Statins in Intracerebral Hemorrhage

Lauer, Arne; Greenberg, Steven M.; Gurol, M. Edip

doi:10.1007/s11883-015-0526-5

Cited by 37 publications

(27 citation statements)

References 69 publications

(71 reference statements)

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“…Although the benefits of statin treatment in primary and secondary prevention of ischemic stroke are widely recognized, the association between these molecules and the risk of cerebral bleeding is still controversial. 10 Although this study was not specifically designed to investigate this hypothesis, our results are in agreement with previous reports suggesting a possible relationship between statin therapy and increased risk of ICH. 10 Statins pleiotropic effects, including reduction of platelet aggregation and inhibition of the coagulation cascade, 11 make the relation between statins and cerebral bleeding in subjects with underlying SVD biologically plausible.…”

Section: Discussionsupporting

confidence: 92%

Risk Profile of Symptomatic Lacunar Stroke Versus Nonlobar Intracerebral Hemorrhage

Morotti

Paciaroni²,

Zini³

et al. 2016

Stroke

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T he term cerebral small vessel disease (SVD) encompasses a wide spectrum of pathological processes affecting the small vessels of the brain, 1 among which, arteriolosclerosis, also known as hypertensive microangiopathy, is the most common. Lacunar strokes (LS) and hemorrhages located in the deep brain regions (nonlobar or deep intracerebral hemorrhage [dICH]) represent the acute symptomatic consequences of this progressive microangiopathy. Because these two phenotypes share the same pathological substrate, 1 it is still matter of debate why some individuals are more prone to develop acute small vessel occlusion, whereas others are more susceptible to vascular rupture. To date, few studies have attempted to address this issue, with conflicting results. Most of the inconsistency arise from methodological drawbacks of the study designs, including the relatively small number of subjects in some analyses, the exclusion of subjects without hypertension in others, as well as the lack of a clear distinction between ischemic stroke subtypes and between lobar and dICH.2-5 Therefore, in this study we aimed at investigating whether differences in individual risk factor profile underlie the propensity for developing dICH, rather than LS.Background and Purpose-Although lacunar stroke (LS) and deep intracerebral hemorrhage (dICH) represent acute manifestations of the same pathological process involving cerebral small vessels (small vessel disease), it remains unclear what factors predispose to one phenotype rather than the other at individual level. Methods-Consecutive patients with either acute symptomatic LS or dICH were prospectively enrolled as part of a multicenter Italian study. We compared the risk factor profile of the 2 subgroups using multivariable logistic regression.

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Section: Discussionsupporting

confidence: 92%

Risk Profile of Symptomatic Lacunar Stroke Versus Nonlobar Intracerebral Hemorrhage

Morotti

Paciaroni²,

Zini³

et al. 2016

Stroke

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“…29 The diagnosis of CAA might similarly affect other clinical decisions suggested to increase ICH risk such as statins for secondary stroke prevention. [31][32][33] The diagnosis of probable CAA by the Boston criteria has high specificity, but currently available methods are insensitive to the presence of CAA in situations such as occurrence of an isolated lobar ICH without microbleeds, hemorrhagic lesions in both deep and lobar locations, or cerebellar hemorrhages. 19,20 In our largest analyzed series of consecutive primary ICH patients who had MRI (n 5 526), patients with uncertain diagnoses were common (isolated lobar ICH, n 5 122, 23.2%; mixed location or cerebellar ICH, n 5 76, 14.5%) relative to the more definite diagnostic categories (probable CAA, n 5 191, 36.3%; HTN-ICH, n 5 137, 26%).…”

Section: Resultsmentioning

confidence: 99%

Florbetapir-PET to diagnose cerebral amyloid angiopathy

et al. 2016

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Objective: We hypothesized that florbetapir, a Food and Drug Administration-approved PET tracer, could distinguish cerebral amyloid angiopathy (CAA)-related intracerebral hemorrhage (ICH) from hypertensive ICH (HTN-ICH). Methods:We prospectively enrolled survivors of primary ICH related to probable CAA (per Boston Criteria, n 5 10) and HTN-ICH (n 5 9) without dementia. All patients underwent florbetapir-PET and multimodal MRI, and patients with CAA had additional Pittsburgh compound B (PiB) PET. Amyloid burden was assessed quantitatively (standard uptake value ratio [SUVR]) and visually classified as positive or negative. Results:The CAA and HTN-ICH groups had similar age (66.9 vs 67.1), sex, and leukoaraiosis volumes (31 vs 30 mL, all p . 0.8). Florbetapir uptake and PiB retention strongly correlated in patients with CAA both globally within cerebral cortex (r 5 0.96, p , 0.001) and regionally in lobar cortices (all r . 0.8, all p # 0.01). Mean global cortical florbetapir uptake was substantially higher in CAA than HTN-ICH (SUVR: 1.41 6 0.17 vs 1.15 6 0.08, p 5 0.001), as was mean occipital SUVR (1.44 6 0.12 vs 1.17 6 0.08, p , 0.001), even after correcting for global SUVR (p 5 0.03). Visual rating for positive/negative florbetapir demonstrated perfect interrater agreement (k 5 1) and was positive for all 10 patients with CAA vs 1 of 9 HTN-ICH patients (sensitivity 100%, specificity 89%).Conclusions: Florbetapir appears to label vascular amyloid in patients with CAA-related ICH. The approved florbetapir binary visual reading method can have diagnostic value in appropriate clinical settings. Classification of evidence:This study provides Class II evidence that florbetapir-PET provides a sensitivity of 100% (95% confidence interval [CI] 66%-100%) and specificity of 89% (95% CI 51%-99%) for determination of probable CAA among cognitively normal patients. Cerebral amyloid angiopathy (CAA), characterized by accumulation of b-amyloid (Ab) proteins in the walls of cortical/leptomeningeal vessels, is a common cause of vessel wall breakdown and vascular dysfunction in older adults, making it a major contributor to fatal or disabling intracerebral hemorrhages (ICH) as well as ischemic injury and dementia. 1,2 There currently is no specific treatment for CAA, in part because of our inability to identify this condition at early phases prior to appearance of multiple hemorrhagic brain lesions. 3 Accurate early diagnosis of CAA also has direct implications for stroke prevention, as this pathology is an important cause of anticoagulant-associated ICH and might dictate use of alternative nonpharmaceutical approaches such as left atrial appendage closure for patients with nonvalvular atrial fibrillation. 4,5

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“…Among some patients with stroke, however, and particularly those with prior hemorrhage, small vessel disease, or cerebral amyloid angiopathy, statins may be associated with an increased risk of intracerebral hemorrhage. 105, 106 …”

Section: Stroke Risk Factorsmentioning

confidence: 99%

Stroke Risk Factors, Genetics, and Prevention

Boehme

Esenwa

Elkind

2017

Circulation Research

1,228

895

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Stroke is a heterogeneous syndrome, and determining risk factors and treatment depends on the specific pathogenesis of stroke. Risk factors for stroke can be categorized as modifiable and nonmodifiable. Age, sex, and race/ethnicity are nonmodifiable risk factors for both ischemic and hemorrhagic stroke, while hypertension, smoking, diet, and physical inactivity are among some of the more commonly reported modifiable risk factors. More recently described risk factors and triggers of stroke include inflammatory disorders, infection, pollution, and cardiac atrial disorders independent of atrial fibrillation. Single-gene disorders may cause rare, hereditary disorders for which stroke is a primary manifestation. Recent research also suggests that common and rare genetic polymorphisms can influence risk of more common causes of stroke, due to both other risk factors and specific stroke mechanisms, such as atrial fibrillation. Genetic factors, particularly those with environmental interactions, may be more modifiable than previously recognized. Stroke prevention has generally focused on modifiable risk factors. Lifestyle and behavioral modification, such as dietary changes or smoking cessation, not only reduces stroke risk, but also reduces the risk of other cardiovascular diseases. Other prevention strategies include identifying and treating medical conditions, such as hypertension and diabetes, that increase stroke risk. Recent research into risk factors and genetics of stroke has not only identified those at risk for stroke but also identified ways to target at-risk populations for stroke prevention.

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Statins in Intracerebral Hemorrhage

Cited by 37 publications

References 69 publications

Risk Profile of Symptomatic Lacunar Stroke Versus Nonlobar Intracerebral Hemorrhage

Risk Profile of Symptomatic Lacunar Stroke Versus Nonlobar Intracerebral Hemorrhage

Florbetapir-PET to diagnose cerebral amyloid angiopathy

Stroke Risk Factors, Genetics, and Prevention

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