TIA as Acute Cerebrovascular Syndrome (Frontiers of Neurology and Neuroscience)

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In , the stratification system was modified, for screening and treatment of patients with dyslipidemia Among the changes, the "diabetes mellitus" item was eliminated from the algorithm because this disease was considered as a coronary equivalent. A caveat of using the Framingham risk stratification in patients with IS or TIA is that the system was created for evaluation of the general population and not to individual patients with cardiovascular disease. In the Framingham cohort, the number of risk factors associated with greater likelihood of CHD was lower in patients with history of CHD or stroke, than in patients without cardiovascular disease Also, stroke etiologies are heterogeneous.

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Patients with IS caused by extracranial internal carotid artery atherosclerosis are known to have greater CHD risk than the general population, but CHD risks have been less investigated in IS caused by other etiologies, such as intracranial atherosclerosis or non-atherosclerotic causes.

Considering that not all IS or TIA are caused by atherosclerosis, this strategy is open to discussion The absence of significant differences in burden of asymptomatic CHD in autopsies of patients with different IS etiologies may indicate that indeed, patients with any IS are at increased risk, or may reflect low power due to small sample sizes in IS subgroups In theory, it is possible that cut-off values for estimation of CHD risk may be lower in patients with IS compared to the general population, or in miscigenated populations compared to North-American and European populations.

The Framingham stratification system was validated in countries of predominantly European ancestry, and its predictive value in miscigenated populations remains to be determined. The inclusion of additional criteria or biomarkers such as family history of early CHD, chronic renal insufficiency or calcium scores, among others, may refine stratification but this approach has not been thoroughly tested in patients with IS Another defying task for physicians that treat patients with stroke is to properly investigate and diagnose atherosclerosis as a cause of IS or TIA, in the absence of extracranial internal carotid artery atherosclerosis.

Appropriate interpretation of clinical, laboratory and imaging findings is crucial to diagnose IS caused by atherosclerosis in the extracranial vertebral artery, or in intracranial arteries. Tests such as intracranial magnetic resonance or computed tomography angiography and transcranial Doppler are key for diagnosis of intracranial artery disease If physicians do not acknowledge intracranial artery disease as a cause of IS that deserves investigation, such tests may never be ordered, leading to underdiagnosis of this condition.

For instance, diagnosis of basilar artery occlusive disease may be missed if investigation of intracranial arteries is not performed in a patient with TIAs presenting with pure motor hemiparesis and mild or absent extracranial internal carotid artery atherosclerosis Considering that patients with intracranial artery occlusive disease are considered to be at high risk of recurrence and death from cardiovascular events, and that aggressive treatment of atherosclerosis has been suggested to be key in these cases, underdiagnosis of this condition may have serious consequences for overall vascular risk.

The fact that the relation between extracranial internal carotid artery atherosclerosis and CHD has been well recognized should not cloud the need to determine if there is a similar association between atherosclerosis in other cervicocranial arteries, including intracranial arteries, and CHD risk. Few studies have addressed this issue over the past years. The composition of the arterial wall and the magnitude of hemodynamic stress sustained by coronary and large intracranial arteries are different.

In autopsies from Japanese individuals, the amounts of esterified to total cholesterol, and of chondroitin sulfate in total glycosaminoglycans were lower, while heparin sulfate content was higher in normal intima of intracranial arteries than in coronary arteries and the aorta In autopsies, lipids have been reported to be predominant components of coronary plaques, while fibrotic content seems to predominate in intracranial plaques.

Plaques rich in lipids are more likely to ulcerate, triggering acute thrombosis, than fibrous plaques 5. Also, it has been suggested that atherosclerosis may often affect either extra- or intracranial arteries, instead of involving both arterial beds. It has been proposed that pathogenesis of intracranial and extracranial atherosclerosis may differ, for example concerning metabolic abnormalities and inflammation Correlations between coronary and internal carotid artery plaques have been widely described, but few studies have explored the coexistence of coronary and intracranial atherosclerosis.

History of CHD has been reported to be more frequent in patients with extracranial carotid artery atherosclerosis than in those with middle cerebral artery stenosis but overall, insufficient information is available about intracranial atherosclerosis In Japan, autopsies performed in the s revealed a lower degree of atherosclerosis in the coronary arteries, and a higher burden in the circle of Willis, with respect to Americans. On the other hand, in India intracranial and coronary atherosclerosis were found to be significantly correlated Consistent with other reports, coronary atherosclerosis was more frequent than intracranial atherosclerosis in younger individuals, and the correlation between the progression of atherosclerosis with age was more marked for coronary than for cerebral atherosclerosis.

While coronary atherosclerotic burden increased gradually until age 40 and then evolved sharply with age, intracranial atherosclerosis was more evident after age 40 and continued to build gradually until the eight decade. Moreover, calcified and complicated plaques were common in coronary but not in intracranial plaques after age Characteristics and distribution of plaques in coronary and intracranial arterial beds may differ according to ethnicity and exposure to risk factors. In contrast with the results reported in India, fatty streaks and fibrous plaques were present in intracranial arteries already in the second decade of life, in autopsies performed in New Orleans in the s and early s 43 , In regard to coronary atherosclerosis, ethnic and regional differences are also well established.

Imaging Diagnosis of Transient Ischemic Attack in Clinic and Traditional Chinese Medicine

For instance, in a study that included more than 17, asymptomatic Brazilian, Portuguese and American subjects, Santos et al. Dissimilarities remained significant even after adjustments were made for traditional risk factors for atherosclerosis Genetic factors have been pointed out as candidate reasons to explain the "Hispanic paradox", i. It is possible that genetic and environmental factors modulate the involvement of coronary and cervicocephalic arteries by different mechanisms and at different degrees in various populations.

Therefore, the coexistence, severity and progress of atherosclerotic lesions in diverse arterial beds may be more frequent in some populations than in others, with likely implications on causes of vascular death. Until now, this remains an open question. In these patients, intracranial internal carotid artery stenosis, symptomatic vertebrobasilar stenosis and presence of high levels of lipoprotein and homocysteine were independently associated with silent myocardial ischemia. In another study, lipoprotein-associated phospli-phase A 2 , a novel cardiovascular risk biomarker, was found to be the only predictor of new vascular events in patients with IS or TIA and intracranial atherosclerosis In Korea, 71 patients with IS of various etiologies and no history of CHD underwent computed tomography coronary angiography Patients with coronary stenosis had greater rates of IS caused by atherosclerosis Older age and extracranial internal carotid artery atherosclerosis, but not intracranial atherosclerosis, were independent predictors of CHD.

However, statistical power for detection of a significant association between CHD and IS caused by intracranial atherosclerosis was low, since only 14 patients were diagnosed with IS caused by atherosclerosis extra- or intracranial. Contraindications for computed tomography coronary angiography renal failure, inability to cooperate with the test or for extracranial and intracranial magnetic resonance angiography limited sample size.

Significant correlations were found between coronary atherosclerosis and stenosis of the extracranial carotid, intracranial vertebral and basilar arteries, but not with anterior, middle and posterior cerebral arteries. These results suggested that the relation between coronary and intracranial atherosclerosis may be present for some, but not all intracranial arteries. Therefore, studying "intracranial atherosclerosis" instead of disease in distinct intracranial arteries may bias results, obscuring the relation between intracranial and coronary lesions.

In addition, a Japanese study that evaluated patients with IS patients with no symptoms of CHD reported intracranial atherosclerosis and the metabolic syndrome as the strongest predictors of CHD, diagnosed by coronary computed tomography or coronary angiography Differences in methodology, sample size, genetic as well as environmental factors may explain the discrepancies found in literature.

CHD and IS are frequent coexistent conditions that share risk factors and pose major burdens to global health. Intracranial atherosclerosis, the most frequent cause of IS in Asia and possibly the most likely cause worldwide, is associated with high risks for stroke recurrence and vascular death.

What Happens During an Ischemic Stroke

Even though a clear relation has been established between extracranial internal carotid artery atherosclerosis and symptomatic or asymptomatic CHD, there is a gap in knowledge about the association between intracranial atherosclerosis, and CHD. Intracranial atherosclerosis is associated with high risk for stroke recurrence and vascular death. There is a need for more research in this field, as well as for clinical trials that answer whether early diagnosis of asymptomatic CHD and aggressive treatment, whether or not be restricted to medical treatment, can decrease the risk of vascular death in patients with IS caused by intracranial atherosclerosis.

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Geneva, Switzerland: World Health Organization. Last accessed September 5th, Worldwide stroke incidence and early case fatality reported in 56 population-based studies: a systematic review. Lancet Neurol ; Incidence of stroke subtypes, prognosis and prevalence of risk factors in Joinville, Brazil: a 2-year community based study.

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Lancet ;— Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries the interheart study : case-control study. Lancet ; Antithrombotic and thrombolytic therapy for ischemic stroke. Chest ;SS. Advances in the diagnosis of etiologic subtypes of ischemic stroke. Curr Neurol Neurosci Rep ; Yamamoto FI. Ischemic stroke in young adults: an overview of etiological aspects. Arq Neuropsiquiatr ; Risk factors, outcome, and treatment in subtypes of ischemic stroke: the German Stroke Data Bank.

Stroke ; Large artery intracranial occlusive disease: a large worldwide burden but a relatively neglected frontier.

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Arenillas JF. Intracranial atherosclerosis: current concepts. Stroke ;42 Suppl :SS Race-ethnicity and determinants of intracranial atherosclerotic cerebral infarction: the Northern Manhattan Stroke Study. Autopsy prevalence of intracranial atherosclerosis in patients with fatal stroke. A possible explanation for the racial difference in distribution of large-arterial cerebrovascular disease; ancestral European settlers evolved genetic resistance to atherosclerosis, but confined to the intracranial arteries. Med Hypotheses ; Basilar artery occlusive disease in stroke survivors in a multiethnic population.

Clin Neurol Neurosurg ; Long-term outcomes of ischemic stroke patients with concurrent intracranial and extracranial stenoses and ischemic heart disease. Cerebrovasc Dis ; Comparison of warfarin and aspirin for symptomatic intracranial stenosis. N Engl J Med ; Stenting versus aggressive medical therapy for intracranial arterial stenosis.

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This Research Topic aims at a multifaceted approach to evaluating recent progress in our understanding of the cellular and molecular biology of these diseases. Research articles and review papers are welcome from scientists working in the areas of i brain cellular and vascular biochemistry and molecular biology and their relationships to brain development; ii morphological analysis of brain structure after cerebrovascular and neurodegenerative diseases; iv the molecular and cellular events underlying the development of cerebral blood vessels and their relationships to brain development; v the factors controlling the functional interaction between endothelial cells, neurons and glia; vi studies of membrane channels and proteins; vii perivascular status of the brain and functions of the blood brain barrier in health and disease; viii protective mechanism of brain and new therapeutic targets.

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