Giant cell arteritis as a cardiovascular entity

Abstract

Giant cell arteritis as a cardiovascular entityGiant cell arteritis (GCA) is a relatively infrequent disorder that is underdiagnosed and little appraised in the field of general cardiology. However, it is important to be familiar with the clinical picture of this disease, especially because of the risk of developing fatal aortic aneurysms. If the disease is suspected after a thorough history and clinical examination combined with laboratory investigation, the diagnosis can be confirmed with 18 F-2-deoxy-glucose positron emission tomographic (FDG-PET) imaging. Early recognition of giant cell arteritis followed by prompt treatment with glucocorticosteroids will decrease the risk of developing large-vessel complications. (Neth Heart J 2009;17:281-3.)Keywords: giant cell arteritis, large-vessel disease, aortitis A 66-year-old previously healthy female patient presented with symptoms of fatigue, anorexia and low-grade fever. She had no claudication, headache or muscle weakness. She was a non-smoker, did not use any alcohol and had no family history of cardiovascular disease. On clinical examination we saw an anaemic Caucasian woman with a blood pressure of 145/75 mmHg with a regular pulse of 75 beats/min. On examination of the heart there were normal heart sounds with a grade III early systolic murmur radiating to the carotid arteries. Peripheral pulsations were palpable and of normal volume. Examination of the lungs and abdomen was unremarkable and on inspection of the skin we found no stigmata of endocarditis. Laboratory investigation revealed a normocytic anaemia (haemoglobin 4.7 mmol/l) and an acute phase reaction with thrombocytosis (535/nl), elevated erythrocyte sedimentation rate (ESR, 128 mm/h) and elevated C-reactive protein (135 mg/l). Electrocardiogram and chest X-ray were normal. In two anaerobic bottles out of six blood cultures Bacterium proprioni acnes was grown. Transthoracic echocardiography showed a hyperdynamic left ventricle and severe concentric myocardial hypertrophy. The ascending aorta was not dilated. The aortic valve was tricuspid with calcified cusps and a moderate aortic insufficiency. On the aortic side of the valve a possible vegetation was visualised.The diagnosis of endocarditis of the aortic valve caused by Bacterium proprioni acnes was made in this patient and treatment was started with intravenous penicillin and gentamycin. Despite 14 days of therapy there was no improvement in the clinical picture or laboratory results. A transoesophageal echocardiography was performed and showed no evidence of vegetations on any of the valves. The diagnosis of endocarditis was questioned and other causes of a chronic inflammatory syndrome were carefully reviewed. Subsequential laboratory analysis was negative for antinuclear antibodies, antineutrophil cytoplasmic antibodies, cryoglobulin and monoclonal antibodies. Computer tomography of the thorax and abdomen showed marked thickening of the wall of the thoracic and abdominal aorta, raising the suspicion of aortitis. 18F-2-deoxy-glucose positron em...

Fatal Aortic Dissection in a Patient with Giant Cell Arteritis: A Case Report and Review of the Literature

“…As per guidelines, the initial evaluation of giant cell arteritis should include computed tomographic or magnetic resonance imaging of the thoracic aorta and branch vessels to assess aneurysm or occlusive disease [2]. Alternatively, the 18-fluorodeoxyglucose positron emission tomography (18-FDG PET) has been proposed as both a sensitive and specific diagnostic test that confirms an active vascular process when clinical symptoms and inflammatory markers are ambiguous or equivocal [27, 28]. In patients with confirmed or suspected temporal arteritis or polymyalgia rheumatica (PMA), PET was positive in 76% of patients with confirmed disease, in 23% with suspected disease, and in 2% of healthy controls, demonstrating the low rate of false positivity [29].…”

“…In patients with confirmed or suspected temporal arteritis or polymyalgia rheumatica (PMA), PET was positive in 76% of patients with confirmed disease, in 23% with suspected disease, and in 2% of healthy controls, demonstrating the low rate of false positivity [29]. Suggested screening for aneurysms in patients with GCA includes baseline and annual abdominal ultrasound, chest radiography, and transthoracic echocardiography [28]. …”

“…Diagnosis and immediate corticosteroid treatment should be based on high clinical suspicion, and surveillance imaging should follow initial assessment for large-vessel involvement [41]. At this time, surgical treatment of asymptomatic aneurysm and suspected dissection is as per atherosclerotic guidelines [28]. However, further research is indicated regarding the surveillance and treatment of aortic aneurysms and dissections in patients with GCA.…”

Case histories: increasing role for major journals

“…[3][4][5][6][7][8][9][10][11] The nine cases have been selected based on originality and potential educational interest to the reader. Topics of the case histories are the various manifestations of ischaemic heart disease varying from drug-induced myocardial infarction to aneurysms of coronary artery bypass grafts.…”