A 43-year-old homosexual man was referred to our hospital for chest pain and loss of consciousness. He was hypertensive, and had an uncontrolled viral load. Serum creatinine revealed acute renal failure, and he died 3 days later. On autopsy, aortic dissection (TypeB) was found. No obvious inflammatory change, granulation, bacterial or fungal infection, or medionecrosis were seen at the dissection site. To our knowledge, this was the first case with HIV in whom aortic dissection was diagnosed at autopsy. Aortic dissection is a potential differential diagnosis even in young patients presenting with hypertension and chest pain

Hirai, Nobuyasu

Hirata, Kazuki

Hishiya, Naokuni

Imai, Yuichiro

Imakita, Natsuko

Kajita, Akihiro

Kasahara, Kei

Konishi, Mitsuru

Mikasa, Keiichi

Nakai, Tokiko

Nakamura-Uchiyama, Fukumi

Ogawa, Taku

Ogawa, Yoshihiko

Ohbayashi, Chiho

Uno, Kenji

Yonekawa, Shinsuke

English

Global Institutional repository of Nara Medical University

(47) AORTIC DISSECTION IN A PATIENT WITH HUMAN IMMUNODEFICIENCY VIRUS INFECTION THAT WAS DIAGNOSED AT AUTOPSY: A CASE REPORT KENJI UN01 . 2, KEI KASAHARA2• AKIHIRO KAJITA3, NAOKUNI HISHIYA\ NATSUKO IMAKITA2, YUICHIRO IMAI2, MITSURU KONISHI2, YOSHIHIKO 0GAWA2, NOBUYASU HIRAI2, TAKU 0GAWA2, FUKUMI NAKAMURA-UCHIYAMA4, SHINSUKE YONEKAWA2, KAZUKI HIRATA3, TOKIKO NAKAI5, Abstract CHIHO OHBA YASHI5 and KEIICHI MIKASA2 Infectious Disease Department, Minami-Nara General Medical Cente.Y Center for Infectious Diseases, Nara Medical University2 Internal medicine, Saiseikai Chuwa Hospitaf Infectious disease department, Ebara Hospitaf Department of Pathology, Nara Medical University5 Received October 20, 2017 A 43-year-old homosexual man was referred to our hospital for chest pain and loss of consciousness. He was hypertensive, and had an uncontrolled viral load. Serum creatinine revealed acute renal failure, and he died 3 days later. On autopsy, aortic dissection (Type B) was found. No obvious inflammatory change, granulation, bacterial or fungal infection, or medionecrosis were seen at the dissection site. To our knowledge, this was the first case with HIV in whom aortic dissection was diagnosed at autopsy. Aortic dissection is a potential differential diagnosis even in young patients presenting with hypertension and chest pain. Key words: HIV infection, Aortic dissection, Hypertension, Autopsy, Acute renal failure Introduction The prognosis of patients with human immunodeficiency virus (HIV) infection has dramatically improved over the past 20 years because of improved antiviral therapy. The causes of death in HIV patients have been changing from AIDS-related causes to non AIDS-related causes such as cardiovascular diseases or non-AIDS related malignancies [1]. We experienced a case with HIV and fatal aortic dissection diagnosed at autopsy. To our knowledge, this is the first case of HIV in whom aortic dissection was diagnosed at autopsy. We report the detailed pathological analysis. Case report A 43-year-old man was admitted as an emergency to our hospital due to loss of consciousness. He was diagnosed with HIV infection eight years before the emergency transfer but was lost (48) Kenji UNO et al. to follow-up for three years. He was referred to the previous hospital because of pneumocystis pneumonia, and combination antiretroviral therapy (cART) was started four years before the emergency transfer. He developed various side effects with cART, and only tolerated tenofovir (TDF) + lamivudine(3TC) + raltegravir (RAL), but was poorly compliant because of his fear of side effects. Therefore, he was referred to our hospital. which was located near his residence three years before the emergency transfer to improve his compliance and to receive more familial support. The patient was a known asthmatic since the age of 15 years and had been receiving inhalational steroid therapy. He also had atopic dermatitis since childhood. His medical history was relevant for the following; hepatitis A virus infection at 27 years old, herpes zoster infection at 30 years old, amoebic colitis at 31 years old, gastric ulcer at 33 years old, and candida esophagitis at 40 years old. He had anaphylactic reactions to sulfamethoxazole-trimethoprim, pentamidine, alcohol, and contrast medium. He did not have diabetes mellitus or hyperlipidemia. He had smoked 20 cigarettes per day for 20 years. His BMI was 20 kg/ rrl . Family history was negative for Marfan syndrome. Since referral to our hospital. his compliance did not improve and his HIV status was uncontrolled. His CD4 positive cell count was persistently under 50/ mm3• His asthma and hypertension were also uncontrolled, for which oral antihypertensives and corticosteroids were initiated, but he often stopped taking the antihypertensive because of fear of allergy, and consequently his hypertension was uncontrolled. Moreover, he was diagnosed with ileus and diffuse peritonitis due to perforation and septic shock, necessitating surgical intervention one year before the emergency transfer. Since then, he had to take daily morphine to achieve pain control. He had been hospitalized several times, and was finally discharged against medical advice, and refused to take any further medications one month before the emergency transfer. Two weeks before the emergency transfer, he complained of chest pain and came to seek our medical advice. On examination, he was fully conscious with a blood pressure of 188/ 90 mmHg. He refused re-admission and did not take any treatment. After that. he was referred to our hospital by ambulance due to loss of consciousness. On examination, his body temperature was 36.6oC , heart rate was 100 beats/ min. blood pressure was 169/ 96 mmHg, and oxygen saturation was 100% on 5 liter/ min oxygen by mask. His Japan coma scale was !I -10. Asystolic murmur (3/ 6) was auscultated over the left sterna! border, and there were coarse crackles over both lung fields. Laboratory data on admission revealed a white blood cell count of 10600 cells/ 11L with 94% neutrophils, serum C-reactive protein (CRP) level of 24.6 mg/dL, blood urea nitrogen level of 133 mg/ dL, serum creatinine level of 13.76 mg/ dL (Table 1). The serum creatinine level was 1.07 mg/ dL, and serum CRP level was 1.1 mg/ dL two weeks before. His admission chest radiograph (Fig. 1) revealed bilateral lung infiltrates reaching the pleura with no mediastinal extension. No aortic calcification was seen. No intracranial hemorrhage or infarction was detected on a brain computed tomography (CT) image. Contrast enhanced CT was not performed because of the anaphylactic reaction to contrast medium. He did not wish to receive any treatment before he lost consciousness, and he died 3 days after admission secondary to respiratory failure. The direct cause of death was clinically diagnosed as acute renal failure. AORTIC DISSECTION IN A PATIENT WITH HUMAN IMMUNODEFICIENCY VIRUS INFECTION THAT WAS DIAGNOSED AT AUTOPSY: A CASE REPORT (49) Table 1. Laboratory Findings at admission (Peripheral Blood] [ Biochemistry] [ Electrolyte] WBC 10600 /"l CRP 24.6 mg/dl "' 130 mEq/L Stab 9.0 % TP 5.2 g/dl 6.1 mEq/L Seg 85.0 % Alb 2.7 g/dl Cl 86 mEq/L lym 2.0 % AMY 256 U/l c. 7.4 mEq/dL Mono 2.0 % AST 66 U/l Eo> 0.0 % ALT 24 U/l [Infection] Hb 6.1 g/dl CK 237 U/l C7-HRP negative Pit 13.6X 104 M ALP 426 U/l Aspergillus antigen negative [Coagulation test] r-GTP 61 U/l ChE 92 U/l Toxoplasma lgG negative PT·INR 1.30 Gl" 78 mg/d l Cryptococcus Antigen negative APTI 35.4 UA 17.3 mg/dl RPR negative BUN 133 mg/dl Cce 13.76 mg/dl TPHA 17.7 COl NH3 28.8 "g/d l • Two weeks before admission On admission • sitting position m Fig. 1. Chest radiographs at two weeks before admission and at admission An autopsy was performed on the day after death. Aortic dissection (Type B) was seen from the left subclavian artery to the r ight arteria iliaca communis. On hematoxylin-eosin (HE) staining, no obvious inflammatory changes, granulation tissue, bacterial infection, fungal infection or medionecrosis were seen at the dissection area (Fig. 2). Cytomegalovirus (CMV), human herpesvirus 6 (HHV-6), and human herpesvirus 8 (HHV-8) special stains were negative. a ) b) Fig. 2. Autopsy examination of the aorta c) d) vascular intima \ (50) Kenji UNO et al. Aortic dissection was absent in both renal arteries. Mild focal sclerosing glomerulonephritis was detected, which did not cause acute renal failure. Other findings that may have caused the acute renal dysfunction, such as acute tubular necrosis, were not detected. Hyaline membrane formation was seen in both lungs, suggesting diffuse alveolar damage. The direct cause of death was likely circulatory failure secondary to aortic dissection, and respiratory failure secondary to diffuse alveolar damage. Discussion To our knowledge, this was the first case with HIV in whom aortic dissection was diagnosed at autopsy. We could not find any articles in the published literature reporting aortic dissection in patients with HIV before the era of highly active antiviral therapy (HAART). even when there were many opportunistic complications. In our case. contrary to our expectations, aortic inflammation was not seen in the autopsy despite the uncontrolled HIV status. This finding might shed light on the fact that aortic dissection in HIV patients may not be due to the immunocompromised status, but due to general risk factors such as hypertension and smoking. Patients with HIV are expected to have a longer life span nowadays; therefore, control of hypertension and smoking cessation also seemed to be important to prevent aortic dissection even in HIV patients. Aortic dissection was seen from the left subclavian artery to the right arteria iliaca communis, but not in the renal arteries, and findings suggestive of acute renal dysfunction, such as acute tubular necrosis, were not seen in the kidneys. Therefore, acute renal failure was thought to be triggered by decreased renal blood flow due to bilateral obstruction of the renal arteries, and loss of consciousness might be explained by uremia Aortic dissection is caused by a tear in the aortic vascular media. In Japan, the prevalence of aortic dissection at autopsies was 1.5% from 2003 to 2008, and the peak incidence of aortic dissection occurred at 70 years of age among the general population [2]. Predisposing factors for aortic dissection are hypertension, disorders of collagen such as Marfan's syndrome, preexisting aortic aneurysm, bicuspid aortic valve, aortic instrumentation and surgery, aortic coarctation, Turner syndrome, pregnancy and delivery, and inflammatory diseases that cause vasculitis such as Takayasu's arthritis, rheumatoid arthritis. and infective aortitis [3]. It is known that HIV patients have a high prevalence of cardiovascular diseases [4,5]. which is caused by hypertension, dyslipidemia, smoking, and diabetes mellitus as clinical factors [6,7]; and persistent inflammation [8]. protease inhibitor administration [9]. and low CD 4 positive cell count as HIV related conditions [10]. Nevertheless. the incidence of vasculitides remains low (1%) in the HIV population [11]. The mechanism of HIV-associated vasculitides is heterogeneous and multifactorial with a complex pathogenesis. N air et al. [12] studied the histopathological features of the aneurysm wall in detail in 10 patients with HIV. The common theme was inflammation of the vessel walls with the vasa vasora being the epicenter of this inflammatory process. and adventitia demonstrated evolving inflammatory changes, characterized by macrophage infiltration with haemosiderin deposits. Giant cell arteritis (GCA). Takayasu's arthritis, and Behcet's syndrome were also reported as the cause of large-vessel vasculitides AORTIC DISSECTION IN A PATIENT WITH HUMAN IMMUNODEFICIENCY VIRUS INFECTION THAT WAS DIAGNOSED AT AUTOPSY: A CASE REPORT (51) in patients with HIV [13, 14]. In our case, autopsy revealed no cellular infiltration around the aorta; hence, aortic dissection was not due to GCA or vasculitis. We could not find a relationship between the chronic inflammation seen in patients with HIV and aortic dissection. Two cases of HIV infection and aortic dissection were previously reported (Table 2) [15, 16]. The age at presentation was between 40 and 50 years including our case, and all the reported cases were hypertensive. On the other hand, the other 2 cases were receiving cART and HIV was under control. Aortic dissection in our case was diagnosed on autopsy, while the other cases were diagnosed while alive as having DeBakey I, and one of them underwent surgery. Table 2. Record of HIV and Aortic Dissection Baciewicz 2003 Shen 2012 Our case Age, gender 57, male 46, male 43, male signs Weakness of right Chest pain, back Unconsciousness, leg pain chest pain Hypertension history Yes Yes Yes Smoke habitant No record No Yes Family history No No record No Diagnosis method CT CT Autopsy Debekey llib Stanford A A cART 3TC+RTV d4T+3TC+EFV Not received CD4 (/~L) at diagnosis 390 150 16 Viral load (copies/mU < 40 <40 7000 Therapy operation conservative No therapy prognosis Aliive Dead 8months death (found at after diagnosis autopsy) Acute respiratory distress syndrome (ARDS) was diagnosed clinically, and was considered one of the direct causes of death, which was confirmed by the pathological findings on autopsy. Septic shock and trauma were reported as causes of ARDS [17]. Sugano et al. reported that serum CRP level > 15 mg/ dL in patients with aortic dissection was an independent factor for respiratory failure at Pa0/ FI02 ~ 200 mmHg [18]. In our case, hence, respiratory failure seems to have followed the aortic dissection despite the fact that we could rule out septic shock. In conclusion, aortic dissection should be considered as a differential diagnosis in hypertensive HIV patients presenting with symptoms such as chest pain, even in the young. Acknowledgements We would like to thank Editage (www.editage.jp) for English language editing. Conflict of interest There were no conflicts of interest to declare. References 1) Smith C] , Ryom L, Weber R, Morlat P, Pradier C, Reiss P et al. Trends in underlying causes of death in (52) Kenji UNO et al. people with HIV from 1999 to 2011 (D:A:D): a multicohort collaboration. Lancet 384: 241-248, 2014. 2) Triant V A. Regan S. Lee H. Sax PE. Meigs ]B, Grinspoon SK. Association of immunologic and virologic factors with myocardial infarction rates in a US healthcare system. J Acquir Immune Defic Syndr 55:615-619, 2010. 3) Hiratzka LF, Bakris GL, Beckman JA. et al. 2010 ACCF/ AHA/AATS/ ACR/ ASA/ SCA/ SCAIISIR/ STS/ SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation 121: e266-e369, 2010. 4) JCS Joint Working Group. Guidelines for Diagnosis and Treatment of Aor tic Aneurysm and Aortic Dissection (]CS 2011). Circ J 77:789-828, 2013. 5) Islam FM, Wu J. Jansson J. Wilson DP. Relative risk of cardiovascular disease among people living with HIV: a systematic review and meta-analysis. HIV Med 13:453-468, 2012. 6) Freiberg MS, Chang CC, Kuller LH, Skanderson M, Lowy E. Kraemer KL. HIV infection and the risk of acute myocardial infarction. JAMA Intern Med 173:614-622, 2013. 7) DAD Study Group, Friis-M0ller N. Reiss P, Sabin CA. et al. Class of antiretroviral drugs and the risk of myocardial infarction. N Engl J Med 356:1723-1735, 2007. 8) Stein JH. Brown TT, Ribaudo HJ. et al. Ultrasonographic measures of cardiovascular disease r isk in antiretroviral treatment-naive individuals with HIV infection. AIDS 27:929-937, 2013. 9) Friis-M0ller N, Sabin CA, Weber R, et al. Combination antiretroviral therapy and the risk of myocardial infarction. N Engl J Med 349:1993-2003, 2003. 10) Hunt PW, Martin JN. Sinclair E. et al. T cell activation is associated with lower CD4+ T cell gains in human immunodeficiency virus-infected patients with sustained viral suppression during antiretroviral therapy. J Infect Dis 187:1534-1543, 2003. 11) Pate! N. Pate! N. Khan T. Pate! N. Espinoza LR HIV infection and clinical spectrum of associated vasculitides Curr Rheumatol Rep. 2011;13:506-12 12) Nair R, Abdool-Carrim A, Chetty R, Robbs ]. Arterial aneurysms in pat ients infected with human immunodeficiency virus: a distinct clinicopathology entity? J Vase Surg. 1999;29:600-7. 13) Pillay B. Ramdial PK, Naidoo DP. HIV-associated large-vessel vasculopathy: a review of the current and emerging clinicopathological spectrum in vascular surgical practice Cardiovasc J Afr. 2015 26:70-81. 14) Loic Guillevin. Vasculitides in the context of HIV infection. AIDS 22 (suppl 3):S27-33, 2008. 15) Baciewicz FA Jr. MacArthur RD. Crane LR. Repair type I aortic dissection in a patient with human immunodeficiency virus infection. Ann Thorac Surg 76:917-919, 2003. 16) Shen YZ. Song W. Lu HZ. T ype I aortic dissection in a patient with human immunodeficiency virus infection. Biosci Trends 6:143-146, 2012. 17) JRS Guideline Clinical practical guideline for acute lung injury and acute respiratory distress syndrome second edition 2010. 18) Sugano Y, Anzai T, Yoshikawa T et al. Serum C-reactive protein elevation predicts poor clinical outcome in patients with distal type acute aortic dissection: association with the occurrence of oxygenation impairment. Int J Cardiol102:39-45, 2005. 

Aortic Dissection in a Patient with Human Immunodeficiency Virus Infection That was Diagnosed at Autopsy : A Case Report.

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Aortic Dissection in a Patient with Human Immunodeficiency Virus Infection That was Diagnosed at Autopsy : A Case Report.

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