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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors reported causes of death and searched for prognosis factors in Giant Cell Arteritis (GCA). The diagnosis was confirmed by temporal biopsy in all cases. Fourteen patients died during treatment; thirty-six patients had completely recovered (follow up > 6 months after withdrawal of steroid therapy). The commonest causes of death were cardiovascular (n = 7) and digestive (n = 4); they occurred after an average of 195 days of treatment, half of them during the first three months. One death was due to GCA (autopsy) and five deaths were attributed to the treatment with corticosteroids. The prognosis factors were searched for by comparing age, sex, clinical signs, laboratory data before treatment, past medical history in the both series; further more initial dose of Prednisone and the dose after 180 days of steroid therapy were compared in the two groups. The adverse prognosis factors revealed by this study were: advanced age (p < 0.01), previous ischaemic heart disease (p < 0.05) and higher dose of corticosteroids administered at 6 months of treatment (< 0.01).
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PMID:[Death in Horton disease. Prognostic factors]. 141 Aug 98

A 67-year-old man well while receiving steroid therapy for giant cell arteritis, developed symptoms of ischemic heart disease and was found to have critical left main coronary stenosis. An aortic biopsy at the time of bypass grafting revealed giant cell aortitis. We discuss the finding of clinically discordant aortitis; the etiology of the concurrent coronary stenosis and therapy with prednisone-dapsone.
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PMID:Antemortem diagnosis of giant cell aortitis. 235 86

Coronary artery disease is overwhelmingly atherosclerotic in nature, but inflammatory disease of the coronary arteries can be just as life-threatening a cause of ischemic heart disease in all age groups. Coronary vasculitis is not short in variety; as a clinicopathologic entity it spans the entire spectrum of systemic vasculitides. Coronary vasculitis is most closely associated with the polyarteritis group of necrotizing angiitis, vasculitis of collagen-vascular disease, and granulomatous giant cell arteritis. This article provides an overview of coronary vasculitis as an independent entity as well as a manifestation of systemic vasculitis, both the common and the uncommon varieties.
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PMID:Coronary vasculitis. A review in the current scheme of classification of vasculitis. 354 44

This study was made to evaluate the usefulness of various non-invasive methods such as electrocardiography, echocardiography and 201T1 myocardial scintigraphy in the differential diagnosis of idiopathic congestive cardiomyopathy (CCM) and ischemic heart disease (IHD). Eighteen cases with CCM and 9 cases with IHD were subjected. For this study patients with IHD showing dilated cavity (LVDd over 66 mm) and diffuse hypokinesis of the left ventricle in the echocardiogram were selected. For echocardiographic study, cross-sectional sector-scan instrument, Toshiba SSH-11A was used, and 201T1 myocardial scintigraphy was performed using Toshiba jumbo gamma camera GCA-401. Cardiothoracic ratio of CCM and IHD were 59.6 +/- 6.3% and 58.3 +/- 6.3% in average, respectively. In CCM, mean LVDd was 76.0 +/- 5.6 mm and mean LVDs was 63.4 +/- 7.3 mm. In IHD, mean LVDd was 74.7 +/- 8.1 mm and mean LVDs as 63.2 +/- 4.6 mm. Both cardiothoracic ratios and echocardiographic findings showed no difference between CCM and IHD. Incidence of an abnormal Q wave in ECG was higher in IHD (2.72 leads per a case) than that in CCM (1.33 leads per a case). An abnormal Q wave in aVL was frequently (28%) observed in CCM but none in IHD. However, these ECG findings did not seem to be contributory to the differential diagnosis. Myocardial scintigraphic study revealed that 10 of 18 cases with CCM showed no perfusion defect or sparse uptake and others showed small and isolated defect in the apex or postero-lateral wall of the left ventricle, while 7 of 9 cases with IHD showed large perfusion defect over 15% in the anterior and inferior areas. However, small localized defects less than 14% in the apex were observed in both groups, 5 cases (27.8%) with CCM, and 2 cases (22.2%) with IHD, suggesting limitation of this method for the differential diagnosis.
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PMID:[Differential diagnosis of idiopathic congestive cardiomyopathy and ischemic heart disease by echocardiography and 201Tl-myocardial scintigraphy (author's transl)]. 734 20

It is generally accepted that myocardial ischemia, and its extreme consequence, acute myocardial infarction, can result from transient or permanent disproportion between myocardial oxygen demand and coronary artery blood supply. Insufficient coronary artery blood supply may have many reasons. The aim of the study is to point to the clinical features of the coronary vasculitides as well as to the diagnostic and therapeutic possibilities. Coronary artery involvement in infectious angiitis, in Takayasu's arteritis, in granulomatous giant cell arteritis, in thromboangiitis obliterans, in polyarteritis nodosa, in Wegener's granulomatosis and in Churg--Strauss syndrome is discussed. The diagnosis of coronary vasculitis must be supposed in every patient with primary or secondary vasculitis in whom chest pain or cardiac failure appear. In young patients with clinical, electrocardiographic or laboratory signs of coronary artery disease, especially in absence of risk factors for atherosclerosis, the diagnosis of coronary vasculitis must be considered in differential diagnosis. (Fig. 4, Tab. 1, Ref. 32.).
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PMID:[Vasculitides of the coronary arteries]. 862 Mar 25

Vasospasm can have many different causes and can occur in a variety of diseases, including infectious, autoimmune, and ophthalmic diseases, as well as in otherwise healthy subjects. We distinguish between the primary vasospastic syndrome and secondary vasospasm. The term "vasospastic syndrome" summarizes the symptoms of patients having such a diathesis as responding with spasm to stimuli like cold or emotional stress. Secondary vasospasm can occur in a number of autoimmune diseases, such as multiple sclerosis, lupus erythematosus, antiphospholipid syndrome, rheumatoid polyarthritis, giant cell arteritis, Behcet's disease, Buerger's disease and preeclampsia, and also in infectious diseases such as AIDS. Other potential causes for vasospasm are hemorrhages, homocysteinemia, head injury, acute intermittent porphyria, sickle cell disease, anorexia nervosa, Susac syndrome, mitochondriopathies, tumors, colitis ulcerosa, Crohn's disease, arteriosclerosis and drugs. Patients with primary vasospastic syndrome tend to suffer from cold hands, low blood pressure, and even migraine and silent myocardial ischemia. Valuable diagnostic tools for vasospastic diathesis are nailfold capillary microscopy and angiography, but probably the best indicator is an increased plasma level of endothelin-1. The eye is frequently involved in the vasospastic syndrome, and ocular manifestations of vasospasm include alteration of conjunctival vessels, corneal edema, retinal arterial and venous occlusions, choroidal ischemia, amaurosis fugax, AION, and glaucoma. Since the clinical impact of vascular dysregulation has only really been appreciated in the last few years, there has been little research in the according therapeutic field. The role of calcium channel blockers, magnesium, endothelin and glutamate antagonists, and gene therapy are discussed.
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PMID:Vasospasm, its role in the pathogenesis of diseases with particular reference to the eye. 1128 96

Giant cell arteritis is a medium- and large-vessel vasculitis, the most prevalent systemic vasculitis in subjects over age 60. Clinical features are miscellaneous and sometimes misleading. Elevated acute-phase responses, such as a high erythrocyte sedimentation rate and increased levels of C-reactive protein, are important clues to the diagnosis, which is ensured by a positive temporal artery biopsy. Non invasive imaging techniques such as colour duplex ultrasonography, high resolution tomodensitometry, magnetic resonance imaging, and positron emission tomography (or 18-fluorodeoxyglucose scintigram) assist meaningfully the diagnosis in patients with aortitis and/or aortic arch syndrome. The frequent and fearsome visual complications (monocular or even binocular blindness) highlight the urgency of treatment, based mainly on prolonged corticosteroid treatment, with its frequent, at times severe, side effects. These patients can often become free of treatment, in 2 to 3 years in average, but are prone to develop lately vascular complications such as ischemic heart disease or aortic aneurysm so that a close follow-up far beyond the clinical recovery is needed.
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PMID:[Giant cell arteritis]. 1852 8

Premature atherosclerosis has been observed during the course of different systemic inflammatory diseases such as rheumatoid arthritis and sytemic lupus erythematosus. Remarkably, relatively few studies have been published on the occurrence of accelerated atherosclerosis in patients with vasculitis. In giant cell arteritis (GCA), mortality because of ischaemic heart disease is not increased. In addition, intima media thickness (IMT) is lower in patients with GCA than in age-matched controls. In contrast, IMT is increased significantly in Takayasu arteritis, another form of large vessel vasculitis occurring in younger patients. In Takayasu arteritis and in Kawasaki disease, a form of medium-sized vessel vasculitis, accelerated atherosclerosis has been well documented. In small vessel vasculitis because of anti-neutrophil cytoplasmic autoantibodies-associated vasculitis, cardiovascular diseases are a major cause of mortality. IMT measurements reveal conflicting results. During active disease these patients experience acceleration of the atherosclerotic process. However, when inflammation is controlled, these patients have atherosclerotic development as in healthy subjects. Several risk factors, such as diabetes and hypertension, are present more often in patients with vasculitis compared with healthy controls. In addition, steroids may be pro-atherogenic. Most importantly, many patients have impaired renal function, persistent proteinuria and increased levels of C-reactive protein, well-known risk factors for acceleration of atherosclerosis. Enhanced oxidation processes, persistently activated T cells and reduced numbers of regulatory T cells are among the many pathophysiological factors that play a role during acceleration of atherogenesis. Finally, autoantibodies that may be relevant for acceleration of atherosclerosis are found frequently in elevated titres in patients with vasculitis. Because patients have an increased risk for cardiovascular events, vasculitis should be treated with as much care as possible. In addition, treatment should be considered with angiotensin-converting-enzyme inhibitors and/or angiotensin receptor-1 blockers, statins and acetylsalicyl acid. Finally, classical risk factors for cardiovascular disease should be monitored and treated as much as possible.
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PMID:Translational mini-review series on immunology of vascular disease: accelerated atherosclerosis in vasculitis. 1930 50

Ischaemic heart disease is a common cause of morbidity and mortality worldwide. Patients typically present with chest pain and breathlessness either on exertion or at rest. Cardiac ischaemia can also lead to headache, although this is very rarely its only manifestation. Headache is mostly associated with migraine, cluster and tension headache disorders. More sinister causes include subarachnoid haemorrhage, temporal arteritis, meningitis, venous sinus thrombosis as well as vertebral and carotid artery dissection. A case of headache is presented where the underlying cause was cardiac ischaemia, itself the result of triple vessel coronary artery disease. This, also referred to as cardiac cephalgia, should be suspected in the older patient with risk factors for atherosclerotic disease presenting with recent-onset headache. Diagnosis of this requires high clinical suspicion and is essential for correct patient management.
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PMID:Acute coronary syndromes can be a headache. 2096 32

Patients with different forms of systemic vasculitis experience long-term morbidity and mortality caused by cardiovascular disease due to premature atherosclerosis. Epidemiologic reports of patients with GCA suggest that long-term mortality in this disease is not increased compared with the general population of the same age. The risk of a stroke, however, in particular in the vertebrobasilar territory, is increased. In addition, the occurrence of aortic aneurysmal disease and aortic dissection is also clearly increased in GCA. Mortality due to ischaemic heart disease, however, is not increased. In Takayasu arteritis accelerated atherosclerosis has been clearly documented both clinically and in autopsy reports. Atherosclerotic plaques in the carotid artery may be present in the carotid arteries especially in patients with a documented history of arteritis involving the carotid artery. It is controversial whether Kawasaki disease is associated with accelerated atherosclerosis. Young adults with a history of Kawasaki disease may have abnormal brachial artery reactivity, increased carotid IMT values and increased arterial stiffness. At autopsy examinations of KD patients, however, no significant atherosclerotic lesions are detected and carotid IMT measurements were found to be clearly different from those in young adults with familiar hypercholesterolaemia, suggesting that the remodeling process in KD is different from atherosclerosis. In ANCA-associated vasculitis (AAV), an increased mortality as a consequence of cardiovascular disease is well-documented. In these patients the relative risk for coronary heart disease is two- to fourfold that in control subjects. In addition, a similar relative risk has been found for stroke. Diabetes, hypertension, dyslipidemia, abdominal obesity (metabolic syndrome), impaired renal function, persistent proteinuria and increased production of C-reactive protein are common risk factors for premature atherosclerosis in patients with systemic vasculitis. Furthermore, cholesterol and its modifications play a pivotal role in the pathogenesis of accelerated atherosclerosis in vasculitis. The (preventive) therapy for accelerated atherosclerosis in systemic vasculitis is based on an aggressive approach against inflammation and against risk factors of premature atherosclerosis such as smoking, inactivity, obesity and unhealthy diet. In addition, patients should be treated with angiotensin-converting enzyme inhibitors and/or angiotensin receptor-1 blockers for hypertension and statins for dyslipidemia. Finally, low dose acetylsalicylic acid should be prescribed in patients with large vessel vasculitis, i.e., both in GCA and TA, who do not have contraindications for ASA.
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PMID:Cardiovascular disease due to accelerated atherosclerosis in systemic vasculitides. 2350 55


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