Giant Cell Arteritis: Stroke Risk And Prevention

does giant cell arteritis can lead to stroke

Giant cell arteritis (GCA) is a rare cause of stroke, but it is difficult to differentiate from other, more common causes of stroke, such as atherosclerosis, as they share similar characteristics and risk factors. GCA is an immune-mediated inflammatory disease of medium and large arteries, typically affecting people over 50 years old. It is the most common form of vasculitis in adults and the elderly, and if left untreated, can lead to permanent vision loss and even death.

The diagnosis of GCA can be challenging and requires a high level of suspicion since no single test has perfect sensitivity. Clinical decision-making should be driven by a high index of suspicion, and a combination of tests may be needed to improve diagnostic accuracy. These tests include elevated inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), as well as imaging techniques such as Doppler ultrasound, magnetic resonance imaging (MRI) angiography, and positron emission tomography-computed tomography (PET-CT). Temporal artery biopsy remains the gold standard for diagnosis but may have false-negative results due to the segmental involvement of vessel walls.

The prognosis of GCA-related stroke is poor, with high morbidity and mortality rates. Early diagnosis and treatment with corticosteroids are crucial to improving outcomes. However, even with treatment, some patients may continue to experience strokes. Endovascular treatment, such as angioplasty, may be a valid therapeutic option in selected cases.

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Giant cell arteritis (GCA) is a rare cause of stroke

GCA is a rare cause of stroke, accounting for 0.15% to 0.4% of patients admitted for stroke and 0.76 per 100,000 inhabitants per year. However, stroke is a severe complication of GCA, and it is one of the leading factors influencing the mortality and disability rates of GCA patients. GCA-related stroke typically develops in the vertebrobasilar territory and is more frequent in patients who have ophthalmic ischemic symptoms.

The risk of GCA-related stroke is higher in patients with ophthalmic signs (transient or irreversible), vascular risk factors (chronic hypertension, diabetes, dyslipidemia, smoking, atrial fibrillation, age at diagnosis), and aortic branch lesions. GCA patients with general signs or symptoms such as constitutional syndrome or fever, and inflammatory systemic response are less likely to experience stroke.

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GCA is difficult to differentiate from other causes of stroke

GCA is a rare cause of stroke, but it is difficult to differentiate from other, more common etiologies, such as atherosclerosis because their characteristics and risk factors are similar.

The diagnosis of GCA in stroke patients may be challenging, especially if stroke is the first clinical manifestation. Anorexia, malaise, weight loss, fever, headache or arthralgia in the prior medical history of the patient may turn attention to the diagnosis of GCA, but these nonspecific symptoms could easily be overlooked in case of acute stroke. Both C-reactive protein level and the erythrocyte sedimentation rate are significantly higher in the majority of the GCA cases, but these findings are also nonspecific. However, duplex ultrasonography, which is a standard diagnostic tool in acute stroke, could help to establish the diagnosis of CGA.

The presence of the halo sign at the level of the cervical vessels, mainly in the vertebral arteries and less often in the carotid arteries may be the first proof of GCA. In these cases, the Doppler ultrasound examination of the superficial temporal arteries is mandatory, because the classic sonography signs, e.g., hypoechoic halo sign, compression sign, of GCA are usually present at this level in the majority of cases.

The halo sign was first described by Schmidt et al in 1995. The swollen vessel wall of the temporal arteries is characterised by ultrasound as a hypoechoic circumferential mural thickening localised around the lumen, with a diameter ranging from 0.3 to 0.5 mm. The halo sign can be present, not only at the level of the superficial temporal arteries, but at the level of the vertebral, occipital, subclavian or axillary arteries too, and in rare cases, at the level of the carotid arteries. Vessel stenosis or occlusion can also be evidenced at the level of temporal arteries, but the diagnostic value of such is lower. The ultrasound examination can also help to navigate or to plan the precise localization of biopsy.

The other temporal arteritis related ultrasound sign is the so-called ‘compression sign’. This term refers to the continuous feature of a hypoechoic halo during the compression of the vessel lumen by the ultrasound transducer. This sign has high specificity for the diagnosis.

The main advantages of the ultrasound examination are its non-invasive nature, fast availability, lack of radiation exposure and the possibility of simultaneous image acquisition and interpretation. Conversely, the disadvantage of this method is its operator-dependent nature, the need for high-quality equipment, the adequate probe setting and the standardisation requirement.

The so-called ‘fast-track clinics’ in Europe and in the United States with well-trained ultrasound specialists may help to initiate treatment before the appearance of severe complications.

Temporal artery biopsy remains the gold standard of the diagnosis; however, it is more time-consuming compared to ultrasonography. Moreover, false-negative results are not uncommon, due to the segmental involvement of the vessel walls. The mural edema and vessel wall enhancement were demonstrated with high-resolution contrast-enhanced MRI and MR angiography.

Finally, positron-emission tomography can also be useful in diagnosis in selected cases.

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Giant cell arteritis (GCA) is an immune-mediated inflammatory disease of medium and large arteries that typically affects people over 50 years old. GCA presents with symptoms such as headache, scalp tenderness, jaw claudication, and sudden vision loss. It is commonly associated with polymyalgia rheumatica, which causes aches and pains in the shoulders, neck, and hips.

People with GCA have a higher risk of developing strokes, with GCA being an uncommon but recognised cause of stroke. The majority of studies have shown that GCA-related strokes mostly occur between the onset of symptoms and one month after starting steroid therapy. This timing of stroke occurrence is critical and requires careful consideration.

In a large-scale study, Gonzalez-Gay et al. retrospectively analysed data from 287 biopsy-proven GCA patients over 27 years. Of these, 2.8% experienced a stroke between the onset of symptoms and four weeks after starting steroid treatment. The frequency of stroke was significantly higher in male patients, and permanent vision loss and a history of hypertension were the best predictors of stroke.

The active phase of the disease, marked by the onset of symptoms and the first month of steroid therapy, is a critical window for stroke risk. During this period, GCA-related strokes primarily develop in the vertebrobasilar (VB) territory. This localisation is a significant finding, as GCA-related strokes are the main cause of mortality in these patients.

The early initiation of steroid therapy is crucial in managing GCA and reducing stroke risk. However, even with treatment, GCA patients still have a slightly higher risk of stroke than those without GCA. Additionally, stroke recurrence may occur after treatment initiation, highlighting the need for careful monitoring and patient education to recognise and promptly report any signs or symptoms.

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GCA is the most common form of vasculitis in adults

Giant cell arteritis (GCA), also known as temporal arteritis, is the most common form of vasculitis in adults. Vasculitis is a family of rare disorders characterised by inflammation of the blood vessels, which can restrict blood flow and damage vital organs and tissues. GCA typically affects the arteries in the neck and scalp, especially the temples, and often the aorta and its large branches to the head, arms, and legs.

GCA is a disease of older people, with an average age of onset of 72, and almost all people with the disease are over 50. It is more common in women, who are afflicted two to three times more often than men. The condition can occur in every racial group but is most common in people of Scandinavian descent.

The most common symptoms of GCA include persistent, throbbing headaches, tenderness of the temples and scalp, jaw pain, fever, joint and/or muscle pain, and vision problems. GCA can lead to blindness or stroke if left untreated. Early treatment is vital to prevent serious complications.

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In the general population, the carotid-territory strokes are more frequent than the vertebrobasilar (VB) territory strokes; in population-based epidemiologic stroke studies, their ratio was 5:1, respectively. However, in the active phase of GCA, the stroke cases primarily developed in the VB territory. For example, Gonzalez-Gay et al. reported in a population-based study including a total of 287 GCA patients that seven out of the eight stroke cases occurred in VB territory. Moreover, in six of the seven cases, the patients were male. In a population-based cohort study published by Salvarani et al., all of the five stroke cases among a series of 180 patients with biopsy-proven GCA showed VB localisation. Similar results were reported by Samson et al. (75% of GCA-related strokes) and by Pariente et al. (11/18 stroke cases). Notably, studies that include all cases of stroke in GCA patients, regardless of whether it occurs in the active stage of the disease or not, tend to report higher frequency of stroke in the carotid localisation, similar to the data of the general population.

Frequently asked questions

Giant cell arteritis (GCA) is an immune-mediated inflammatory disease of medium and large arteries, which typically affects people over 50 years old.

Symptoms of GCA include headache, scalp tenderness, jaw claudication, and sudden vision loss. Other symptoms include dysarthria, dysphagia, facial drop, and generalised weakness.

Yes, GCA can lead to stroke, although it is a rare complication. GCA is a cause of stroke in around 0.15% of cases.

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