scholarly journals Silent Brain MRI Infarcts and Subsequent Stroke Type In the Cardiovascular health Study

Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 363-363
Author(s):  
Charles B Bernick ◽  
Lewis H Kuller ◽  
Will T Longstreth ◽  
Corinne Dulberg ◽  
Teri A Manolio ◽  
...  

P136 Objective: Silent infarcts seen on cranial MRI scans are a risk factor for subsequent clinical stroke in the elderly. This study examines the type of clinical strokes seen in those with silent infarcts. Methods: Cranial MRI examination was completed on 3324 Cardiovascular Health Study (CHS) participants aged 65+ who were without a prior history of clinical stroke. Incident strokes were identified over an average follow-up of 4 years and classified as hemorrhagic or ischemic. Ischemic strokes were further subdivided into lacunar, cardioembolic, atherosclerotic or other/unknown. Results: Silent MRI infarcts >3mm were found in approximately 28% (n=923). Of these, 7% (n=67) subsequently had a clinically evident stroke. The characteristics of the silent MRI infarcts in those who sustained an incident stroke were as folows: 56 had only subcortical infarcts, of which 55 were <20mm; 4 had only cortical infarcts; and 7 had both cortical and subcortical infarcts. Of those with only subcortical silent MRI infarcts, 16% (n=9) went on to a hemorrhagic stroke and 84% (n=47) sustained an ischemic stroke. The ischemic strokes were subtyped as 12 cardioembolic, 3 lacunar, 2 atherosclerotic and 30 unknown/other. Considering only those with cortical silent infarcts, either alone or in combination with subcortical infarcts, there was 1 hemorrhagic stroke and 10 ischemic strokes. Half of the ischemic strokes were cardioembolic and half were unknown type. Conclusion: Elderly individuals with silent subcortical infarcts who go onto subsequent stroke may be at risk not only for lacunar infarcts but also cardioembolic or hemorrhagic strokes.

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Dean Shibata ◽  
Therese Tillin ◽  
Norman Beauchamp ◽  
John Heasman ◽  
Wadyslaw Gedroyc ◽  
...  

Introduction: Stroke mortality is doubled in people of Black African descent compared with Whites, but factors responsible for this excess are unclear. We wished to compare infarct like lesions (ILL) on MRI by ethnicity and the role of risk factors. Methods: SABRE is a UK community based multi-ethnic cohort of men and women aged 40-69 years at baseline (1988-1990), and 58-86 years at follow up (2008-2011). At follow up, a questionnaire was completed and investigations performed including resting and ambulatory BP, anthropometry, and bloods for glucose and lipids. Cerebral MRI scans were scored for infarcts independently by two readers according to the Cardiovascular Health Study protocol. Results: Of 2346 Whites, 684 attended follow up, and 590 completed cerebral MRI. Of 801 Blacks (first generation migrants of Black African descent to the UK), 232 attended clinic and 207 completed MRI. Mortality loss was greater in Whites (605, 25%) than Blacks (121, 15%)(p<0.0001), although stroke was more likely the underlying cause in Blacks (23, 19%), than Whites (43, 7%)(p<0.0001) . Baseline systolic/diastolic BP was similarly higher in Blacks than Whites in attendees (8/5 mmHg), non-responders (7/6 mm Hg), and those who died (8/5 mmHg). At follow up stroke risk factors were adverse in Blacks, apart from smoking ( table ). Prevalence of ILL was similar by ethnicity, not differing when those <65 years were analysed separately, or when those with stroke/TIA history were excluded. Associations between ILL and risk factors did not differ by ethnicity. But prescribed treatment in those with elevated clinic BP (≥140 mmHg systolic, or ≥90 mmHg diastolic) was 83% in Blacks, 63% in Whites (p<0.0001). Further, in those with an ILL, 95% of Blacks, and 69% (p<0.0001) of Whites were on treatment. Conclusion: Equivalence of ILL rates in Blacks and Whites was unanticipated, given the greater stroke mortality in Blacks. Mitigating against selective mortality as the explanation of our findings is the similar ethnic differential in baseline BP in survivors and non-survivors, the lower overall mortality in Blacks, and overall small numbers of stroke deaths. A more likely explanation is that better targeted more aggressive treatment is now occurring in Blacks than Whites, reducing their potential burden of ILL.


Neurology ◽  
2018 ◽  
Vol 91 (13) ◽  
pp. e1237-e1244 ◽  
Author(s):  
Shadi Yaghi ◽  
Traci M. Bartz ◽  
Richard Kronmal ◽  
Hooman Kamel ◽  
John Gottdiener ◽  
...  

ObjectiveTo determine the association left atrial diameter (LAD) and vascular brain injury on brain MRI.MethodsWe analyzed data from the Cardiovascular Health Study (CHS), a prospective cohort of community-dwelling adults ≥65 years old. LAD was measured from 2-dimensional transthoracic echocardiograms. Among CHS participants who underwent brain MRI, we examined associations of LAD with brain infarcts and leukoaraiosis. Primary outcomes (number for analysis) were prevalent infarcts (2,327) and degree of leukoaraiosis on initial MRI (2,315). Secondary outcomes were prevalent nonlacunar infarcts (2,327), incident infarcts (939), incident nonlacunar infarcts (1,185), and degree of leukoaraiosis on follow-up MRI adjusted for initial MRI (1,158). Relative risk (RR) and linear regression models were adjusted for demographics, vascular risk factors, and potential confounders.ResultsMean age of the 2,335 participants with initial brain MRI was 72.0 ± 4.8 years; 38.7% were men; and 29.0% participants had prevalent infarcts. In multivariable, fully adjusted models, LAD was associated with prevalent infarcts (RR 1.20, 95% confidence interval [CI] 1.08–1.34) and prevalent nonlacunar infarcts (RR 1.28, 95% CI 1.06–1.54) but not with leukoaraiosis (−0.08, 95% CI −0.17 to 0.07), incident infarcts (RR 1.00, 95% CI 0.78–1.29), nonlacunar infarcts (RR 0.98, 95% CI 0.67–1.42), or worsening leukoaraiosis (−0.04, 95% CI −0.10 to 0.02).ConclusionLAD is independently associated with prevalent brain infarcts, particularly nonlacunar infarcts, but not leukoaraiosis. Larger studies are needed to determine associations with incident infarct risk and whether this risk in patients with left atrial enlargement can be reduced with anticoagulant agents.


1998 ◽  
Vol 79 (05) ◽  
pp. 912-915 ◽  
Author(s):  
Mary Cushman ◽  
Frits R. Rosendaal ◽  
Bruce M. Psaty ◽  
E. Francis Cook ◽  
J. Valliere ◽  
...  

SummaryCoagulation factor V Leiden is a risk marker for venous thrombosis. For arterial thrombosis no large study to date has included population-based elderly patients. The Cardiovascular Health Study is a longitudinal study of 5,201 men and women over age 65. With 3.4-year follow-up, we studied 373 incident cases of myocardial infarction (MI), angina, stroke, or transient ischemic attack (TIA), and 482 controls. The odds ratios for each event with heterozygous factor V Leiden were: MI, 0.46 (95% CI 0.17 to 1.25); angina, 1.0 (95% CI 0.45 to 2.23); stroke, 0.77 (95% CI 0.35 to 1.70); TIA, 1.33 (95% CI 0.5 to 3.55); any outcome, 0.83 (95% CI 0.48 to 1.44). Adjustment for cardiovascular risk factors did not change relationships. In older adults factor V Leiden is not a risk factor for future arterial thrombosis.


2019 ◽  
Vol 74 (4) ◽  
pp. 501-509 ◽  
Author(s):  
Dominik Steubl ◽  
Petra Buzkova ◽  
Pranav S. Garimella ◽  
Joachim H. Ix ◽  
Prasad Devarajan ◽  
...  

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3448-3448
Author(s):  
Neil A Zakai ◽  
Benjamin French ◽  
Alice Arnold ◽  
Anne Newman ◽  
Linda F. Fried ◽  
...  

Abstract Introduction: Anemia is associated with increased morbidity and mortality in the elderly, though the risk factors for and the consequences of hemoglobin (HGB) decline are poorly characterized. Methods: We studied 5201 men and women ≥65 participating in the Cardiovascular Health Study. The cohort was followed biannually and had baseline and repeat hemograms 3 years later. HGB decline was defined as >1g/dL HGB drop, or incident anemia at 3 years by WHO criteria. Results: 4006 participants survived to 3 years and had two HGB measures. The median HGB change was −0.2g/dL (IQR-0.8, 0.1). 961 (24%) participants had a >1g/dL HGB drop and 335 (8%) developed incident anemia. The left side of the table presents adjusted logistic regression models of baseline risk factors for HGB decline. Those with baseline cardiovascular disease (CVD), diabetes and kidney disease were more likely to develop >1g/dL HGB drop while only baseline kidney disease was associated with incident anemia. The table also shows the adjusted risk of HGB decline with concurrent development of co-morbid conditions. A >1g/dL drop in HGB was more likely in those who concurrently developed incident CVD, hypertension or inflammation. Incident anemia was more likely in participants with concurrent development of kidney disease or inflammation. Both incident anemia and a HGB drop >1g/dL were associated with subsequent 9-year mortality adjusting for age, race, gender, year 3 HGB, hypertension, CVD, diabetes, and renal disease; HRs (95% CI) 1.4 (1.2, 1.6) and 1.2 (1.1, 1.4) respectively. Discussion: Among studied factors, baseline CVD, diabetes and kidney disease were risk factors for >1g/dL HGB drop while only baseline kidney disease was a risk factor for incident anemia. Incident CVD and hypertension were associated concurrently with >1g/dL HGB drop while kidney disease was associated with concurrent incident anemia. Inflammation development was the strongest risk factor accompanying HGB decline. HGB decline, especially a 1g/dL drop, was associated with subsequent mortality irrespective of HGB concentration. These data suggest that small HGB changes not captured by the WHO anemia criteria are associated with poor health outcomes and that inflammation is a major correlate of HGB decline in the elderly. Table: Risk Factors for HGB Decline in Age-, Race-, Gender, and Baseline HGB-Adjusted Logistic Regression Models Baseline Risk Factors for HGB Decline Risk of HGB Decline with Concurrent Conditions HGB Drop >1g/dL Incident Anemia HGB Drop >1g/dL Incident Anemia CVD 1.2 (1.1, 1.4) 1.0 (0.8, 1.3) 1.3 (1.1, 1.6) 1.0 (0.7, 1.3) Hypertension 1.1 (0.99, 1.3) 1.1 (0.8, 1.2) 1.4 (1.1, 1.7) 1.1 (0.8, 1.5) Diabetes 1.3 (1.1, 1.5) 1.1 (0.8, 1.4) 0.9 (0.6, 1.4) 0.8 (0.4, 1.7) Kidney Disease (GFR <60ml/min/1.73m2) 1.2 (1.0, 1.3) 1.3 (1.1, 1.7) 1.1 (0.8, 1.4) 1.5 (1.0, 2.1) Inflammation CRP ≥10mg/dL or WBC≥15×109/mm3 1.0 (0.8, 1.3) 1.3 (0.99 1.8) 2.3 (1.8, 2.8) 2.3 (1.8, 3.0)


2004 ◽  
Vol 13 (2) ◽  
pp. 61-68 ◽  
Author(s):  
Sunil T. Mathew ◽  
John S. Gottdiener ◽  
Dalane Kitzman ◽  
Gerard Aurigemma ◽  
Julius M. Gardin

2010 ◽  
Vol 65A (11) ◽  
pp. 1242-1249 ◽  
Author(s):  
D. B. Welmerink ◽  
W. T. Longstreth ◽  
M. F. Lyles ◽  
A. L. Fitzpatrick

2014 ◽  
Vol 99 (4) ◽  
pp. 1220-1226 ◽  
Author(s):  
Margaret C. Garin ◽  
Alice M. Arnold ◽  
Jennifer S. Lee ◽  
Russell P. Tracy ◽  
Anne R. Cappola

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