Sudden death due to isolated segmentary coronary vasculitis.

CASE REPORT

Sudden Death Due to Isolated Segmentary Coronary Vasculitis Dan Dermengiu, PhD,*† Sorin Hostiuc, PhD,*† George Cristian Curca, PhD,*† Mugurel Constantin Rusu, MD, PhD,‡ Cristian Paparau,† and Mihai Ceausu, PhD§∥ Abstract: Coronary vasculitis is a group of conditions occurring either independently or associated with another diseases characterized by an inflammation of the blood vessel's wall and subsequent fibrinoid necrosis, occlusion, stenosis, or aneurismal dilatations. Coronary vasculitis leading to sudden cardiac death has rarely been described in the scientific literature. We present the case of an 18-year-old football player who collapsed when playing football. The patient remained in a deep coma (glasgow coma scale = 3) in the hospital for another 4 hours before dying. During hospitalization, he was diagnosed with acute anterolateral myocardial infarction with ST elevation. An autopsy was performed the next day, and on the coronary vessels were identified a dilatation with luminal extension, which, based on clinical and pathological criteria, was considered to be an isolated, coronary polyarteritis nodosa. Key Words: autopsy, adolescent, forensic pathology, sudden cardiac death, isolated coronary vasculitis, isolated coronary polyarteritis nodosa (Am J Forensic Med Pathol 2014;35: 223–231)

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asculitis (vasculidites) is a group of conditions occurring either independently (primary vasculidites) or associated with another diseases (secondary vasculidites), characterized by inflammation of the blood vessel's wall and subsequent fibrinoid necrosis,1 occlusion, stenosis, or aneurismal dilatations.2 They are usually classified according to the dominant vessel size, type (primary or secondary), and association with antineutrophil cytoplasmic antibodies.3 Sudden death (SD) caused by coronary vasculitis is rarely identified, as clinical, systemic symptoms usually appear before the vasculitic process is severe enough to cause death. However, vasculitis affecting the coronary vessels, either isolated or associated with noncoronarian locations, was described in the scientific literature as being associated with SD. There are various types of vasculitis being associated with SD: eosinophilic (either associated4 or not5,6 with Churg-Strauss syndrome7); lymphoplasmacytic7,8; idiopathic giant cell arteritis7,9–11; vasculitis associated with systemic lupus erythematosus12; Kawasaki, usually in children13–17; Takayasu disease18; polyarteritis nodosa19; and so forth. We describe in this article a case of an SD caused by an isolated coronary vasculitis.

CASE REPORT Clinical Data A male patient, 18 years old, while playing football, suddenly felt very fatigued, went to sit on a bench, and immediately collapsed. Cardiopulmonary resuscitation was conducted for Manuscript received January 21, 2013; accepted August 25, 2013. From the *Department of Legal Medicine and Bioethics, Carol Davila University of Medicine and Pharmacy; †Department of Forensic Pathology, National Institute of Legal Medicine; Departments of ‡Anatomy and §Pathology, Carol Davila University of Medicine and Pharmacy; and ∥Department of Pathology, National Institute of Legal Medicine, Bucharest, Romania. The authors report no conflicts of interest. Reprints: Sorin Hostiuc, PhD, Department of Forensic Pathology, National Institute of Legal Medicine, No 9 Vitan Barzesti Street, 042122 Sector 4 Bucharest, Romania. E-mail: [email protected]; [email protected]. Copyright © 2014 by Lippincott Williams & Wilkins ISSN: 0195-7910/14/3504–0223 DOI: 10.1097/PAF.0000000000000125

Am J Forensic Med Pathol • Volume 35, Number 4, December 2014

approximately 30 minutes before stable heart beating was obtained. The patient remained in a deep coma (glasgow coma scale = 3) in the hospital for another 4 hours before dying. During the hospitalization, he was diagnosed with acute anterolateral myocardial infarction with ST elevation. The patient had a negative medical history for cardiovascular diseases, and he did not say anything to his family or colleagues about any symptoms before his death.

Autopsy Findings An autopsy was performed the next day and identified a mild cerebral edema, interstitial pulmonary edema, thymus hyperplasia, and a mildly nodular goiter. The heart had a weight of 320 g; the epicardium was smooth, with a thin, inconstant, adipose layer; and the endocardium (including the heart valves) was smooth and semitransparent. The coronary system had a left predominance with a short right coronary and a well-developed circumflex artery. The left coronary artery has a short course before the emergence of the left interventricular and circumflex arteries. During cardiac dissection, a focal nodular area was identified on the anterior interventricular artery (AIVA) followed by another three with a mean length of 0.5 to 0.7 cm on the circumflex artery (Fig. 1). By sectioning each focal nodular area, we found a luminal obstruction of a minimum of 80% by fibrous caps (Fig. 1). Such focal nodular areas were not identified on other vessels. On cut section, the left ventricle contained numerous myocardial scars, the largest of which was approximately 2.5/1.5/1 cm and located in the posterior basal area of the left ventricle (Fig. 2). Anterolateral in the proximal and middle third of the left ventricle, a recent myocardial infarction was suggested by the gross appearance.

MATERIALS AND METHODS Histopathology Investigation Tissue Sampling and Stains Specimens of the left coronary artery (2 segments from the AIVA), 4 segments from the circumflex artery, and tissues from the left and right coronary ostia were taken for histopathology investigation. In addition, samples of myocardial tissue from different areas of the anterior and lateral walls of the left ventricle and the interventricular septum were taken as well. Other fragments were harvested from the lungs, liver, kidney, pancreas, spleen, and thymus. The selected tissue samples were fixed in 10% of neutral buffered formalin (pH, 7) for 24 to 48 hours and were paraffin embedded. Sections were cut at 5 μm and stained with standard hematoxylin-eosin (HE) and van Gieson. In addition, special stains such as Weigert elastic, Masson trichrome, Mallory phosphotungstic acid hematoxylin (PTAH), periodic acid-schiff, Alcian Blue pH 2.5, and Lie have been done.

Immunohistochemistry Immunohistochemical analysis (IHC) was done using sections displayed on slides treated first with poly-L-lysine. The www.amjforensicmedicine.com

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FIGURE 1. A, Anterior, superior, and left lateral views of the AIVA, which present a dilated segment (arrows) at 1 cm distally to its origin from the left coronary artery. B, The right coronary artery continues as the right marginal artery; it does not send the posterior interventricular artery. C, Serially successive dilations are identified (arrows) on the circumflex artery on the diaphragmatic surface of the heart; the circumflex artery sends off the posterior interventricular artery and the right retroventricular artery, proof for the left coronary dominance.

IHC was performed on 3-μm-thick sections from formalin-fixed paraffin-embedded specimens, according to the indirect tristadial Avidin-Biotin-Complex method of Hsu et al,20 modified by Bussolati and Gugliotta.21 Briefly, the procedure is composed of deparaffination in xylene and alcohol series, rehydration, washing in phosphate buffer saline, blocking with normal serum for 20 minutes, incubation with primary antibody overnight and then with standard labeled streptavidin antibody biotin (LSAB kit; DAKO, Denmark), washing in carbonate buffer, and developing in 3,3'-DAB hydrochloride/H2O2. The antibodies used for IHC were CD20, CD45RO, CD68, CD30, Vim, and smooth muscle actin (SMA) (for details, see Table 1). Antigen retrieval techniques (thermal or enzymatic pretreatment) for some of the aforementioned antibodies were done,

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according to the producer’s specifications. Both positive and negative controls were used. All slides were examined and photographed on a Zeiss AxioImager microscope (Gottingen, Germany). Digital images acquired with Zeiss Axio Vision program have been processed and analyzed with ACDSee Pro Photo Manager (Washington, DC), running under Windows Vista.

RESULTS The examination of the heart samples has revealed a transmural myocardial infarction, localized on the anterolateral wall of the left ventricle and extended to the interventricular septum, © 2014 Lippincott Williams & Wilkins



SD due to Isolated Segmentary Coronary Vasculitis

The IHC reactions revealed many spindle cells (fibroblasts) positive to vimentin and numerous elongated, plump, spindleshaped cells positive to SMA (possible myofibroblasts or myointimal cells) (Fig. 10). The involvement of arteries was segmental, and healing lesions were present in the same time with chronic and active lesions, with significant stenosis of the lumen. The diagnosis was of a segmental coronary vasculitis, in various stages of evolution, with multiple stenosis of the lumen and with isolated thrombosis of the proximal part of the AIVA. In the both coronary ostia, a nodular subintimal hyperplasia was found associated with substitution fibrosis and focal myxoid degeneration. In the liver, a nonspecific granulomatous hepatitis with multinucleated giant cells was found (Fig. 11). In the kidney, in the cortical area, various degrees of glomerulosclerosis were noticed, predominantly subcapsular, associated with marked interstitial inflammatory infiltrate, consisting of lymphocytes and plasma cells (Fig. 11). The spleen and the thymus were enlarged, showing lymphoid follicular hyperplasia and reactive histiocytosis. The lungs showed congestion and edema, and the pancreas was normal. FIGURE 2. Top, Coronary lumen narrowing. Bottom, Extensive myocardial infarct of the anterior and lateral walls of the left ventricle (frame).

approximately 7 to 14 days (Fig. 3), associated with disseminated subendocardial microinfarcts approximately 4 to 7 days (Fig. 4). The AIVA coronary artery wall showed segmental fibrinoid necrosis and variable infiltration of inflammatory cells, on a background of marked subintimal hyperplasia, with disruption of normal architecture of the vessel wall. In addition, isolated necrosis of smooth muscle cells of the media associated with destruction of the internal elastic lamina was noticed. The proximal part of AIVA showed a thickened vessel wall due to subintimal hyperplasia, associated with fibrinoid necrosis and mixed inflammatory infiltrate, on a background of granulation tissue in various stages of evolution. Disruption of internal and external elastic laminae, with fragmentation of elastic fibers, was also noticed. The extensive damage of the intima led to thrombus formation, with subtotal stenosis of coronary lumen (Fig. 5). The inflammatory infiltrate was composed mainly by chronic cells, sometimes forming nonspecific granulomas, with dispersed epithelioid and isolated multinucleated giant cells surrounding the area of fibrinoid necrosis. The IHC reactions showed numerous T lymphocytes (CD45RO positive); rare B lymphocytes (CD20 positive) in the inflammatory infiltrate, associated with scattered epithelioid cells; and isolated multinucleated giant cell (CD68 positive) (Fig. 6). CD30 for neutrophils was negative. The distal part of the AIVA showed also fibrinoid necrosis of the vessel wall associated with marked inflammation, on a background of diffuse subintimal hyperplasia, and focal disruption of the internal elastic lamina (Fig. 7). The populations of leucocytes from the inflammatory infiltrate consisted of numerous T lymphocytes (positive to CD45RO), few B lymphocytes (positive to CD20), and frequent macrophages (positive to CD68) (Fig. 8). CD30 for neutrophils was negative. In the 4 serial segments of circumflex artery, various degrees of stenosis have been noticed because of subintimal hyperplasia, with eccentric thickening of the vessel wall, in the context of vasculitis (Fig. 9). In some segments of the circumflex artery, besides patchy fibrinoid necrosis, organizing granulation tissue with healing was found, followed by fibrous replacement of specialized structures. © 2014 Lippincott Williams & Wilkins

Thanatochemistry Pericardium liquid and blood samples were taken for biochemistry analysis. The enzyme-linked immunosorbent assay method for quantitative detection of T3 and T4 hormones, thyroid-stimulating hormone, hepatitis B antigen, autoantibodies c-ANCA and p-ANCA, antinuclear antibodies, and rheumatoid factor in centrifugated blood serum was done. One-step, rapid, immunochromatograpic test for the qualitative detection of troponin I, myoglobin, and creatine phosphokinase-MB isoenzyme in serum pericardium liquid was carried out. The recorded data were the following: • thyroid-stimulating hormone = 85.26 μIU/mL (reference interval, 0.35–4.94) • T4 = 4.08 μg/dL (reference interval, 487–11.72 μg/dL), normal T3 • creatine phosphokinase-MB isoenzyme = 4688 UI (reference interval, 105–154 UI) • Positive troponin I, negative myoglobin • Negative hepatitis B antigen • Negative c-ANCA and p-ANCA • Negative antinuclear antibodies and rheumatoid factor

DISCUSSION Coronary vasculitis leading to sudden cardiac death is rarely described in the scientific literature, with the coronary pathology most often associated with SD being atherosclerosis,22,23 followed by congenital coronary anomalies.24–27 Identification of vasculitis TABLE 1. Antibodies Used for IHC Tests Antibody

Clone

Dilution

Producer

Specificity

CD20 CD45RO CD68 CD30 Vimentin SMA

L26 UCHL1 514H12 1G12 V9 Alpha-SM1

RTU RTU RTU RTU 1:100 RTU

Novocastra BioGenex Novocastra Novocastra Novocastra Novocastra

B lymphocytes T lymphocytes Macrophages Neutrophils Fibroblasts Smooth muscle



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FIGURE 3. Extensive myocardium infarct (approximately 7-14 days) of the left ventricle, in the anterior wall (A) and lateral wall (B); scarring in progress, with organizing granulation tissue and interstitial collagen deposition (van Gieson, 100).

(and especially the type of vasculitis) is often difficult, especially in atypical cases or when the cause of death is sudden, as the diagnosis is usually reached during the histopathological examination. As a result, there is often not enough vascular tissue to obtain a correct diagnosis, especially regarding all the locations of the vasculitic process.7 To properly characterize the type of vasculitis, both specialized histopathological techniques and clinical data are needed, as most definition criteria for vasculitis include both types of data in the definition criteria. Only histopathological criteria, although it may suggest a specific type of vasculitis, must be interpreted with caution as there is significant overlap between the histological pattern of different vasculitis different stages of vasculitis.28 This is the main reason some authors only classify vasculitis identified after death according to the type of inflammatory reaction.7 According to the Chapel Hill Nomenclature and Definitions of Vasculitis, they can be classified in large vessel vasculitis (giant cell and Takayasu arteritis), medium vessel (polyarteritis nodosa and Kawasaki), and small vessel vasculitis (Wegener granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis, HenochSchonlein purpura, cryoglobulinemic vasculitis, and cutaneous leukocytoclastic angiitis).29 Most often, coronary involvement was cited in medium vessel vasculitis (especially Kawasaki disease), but cases of large or small coronary vasculitis have also been cited in the scientific literature. Giant cell arteritis is rarely found in people younger than 50 years and usually involves cranial arteries (typically the temporal artery), although it was identified in the aorta and its major thoracic and abdominal branches as well30 in approximately 15% of all cases. Takayasu arteritis usually affects women in their reproductive ages (younger than 40 years) and involves the aorta and its main branches. The histology of both is similar—a panarteritis with intimal proliferation, inconstant fibrinoid necrosis, acute inflammation of the adventitia and media with CD4- and CD8positive lymphocytes, some CD68-positive macrophages, and rare B lymphocytes. Takayasu arteritis associated elastic tissue replacement with fibrotic tissue, the obliteration of vasa vasorum, and irregular thickening of the intima.30 Giant cell arteritis is often

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associated with giant multinucleated giant cells, extensive fragmentation of the internal elastic lamina, and endothelial proliferation.30 The age and sex of our patient, the type of inflammatory reaction (mixed), the temporal variability of the lesions as suggested by the different evolutive stages, and the absence of aortitis made, however, the diagnosis of large vessel vasculitis less likely. The absence of small vessel (arterioles and capillaries) involvement, the absence of glomerulonephritis, and a negative c-ANCA pattern suggest that a small vessel vasculitis is less likely in this case. Another possible differential diagnosis is with systemic lupus erythematosus with a vasculitic granulomatous reaction, as suggested by the association of coronary vasculitis with granulomatous hepatitis and sclerotic glomerular lesions. Several cases of lupus associated with coronary vasculitis have been described in the scientific literature,31–36 affecting both men and women and potentially leading to sudden cardiac death. However, in our case,

FIGURE 4. Acute subendocardial infarction. © 2014 Lippincott Williams & Wilkins




FIGURE 5. Coronary vasculitis (AIVA, proximal part). Left, Thickened vessel wall due to marked subintimal hyperplasia associated with fibrinoid necrosis and mixed inflammatory infiltrate, on a background of granulation tissue in various stages of evolution and thrombosis with subtotal stenosis of coronary lumen (HE, 50) (inset, extensive area with deposits of fibrin in vessel wall [asterisk], PTAH stain, 100). Right, Disruption of internal elastic lamina and external elastic lamina (arrows), with fragmentation of elastic fibers (Weigert stain, 50).

we could not identify other clinical markers of systemic lupus erythematosus, and glomerulosclerosis tends to appear in this disease at later stages, usually associated with other clinical signs. Therefore, the most likely diagnosis in our case seemed to be either Kawasaki disease or polyarteritis nodosa. The presence of an inflammatory reaction with T lymphocytes and CD68-positive macrophages was described in both Kawasaki and polyarteritis nodosa (PAN) in later stages of evolution. However, the absence of mucocutaneous lymph node syndrome,

specific for Kawasaki disease; the age (18 years); and the absence of pulmonary involvement suggest a high-probability diagnosis of polyarteritis nodosa. The PAN is characterized, in the acute phase, by an extensive fibrinoid necrosis with neutrophils surrounding or within them. After a few days, however, the inflammatory reaction becomes mixed as it contains mostly lymphocytes, monocytes, and macrophages, sometimes associated with the presence of multinucleated and giant cells.37,38 Later on, the acute infiltrate is replaced by a proliferation of

FIGURE 6. Coronary vasculitis (AIVA, proximal part): populations of leucocytes illustrated by IHC. Left, Subintimal inflammatory infiltrate with numerous T lymphocytes positive to CD45RO (UCHL1), 200. Top right, Scattered B lymphocytes in the inflammatory infiltrate, CD20 (L26), 400. Bottom right, Multinucleated giant cell and dispersed epithelioid cells positive to CD68, 400. © 2014 Lippincott Williams & Wilkins



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FIGURE 7. Coronary vasculitis (AIVA, distal part). Left, Fibrinoid necrosis of the vessel wall associated with marked inflammation on a background of diffuse subintimal hyperplasia, which significantly narrows the arterial lumen (HE, 25; digital reconstruction of the coronary vessel) (inset, large amounts of fibrin deposits in the vascular wall [thick yellow arrows]; PTAH stain, 100). Right, Focal disruption of the internal elastic lamina (thin black arrows) with destruction of media (Weigert stain, 50).

fibroblasts with progressive narrowing of the lumen.39 In our case, the vasculitis was older, as suggested by the coronary histology, with a predominance of T lymphocytes and macrophages and fibroblastic proliferation within the arterial wall, and by the presence of various areas of old myocardial infarction located all over the left ventricle. The PAN usually involves medium (sometimes also small) arteries located in the gastrointestinal tract, kidneys, skin, nervous system, joints, and muscles and is by definition

a disease affecting multiple organs or territories. Coronary involvement in PAN was usually identified in association with other locations.40–44 Isolated PAN has been described as well but is an exclusion diagnosis and has been described in the central nervous system, peripheral nerves, or skin.45 Isolated coronary PAN has been described as well.39,42 Usually, PAN causes vascular aneurisms, but there have been cited cases in which it was associated with extreme narrowings of the coronary lumen.39

FIGURE 8. Coronary vasculitis (AIVA, distal part): populations of leucocytes illustrated by IHC. Left, Numerous T lymphocytes positive to CD45RO (UCHL1), 100. Top right, Few B lymphocytes positive to CD20 (L26), 400. Bottom right, Frequent macrophages positive to CD68, 200.

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FIGURE 9. Coronary vasculitis (circumflex artery, 2 segments with various degrees of stenosis). Left, Subintimal hyperplasia and fibrinoid necrosis and fibrosis, with moderate stenosis of the lumen; Masson trichrome, 50. Right, Marked eccentric thickening of the vessel wall, with severe stenosis due to subintimal hyperplasia and fibrosis, in the context of vasculitis (Masson trichrome, 50).

For example, Cassling et al39 described the case of a 30-yearold man with isolated coronary PAN in which he have identified 80% of narrowing on the second diagonal branch and the proximal right artery and 98% of luminal reduction at the origin of the first diagonal. The PAN is known to be often associated with hepatitis B.46,47 The most likely causes of this association seem to be a direct injury of the vessel wall caused by viral replication and the appearance of vascular lesions resulting from deposition of circulating immune complexes and/or in situ formation of such complexes, leading to complement activation and subsequent release

of neutrophil chemoattractant factors.46 Reports have correlated PAN with hepatitis B vaccines48and other infective agents such as parvovirus B19, group A streptococcus, hepatitis C,49 human immunodeficiency virus, human T-lymphotropic virus 1, cytomegalovirus, and so on, but a definite correlation still needs to be proven. In our case, however, a rapid serum test for the hepatitis B antigen was negative. As a conclusion, we presented a rare particular case of SD due to a segmentary coronary vasculitis (most likely an isolated polyarteritis nodosa with coronary involvement), which

FIGURE 10. Coronary vasculitis (circumflex artery, same segments as described in Fig. 7): cell populations illustrated by IHC. Left, Subintimal hyperplasia with many spindle-shaped cells positive to vimentin, 200. Right, Marked subintimal hyperplasia, with numerous elongated, spindle-shaped plump cells, positive to SMA, 200. © 2014 Lippincott Williams & Wilkins



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FIGURE 11. Left, Nonspecific granulomatous hepatitis: nodular aggregate with multinucleated giant cells, epithelioid cells, and lymphocytes; HE, 100. Right, Cortical area of the kidney with various degrees of glomerulosclerosis, associated with marked interstitial inflammatory infiltrate, consisting of lymphocytes and plasma cells; HE, 100.

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