Risk Factors for Lacunar Infarcts

Besson, Gérard; Hommel, Marc; Perret, J

doi:10.1159/000016095

Cited by 19 publications

(10 citation statements)

References 10 publications

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“…17,18,22 Despite these findings, the role of hypertension in LI has been questioned, mainly because other causal factors for LI such as embolus of cardiac or carotid origin have been found recently. 3,4,6,7,9,16,23,24 Kappelle and van Gijn 7 revised 14 LI studies and found that 43% to 83% of the patients were hypertensive. In a study of isolated systolic hypertension, Davis et al 25 found that diabetes mellitus and smoking are particularly associated with LI.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] They are traditionally associated with risk factors, natural history, and clinical management that are significantly different from those of other types of brain infarcts. [2][3][4][5][6][7][8] Recently, Boiten et al 9 proposed that 2 distinct LI entities can be distinguished: (1) patients with a single LI and the usual vascular risk factors and (2) patients with multiple LI and a high frequency of hypertension and leukoaraiosis, in which the underlying small-vessel vasculopathy may be different. Although speculative, distinguishing these 2 clinical LI entities may enable more appropriate therapy.…”

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confidence: 99%

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Prospective Study of Single and Multiple Lacunar Infarcts Using Magnetic Resonance Imaging

Araúz

Murillo

Cantú

et al. 2003

Stroke

103

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Prospective Study of Single and Multiple Lacunar Infarcts Using Magnetic Resonance Imaging

Araúz

Murillo

Cantú

et al. 2003

Stroke

103

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“…However, atypical lacunar syndromes represent a less studied group of LI, and although it is supposed that in such a subgroup the lacunar hypothesis is also met, we have fewer available data. Using multivariate analysis, Besson et al [45]did not find a difference between the frequency of risk factors and vascular concomitants between classic lacunar syndromes and an atypical or miscellaneous lacunar group, concluding that atypical lacunar syndrome is a true variant of lacunar stroke.…”

Section: Recent Advancesmentioning

confidence: 99%

New Concepts in Lacunar Stroke Etiology: The Constellation of Small-Vessel Arterial Disease

Arboix

Martí-Vilalta

2003

Cerebrovasc Dis

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Objective: To update the less frequent etiologies causing lacunar infarcts (LIs). To highlight recent advances in risk factors, clinical syndromes, topography, complementary tests and long-term prognosis in this subtype of ischemic stroke. Patients and Methods: The most important studies are analyzed, from CM Fisher works, selecting those referring to LIs of unusual etiology, and recent advances and controversies in the clinical management of LI are discussed. Results: LIs are found in approximately 11% of patients admitted with stroke. The pure motor hemiparesis (55%) constitutes the most usual lacunar syndrome. However, lacunar syndromes may not be caused by LIs in 10–20% of cases. LIs caused by microembolism and cholesterol embolism from the aortic arch are reviewed. Hematological diseases can also cause LI, such as polycythemia rubra vera, essential thrombocythemia and primary antiphospholipidic antibody syndrome. Other etiologies are carotid plaque embolism, severe stenosis of a perforated arteriole and amyloid angiopathy. Infectious arteritis by neurolues, neurocysticercosis, neuroborreliosis, by AIDS or Helicobacter pylori infection have also been associated with the presence of LIs. Likewise, inflammatory arteritis in systemic lupus erythematosus or granulomatous angiitis, cocaine abuse and panarteritis nodosa have been related to LI, although in the latter LI would be caused by a thrombotic microangiopathy and not by vasculitis. Conclusions: LI is an ischemic stroke subtype with a characteristic clinical presentation and a short-term favorable prognosis. Although high blood pressure constitutes the main risk factor and the main etiology, LIs may be caused, in less than 5% of cases, by various etiologies, mainly hematological diseases and infectious or inflammatory arteritis. It is essential to make a correct etiological diagnosis for LI as treatment will be different according to its etiology.

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“…Lacunar infarction possesses several noteworthy characteristics including low mortality rate [12, 13, 14]. Although its symptoms are well known as lacunar syndromes, lacunar infarction is more often silent [15, 16].…”

Section: Introductionmentioning

confidence: 99%

Genetic Predisposition to Neurological Symptoms in Lacunar Infarction

et al. 2004

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Objective: Lacunar infarction is a unique stroke entity with characteristic symptoms. However, it is often silent clinically. The possible genetic predisposition to symptoms of lacunar infarction was investigated. Methods: One-hundred and fifty-one patients with lacunar stroke were consecutively recruited. Lacunar stroke was diagnosed based on both neurological symptoms and lacunar lesion(s), demonstrated by MRI, that were responsible for the symptoms. One-hundred and fifty control subjects with MRI-proven lacunar lesions without neurological symptoms served as controls. There was no significant difference in age, sex and prevalence of known risk factors between cases and controls. Insertion and deletion polymorphisms of the angiotensin-converting enzyme gene (ACE), M235T substitution of the angiotensinogen gene (AGT), and A1133C substitution of type 1 receptor of the angiotensin II gene were determined. Results: The frequency of ACE D allele was significantly higher in symptomatic patients compared with asymptomatic subjects (0.44 vs. 0.36, p < 0.05). The genotype distribution of AGT was significantly different between symptomatic and asymptomatic patients (χ² = 6.6, p = 0.037). Multiple logistic regression analysis revealed that ACE gene and AGT genotypes were independently associated with the neurological manifestation of lacunar infarction. In subjects with 1 lacuna, the odds ratio of the ACE DD genotype for symptomatic manifestation was 4.98 (95% CI 1.25–19.9). In subjects with 4 or more lacunae, the odds ratio of the ACE II genotype for symptomatic manifestation was 0.24 (95% CI 0.10–0.56). Furthermore, the ACE gene polymorphism was significantly different between symptomatic patients with a single lacuna and asymptomatic subjects with 4 or more multiple lacunar infarctions (χ² = 10.6, p = 0.005). Conclusion: These findings suggest that 2 subtypes of lacunar infarction, single symptomatic lacuna and multiple asymptomatic lacunae, may possess different genetic backgrounds. Subjects with the ACE DD genotype could be more predisposed to be symptomatic in first-ever lacunar stroke, while the ACE II genotype may convey resistance to symptoms even after multiple lacunar strokes. Polymorphism of genes of the renin-angiotensin system could be involved in the manifestation of neurological symptoms of lacunar infarction.

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Risk Factors for Lacunar Infarcts

Cited by 19 publications

References 10 publications

Prospective Study of Single and Multiple Lacunar Infarcts Using Magnetic Resonance Imaging

Prospective Study of Single and Multiple Lacunar Infarcts Using Magnetic Resonance Imaging

New Concepts in Lacunar Stroke Etiology: The Constellation of Small-Vessel Arterial Disease

Genetic Predisposition to Neurological Symptoms in Lacunar Infarction

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