Associations Between Vascular Risk Factor Levels and Cognitive Decline Among Stroke Survivors

被引:11
|
作者
Levine, Deborah A. [1 ,2 ,3 ,4 ]
Chen, Bingxin [5 ]
Galecki, Andrzej T. [1 ,2 ,8 ]
Gross, Alden L. [6 ]
Briceno, Emily M. [1 ,2 ,7 ]
Whitney, Rachael T. [1 ,2 ]
Ploutz-Snyder, Robert J. [5 ]
Giordani, Bruno J. [9 ,10 ]
Sussman, Jeremy B. [1 ,2 ,4 ,11 ]
Burke, James F. [12 ]
Lazar, Ronald M. [13 ,14 ]
Howard, Virginia J. [15 ]
Aparicio, Hugo J. [16 ,17 ]
Beiser, Alexa S. [16 ,17 ,18 ]
Elkind, Mitchell S. V. [19 ,20 ]
Gottesman, Rebecca F. [21 ]
Koton, Silvia [6 ,22 ]
Pendlebury, Sarah T. [23 ,26 ,27 ]
Sharma, Anu [1 ,2 ]
Springer, Mellanie V. [3 ,4 ]
Seshadri, Sudha [17 ,24 ,25 ]
Romero, Jose R. [16 ,17 ]
Hayward, Rodney A. [1 ,2 ,4 ,11 ]
机构
[1] Univ Michigan, Dept Internal Med, Ann Arbor, MI USA
[2] Univ Michigan, Cognit Hlth Serv Res Program, Ann Arbor, MI USA
[3] Univ Michigan, Dept Neurol & Stroke Program, Ann Arbor, MI USA
[4] Univ Michigan, Inst Healthcare Policy & Innovat, Ann Arbor, MI USA
[5] Univ Michigan, Dept Nursing, Ann Arbor, MI USA
[6] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA
[7] Univ Michigan, Dept Phys Med & Rehabil, Ann Arbor, MI USA
[8] Univ Michigan, Dept Biostat, Ann Arbor, MI USA
[9] Univ Michigan, Dept Psychiat, Ann Arbor, MI USA
[10] Univ Michigan, Michigan Alzheimers Dis Ctr, Ann Arbor, MI USA
[11] VA Ann Arbor Healthcare Syst, Ann Arbor, MI USA
[12] Ohio State Univ, Dept Neurol, Coll Med, Columbus, OH USA
[13] Univ Alabama Birmingham, Dept Neurol, Birmingham, AL USA
[14] Univ Alabama Birmingham, Evelyn F McKnight Brain Inst, Heersink Sch Med, Birmingham, AL USA
[15] Univ Alabama Birmingham, Dept Epidemiol, Sch Publ Hlth, Birmingham, AL USA
[16] Boston Univ, Dept Neurol, Sch Med, Boston, MA USA
[17] Natl Heart Lung & Blood Inst, Framingham Heart Study, Framingham, MA USA
[18] Boston Univ, Dept Biostat, Sch Publ Hlth, Boston, MA USA
[19] Columbia Univ, Dept Neurol, Vagelos Coll Phys & Surg, New York, NY USA
[20] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA
[21] Natl Inst Neurol Disorders & Stroke, Stroke Branch, Bethesda, MD USA
[22] Tel Aviv Univ, Stanley Steyer Sch Hlth Profess, Dept Nursing, Tel Aviv, Israel
[23] Univ Oxford, Nuffield Dept Clin Neurosci, Wolfson Ctr Prevent Stroke & Dementia, Oxford, England
[24] Univ Texas San Antonio, Dept Neurol, San Antonio, TX USA
[25] Univ Texas San Antonio, Glenn Biggs Inst Alzheimers & Neurodegenerat Dis, Joe R & Teresa Lozano Long Sch Med, San Antonio, TX USA
[26] Oxford Univ Hosp NHS Fdn Trust, NIHR Biomed Res Ctr, Dept Med, Oxford, England
[27] Oxford Univ Hosp NHS Fdn Trust, NIHR Biomed Res Ctr, Dept Geratol, Oxford, England
基金
美国国家卫生研究院;
关键词
TRANSIENT ISCHEMIC ATTACK; DENSITY-LIPOPROTEIN-CHOLESTEROL; BLOOD-PRESSURE; CLINICAL DETERMINANTS; RACIAL-DIFFERENCES; DEMENTIA; IMPAIRMENT; PREVALENCE; HARMONIZATION; PREVENTION;
D O I
10.1001/jamanetworkopen.2023.13879
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
IMPORTANCE Incident stroke is associated with accelerated cognitive decline. Whether poststroke vascular risk factor levels are associated with faster cognitive decline is uncertain. OBJECTIVE To evaluate associations of poststroke systolic blood pressure (SBP), glucose, and low-density lipoprotein (LDL) cholesterol levels with cognitive decline. DESIGN, SETTING, AND PARTICIPANTS Individual participant data meta-analysis of 4 US cohort studies (conducted 1971-2019). Linear mixed-effects models estimated changes in cognition after incident stroke. Median (IQR) follow-up was 4.7 (2.6-7.9) years. Analysis began August 2021 and was completed March 2023. EXPOSURES Time-dependent cumulative mean poststroke SBP, glucose, and LDL cholesterol levels. MAIN OUTCOMES AND MEASURES The primary outcome was change in global cognition. Secondary outcomes were change in executive function and memory. Outcomes were standardized as t scores (mean [SD], 50 [10]); a 1-point difference represents a 0.1-SD difference in cognition. RESULTS A total of 1120 eligible dementia-free individuals with incident stroke were identified; 982 (87.7%) had available covariate data and 138 (12.3%) were excluded for missing covariate data. Of the 982, 480 (48.9%) were female individuals, and 289 (29.4%) were Black individuals. The median age at incident stroke was 74.6 (IQR, 69.1-79.8; range, 44.1-96.4) years. Cumulative mean poststroke SBP and LDL cholesterol levels were not associated with any cognitive outcome. However, after accounting for cumulative mean poststroke SBP and LDL cholesterol levels, higher cumulative mean poststroke glucose level was associated with faster decline in global cognition (-0.04 points/y faster per each 10-mg/dL increase [95% CI, -0.08 to -0.001 points/y]; P=.046) but not executive function or memory. After restricting to 798 participants with apolipoprotein E4 (APOE4) data and controlling for APOE4 and APOE4 x time, higher cumulative mean poststroke glucose level was associated with a faster decline in global cognition in models without and with adjustment for cumulative mean poststroke SBP and LDL cholesterol levels (-0.05 points/y faster per 10-mg/dL increase [95% CI, -0.09 to -0.01 points/y]; P=.01; -0.07 points/y faster per 10-mg/dL increase [95% CI, -0.11 to -0.03 points/y]; P=.002) but not executive function or memory declines. CONCLUSIONS AND RELEVANCE In this cohort study, higher poststroke glucose levels were associated with faster global cognitive decline. We found no evidence that poststroke LDL cholesterol and SBP levels were associated with cognitive decline.
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页数:17
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