Shifting the paradigm from stroke to global vascular risk estimation

被引:19
作者
Sacco, Ralph L. [1 ]
机构
[1] Univ Miami, Miller Sch Med, Dept Neurol, Miami, FL 33136 USA
关键词
cerebrovascular disease; epidemiology; prevention; risk factors;
D O I
10.1161/STROKEAHA.106.481143
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
By the year 2010, it is estimated that 18.1 million people worldwide will die annually because of cardiovascular diseases and stroke. "Global vascular risk" more broadly includes the multiple overlapping disease silos of stroke, myocardial infarction, peripheral arterial disease, and vascular death. Estimation of global vascular risk requires consideration of a variety of variables including demographics, environmental behaviors, and risk factors. Data from multiple studies suggest continuous linear relationships between the physiological vascular risk modulators of blood pressure, lipids, and blood glucose rather than treating these conditions as categorical risk factors. Constellations of risk factors may be more relevant than individual categorical components. Exciting work with novel risk factors may also have predictive value in estimates of global vascular risk. Advances in imaging have led to the measurement of subclinical conditions such as carotid intima-media thickness and subclinical brain conditions such as white matter hyperintensities and silent infarcts. These subclinical measurements may be intermediate stages in the transition from asymptomatic to symptomatic vascular events, appear to be associated with the fundamental vascular risk factors, and represent opportunities to more precisely quantitate disease progression. The expansion of studies in molecular epidemiology and detection of genetic markers underlying vascular risks also promises to extend our precision of global vascular risk estimation. Global vascular risk estimation will require quantitative methods that bundle these multi-dimensional data into more precise estimates of future risk. The power of genetic information coupled with data on demographics, risk-inducing behaviors, vascular risk modulators, biomarkers, and measures of subclinical conditions should provide the most realistic approximation of an individual's future global vascular risk. The ultimate public health benefit, however, will depend on not only identification of global vascular risk but also the realization that we can modify this risk and prove the prediction models wrong.
引用
收藏
页码:1980 / 1987
页数:8
相关论文
共 33 条
[1]  
[Anonymous], 2004, ATLAS HEART DIS STRO
[2]  
Boden-Albala B, 2004, STROKE, V35, P243
[3]   The effect of including C-reactive protein in cardiovascular risk prediction models for women [J].
Cook, Nancy R. ;
Buring, Julie E. ;
Ridker, Paul M. .
ANNALS OF INTERNAL MEDICINE, 2006, 145 (01) :21-29
[4]   Interleukin-2 levels are associated with carotid artery intima-media thickness [J].
Elkind, MS ;
Rundek, T ;
Sciacca, RR ;
Ramas, R ;
Chen, HJ ;
Boden-Albala, B ;
LeRoy, R ;
Sacco, RL .
ATHEROSCLEROSIS, 2005, 180 (01) :181-187
[5]   Tumor necrosis factor receptor levels are associated with carotid atherosclerosis [J].
Elkind, MS ;
Cheng, JF ;
Boden-Albala, B ;
Rundek, T ;
Thomas, J ;
Chen, H ;
Rabbani, LE ;
Sacco, RL .
STROKE, 2002, 33 (01) :31-37
[6]   Moderate alcohol consumption reduces risk of ischemic stroke - The Northern Manhattan Study [J].
Elkind, MSV ;
Sciacca, R ;
Boden-Albala, B ;
Rundek, T ;
Paik, MC ;
Sacco, RL .
STROKE, 2006, 37 (01) :13-19
[7]   Implications of stroke prevention trials - Treatment of global risk [J].
Elkind, MSV .
NEUROLOGY, 2005, 65 (01) :17-21
[8]   Relative elevation in baseline leukocyte count predicts first cerebral infarction [J].
Elkind, MSV ;
Sciacca, RR ;
Boden-Albala, B ;
Rundek, T ;
Paik, MC ;
Sacco, RL .
NEUROLOGY, 2005, 64 (12) :2121-2125
[9]   Preventing cancer, cardiovascular disease, and diabetes - A common agenda for the American Cancer Society, the American Diabetes Association, and the American Heart Association [J].
Eyre, H ;
Kahn, R ;
Robertson, RM .
STROKE, 2004, 35 (08) :1999-2010
[10]  
Goldstein LB, 2006, STROKE, V37, P1583, DOI 10.1161/01.STR.0000223048.70103.F1