which it arises; what is currently considered subclinical progression of cardiac involvement could potentially, in the
future, be handily identified. Nevertheless, due to its rarity, screening is unlikely to be feasible and thus the scenario described in the case remains a continued risk for some individuals. 4. Conclusion To our knowledge, we present the first documented case of SCAD secondary to undiagnosed and subclinical cardiac sarcoidosis in a male. The decedent had a relatively innocuous past medical history and reported no concerning symptoms prior to his death. Due to the risk of sudden cardiac death, cardiac involvement should be ruled out in the context of systemic sarcoidosis. Furthermore, SCAD is not exclusive to females and, though rare, is a cause of sudden cardiac death to be considered by the pathologist at autopsy. Acknowledgements None. References [1] Ehya H, Weitznes S. Postpartum dissecting aneurysm of coronary arteries in a patient with sarcoidosis. South Med J 1980;73(1):87–8. [2] Hayes SN. Spontaneous coronary artery dissection (SCAD): new insights into this not-so-rare condition. Tex Heart Inst J 2014;41(3):295–8. [3] Saw J. Spontaneous coronary artery dissection. Can J Cardiol 2013;29(9):1027–33. [4] Sekhri V, Sanal S, Delorenzo LJ, Aronow WS, Maguire GP. Cardiac sarcoidosis: a comprehensive review. Arch Med Sci 2011;7(4):546–54. [5] Lagana SM, Parwani AV, Nichols LC. Cardiac sarcoidosis: a pathology-focused review. Arch Pathol Lab Med 2010;143:1039–46. [6] Pretty HC. Dissecting aneurysm of coronary artery in a woman aged 42: rupture. Br Med J 1931;1:667. [7] McCann AB, Whitbourn RJ. Spontaneous coronary artery dissection: a review of the etiology and available treatment options. Heart Vessels 2009;24(6):463–5. [8] Mortensen KH, Thuesen L, Kristensen IB, Christiansen EH. Spontaneous coronary artery dissection: a Western Denmark Heart Registry study. Catheter Cardiovasc Interv 2009;74(5):710–7. [9] Newman LS, Rose CS, Maier LA. Sarcoidosis. N Engl J Med 1997;336(17):1224–34. [10] Saidha S, Sotirchos ES, Eckstein C. Etiology of sarcoidosis: does infection play a role? Yale J Biol Med 2012;85:133–41. [11] Byard RW, Manton N, Tsokos M. Sarcoidosis and mechanisms of unexpected death. J Forensic Sci 2008;53(2):460–4. [12] Erdal BS, Clymer BD, Yildiz VO, Julian MW, Crouser ED. Unexpectedly high prevalence of sarcoidosis in a representative U.S. Metropolitan population. Respir Med 2012;106(6):893–9. [13] Butany J, Bahl NE, Morales K, Thangaroopan M, Ross H, Rao V, et al. The intricacies of cardiac sarcoidosis: a case report involving the coronary arteries and a review of the literature. Cardiovasc Pathol 2006;15(4):222–7. [14] Bagwan IN, Hooper LV, Sheppard MN. Cardiac sarcoidosis and sudden death. The heart may look normal or mimic other cardiomyopathies. Virchows Arch 2011; 458(6):671–8.
Contents lists available at ScienceDirect
Cardiovascular Pathology
Clinical Case Report
Sudden cardiac death due to coronary artery dissection as a complication of cardiac sarcoidosis Savas Kanaroglou a,1, Vidhya Nair b,c,⁎, John R Fernandes b,c,2 a b c
Hamilton Centre for Kidney Research, St. Joseph's Hospital, Hamilton, Ontario, Canada L8N 4A6 Hamilton General Hospital, Hamilton Health Sciences, Hamilton, Ontario, Canada L8L2X2 Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada L8N3ZS
a r t i c l e
i n f o
Article history: Received 11 November 2014 Received in revised form 31 December 2014 Accepted 1 January 2015 Keywords: Sarcoidosis Vasculitis Spontaneous coronary artery dissection Sudden cardiac death
a b s t r a c t Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome (ACS), cardiac tamponade and sudden cardiac death that typically affects young women in the postpartum period. Rarely, it can be caused by systemic inflammatory conditions such as sarcoidosis. Sarcoidosis is an inflammatory disease most often affecting the lung and lymph nodes that can sometimes affect the heart. The authors report a case of sudden cardiac death caused by SCAD in the context of undiagnosed and subclinical cardiac sarcoidosis. The decedent was a 47-year-old male with a relatively innocuous past medical history. He was found dead in bed. At autopsy, there was a lethal hemopericardium resulting in cardiac tamponade. Gross examination of the heart revealed dissection of the posterior descending coronary branch of the right coronary artery. Histologically, the coronary artery showed acute and organizing dissection with evidence of vasculitis. A chronic inflammatory infiltrate consisting of lymphocytes, histiocytes, eosinophils and giant cells was seen. Sections of the myocardium showed myocarditis with a nonnecrotizing granuloma. The death was attributed to cardiac tamponade secondary to SCAD in the context of systemic sarcoidosis. The presented case demonstrates two concurrent rare pathologies and highlights the importance of considering SCAD in cases of sudden cardiac death at autopsy. © 2015 Elsevier Inc. All rights reserved.
1. Introduction Spontaneous coronary artery dissection (SCAD) refers to cases of coronary artery dissection without a traumatic or iatrogenic cause. SCAD is a rare entity in its own right and has only once been described as a complication of cardiac sarcoidosis. Of particular note is that this is a case of a postpartum female [1]. Nonsarcoid SCAD accounts for 0.1–4% of acute coronary syndromes (ACSs) and has a multifactorial etiology most typically involving an arteriopathy [2]. Examples of arteriopathies that can lead to SCAD include atherosclerosis, the peripartum state, connective tissue disorders, systemic inflammatory conditions and coronary artery spasm [3]. Sarcoidosis is a systemic granulomatous disease that has no known etiology. It is characterized microscopically by noncaseating granulomata and most typically involves the lungs and lymph nodes, though it can affect almost any organ. Cardiac sarcoidosis can manifest as conduction abnormalities, congestive heart failure, ventricular aneurysm, pericardial
Funding: There were no external sources of funding for this case report. The authors report no conflict of interest. The autopsy case was carried out by Dr. John Fernandes at the Hamilton General Hospital. ⁎ Corresponding author. Hamilton General Hospital, 237 Barton Street East, Hamilton, Ontario, Canada L8L 2X2. Tel.: +1-905-527-4322x46170. E-mail addresses: [email protected] (S. Kanaroglou), [email protected] (V. Nair), [email protected] (J.R. Fernandes). 1 Tel.: +1-905-512-8578. 2 Tel.: +1-905-527-4322x46530. http://dx.doi.org/10.1016/j.carpath.2015.01.001 1054-8807/© 2015 Elsevier Inc. All rights reserved.
effusion and pulmonary hypertension [4]. Cardiac manifestations are responsible for up to 50% of deaths associated with sarcoidosis [5]. We describe the case of a man who succumbed to SCAD as a complication of cardiac sarcoidosis. 2. Case description A 47-year-old male was found lifeless in bed. On the previous day, the decedent did gardening for up to 4 h then fell asleep watching television. His past medical history was significant for a previous pulmonary embolism and his medications consisted of tylenol 3 and meloxicam. There was no evidence of trauma or disturbance at the scene. At autopsy, there was a lethal hemopericardium. Cardiac examination revealed a 457-g heart. There was abnormality of the posterior myocardium with possible dissection of the posterior descending branch of the coronary artery (Fig. 1). There was hemorrhage posteriorly involving the posterior right and left ventricles without any grossly evident myocardial infarction (Fig. 1). There were no findings on gross examination indicating a cause for the dissection of the posterior descending coronary branch and hemorrhage of the myocardium. Sections from the myocardium showed variable myocyte hypertrophy and increased interstitial fibrosis. There were multifocal lymphocytic infiltrates with associated myocyte necrosis (Fig. 2A). A nonnecrotizing granuloma composed of giant cells and histiocytes was seen in the posterior wall of the left ventricle (Fig. 2B). Special stains (Gram for bacteria, Grocott methenamine silver for fungus and Ziehl–Neelsen stain for acid fast bacilli) did
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not reveal any microorganisms. The hilar lymph nodes and the lungs showed numerous hyalinized nonnecrotizing granulomata. Special stains were also negative using the same staining panel for microorganisms. Sections from the left anterior descending coronary artery showed atherosclerosis with luminal stenosis of 40%. Sections from the left circumflex coronary artery showed intimal hyperplasia and luminal stenosis of 30%. Sections from the proximal part of the right coronary artery showed atherosclerosis with stenosis of 40%. The posterior descending branch of the right coronary artery showed acute and organizing dissection of the media (Fig. 3A and B). The periadventitial fat showed an infiltrate composed of giant cells, histiocytes and eosinophils (Fig. 4). There was recent hemorrhage into the epicardial fat suggesting external rupture. There was evidence of vasculitis in the distal segment of the posterior descending coronary artery with an organizing thrombus in the lumen and destruction of the media. There was evidence of organization with fibrosis and chronic inflammation involving the media and the periadventitial epicardial fat (Fig. 5).
3. Discussion Fig. 1. Gross photograph showing the hemorrhage along the posterior surface of the heart (white arrow).
The link between SCAD and sarcoidosis has been described previously, yet there is a paucity of case reports in the literature linking the
Fig. 2. (A) Photomicrograph showing lymphocytic infiltration with myocyte necrosis. (Stain: hematoxylin and eosin. Original magnification: ×100.) (B) Photomicrograph showing cardiac myocytes consistent with a nonnecrotizing granuloma composed of giant cells (white arrow) and histiocytes. (Stain: hematoxylin and eosin. Original magnification: ×200.)
Fig. 3. (A) Photomicrograph of the posterior descending coronary artery showing acute and organizing dissection of the tunica media. (B) Photomicrograph showing acute dissection (Stain A and B: hematoxylin and eosin. Original magnification: A is ×40 and B is ×200.)
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S. Kanaroglou et al. / Cardiovascular Pathology 24 (2015) 244–246
Fig. 4. Photomicrograph showing periadventitial fat with an inflammatory infiltrate composed of giant cells (white arrow), histiocytes (black arrow) and eosinophils (black arrow head). (Stain: hematoxylin and eosin. Original magnification: ×200.)
Fig. 5. Photomicrograph of the distal right coronary artery showing dissection of the media with the presence of granulation tissue and chronic inflammation consistent with vasculitis. (Stain: hematoxylin and eosin. Original magnification: ×40.)
two [3]. A solitary case describes SCAD in a 27-year-old postpartum female with systemic sarcoidosis [1]. Our case is thus remarkable as the effects of hormonal fluctuation on connective tissue due to pregnancy are absent and thus it is likely that the patient's SCAD is solely due to vasculitis associated with cardiac sarcoidosis. SCAD is defined as the creation of a false lumen through the coronary arterial wall following the separation of its layers. Generally, this causes a hematoma that then compresses the coronary artery leading to ACS [3]. The oldest known case was reported in 1931 and is that of a 42-yearold woman who succumbed to sudden cardiac death [6]. The most susceptible individuals are thought to be females under the age of 50 years in the postpartum period with up to one third of women who develop SCAD either pregnant or postpartum [7]. In a retrospective case identification study of 11,175 cases of ACS, 17/22 (77%) cases of SCAD were females, all of which had a gravidity of at least one [8]. Of the males identified in this study, only two had no cardiac risk factors [8]. While SCAD is a rare cause of ACS, rarer still is sarcoidosis as a cause of SCAD. Sarcoidosis is a nebulous entity with an obscure etiology. It is known to be a systemic disease characterized by granulomatous inflammation and giant cell formation that is not due to foreign bodies or infection [9]. The most prominent theory on the etiology of sarcoidosis describes it as an aberrant immune response to a heretofore unidentified antigen in the context of genetic predisposition [10]. The epidemiology of sarcoidosis lends itself well to this multifactorial explanation. The incidence is variable based on country: It has an incidence of 1–40 per 100,000 in the United States, 64/10000 in Sweden and 1/100000 in Japan [11]. Prevalence has been increasing steadily, from 164/100000 in 1995 to 330/10000 in 2010 in the United States [12]. It also shows a predilection for the female gender and Afro-American ethnicity. Sarcoidosis remains particularly difficult to diagnose due to its nonspecific presentation, and as such, the stated prevalence is likely to be an underestimation of its true extent in the population. Cardiac involvement is a dreaded manifestation of disease; it is found in up to 30% of systemic sarcoidosis cases at autopsy and can lead to sudden cardiac death [13]. To further complicate matters, diagnosis of cardiac involvement in vivo by biopsy is technically difficult due to patchy distribution and predilection for affecting the left ventricle that is challenging to access [13]. What is clear is that cardiac involvement can remain subclinical in the context of sarcoidosis [14]. Even more concerning is the existence of isolated cardiac involvement in which the nonspecific symptoms of lung involvement fail to manifest to encourage investigation [13]. Further research into the pathogenesis of sarcoidosis may yield an understanding of the context in which it arises; what is currently considered subclinical progression of cardiac involvement could potentially, in the
future, be handily identified. Nevertheless, due to its rarity, screening is unlikely to be feasible and thus the scenario described in the case remains a continued risk for some individuals. 4. Conclusion To our knowledge, we present the first documented case of SCAD secondary to undiagnosed and subclinical cardiac sarcoidosis in a male. The decedent had a relatively innocuous past medical history and reported no concerning symptoms prior to his death. Due to the risk of sudden cardiac death, cardiac involvement should be ruled out in the context of systemic sarcoidosis. Furthermore, SCAD is not exclusive to females and, though rare, is a cause of sudden cardiac death to be considered by the pathologist at autopsy. Acknowledgements None. References [1] Ehya H, Weitznes S. Postpartum dissecting aneurysm of coronary arteries in a patient with sarcoidosis. South Med J 1980;73(1):87–8. [2] Hayes SN. Spontaneous coronary artery dissection (SCAD): new insights into this not-so-rare condition. Tex Heart Inst J 2014;41(3):295–8. [3] Saw J. Spontaneous coronary artery dissection. Can J Cardiol 2013;29(9):1027–33. [4] Sekhri V, Sanal S, Delorenzo LJ, Aronow WS, Maguire GP. Cardiac sarcoidosis: a comprehensive review. Arch Med Sci 2011;7(4):546–54. [5] Lagana SM, Parwani AV, Nichols LC. Cardiac sarcoidosis: a pathology-focused review. Arch Pathol Lab Med 2010;143:1039–46. [6] Pretty HC. Dissecting aneurysm of coronary artery in a woman aged 42: rupture. Br Med J 1931;1:667. [7] McCann AB, Whitbourn RJ. Spontaneous coronary artery dissection: a review of the etiology and available treatment options. Heart Vessels 2009;24(6):463–5. [8] Mortensen KH, Thuesen L, Kristensen IB, Christiansen EH. Spontaneous coronary artery dissection: a Western Denmark Heart Registry study. Catheter Cardiovasc Interv 2009;74(5):710–7. [9] Newman LS, Rose CS, Maier LA. Sarcoidosis. N Engl J Med 1997;336(17):1224–34. [10] Saidha S, Sotirchos ES, Eckstein C. Etiology of sarcoidosis: does infection play a role? Yale J Biol Med 2012;85:133–41. [11] Byard RW, Manton N, Tsokos M. Sarcoidosis and mechanisms of unexpected death. J Forensic Sci 2008;53(2):460–4. [12] Erdal BS, Clymer BD, Yildiz VO, Julian MW, Crouser ED. Unexpectedly high prevalence of sarcoidosis in a representative U.S. Metropolitan population. Respir Med 2012;106(6):893–9. [13] Butany J, Bahl NE, Morales K, Thangaroopan M, Ross H, Rao V, et al. The intricacies of cardiac sarcoidosis: a case report involving the coronary arteries and a review of the literature. Cardiovasc Pathol 2006;15(4):222–7. [14] Bagwan IN, Hooper LV, Sheppard MN. Cardiac sarcoidosis and sudden death. The heart may look normal or mimic other cardiomyopathies. Virchows Arch 2011; 458(6):671–8.
