CASE REPORT AND LITERATURE REVIEW
Spontaneous Coronary Artery Dissection Report of 3 Cases and Literature Review Hormonal, Autoimmune, Morphological Factors İpek Esen Melez, MD,* Murat Nihat Arslan, MD,† Deniz Oğuzhan Melez, MD,† Arzu Akçay, MD,† Yalçin Büyük, MD,† Abdullah Avşar, MD,‡ Bahadir Kumral, MD,§ Gözde Şirin, MD,† Ferah Anıl Karayel, MD,† Taner Daş, MD,† Yasemin Erenç Dokudan, MD,k and Bülent Şam, MD† Abstract: The number of cases with spontaneous coronary artery dissection (SCAD) is considered to be being underestimated because of a large amount of SCAD leading to sudden death without previous diagnosis. Besides, not only in clinics but also in autopsy practice, correct diagnosis of SCAD is important to prevent forensic malpractice. The article is intended to discuss the pathological findings through the forensic point of view for improving the malpractice expertise in scope of clinicians' timely antemortem diagnosis according to risk factors and in scope of forensic pathologists' the cause of death determination ability according to macroscopical and microscopical findings of the autopsy. In 3 cases reported, the main characteristics were the female sex, pregnancy history and a sudden death without any trauma. However, although there are many women giving birth or using oral contraceptives, only some of them are facing with SCAD. This suggests the possibility of some hereditary factors, whereas hereditary characteristics may be understood in many different ways like hormone-releasing regulating mechanisms as well as immunity, morphology, or any other mechanism. For instance, autoimmunity has been also a hereditary underlying factor for vessel injury considered in presented cases. Key Words: coronary artery dissection, autopsy, pregnancy, autoimmunity, morphology, malpractice (Am J Forensic Med Pathol 2015;36: 188–192)
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pontaneous coronary artery dissection (SCAD), first described in 1931, is explained briefly as the dissection between the layers of media and adventitia in the coronary artery wall.1 The detection of SCAD is usually done by coronary angiography in clinical studies, and confirmation of this diagnosis is possible by a novel method, intravascular ultrasound.2–4 The incidence of SCAD has been reported as 0.1% to 0.2% in the angiographic series increasing to 1.1% or even 10.8% in patient groups with acute coronary syndrome.2–5 However, the correct number of cases is considered to be being underestimated due to a large amount of SCAD leading to sudden death without previous diagnosis. Some of these undiagnosed cases are detected by postmortem examination. Different postmortem diagnosis ratios have been given in different autopsy studies, yet the success ratio of detection in
Manuscript received May 16, 2013; accepted October 23, 2014. From the *Department of Forensic Medicine, Medical Faculty, Bezmialem Vakıf University; †The Ministry of Justice Council of Forensic Medicine, İstanbul; ‡Department of Forensic Medicine, Medical Faculty, Kahramanmaraş Sütçü İmam University, Kahramanmaraş; §Department of Forensic Medicine, Medical Faculty, Namık Kemal University, Tekirdağ; kDepartment of Forensic Medicine, İstanbul Medical Faculty, Istanbul University, İstanbul, Turkey. The authors report no conflict of interest. Reprints: İpek Esen Melez, MD, Bezmialem Vakıf University, Adnan Menderes Bulvarı, Vatan Caddesi, 34093 Fatih, İstanbul, Turkey. E-mail: [email protected]. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0195-7910/15/3603-0188 DOI: 10.1097/PAF.0000000000000167
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autopsy is still unclear because it is impossible to know the correct number of undetected cases.6–10 The common postmortem histopathological findings of the SCAD cases are subadventitial dissection with hematoma and mixed inflammatory cell infiltration dominated by eosinophils in the adjacent adipose tissue.11,12 Among the diagnosed SCAD cases, approximately 3/4 of the cases are women and typically in the middle age group.3–6,8,13 Besides, the left anterior coronary artery (LAD) involvement is reported to be seen commonly in females, while the right coronary artery (RCA) involvement is more frequently seen in men.3,5,6,14,15 Surgical, medical, or palliative treatment options are considered according to the clinical picture and features of the dissection.2,3,5,15 We present 3 SCAD cases with their clinical picture and pathological findings through the forensic point of view for improving the malpractice expertise in scope of the clinicians' timely antemortem diagnosis according to risk factors and in scope of forensic pathologists' cause of death determination ability according to the macroscopical and microscopical findings of the autopsy.
CASES Case 1 A 38-year-old woman, with no known disease, went to a pharmacy with chest pain, collapsed in the pharmacy, and despite the cardiopulmonary resuscitation, she suddenly died. The body was referred to the Council of Forensic Medicine Morgue Department (CFM-MD) for autopsy to determine the cause of death. Her relatives reported that she had taken time off from work since she had been feeling unwell on the day she died. According to the information received from her relatives, the mother of the case had similarly died from an unknown cause at the age of 37 years, the father of the case had died from cardiovascular problems at the age of 51 after a mitral valve replacement at the age of 30 years, the case had never smoked cigarette and had given birth by cesarean section to her only child 5 years before her death. Her husband refused to share the contraception method/s that they had used. The external examination revealed horizontally located 18 cm long cesarean section scar tissue on the suprapubic region. The macroscopical examination of the heart showed luminal narrowing of the left anterior descending coronary artery and circumferential hematoma in the arterial wall. It was noted that there were 2 adjacent ostia of the RCA while the right coronary and the left circumflex coronary arteries were patent. During the macroscopical examination of the other organs, hyperemia in the corpus region of the stomach, loss of the gastric folds in the gastric mucosa, and enlargement of the spleen (spleen weighed 530 g) were determined. Histopathologically, there were slight hypertrophy, slight perivascular fibrosis, subadventitial dissection together with hematoma formation on the left anterior descending coronary artery Am J Forensic Med Pathol • Volume 36, Number 3, September 2015
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Spontaneous Coronary Artery Dissection
wall, and mixed inflammatory cell infiltration dominated by eosinophils in the adjacent adipose tissue (Fig. 1). All of these findings were interpreted as the elements of a coronary artery dissection with subadventitial hematoma formation. Pulmonary edema, non-necrotizing granulomas in the liver and in the lung, chronic gastritis, and lymphoid hyperplasia in the spleen were also noted as other histopathological diagnoses.
Case 2 A 39-year-old woman, with no known disease, was found unconscious lying on prone position at her home, taken to hospital, pronounced to be dead on arrival, and presented to the CFM-MD to determine the cause of death. According to the information received from her husband, the mother or father of the case was not having any known cardiovascular disease, he did not know if her other relatives had died from cardiovascular problems or not, she had never smoked cigarette, she had been suffering from headache for many years even before their marriage, thus she had been using painkillers frequently, they had 4 children born in 12 years until 3 years before her death, she had used oral contraceptives for 1 year before her second pregnancy, at other times they had been using natural methods of contraception, this second child was born with cardiovascular problems and still having cardiovascular problems, only the last birth had been performed by cesarean section, and before their last child, they had a willful abortion. The external examination of the case revealed a horizontally located 11 cm long cesarean section scar tissue on the suprapubic region, no other lesion was detected. Left anterior descending coronary artery was found to be embedded in the myocardium 1 cm after its origin continuing in 0.3 cm depth and lying totally 1.5 cm in the myocardial tissue. Then, it was going on toward the epicardial adipose tissue superficially. A hematoma, almost totally occluding the lumen, was detected 1 cm after the artery's reaching the epicardial adipose tissue. The right and the left circumflex coronary arteries were patent. The histopathological examination revealed hypertrophy and congestion of the myocardium, subadventitial dissection together with hematoma formation in the cross-section of the left anterior descending coronary artery and mixed inflammatory cell infiltration dominated by eosinophils in the adjacent adipose tissue (Fig. 2). These findings were inferred as a coronary artery dissection with subadventitial hematoma formation. Pulmonary edema, chronic pyelonephritis, and renal retention cyst were also detected as other histopathological diagnoses.
FIGURE 2. Histopathological section in case 2.
Case 3 A 49-year-old woman, with no known disease, felt ill, and decided to go to bed after cleaning the house and having lunch. Because she became worse and lost her consciousness, she was taken to hospital after the first aid. However, she was pronounced to be dead on arrival in the hospital. The body was presented to the CFM-MD to determine the cause of death. According to the information received from her husband, they had 7 children born in 16 years until 10 years before her death, all by vaginal delivery, besides she had been having no family history of cardiovascular diseases, and they had been using natural methods of contraception. At the external examination in the autopsy, extensive vitiligo lesions, especially concentrated on the hands and the lower extremities, were seen all over the body. The macroscopic examination of the heart showed increased epicardial fat tissue and sporadic accumulations of raised atheromatous plaques initiating from the aortic valves in the ascending aorta. On the wall of the distal RCA, slight atheromatous plaques and a hematoma were detected. In addition, slight fibrous thickening of the mitral valves was noted at the macroscopic examination. During the macroscopic examination of the other organs, hyperemia and flattening of the gastric folds, and a 5 5 5 cm cystic formation of the left ovary were determined. The histopathological examination revealed congestion and focal interstitial fibrosis in the myocardium, hematoma in the RCA, and mixed inflammatory cell infiltration dominated by eosinophils in the adjacent adipose tissue (Fig. 3). Again, these findings were inferred as a coronary artery dissection with subadventitial hematoma formation. Pulmonary edema was also detected. There was no traumatic pathological finding at the external examinations of each 3 cases, and also there was no history of trauma. Besides, no toxic substance was found in the toxicological analyses of blood and internal organs of each 3 cases. The causes of the sudden deaths for each 3 cases were concluded as heart failure due to SCAD.
DISCUSSION
FIGURE 1. Histopathological section in case 1. © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Spontaneous coronary artery dissection, described as the dissection between the layers of media and adventitia in the coronary artery wall, has the histopathological characteristics of subadventitial dissection, hematoma formation in the cross-section of the coronary artery, and mixed inflammatory cell infiltration dominated by eosinophils in the adjacent adipose tissue.1,10,12 www.amjforensicmedicine.com
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FIGURE 3. Histopathological section in case 3.
The female sex, the presence of the accompanying atherosclerotic artery diseases, the family history of coronary artery disease, pregnancy, postpartum period, history of oral contraceptive use, collagen tissue disease, and some of the inflammatory diseases are suggested among the factors increasing the risk of SCAD.2–6,8,13,16–18 On the other hand, it is reported that SCAD can be concurrent with smoking, diabetes, hypertension, dyslipidemia, obesity, coronary artery anomalies, migraine, lupus, use of cocaine, use of cyclosporine, use of ergotamine, and autosomal dominant renal diseases.2,3,14–17,19–21 Except the given factors specific to SCAD, the other arteriopathic factors reported in the literature can also be taken into account for SCAD predisposition. These factors in addition to abovementioned ones are hyperhomocysteinemia, α-1-antitrypsin deficiency, protease hyperactivity, and myocardial bridging.22–25 The cases we present are 38-, 39-, and 49-year-old women having pregnancy and/or oral contraceptive use histories and no finding of any trauma or intoxication which may cause death. Besides, all 3 cases died suddenly and unexpectedly. When these common features of the cases are considered together with the findings obtained from the autopsies, the causes of the sudden death for each 3 cases were concluded as heart failure due to SCAD. The fact that SCADs are reported mostly in women with pregnancy or with a history of pregnancy and the hypothesis indicating a correlation between hormonal factors and pregnancy-induced vascular wall changes are supportive for each other.2–6,8,13,16,26 According to the literature, proliferation in the smooth muscle, irregular collagen synthesis, and the changes in proteins and acid mucopolysaccharides in the tunica media are all associated with hormonal changes in women.9,26,27 In the presence of these structural changes, increased blood pressure during pregnancy, childbirth, increased cardiac output and shearing stress (circulation stress) are accounted for the occurrence of SCAD during pregnancy or during lactation.3,7,9,13,26,28 The first case in this study was a 38-year-old woman with a cesarean section scar supporting her pregnancy history of 1 child and without an intrauterine device at least slightly supporting the possibility of oral contraceptive use despite the fact that her husband refused to give information about the contraception method they had been using. The second case was a 39-year-old woman, with a cesarean section scar, without an intrauterine device, having the history of 1-year oral contraceptive use in the past and 4 children. The third case had 7 children despite having no history of oral contraceptive use.
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All 3 cases being middle-aged women and having the possible influence of hormonal factors on their vessel walls may have put them at high risk for SCAD. However, although there are many women giving birth or using oral contraceptives in some periods in their lives, only some of them are facing with SCAD.2–5,29,30 This suggests the possibility of some hereditary factors. In the literature, although there are studies supporting family history of coronary diseases in SCAD cases like the studies of Çolak et al and Dhawan et al, there are also some other SCAD case reports not indicating family history of coronary diseases.5,18,26,31–35 Among 3 cases, we present, the first case's mother was learnt to have died suddenly at the age of 37 years without any clear cause of death, in addition to her mother, her father was also learnt to have died from cardiovascular problems at the age of 51 years after a mitral valve replacement at the age of 30 years, supporting a possible hereditary background of SCAD. Also, the cardiovascular problems stated for the second child of the second case can be considered in scope of hereditary links as well as the possible adverse effects of the oral contraceptives used by the mother before pregnancy. The question of possible hereditary links should be checked in a more detailed way through genetic studies. If a correlation can be found, especially women of the upcoming generation may be important to manage early diagnosis. Which inherited characteristic causing predisposition for SCAD can be more predominant also seems to be unclear. Autoimmunity may be a hereditary underlying factor for vessel injury.36 The presence of the pathologies which can be seen in autoimmune diseases with the focal effect of autoantibodies involving various layers of the arterial wall, such as cervical artery dissection and aortic aneurism, suggests the possibility of an autoimmune mechanism in the etiopathogenesis of SCAD. In fact, this effect is believed to be a result of an arterial wall damage arising from the cross-reaction between the antibodies specific to nonendothelial tissues, such as thyroid, and the endothelial proteins.37–41 Atherosclerosis—as one of the factors increasing the risk of SCAD—is also being discussed to occur as a result of autoimmune mechanisms. In the literature, there are supporting and nonsupporting findings in different studies related with the effect of autoimmunity on atherosclerosis formation.42–44 Although there is a possibility of age-related atherosclerotic formation in the third case, autoimmune mechanisms may have a role in inducing the arterial wall damage. Additionally, vitiligo, an autoimmune disease that is characterized by the loss of melanocytes and clinically significant with hypopigmented well-demarcated lesions, was observed as widespread lesions all over the body of the third case, again supporting the presence of an autoimmune reaction in the body. When we consider the first case, non-necrotizing granulomas in the liver and lungs, gastritis in the stomach, and lymphoid hyperplasia in the spleen may all be the signs of an autoimmune process.45–53 These findings are supporting the possibility of a SCAD autoimmune process coexistence.28,54–56 Myocardial bridging may be another predisposing factor for SCAD.25 At each systole, the turbulent flow resulting from the disruption of the laminar flow with contraction of the bridging segment will result in stress on the vascular wall of the distal segment. The fact that distal segment tunica media is thinner when compared to the other segments in myocardial bridging and the presence of turbulent flow in the myocardial compressioninduced narrowed tunnel segment of the bridging region can lead to endothelial injury.24,25,54,57 In the second case, we present, myocardial bridging of the left anterior descending artery along with myocardial hypertrophy, and the presence of SCAD in the distal section of the bridging is noteworthy. The involved artery of SCAD was the left anterior coronary artery in the first and © 2015 Wolters Kluwer Health, Inc. All rights reserved.
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second cases while the involved artery was the RCA in the third case similar to the predominance of the left coronary artery in the literature.5 As we have discussed the dominance of possibility for “hereditary” mechanisms, we also should not forget to consider the acquired factors. For example, the third case had cleaned the house before facing with death, reminding us of the exerciseinduced shearing stress (circulation stress).3,7,9,26,28,58 Actually, autoimmunity is sometimes explained with acquired mechanisms instead of the abovementioned hereditary point of view.38,59–62 In addition, some theories state that the apparent chronicity of an inflammatory infiltrate represents a reaction to arterial wall that has occurred gradually because of detection before any inflammatory process. Such theories support acquired mechanisms as much as hereditary mechanisms.11 The importance of early diagnosis for SCAD is undeniable and crucial for life saving.11 However, all those mechanisms discussed above, together with valid risk factors and histopathological examinations, are surely important not only in scope of cardiology or cardiovascular surgery diagnoses but also for forensic medicine diagnoses. Because determining the correct cause of death by means of trying to consider all details is the responsibility of forensic medicine and pathology. Slight changes in the expressions related with the cause of death or death mechanism in a forensic pathology report may change a lot in determining the origin of an act.63–66 For instance, such expression details may be important for a malpractice decision in a SCAD case after an angioprocess of a cardiologist.9,67 If the forensic pathologist is not able to consider SCAD and instead of SCAD sees only a ‘thrombosis’ artifact as a misdiagnosis during the autopsy, this leads the forensic pathologist not to take sample for histopathological examination from the artery wall to determine SCAD. Thus, that forensic pathologist may give the result in a wrong way through an “emboli” point of view.11 In the future, these differences in postmortem diagnosis may differ more and more in scope of insurance companies. Because, for legal actions taken between an insurer and an insured party, forensic expertise reports are important for the determination of the fault degree as in the above given example, that is, a wrong “thrombosis” report for a SCAD death after an angioprocess malpractice. Besides, either coming from insurance companies or from individuals, forensic malpractice allegations, especially related with wrong cause of death decisions by forensic pathologists, are increasing fast and seems to continue fast in the future. In conclusion, for a forensic pathologist, details are important for improving differential diagnosis not only in clinics but also in postmortem evaluation, to avoid forensic malpractice allegations and to be able to provide justice between parties. REFERENCES 1. Pretty HC. Dissecting aneurysm of coronary artery in a woman aged 42: rupture. BMJ. 1931;1:667. 2. Vanzetto G, Berger-Coz E, Barone-Rochette G, et al. Prevalence, therapeutic management and medium-term prognosis of spontaneous coronary artery dissection: result from a database of 11,605 patients. Eur J Cardiothorac Surg. 2009;35:250–254. 3. Maeder M, Ammann P, Angehrn W, et al. Idiopathic spontaneous coronary artery dissection: incidence, diagnosis and treatment. Int J Cardiol. 2005; 101:363–369. 4. Maehara A, Mintz GS, Castagna MT, et al. Intravascular ultrasound assessment of spontaneous coronary artery dissection. Am J Cardiol. 2002; 89(4):466–468. 5. Çolak N, Nazlı Y, Alpay F, et al. Spontaneous coronary artery dissections: four cases and literature review. Dicle Med J. 2009;36(4):294–300.
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Spontaneous Coronary Artery Dissection Report of 3 Cases and Literature Review Hormonal, Autoimmune, Morphological Factors İpek Esen Melez, MD,* Murat Nihat Arslan, MD,† Deniz Oğuzhan Melez, MD,† Arzu Akçay, MD,† Yalçin Büyük, MD,† Abdullah Avşar, MD,‡ Bahadir Kumral, MD,§ Gözde Şirin, MD,† Ferah Anıl Karayel, MD,† Taner Daş, MD,† Yasemin Erenç Dokudan, MD,k and Bülent Şam, MD† Abstract: The number of cases with spontaneous coronary artery dissection (SCAD) is considered to be being underestimated because of a large amount of SCAD leading to sudden death without previous diagnosis. Besides, not only in clinics but also in autopsy practice, correct diagnosis of SCAD is important to prevent forensic malpractice. The article is intended to discuss the pathological findings through the forensic point of view for improving the malpractice expertise in scope of clinicians' timely antemortem diagnosis according to risk factors and in scope of forensic pathologists' the cause of death determination ability according to macroscopical and microscopical findings of the autopsy. In 3 cases reported, the main characteristics were the female sex, pregnancy history and a sudden death without any trauma. However, although there are many women giving birth or using oral contraceptives, only some of them are facing with SCAD. This suggests the possibility of some hereditary factors, whereas hereditary characteristics may be understood in many different ways like hormone-releasing regulating mechanisms as well as immunity, morphology, or any other mechanism. For instance, autoimmunity has been also a hereditary underlying factor for vessel injury considered in presented cases. Key Words: coronary artery dissection, autopsy, pregnancy, autoimmunity, morphology, malpractice (Am J Forensic Med Pathol 2015;36: 188–192)
S
pontaneous coronary artery dissection (SCAD), first described in 1931, is explained briefly as the dissection between the layers of media and adventitia in the coronary artery wall.1 The detection of SCAD is usually done by coronary angiography in clinical studies, and confirmation of this diagnosis is possible by a novel method, intravascular ultrasound.2–4 The incidence of SCAD has been reported as 0.1% to 0.2% in the angiographic series increasing to 1.1% or even 10.8% in patient groups with acute coronary syndrome.2–5 However, the correct number of cases is considered to be being underestimated due to a large amount of SCAD leading to sudden death without previous diagnosis. Some of these undiagnosed cases are detected by postmortem examination. Different postmortem diagnosis ratios have been given in different autopsy studies, yet the success ratio of detection in
Manuscript received May 16, 2013; accepted October 23, 2014. From the *Department of Forensic Medicine, Medical Faculty, Bezmialem Vakıf University; †The Ministry of Justice Council of Forensic Medicine, İstanbul; ‡Department of Forensic Medicine, Medical Faculty, Kahramanmaraş Sütçü İmam University, Kahramanmaraş; §Department of Forensic Medicine, Medical Faculty, Namık Kemal University, Tekirdağ; kDepartment of Forensic Medicine, İstanbul Medical Faculty, Istanbul University, İstanbul, Turkey. The authors report no conflict of interest. Reprints: İpek Esen Melez, MD, Bezmialem Vakıf University, Adnan Menderes Bulvarı, Vatan Caddesi, 34093 Fatih, İstanbul, Turkey. E-mail: [email protected]. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0195-7910/15/3603-0188 DOI: 10.1097/PAF.0000000000000167
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autopsy is still unclear because it is impossible to know the correct number of undetected cases.6–10 The common postmortem histopathological findings of the SCAD cases are subadventitial dissection with hematoma and mixed inflammatory cell infiltration dominated by eosinophils in the adjacent adipose tissue.11,12 Among the diagnosed SCAD cases, approximately 3/4 of the cases are women and typically in the middle age group.3–6,8,13 Besides, the left anterior coronary artery (LAD) involvement is reported to be seen commonly in females, while the right coronary artery (RCA) involvement is more frequently seen in men.3,5,6,14,15 Surgical, medical, or palliative treatment options are considered according to the clinical picture and features of the dissection.2,3,5,15 We present 3 SCAD cases with their clinical picture and pathological findings through the forensic point of view for improving the malpractice expertise in scope of the clinicians' timely antemortem diagnosis according to risk factors and in scope of forensic pathologists' cause of death determination ability according to the macroscopical and microscopical findings of the autopsy.
CASES Case 1 A 38-year-old woman, with no known disease, went to a pharmacy with chest pain, collapsed in the pharmacy, and despite the cardiopulmonary resuscitation, she suddenly died. The body was referred to the Council of Forensic Medicine Morgue Department (CFM-MD) for autopsy to determine the cause of death. Her relatives reported that she had taken time off from work since she had been feeling unwell on the day she died. According to the information received from her relatives, the mother of the case had similarly died from an unknown cause at the age of 37 years, the father of the case had died from cardiovascular problems at the age of 51 after a mitral valve replacement at the age of 30 years, the case had never smoked cigarette and had given birth by cesarean section to her only child 5 years before her death. Her husband refused to share the contraception method/s that they had used. The external examination revealed horizontally located 18 cm long cesarean section scar tissue on the suprapubic region. The macroscopical examination of the heart showed luminal narrowing of the left anterior descending coronary artery and circumferential hematoma in the arterial wall. It was noted that there were 2 adjacent ostia of the RCA while the right coronary and the left circumflex coronary arteries were patent. During the macroscopical examination of the other organs, hyperemia in the corpus region of the stomach, loss of the gastric folds in the gastric mucosa, and enlargement of the spleen (spleen weighed 530 g) were determined. Histopathologically, there were slight hypertrophy, slight perivascular fibrosis, subadventitial dissection together with hematoma formation on the left anterior descending coronary artery Am J Forensic Med Pathol • Volume 36, Number 3, September 2015
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wall, and mixed inflammatory cell infiltration dominated by eosinophils in the adjacent adipose tissue (Fig. 1). All of these findings were interpreted as the elements of a coronary artery dissection with subadventitial hematoma formation. Pulmonary edema, non-necrotizing granulomas in the liver and in the lung, chronic gastritis, and lymphoid hyperplasia in the spleen were also noted as other histopathological diagnoses.
Case 2 A 39-year-old woman, with no known disease, was found unconscious lying on prone position at her home, taken to hospital, pronounced to be dead on arrival, and presented to the CFM-MD to determine the cause of death. According to the information received from her husband, the mother or father of the case was not having any known cardiovascular disease, he did not know if her other relatives had died from cardiovascular problems or not, she had never smoked cigarette, she had been suffering from headache for many years even before their marriage, thus she had been using painkillers frequently, they had 4 children born in 12 years until 3 years before her death, she had used oral contraceptives for 1 year before her second pregnancy, at other times they had been using natural methods of contraception, this second child was born with cardiovascular problems and still having cardiovascular problems, only the last birth had been performed by cesarean section, and before their last child, they had a willful abortion. The external examination of the case revealed a horizontally located 11 cm long cesarean section scar tissue on the suprapubic region, no other lesion was detected. Left anterior descending coronary artery was found to be embedded in the myocardium 1 cm after its origin continuing in 0.3 cm depth and lying totally 1.5 cm in the myocardial tissue. Then, it was going on toward the epicardial adipose tissue superficially. A hematoma, almost totally occluding the lumen, was detected 1 cm after the artery's reaching the epicardial adipose tissue. The right and the left circumflex coronary arteries were patent. The histopathological examination revealed hypertrophy and congestion of the myocardium, subadventitial dissection together with hematoma formation in the cross-section of the left anterior descending coronary artery and mixed inflammatory cell infiltration dominated by eosinophils in the adjacent adipose tissue (Fig. 2). These findings were inferred as a coronary artery dissection with subadventitial hematoma formation. Pulmonary edema, chronic pyelonephritis, and renal retention cyst were also detected as other histopathological diagnoses.
FIGURE 2. Histopathological section in case 2.
Case 3 A 49-year-old woman, with no known disease, felt ill, and decided to go to bed after cleaning the house and having lunch. Because she became worse and lost her consciousness, she was taken to hospital after the first aid. However, she was pronounced to be dead on arrival in the hospital. The body was presented to the CFM-MD to determine the cause of death. According to the information received from her husband, they had 7 children born in 16 years until 10 years before her death, all by vaginal delivery, besides she had been having no family history of cardiovascular diseases, and they had been using natural methods of contraception. At the external examination in the autopsy, extensive vitiligo lesions, especially concentrated on the hands and the lower extremities, were seen all over the body. The macroscopic examination of the heart showed increased epicardial fat tissue and sporadic accumulations of raised atheromatous plaques initiating from the aortic valves in the ascending aorta. On the wall of the distal RCA, slight atheromatous plaques and a hematoma were detected. In addition, slight fibrous thickening of the mitral valves was noted at the macroscopic examination. During the macroscopic examination of the other organs, hyperemia and flattening of the gastric folds, and a 5 5 5 cm cystic formation of the left ovary were determined. The histopathological examination revealed congestion and focal interstitial fibrosis in the myocardium, hematoma in the RCA, and mixed inflammatory cell infiltration dominated by eosinophils in the adjacent adipose tissue (Fig. 3). Again, these findings were inferred as a coronary artery dissection with subadventitial hematoma formation. Pulmonary edema was also detected. There was no traumatic pathological finding at the external examinations of each 3 cases, and also there was no history of trauma. Besides, no toxic substance was found in the toxicological analyses of blood and internal organs of each 3 cases. The causes of the sudden deaths for each 3 cases were concluded as heart failure due to SCAD.
DISCUSSION
FIGURE 1. Histopathological section in case 1. © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Spontaneous coronary artery dissection, described as the dissection between the layers of media and adventitia in the coronary artery wall, has the histopathological characteristics of subadventitial dissection, hematoma formation in the cross-section of the coronary artery, and mixed inflammatory cell infiltration dominated by eosinophils in the adjacent adipose tissue.1,10,12 www.amjforensicmedicine.com
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FIGURE 3. Histopathological section in case 3.
The female sex, the presence of the accompanying atherosclerotic artery diseases, the family history of coronary artery disease, pregnancy, postpartum period, history of oral contraceptive use, collagen tissue disease, and some of the inflammatory diseases are suggested among the factors increasing the risk of SCAD.2–6,8,13,16–18 On the other hand, it is reported that SCAD can be concurrent with smoking, diabetes, hypertension, dyslipidemia, obesity, coronary artery anomalies, migraine, lupus, use of cocaine, use of cyclosporine, use of ergotamine, and autosomal dominant renal diseases.2,3,14–17,19–21 Except the given factors specific to SCAD, the other arteriopathic factors reported in the literature can also be taken into account for SCAD predisposition. These factors in addition to abovementioned ones are hyperhomocysteinemia, α-1-antitrypsin deficiency, protease hyperactivity, and myocardial bridging.22–25 The cases we present are 38-, 39-, and 49-year-old women having pregnancy and/or oral contraceptive use histories and no finding of any trauma or intoxication which may cause death. Besides, all 3 cases died suddenly and unexpectedly. When these common features of the cases are considered together with the findings obtained from the autopsies, the causes of the sudden death for each 3 cases were concluded as heart failure due to SCAD. The fact that SCADs are reported mostly in women with pregnancy or with a history of pregnancy and the hypothesis indicating a correlation between hormonal factors and pregnancy-induced vascular wall changes are supportive for each other.2–6,8,13,16,26 According to the literature, proliferation in the smooth muscle, irregular collagen synthesis, and the changes in proteins and acid mucopolysaccharides in the tunica media are all associated with hormonal changes in women.9,26,27 In the presence of these structural changes, increased blood pressure during pregnancy, childbirth, increased cardiac output and shearing stress (circulation stress) are accounted for the occurrence of SCAD during pregnancy or during lactation.3,7,9,13,26,28 The first case in this study was a 38-year-old woman with a cesarean section scar supporting her pregnancy history of 1 child and without an intrauterine device at least slightly supporting the possibility of oral contraceptive use despite the fact that her husband refused to give information about the contraception method they had been using. The second case was a 39-year-old woman, with a cesarean section scar, without an intrauterine device, having the history of 1-year oral contraceptive use in the past and 4 children. The third case had 7 children despite having no history of oral contraceptive use.
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All 3 cases being middle-aged women and having the possible influence of hormonal factors on their vessel walls may have put them at high risk for SCAD. However, although there are many women giving birth or using oral contraceptives in some periods in their lives, only some of them are facing with SCAD.2–5,29,30 This suggests the possibility of some hereditary factors. In the literature, although there are studies supporting family history of coronary diseases in SCAD cases like the studies of Çolak et al and Dhawan et al, there are also some other SCAD case reports not indicating family history of coronary diseases.5,18,26,31–35 Among 3 cases, we present, the first case's mother was learnt to have died suddenly at the age of 37 years without any clear cause of death, in addition to her mother, her father was also learnt to have died from cardiovascular problems at the age of 51 years after a mitral valve replacement at the age of 30 years, supporting a possible hereditary background of SCAD. Also, the cardiovascular problems stated for the second child of the second case can be considered in scope of hereditary links as well as the possible adverse effects of the oral contraceptives used by the mother before pregnancy. The question of possible hereditary links should be checked in a more detailed way through genetic studies. If a correlation can be found, especially women of the upcoming generation may be important to manage early diagnosis. Which inherited characteristic causing predisposition for SCAD can be more predominant also seems to be unclear. Autoimmunity may be a hereditary underlying factor for vessel injury.36 The presence of the pathologies which can be seen in autoimmune diseases with the focal effect of autoantibodies involving various layers of the arterial wall, such as cervical artery dissection and aortic aneurism, suggests the possibility of an autoimmune mechanism in the etiopathogenesis of SCAD. In fact, this effect is believed to be a result of an arterial wall damage arising from the cross-reaction between the antibodies specific to nonendothelial tissues, such as thyroid, and the endothelial proteins.37–41 Atherosclerosis—as one of the factors increasing the risk of SCAD—is also being discussed to occur as a result of autoimmune mechanisms. In the literature, there are supporting and nonsupporting findings in different studies related with the effect of autoimmunity on atherosclerosis formation.42–44 Although there is a possibility of age-related atherosclerotic formation in the third case, autoimmune mechanisms may have a role in inducing the arterial wall damage. Additionally, vitiligo, an autoimmune disease that is characterized by the loss of melanocytes and clinically significant with hypopigmented well-demarcated lesions, was observed as widespread lesions all over the body of the third case, again supporting the presence of an autoimmune reaction in the body. When we consider the first case, non-necrotizing granulomas in the liver and lungs, gastritis in the stomach, and lymphoid hyperplasia in the spleen may all be the signs of an autoimmune process.45–53 These findings are supporting the possibility of a SCAD autoimmune process coexistence.28,54–56 Myocardial bridging may be another predisposing factor for SCAD.25 At each systole, the turbulent flow resulting from the disruption of the laminar flow with contraction of the bridging segment will result in stress on the vascular wall of the distal segment. The fact that distal segment tunica media is thinner when compared to the other segments in myocardial bridging and the presence of turbulent flow in the myocardial compressioninduced narrowed tunnel segment of the bridging region can lead to endothelial injury.24,25,54,57 In the second case, we present, myocardial bridging of the left anterior descending artery along with myocardial hypertrophy, and the presence of SCAD in the distal section of the bridging is noteworthy. The involved artery of SCAD was the left anterior coronary artery in the first and © 2015 Wolters Kluwer Health, Inc. All rights reserved.
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second cases while the involved artery was the RCA in the third case similar to the predominance of the left coronary artery in the literature.5 As we have discussed the dominance of possibility for “hereditary” mechanisms, we also should not forget to consider the acquired factors. For example, the third case had cleaned the house before facing with death, reminding us of the exerciseinduced shearing stress (circulation stress).3,7,9,26,28,58 Actually, autoimmunity is sometimes explained with acquired mechanisms instead of the abovementioned hereditary point of view.38,59–62 In addition, some theories state that the apparent chronicity of an inflammatory infiltrate represents a reaction to arterial wall that has occurred gradually because of detection before any inflammatory process. Such theories support acquired mechanisms as much as hereditary mechanisms.11 The importance of early diagnosis for SCAD is undeniable and crucial for life saving.11 However, all those mechanisms discussed above, together with valid risk factors and histopathological examinations, are surely important not only in scope of cardiology or cardiovascular surgery diagnoses but also for forensic medicine diagnoses. Because determining the correct cause of death by means of trying to consider all details is the responsibility of forensic medicine and pathology. Slight changes in the expressions related with the cause of death or death mechanism in a forensic pathology report may change a lot in determining the origin of an act.63–66 For instance, such expression details may be important for a malpractice decision in a SCAD case after an angioprocess of a cardiologist.9,67 If the forensic pathologist is not able to consider SCAD and instead of SCAD sees only a ‘thrombosis’ artifact as a misdiagnosis during the autopsy, this leads the forensic pathologist not to take sample for histopathological examination from the artery wall to determine SCAD. Thus, that forensic pathologist may give the result in a wrong way through an “emboli” point of view.11 In the future, these differences in postmortem diagnosis may differ more and more in scope of insurance companies. Because, for legal actions taken between an insurer and an insured party, forensic expertise reports are important for the determination of the fault degree as in the above given example, that is, a wrong “thrombosis” report for a SCAD death after an angioprocess malpractice. Besides, either coming from insurance companies or from individuals, forensic malpractice allegations, especially related with wrong cause of death decisions by forensic pathologists, are increasing fast and seems to continue fast in the future. In conclusion, for a forensic pathologist, details are important for improving differential diagnosis not only in clinics but also in postmortem evaluation, to avoid forensic malpractice allegations and to be able to provide justice between parties. REFERENCES 1. Pretty HC. Dissecting aneurysm of coronary artery in a woman aged 42: rupture. BMJ. 1931;1:667. 2. Vanzetto G, Berger-Coz E, Barone-Rochette G, et al. Prevalence, therapeutic management and medium-term prognosis of spontaneous coronary artery dissection: result from a database of 11,605 patients. Eur J Cardiothorac Surg. 2009;35:250–254. 3. Maeder M, Ammann P, Angehrn W, et al. Idiopathic spontaneous coronary artery dissection: incidence, diagnosis and treatment. Int J Cardiol. 2005; 101:363–369. 4. Maehara A, Mintz GS, Castagna MT, et al. Intravascular ultrasound assessment of spontaneous coronary artery dissection. Am J Cardiol. 2002; 89(4):466–468. 5. Çolak N, Nazlı Y, Alpay F, et al. Spontaneous coronary artery dissections: four cases and literature review. Dicle Med J. 2009;36(4):294–300.
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6. Vale PR, Baron DW. Coronary artery stenting for spontaneous coronary artery dissection: a case report and review of the literature. Cathet Cardiovasc Diagn. 1998;45:280–286. 7. Hering D, Piper C, Hohmann C, et al. Prospective study of the incidence, pathogenesis and therapy of spontaneous, by coronary angiography diagnosed coronary artery dissection. Z Kardiol. 1998;87:961–970. 8. DeMaio SJ Jr, Kinsella SH, Silverman ME. Clinical course and long term prognosis of spontaneous coronary artery dissection. Am J Cardiol. 1989; 64:471–474. 9. Mohamed HA, Eshawesh A, Habib N. Spontaneous coronary dissection. A case and review of the literature. Angiology. 2002;53:205–211. 10. Corrado D, Thiene G, Cocco P, et al. Non-atherosclerotic coronary artery disease and sudden death in the young. Br Heart J. 1992;68:601–607. 11. Bateman AC, Gallagher PJ, Vmcenti AC. Sudden death from coronary artery dissection. J Clin Pathol. 1995;48(8):781–784. 12. Robinowitz M, Virmani R, McAllister HA. Spontaneous coronary artery dissection and eosinophilic inflammation: a cause and effect relationship? Am J Med. 1982;72:923–928. 13. Bac DJ, Lotgering FK, Verkaaik APK, et al. Spontaneous coronary artery dissection during pregnancy and postpartum. Eur Heart J. 1995;16: 136–138. 14. Thompson EA, Ferraris S, Gress T, et al. Gender differences and predictors of mortality in spontaneous coronary artery dissection: a review of reported cases. J Invasive Cardiol. 2005;17(1):59–61. 15. Tarhan IA, Yapıcı F, Arslan Y, et al. Spontaneous coronary artery dissections: case report and review of the literature. Arch Turk Soc Cardiol. 2002;30:54–56. 16. Fengping Y, Jue H, Qingchun Y, et al. A case of sudden death due to spontaneous coronary artery dissection. Am J Forensic Med Pathol. 2011; 32(4):312–313. 17. Glamore MJ, Garcia-Covarrubias L, Harrison LH, et al. Spontaneous coronary artery dissection. J Card Surg. 2012;27:56–59. 18. Azam M, Roberts D, Logan W. Spontaneous coronary artery dissection associated with oral contraceptive use. Int J Cardiol. 1995;48:195–198. 19. Garcia Garcia C, Casanovas N, Recasens L, et al. Spontaneous coronary artery dissection in ergotamine abuse. Int J Cardiol. 2007;118:410–411. 20. Hammond AS, Bailey PL. Acute spontaneous coronary artery dissection in the peripartum period. J Cardiothorac Vasc Anesth. 2006;20:837–841. 21. Rekik S, Lanfranchi P, Jacq L, et al. Spontaneous coronary artery dissection in a 35 year-old woman with systemic lupus erythematosus successfully treated by angioplasty. Heart Lung Circ. 2013;22:955–958. 22. Granel B, Rossi P, Bonello L, et al. Rare disease: coronary artery dissection in adult-onset homocystinuria. BMJ Case Rep. 2009;2009. 23. Guillon B, Bousser M. Epidemiology and pathophysiology of spontaneous cervical artery dissection. J Neuroradiol. 2002;29:241–249. 24. Ge J-B, Huang Z-Y, Liu X-B, et al. Spontaneous coronary dissection associated with myocardial bridge causing acute myocardial infarction. Chin Med J. 2008;121:2450–2453. 25. De-Giorgio F, Grassi VM, Abbate A, et al. Causation or coincidence? A case of sudden death due to spontaneous coronary artery dissection in presence of myocardial bridging. Int J Cardiol. 2012;159:e32–e34. 26. Dhawan R, Singh G, Fesniak H. Spontaneous coronary artery dissection: the clinical spectrum. Angiology. 2002;53(1):89–93. 27. Capuano C, Sesana M, Predolini S, et al. Literature review: spontaneous coronary artery dissections. Cardiovasc Revasc Med. 2006;7:231–233. 28. Shufelt CL, Merz CNB. Contraceptive hormone use and cardiovascular disease. J Am Coll Cardiol. 2009;53:221–231. 29. Kalra N, Greenblatt J, Ahmed S. Postpartum spontaneous coronary artery dissection (SCAD) managed conservatively. Int J Cardiol. 2008;129: e53–e55.
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