Abstract 11139: Prevalence, Characteristics and Prognostic Associations of Carotid Plaque Among HIV-infected Subjects Free of Known Cerebrovascular Disease

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Sumbal A Janjua ◽  
Pedro V Staziaki ◽  
Richard A Takx ◽  
Hamed Emami ◽  
Jakob Park ◽  
...  

Introduction: The risk of cerebrovascular events is increased among HIV-infected subjects; this risk is independent of conventional cardiovascular (CV) risk factors and may be related to persistent inflammation leading to accelerated carotid atherosclerosis. However, there are no data characterizing the prevalence, characteristics and prognostic associations of carotid plaque among subjects with HIV. Methods: From a clinical registry, we identified all HIV-infected subjects with a CT neck from 2005-2014. Data collection and CT analysis were performed by blinded independent teams and included CV and HIV specific risk factors. CT variables included presence of carotid plaque, plaque composition (calcified/non-calcified/mixed), degree of stenosis [≥ 50%] and high-risk plaque (HRP) features [low attenuation, spotty calcification]. The outcome was a cerebrovascular event (stroke, transient ischemic event) defined by ICD codes and independently adjudicated by a board certified physician. Association between plaque presence, characteristics and HRP with events was tested by Cox proportional hazard models. Results: Of 231 HIV-infected subjects, 32 had prior cerebrovascular disease,15 had poor image quality leaving an n=184 (46±10 yrs, 21% female,12% diabetics, 19% HTN, smoking in 31%, 14% on statins, average LDL of 90±39mg/dl). On CT, 36% had any carotid plaque and 23% had bilateral plaque. Of those with plaque,15% had a stenosis of ≥50% and 70% had any HRP feature. Both plaque and HRP were increased with age, duration of HIV and anti-retroviral therapy. Over a median of 4 yrs,13 (7%) cerebrovascular events occurred. After adjusting for the number of CV risk factors, a carotid plaque [HR: 3.5 (1.1-11) P =0.03, Fig 1A] and any HRP feature [HR: 3.2 (1.0-10) P =0.04, Fig 1B] were associated with incident cerebrovascular events. Conclusions: Among HIV-infected subjects, free of known cerebrovascular disease, carotid plaque and/or HRP predict cerebrovascular events.

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Donika K Patel ◽  
Seby John ◽  
Neda Hashemi-Sadraei ◽  
Manmeet Ahluwalia

Introduction: Bevacizumab, a humanized monoclonal anti-vascular endothelial growth factor antibody, was FDA approved in 2009 for progressive glioblastoma. Phase II clinical trials suggested an increased risk of ischemic stroke (IS) and intracranial hemorrhage (ICH) while on bevacizumab. The incidence, clinical characteristics, and neuroimaging of glioma patients who developed cerebrovascular events while on treatment is lacking. We report our experience using bevacizumab for glioma patients. Methods: A retrospective review of glioma patients treated with bevacizumab at our institution from July 2005 to June 2011 was studied. Patients with MRI-confirmed IS and/or ICH while on bevacizumab was investigated and compared to historical data. Patient demographics, vascular risk factors, clinical presentations, tumor characteristics, treatments (surgery, chemotherapy, and radiation), and treatment duration were collected. Results: A total of 162 patients (65% male) received bevacizumab and 23 (14%) developed a cerebrovascular event while on treatment, with 3 (2%) IS and 20 (12%) ICH. All IS and ICH patients received prior brain radiation. In the IS group, 2 (66%) patients were symptomatic, with 1 (33%) cardiembolic and 2 (66%) lacunar strokes. None had risk factors besides hypercoagulable state from malignancy. In the ICH group, 3 (15%) patients had a symptomatic bleed and 6 (30%) had associated hypertension. All ICHs were intratumoral and 16 (80%) associated with tumor progression. Median survival after stroke was 9.8 and 3.7 months in the IS and ICH groups, respectively. Length of bevacizumab treatment was not significantly associated with development of IS ( p = 0.6) and ICH ( p = 0.3). Conclusion: Glioma patients have an inherently elevated risk of IS and ICH because of disease- and treatment-related effects. In our study, 78% of the events were asymptomatic and diagnosed on serial imaging. ICHs were more common, but all were small intratumoral bleeds, mostly in the setting of tumor progression. Development of cerebrovascular events was not associated with the duration of bevacizumab treatment. Our study, however, cannot determine causality and randomized controlled studies are needed to determine the risk of IS and ICH with bevacizumab use.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
G Benetos ◽  
K Toutouzas ◽  
G Oikonomou ◽  
I Koutagiar ◽  
M Karmpalioti ◽  
...  

Abstract Introduction The association of carotid plaque inflammation with cerebrovascular events is a matter of rigorous research. Microwave Radiometry (MWR) allows in vivo noninvasive measurement of the internal temperatures of tissues, reflecting inflammation. Purpose To investigate whether increased carotid temperatures in patients with documented coronary artery disease (CAD) are associated with cerebrovascular events. Methods Consecutive patients with significant CAD from three tertiary centers were included in the study. Maximum carotid plaque thickness was assessed in all carotids by ultrasound. ΔT by MWR was assigned as the temperature difference (maximal minus minimum) along the carotid artery. ΔT ≥0.90°C was assigned as high ΔT. All patients were followed-up clinically for two years and all strokes were adjudicated by an independent committee. Transient ischemic attacks were excluded. Results In total 300 patients were included in the study. High ΔT temperatures bilaterally were measured in 47 patients (15.7%). Three patients (1.0%) suffered a stroke, including one fatal. Stoke rate was 4.3% in the group with bilateral high ΔT and 0.4% in non-high ΔT group (p=0.02). In Kaplan-Meier plot patients with bilateral high ΔT showed higher stroke rate (log-rank p=0.004, figure) Conclusions Bilateral high carotid temperatures are associated with increased two-year stroke rate. The potential value of the present finding in risk stratification of intermediate carotid stenosis mandates further investigation.


Author(s):  
Bilal Ahmed ◽  
Ahmed Itrat ◽  
Maria Khan ◽  
Ayeesha Kamal

Background There is a paucity of population based data about the coexistent prevalence of risk factors for stroke in South Asians. Methods In this cross sectional survey performed in an urban slum, individuals 35 years of age or older were invited for participation through simple random sample drawn from baseline census data. For each participant a systematic history and examination was performed to confirm the following risk factors: Diabetes, Hypertension, Obesity, Tobacco Use, Coronary Artery Disease, Family History of Coronary Artery Disease and/or Stroke. Cerebrovascular events (stroke and TIA) were verified by a vascular neurologist. We report the association of risk factor groups and the presence of contemporaneous cerebrovascular event (CVE). Results Five hundred and forty five individuals (49.4% females 269 out of 545) participated in the study. Cerebrovascular event (Stroke and /or TIA) were found in “21.8% (119 out of 545)” individuals. Obesity was found to be the predominant risk factor, occurring in “56.9% (310 out of 545)”, followed by total hypertension “52.1% (284 out of 545)” and tobacco use respectively “39% (213 out of 545)”. There were “63.3% (345 out of 545) individuals with two or more risk factors, with the majority of these being women (54.6%). CVE increased in percentage with quantitative increase in risk factors, with 13% of CVE in individuals with no risk factors to 85.7% CVE among those with 5 risk factors. The combination of Hypertension, Diabetes, Obesity and cigarette smoking conferred the highest odds at 4.9 (p=0.039). Conclusion A systematic screening within South Asians with cerebrovascular disease will uncover multiple preventable risk factors.


2021 ◽  
Vol 12 ◽  
Author(s):  
Sandro Marini ◽  
Marios K. Georgakis ◽  
Christopher D. Anderson

The kidney and the brain, as high-flow end organs relying on autoregulatory mechanisms, have unique anatomic and physiological hemodynamic properties. Similarly, the two organs share a common pattern of microvascular dysfunction as a result of aging and exposure to vascular risk factors (e.g., hypertension, diabetes and smoking) and therefore progress in parallel into a systemic condition known as small vessel disease (SVD). Many epidemiological studies have shown that even mild renal dysfunction is robustly associated with acute and chronic forms of cerebrovascular disease. Beyond ischemic SVD, kidney impairment increases the risk of acute cerebrovascular events related to different underlying pathologies, notably large artery stroke and intracerebral hemorrhage. Other chronic cerebral manifestations of SVD are variably associated with kidney disease. Observational data have suggested the hypothesis that kidney function influences cerebrovascular disease independently and adjunctively to the effect of known vascular risk factors, which affect both renal and cerebral microvasculature. In addition to confirming this independent association, recent large-scale human genetic studies have contributed to disentangling potentially causal associations from shared genetic predisposition and resolving the uncertainty around the direction of causality between kidney and cerebrovascular disease. Accelerated atherosclerosis, impaired cerebral autoregulation, remodeling of the cerebral vasculature, chronic inflammation and endothelial dysfunction can be proposed to explain the additive mechanisms through which renal dysfunction leads to cerebral SVD and other cerebrovascular events. Genetic epidemiology also can help identify new pathological pathways which wire kidney dysfunction and cerebral vascular pathology together. The need for identifying additional pathological mechanisms underlying kidney and cerebrovascular disease is attested to by the limited effect of current therapeutic options in preventing cerebrovascular disease in patients with kidney impairment.


VASA ◽  
2009 ◽  
Vol 38 (4) ◽  
pp. 357-364 ◽  
Author(s):  
Giannoukas ◽  
Sfyroeras ◽  
Griffin ◽  
Saleptsis ◽  
Antoniou ◽  
...  

Background: Severity of stenosis remains the main factor for assessing risk of stroke in patients with internal carotid artery (ICA) disease. This study was conducted to investigate the association of plaque echostructure and other established and emerging cardiovascular risk factors with symptomatic ICA disease. Design: Cross-sectional study of consecutive patients with significant (> 50 %) ICA stenosis. Patients and methods: Carotid plaque echostructure, smoking, hypertension, diabetes mellitus, serum lipoprotein (a), homocysteine, vitamin B12, folate, cholesterol to high-density lipoprotein ratio, triglycerides, C-reactive protein, and the Framingham risk score were assessed in 124 consecutive patients (70 asymptomatic; 54 symptomatic) with significant (> 50 %) ICA stenosis. Results: The asymptomatic and symptomatic groups did not differ in terms of gender distribution (p = 0.76) and severity of stenosis (p = 0.62). Echolucent plaques (type 1 and 2) were more predominant in patients with symptomatic disease (p = 0.004, OR = 2.13, 95 % CI = 1.26-3.6). Patients with plaques type 1 were relatively younger than those with type 4 (p = 0.02). None of the other factors assessed had any significant association with symptomatic disease and any type of carotid plaque. Conclusions: Besides the severity of carotid stenosis, the presence of an echolucent plaque appears as an important factor associated with symptomatic ICA disease. Also, young patients are more likely to have an echolucent plaque suggesting an age-related association with plaque maturation.


2011 ◽  
Vol 3 (1) ◽  
pp. 30
Author(s):  
Anding Xu ◽  
Zefeng Tan ◽  
◽  

Hypertension is the most important of the prevalent and modifiable risk factors for stroke. Based on evidence, blood pressure (BP) lowering is recommended in guidelines for the prevention of stroke. However, there are still some uncertainties in the guidelines for controlling BP and preventing stroke in patients with previous cerebrovascular events, such as the goal BP, who to treat and which class of BP-lowering drugs to use. This article discusses these questions by reviewing guidelines and corresponding clinical trials, with the aim of reducing the gap between guidelines and clinical practice.


Author(s):  
Victoria J. Williams ◽  
Steven E. Arnold ◽  
David H. Salat

Throughout the lifespan, common variations in systemic health and illness contribute to alterations in vasculature structure and function throughout the body, significantly increasing risk for cardiovascular and cerebrovascular disease (CVD). CVD is a prevalent cause of mortality in late life; it also promotes brain alterations, contributing to cognitive decline and, when severe, vascular dementia. Even prior to diseased states, individual variation in CVD risk is associated with structural and functional brain alterations. Yet, how cumulative asymptomatic alterations in vessel structure and function contribute to more subtle changes in brain tissue integrity and function that emerge in late life is unclear. Finally, vascular risk factors are associated with the clinical progression of neurodegenerative diseases such as Alzheimer’s disease (AD); however, recent theory posits that vascular degeneration may serve a contributory role in these conditions. This chapter reviews how lifespan changes in vascular health contribute to degenerative changes in neural tissue and the subsequent development of cognitive impairment and/or vascular dementia. It first discusses associations between vascular risk factors and cognition and also how declining vascular health may lead to cognitive impairment and dementia. Next, it identifies basic aspects of cerebrovascular anatomy and physiology sustaining tissue health and discusses how vulnerabilities of this system contribute to neurodegenerative changes. Finally, it reviews evidence of vascular contributions to AD and presents ideas for future research to better understand the full spectrum of cerebrovascular contributions to brain aging, cognitive decline, and dementia.


2013 ◽  
Vol 70 (11) ◽  
pp. 993-998 ◽  
Author(s):  
Djordje Milosevic ◽  
Janko Pasternak ◽  
Vladan Popovic ◽  
Dragan Nikolic ◽  
Pavle Milosevic ◽  
...  

Background/Aim. A certain percentage of patients with asymptomatic carotid stenosis have an unstable carotid plaque. For these patients it is possible to register by modern imaging methods the existence of lesions of the brain parenchyma - the silent brain infarction. These patients have a greater risk of ischemic stroke. The aim of this study was to analyze the connection between the morphology of atherosclerotic carotid plaque in patients with asymptomatic carotid stenosis and the manifestation of silent brain infarction, and to analyze the influence of risk factors for cardiovascular diseases on the occurrence of silent brain infarction and the morphology of carotid plaque. Methods. This retrospective study included patients who had been operated for high grade (> 70%) extracranial atherosclerotic carotid stenosis at the Clinic for Vascular and Transplantation Surgery of the Clinical Center of Vojvodina over a period of 5 years. The patients analyzed had no clinical manifestation of cerebrovascular insufficiency of the carotid artery territory up to the time of operation. The classification of carotid plaque morphology was carried out according to the Gray-Weale classification, after which all the types were subcategorized into two groups: stable and unstable. Brain lesions were verified using preoperative imaging of the brain parenchyma by magnetic resonance. We analyzed ipsilateral lesions of the size > or = 3 mm. Results. Out of a 201 patients 78% had stable plaque and 22% unstable one. Unstable plaque was prevalent in the male patients (male/female ratio = 24.8% : 17.8%), but without a statistically significant difference (p > 0.05). The risk factors (hypertension, nicotinism, hyperlipoproteinemia, and diabetes mellitus) showed no statistically significant impact on carotid plaque morphology and the occurrence of silent brain infarction. Silent brain infarction was detected in 30.8% of the patients. Unstable carotid plaque was found in a larger percentage of patients with silent brain infarction (36.4% : 29.3%) but without a significant statistical difference (p > 0.05). Conclusions. Even though silent brain infarction is more frequent in patients with unstable plaque of carotid bifurication, the difference is of no statistical significance. The effects of the number and type of risk factors bear no statistical significance on the incidence of morphological asymptomatic carotid plaque.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 775.2-776
Author(s):  
C. W. S. Chan ◽  
P. H. LI ◽  
C. S. Lau ◽  
H. Y. Chung

Background:Cardiovascular (CVS) diseases are the leading cause of death worldwide and patients with rheumatic diseases have an increased CVS risk including stroke and myocardial infarction (MI) (1-3). CVS risk factors and CVS events are common in SpA (4). Delineating the CVS risk and the association with medications in patients with SpA would be useful.Objectives:The objective of this study was to delineate the CVS risk and the association with medications in patients with SpA.Methods:Patients with SpA and patients with non-specific back pain (NSBP) were identified in rheumatology and orthopedics clinics respectively. Clinical information and CVS events were retrieved. Incidence rates were calculated. Association analysis was performed to determine the CVS risk of SpA and other modifiable risk factors.Results:A total of 5046 patients (SpA 2616 and NSBP 2430) were included from eight centers. Over 56 484 person-years of follow-up, 160 strokes, 84 MI and 262 major adverse cardiovascular events (MACE) were identified. Hypercholesterolemia was more prevalent in SpA (SpA 34.2%, NSBP 28.7%, P<0.01). Crude incidence rates of stroke and MI were higher in SpA patients. SpA was associated with a higher risk of MACE (HR 1.66, 95%CI 1.22-2.27, P<0.01) and cerebrovascular events (HR 1.42, 95%CI 1.01-2.00, p=0.04). The use of anti-tumor necrosis factor (TNF) drugs was associated with a reduced risk of MACE (HR 0.37, 95%CI 0.17-0.80, P=0.01) and cerebrovascular events (HR 0.21, 95%CI 0.06-0.78, P=0.02).Conclusion:SpA is an independent CVS risk factor. Anti-TNF drugs were associated with a reduced CVS risk in these patients.References:[1]Crowson CS, Liao KP, Davis JM, 3rd, Solomon DH, Matteson EL, Knutson KL, et al. Rheumatoid arthritis and cardiovascular disease. Am Heart J. 2013;166(4):622-8 e1.[2]Verhoeven F, Prati C, Demougeot C, Wendling D. Cardiovascular risk in psoriatic arthritis, a narrative review. Joint Bone Spine. 2020;87(5):413-8.[3]Liew JW, Ramiro S, Gensler LS. Cardiovascular morbidity and mortality in ankylosing spondylitis and psoriatic arthritis. Best Pract Res Clin Rheumatol. 2018;32(3):369-89.[4]Molto A, Etcheto A, van der Heijde D, Landewe R, van den Bosch F, Bautista Molano W, et al. Prevalence of comorbidities and evaluation of their screening in spondyloarthritis: results of the international cross-sectional ASAS-COMOSPA study. Ann Rheum Dis. 2016;75(6):1016-23.Disclosure of Interests:None declared.


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