Objectives. Mechanisms influencing the course of physical and mental functioning after an atherosclerotic event are unclear. We examined effects of white matter lesion (WML) activity on changes in functioning in patients with symptomatic atherosclerotic disease. Methods. In 486 patients ( years) of the Second Manifestations of ARTerial disease-Magnetic Resonance (SMART-MR) study, volumetric WML measurements on 1.5T MRI were performed at baseline and years followup. Functioning was assessed with the modified Short-Form 12 (SF-12) questionnaire. Associations of WML progression with changes in functioning were adjusted for age, sex, and vascular risk factors. Results. Physical functioning (baseline: 44, 10th–90th percentile 29–55) improved, whereas mental functioning (baseline: 51, 10th–90th percentile 32–60) declined during followup. WML progression (highest quartile versus rest) contributed to a stronger decline in mental functioning ( , 95% CI ?3.11 to ?0.42), but did not influence changes in physical functioning. Conclusions. Progression of WML volume contributes to a decline in mental functioning in patients with symptomatic atherosclerotic disease. 1. Introduction Ischemic heart disease and stroke are leading causes of disability and mortality worldwide [1]. As a result of improved survival and the lifelong aspect of these diseases, health-related quality of life (HRQoL), including physical and mental functioning, has become an increasingly important clinical and research outcome when evaluating burden of disease and treatment benefits. In addition, reduced physical and mental functioning not only interferes with daily living, but also increases the risk of incident ischemic vascular events and mortality [2–4]. Compared to the general population, HRQoL is substantially lower in patients with ischemic heart disease and stroke, especially in the domain of physical functioning [5–7]. A recent study indicated that HRQoL not only is lower in the acute phase of recovery from stroke, but also can decline up to five years after stroke in survivors free of recurrence or myocardial infarction [8]. Also, marked impairments in HRQoL have been observed in patients with other manifestations of atherosclerotic disease, including peripheral arterial disease [9, 10] and abdominal aortic aneurysm [11, 12]. Patients with symptomatic vascular disease frequently have atherosclerotic changes in the small vasculature in the brain, which are characterized by white matter lesions (WMLs) on magnetic resonance imaging (MRI) [13]. Although WMLs are often asymptomatic, they have
References
[1]
A. D. Lopez and C. D. Mathers, “Measuring the global burden of disease and epidemiological transitions: 2002–2030,” Annals of Tropical Medicine and Parasitology, vol. 100, no. 5-6, pp. 481–499, 2006.
[2]
E. L. Idler and Y. Benyamini, “Self-rated health and mortality: a review of twenty-seven community studies,” Journal of Health and Social Behavior, vol. 38, no. 1, pp. 21–37, 1997.
[3]
P. K. Myint, R. N. Luben, P. G. Surtees et al., “Self-reported mental health-related quality of life and mortality in men and women in the European Prospective Investigation into Cancer (EPIC-Norfolk): a prospective population study,” Psychosomatic Medicine, vol. 69, no. 5, pp. 410–414, 2007.
[4]
P. K. Myint, P. G. Surtees, N. W. J. Wainwright et al., “Physical health-related quality of life predicts stroke in the EPIC-Norfolk,” Neurology, vol. 69, no. 24, pp. 2243–2248, 2007.
[5]
J. Xie, E. Q. Wu, Z. J. Zheng, P. W. Sullivan, L. Zhan, and D. R. Labarthe, “Patient-reported health status in coronary heart disease in the United States: age, sex, racial, and ethnic differences,” Circulation, vol. 118, no. 5, pp. 491–497, 2008.
[6]
J. Xie, E. Q. Wu, Z. J. Zheng et al., “Impact of stroke on health-related quality of life in the noninstitutionalized population in the United States,” Stroke, vol. 37, no. 10, pp. 2567–2572, 2006.
[7]
K. S. Hong, J. L. Saver, D. W. Kang et al., “Years of optimum health lost due to complications after acute ischemic stroke: disability-adjusted life-years analysis,” Stroke, vol. 41, no. 8, pp. 1758–1765, 2010.
[8]
M. S. Dhamoon, Y. P. Moon, M. C. Paik et al., “Quality of life declines after first ischemic stroke: the Northern Manhattan Study,” Neurology, vol. 75, no. 4, pp. 328–334, 2010.
[9]
J. C. Dumville, A. J. Lee, F. B. Smith, and F. G. R. Fowkes, “The health-related quality of life of people with peripheral arterial disease in the community: the Edinburgh Artery Study,” British Journal of General Practice, vol. 54, no. 508, pp. 826–831, 2004.
[10]
D. R. Liles, M. A. Kallen, L. A. Petersen, and R. L. Bush, “Quality of life and peripheral arterial disease,” Journal of Surgical Research, vol. 136, no. 2, pp. 294–301, 2006.
[11]
F. Dick, V. Grobéty, F. F. Immer et al., “Outcome and quality of life in patients treated for abdominal aortic aneurysms: a single center experience,” World Journal of Surgery, vol. 32, no. 6, pp. 987–994, 2008.
[12]
B. Aljabri, K. Al Wahaibi, D. Abner et al., “Patient-reported quality of life after abdominal aortic aneurysm surgery: a prospective comparison of endovascular and open repair,” Journal of Vascular Surgery, vol. 44, no. 6, pp. 1182–e2, 2006.
[13]
M. I. Geerlings, A. P. A. Appelman, K. L. Vincken et al., “Brain volumes and cerebrovascular lesions on MRI in patients with atherosclerotic disease. The SMART-MR study,” Atherosclerosis, vol. 210, no. 1, pp. 130–136, 2010.
[14]
D. Inzitari, G. Pracucci, A. Poggesi et al., “Changes in white matter as determinant of global functional decline in older independent outpatients: three year follow-up of LADIS (leukoaraiosis and disability) study cohort,” BMJ (Clinical research ed.), vol. 339, p. b2477, 2009.
[15]
J. C. De Groot, F. E. De Leeuw, M. Oudkerk, A. Hofman, J. Jolles, and M. M. B. Breteler, “Cerebral white matter lesions and depressive symptoms in elderly adults,” Archives of General Psychiatry, vol. 57, no. 11, pp. 1071–1076, 2000.
[16]
A. Kumar, W. Bilker, Z. Jin, and J. Udupa, “Atrophy and high intensity lesions: complementary neurobiological mechanisms in late-life major depression,” Neuropsychopharmacology, vol. 22, no. 3, pp. 264–274, 2000.
[17]
W. M. van der Flier, E. C. W. van Straaten, F. Barkhof et al., “Small vessel disease and general cognitive function in nondisabled elderly: the LADIS study,” Stroke, vol. 36, no. 10, pp. 2116–2120, 2005.
[18]
T. D. Vannorsdall, S. R. Waldstein, M. Kraut, G. D. Pearlson, and D. J. Schretlen, “White matter abnormalities and cognition in a community sample,” Archives of Clinical Neuropsychology, vol. 24, no. 3, pp. 209–217, 2009.
[19]
N. D. Prins, E. J. van Dijk, T. den Heijer et al., “Cerebral small-vessel disease and decline in information processing speed, executive function and memory,” Brain, vol. 128, no. 9, pp. 2034–2041, 2005.
[20]
O. Godin, C. Dufouil, P. Maillard et al., “White matter lesions as a predictor of depression in the elderly: the 3C-Dijon study,” Biological Psychiatry, vol. 63, no. 7, pp. 663–669, 2008.
[21]
R. D. Nebes, C. F. Reynolds, F. Boada et al., “Longitudinal increase in the volume of white matter hyperintensities in late-onset depression,” International Journal of Geriatric Psychiatry, vol. 17, no. 6, pp. 526–530, 2002.
[22]
P. Anbeek, K. L. Vincken, M. J. P. van Osch, R. H. C. Bisschops, and J. van der Grond, “Probabilistic segmentation of white matter lesions in MR imaging,” NeuroImage, vol. 21, no. 3, pp. 1037–1044, 2004.
[23]
P. Anbeek, K. L. Vincken, G. S. van Bochove, M. J. P. van Osch, and J. van der Grond, “Probabilistic segmentation of brain tissue in MR imaging,” NeuroImage, vol. 27, no. 4, pp. 795–804, 2005.
[24]
J. E. Ware, M. Kosinski, and S. D. Keller, “A 12-item short-form health durvey: construction of scales and preliminary tests of reliability and validity,” Medical Care, vol. 34, no. 3, pp. 220–233, 1996.
[25]
J. E. Ware Jr. and C. D. Sherbourne, “The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection,” Medical Care, vol. 30, no. 6, pp. 473–483, 1992.
[26]
B. Gandek, J. E. Ware, N. K. Aaronson et al., “Cross-validation of item selection and scoring for the SF-12 Health Survey in nine countries: results from the IQOLA Project,” Journal of Clinical Epidemiology, vol. 51, no. 11, pp. 1171–1178, 1998.
[27]
“Second European Consensus document on chronic critical leg ischemia,” Circulation, vol. 84, pp. IV1–IV26, 1991.
[28]
J. C. van Swieten, P. J. Koudstaal, M. C. Visser, H. J. A. Schouten, and J. van Gijn, “Interobserver agreement for the assessment of handicap in stroke patients,” Stroke, vol. 19, no. 5, pp. 604–607, 1988.
[29]
E. C. W. van Straaten, F. Fazekas, E. Rostrup et al., “Impact of white matter hyperintensities scoring method on correlations with clinical data: the LADIS study,” Stroke, vol. 37, no. 3, pp. 836–840, 2006.
[30]
D. M. J. van den Heuvel, V. H. Ten Dam, A. J. M. de Craen et al., “Measuring longitudinal white matter changes: comparison of a visual rating scale with a volumetric measurement,” American Journal of Neuroradiology, vol. 27, no. 4, pp. 875–878, 2006.
[31]
M. Yoshita, E. Fletcher, and C. DeCarli, “Current concepts of analysis of cerebral white matter hyperintensities on magnetic resonance imaging,” Topics in Magnetic Resonance Imaging, vol. 16, no. 6, pp. 399–407, 2005.
[32]
J. E. Ware Jr., B. Gandek, M. Kosinski et al., “The equivalence of SF-36 summary health scores estimated using standard and country-specific algorithms in 10 countries: results from the IQOLA Project,” Journal of Clinical Epidemiology, vol. 51, no. 11, pp. 1167–1170, 1998.
[33]
B. D. Thombs, E. B. Bass, D. E. Ford et al., “Prevalence of depression in survivors of acute myocardial infarction: review of the evidence,” Journal of General Internal Medicine, vol. 21, no. 1, pp. 30–38, 2006.
[34]
M. L. Hackett, C. Yapa, V. Parag, and C. S. Anderson, “Frequency of depression after stroke: a systematic review of observational studies,” Stroke, vol. 36, no. 6, pp. 1330–1340, 2005.
[35]
D. K. Hayes, C. H. Denny, N. L. Keenan, J. B. Croft, and K. J. Greenlund, “Health-related quality of life and hypertension status, awareness, treatment, and control: National Health and Nutrition Examination Survey, 2001–2004,” Journal of Hypertension, vol. 26, no. 4, pp. 641–647, 2008.
[36]
L. H. Kuller, K. L. Margolis, S. A. Gaussoin et al., “Relationship of hypertension, blood pressure, and blood pressure control with white matter abnormalities in the Women's Health Initiative Memory Study (WHIMS)—MRI trial,” Journal of Clinical Hypertension, vol. 12, no. 3, pp. 203–212, 2010.
[37]
E. J. van Dijk, N. D. Prins, H. A. Vrooman, A. Hofman, P. J. Koudstaal, and M. M. B. Breteler, “Progression of cerebral small vessel disease in relation to risk factors and cognitive consequences: rotterdam scan study,” Stroke, vol. 39, no. 10, pp. 2712–2719, 2008.
[38]
B. van Harten, J. M. Oosterman, B. J. Potter Van Loon, P. Scheltens, and H. C. Weinstein, “Brain lesions on MRI in elderly patients with type 2 diabetes mellitus,” European Neurology, vol. 57, no. 2, pp. 70–74, 2007.
[39]
L. Pantoni, “Pathophysiology of age-related cerebral white matter changes,” Cerebrovascular Diseases, vol. 13, no. 2, pp. 7–10, 2002.
[40]
G. S. Alexopoulos, B. S. Meyers, R. C. Young, S. Campbell, D. Silbersweig, and M. Charlson, “‘Vascular depression’ hypothesis,” Archives of General Psychiatry, vol. 54, no. 10, pp. 915–922, 1997.