Association of Arterial Stiffness with Silent Cerebrovascular Lesions: The Ohasama Study

Abstract

Background: Arterial stiffness is a risk factor for symptomatic stroke, and is associated with symptomatic cerebral infarction and cognitive impairment. Hence, we hypothesized that arterial stiffness would be a significant determinant of silent cerebrovascular lesions. Methods: The subjects were 363 individuals without symptomatic cerebrovascular lesions who had their arterial stiffness assessed by brachial-ankle pulse wave velocity (baPWV) measurement. The subjects were classified into two groups by the presence or absence of lacunar infarcts, as well as into three groups by grade of white matter hyperintensity (WMH). baPWV was compared among these groups. Results: Eighty-six subjects had lacunar infarcts. Of 138 subjects with WMHs, 102 were classified as having grade 1 and 36 as having grade 2 or 3 WMHs. baPWV was significantly higher in subjects with lacunar infarcts than in those without (17.3 ± 0.3 vs. 16.4 ± 0.2 m/s). baPWV tended to increase with higher WMH grade (16.2 ± 0.2, 16.9 ± 0.3, and 17.8 ± 0.5 m/s in grade 0, 1, and 2 or 3, respectively) after adjustments for confounding factors. The adjusted odds ratio (OR) for lacunar infarcts in subjects with middle-tertile baPWV was significantly higher (OR, 2.37; 95% confidence interval, CI, 1.10–5.11) and the OR in subjects with the highest-tertile baPWV tended to be higher (OR 2.26; 95% CI 0.99–5.45) compared with the lowest-tertile baPWV. The adjusted OR for WMH tended to increase with increased baPWV. Conclusions: Arterial stiffness appeared to be associated with the presence of a lacunar infarct and WMH, independently of the risks for other cerebrovascular diseases.

Silent brain infarct is independently associated with arterial stiffness indicated by cardio-ankle vascular index (CAVI)

“…1-14 Risk factors for SVD include age, hypertension, coronary artery calcification and chronic kidney disease. [7][8][9][10][11][12][13][14][15][16] Likewise, white-matter hyperintensities (WMHs) are associated with cognitive impairment, executive function deficits and gait disturbance. [7][8][9][10][11][16][17][18] The etiology of SBI, a cerebral arterial occlusive lesion, is related to mainly arteriolosclerosis such as lipohyalinosis, microatheroma and fibrinoid necrosis, while the etiology of WMHs is related to cerebral disruption of the blood-brain barrier or leakage of plasma due to SVD or cerebral microvascular arteriosclerosis.…”

“…[7][8][9][10][11][16][17][18] The etiology of SBI, a cerebral arterial occlusive lesion, is related to mainly arteriolosclerosis such as lipohyalinosis, microatheroma and fibrinoid necrosis, while the etiology of WMHs is related to cerebral disruption of the blood-brain barrier or leakage of plasma due to SVD or cerebral microvascular arteriosclerosis. [8][9][10][11][12][13] Therefore, both SBI and WMHs may be associated with arterial stiffness.…”

“…8,[19][20][21][22][23][24] Arterial stiffness, as measured by conventional carotidfemoral pulse wave velocity (PWV) measurement, aortic PWV measurement or non-invasive brachial-ankle PWV (baPWV) measurement, is associated with microvascular early atherosclerotic changes and is an independent predictor for cardiovascular events and deaths. [1][2][3]7,13,14,[25][26][27][28][29] Furthermore, baPWV can be used to assess for the presence of SBI and WMHs. 7,13,14,21,30 However, the relationship between SVD and CAVI is not yet clear.…”

“…[1][2][3]7,13,14,[25][26][27][28][29] Furthermore, baPWV can be used to assess for the presence of SBI and WMHs. 7,13,14,21,30 However, the relationship between SVD and CAVI is not yet clear.…”

Physical Activity Correlates with Arterial Stiffness in Community-dwelling Individuals with Stroke

“…9 Among older adults, elevated arterial stiffness was associated with the presence of lacunar infarcts and white matter hyperintensities, which are markers of silent cerebrovascular disease. 10 Carotid-femoral pulse wave velocity (cfPWV), the criterion standard method for measuring arterial stiffness, reflects the pulse wave propagation model within the arterial tree and can be measured noninvasively using mechanotransducers. 11 It is calculated as D(m)/Δt (sec), where Δt is the transit time of pulse waves between the carotid and femoral arteries (D).…”