Association of Central Systolic Blood Pressure With Intracerebral Small Vessel Disease in Japanese

Ochi, Namiko; Kohara, Katsuhiko; Tabara, Yasuharu; Nagai, Takayuki; Kido, Tomoko; Uetani, Eri; Ochi, Masayuki; Igase, Michiya; Miki, Tetsuro

doi:10.1038/ajh.2010.60

Cited by 53 publications

(55 citation statements)

References 29 publications

(43 reference statements)

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“…19,28,[30][31][32] Our results lend further support to an association of large-artery stiffness with WMH burden, and extend the findings to markers of carotid stiffness, additionally demonstrating that this association is at least in part independent of carotid atherosclerosis. Markers of carotid stiffness were not associated with LIs in our sample, suggesting that carotid stiffness may have an important role in chronic hypoperfusion but not complete infarction in the territory of small arteries.…”

Section: Methods Population and Study Design The 3c-dijonsupporting

confidence: 68%

“…The relationship of pulse wave velocity, a marker of aortic stiffness, with MRI markers of ischemic brain injury was recently assessed, in relatively small samples. 19,[28][29][30][31][32] After accounting for vascular risk factors, pulse wave velocity was consistently associated with WMH burden, [30][31][32] Abbreviations: CCA-IMT 5 common carotid artery intima-media thickness; CI 5 confidence interval; L-WMHV 5 large white matter hyperintensity volume (age-specific top quartile); OR 5 odds ratio (per SD increase); SE 5 standard error; SVD 5 small-vessel disease; WMHV 5 white matter hyperintensity volume. a Log-transformed ratio of WMHV over total white matter volume.…”

Section: Methods Population and Study Design The 3c-dijonmentioning

confidence: 99%

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Large-vessel correlates of cerebral small-vessel disease

et al. 2013

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Objective: Our aim was to investigate the relationship of carotid structure and function with MRI markers of cerebral ischemic small-vessel disease.Methods: The study comprised 1,800 participants (aged 72.5 6 4.1 years, 59.4% women) from the 3C-Dijon Study, a population-based, prospective cohort study, who had undergone quantitative brain MRI and carotid ultrasound. We used multivariable logistic and linear regression adjusted for age, sex, and vascular risk factors.Results: Presence of carotid plaque and increasing carotid lumen diameter (but not common carotid artery intima-media thickness) were associated with higher prevalence of lacunar infarcts: odds ratio ( Conclusions: In addition to and independently of carotid plaque, increasing carotid lumen diameter and markers of carotid stiffness were associated with increasing prevalence of lacunar infarcts and increasing WMHV, respectively. Neurology â 2013;80:662-669 GLOSSARY BI 5 brain infarct; CCA 5 common carotid artery; CI 5 confidence interval; IMT 5 intima-media thickness; LI 5 lacunar infarct; L-WMHV 5 large white matter hyperintensity volume; OR 5 odds ratio; SVD 5 small-vessel disease; WMH 5 white matter hyperintensity; WMHV 5 white matter hyperintensity volume.Brain imaging studies have shown that the impact of ischemic brain injury, a major cause of disability, dementia, and mortality in adults, 1 extends much beyond that of acute clinical events such as stroke. Vascular lesions, including MRI-defined brain infarcts (BIs) and white matter hyperintensities (WMH), are frequently observed in older community-dwelling individuals. The prevalence of BIs ranges between 8% and 28% 2,3

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Section: Methods Population and Study Design The 3c-dijonsupporting

confidence: 68%

Section: Methods Population and Study Design The 3c-dijonmentioning

confidence: 99%

Large-vessel correlates of cerebral small-vessel disease

et al. 2013

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“…35 Finally, other factors may also be associated with SBI and WMHs, including central systolic blood pressure, chronic kidney disease and cerebral microbleeds. 2, 10,11,15,17,25,30 Further research is needed to validate an appropriate stroke prevention strategy for patients with both SBI and WMHs.…”

Section: Arterial Stiffness and Silent Brain Infarct N Saji Et Almentioning

confidence: 99%

“…[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.…”

mentioning

confidence: 99%

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

et al. 2012

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It is still unclear whether silent brain infarct (SBI) and white-matter hyperintensities (WMHs) on magnetic resonance imaging (MRI) scans are associated with cardio-ankle vascular index (CAVI), a novel parameter of arterial stiffness. We studied 220 consecutive patients (mean age, 69 years) without a history of stroke or transient ischemic attack. Patients were assessed for the presence of SBI, WMHs and risk factors. Arterial stiffness was evaluated using CAVI. Patients were categorized into one of two groups according to the presence or absence of SBI and WMHs, and clinical characteristics were compared between the two groups. CAVI was significantly higher in patients with SBI or in patients with WMHs than in those without those respective findings. The CAVI cutoff values for detection of SBI and WMHs were 9.2 and 8.9, respectively. On multivariable analyses, CAVI, a one point increase in CAVI: odds ratio (OR), 1.25; 95% confidence interval (CI), 1.01-1.56; CAVIX9.2: OR, 2.34; 95% CI, 1.16-5.02, was independently associated with SBI, however, CAVI was not independently associated with WMHs. Patients with CAVI X9.2 had higher OR for the presence of both SBI and WMHs (OR, 2.57; 95% CI, 1.15-5.98) when compared with patients with CAVI o9.2 after adjustment for age and sex. SBI is independently associated with arterial stiffness indicated by CAVI.

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“…Currently available data do support this assumption. The central blood pressure has been shown to be associated with cerebral lacunar infarction (Ochi et al 2010), which occurs frequently in the areas of blood supply governed by the perforating arteries. Likewise, the central pressure is associated with white matter hyperintensity lesions (seen on brain MRI), which are manifestations of cerebral microvascular damage, and this association is stronger than that with the brachial pressure (Shrestha et al 2009).…”

Section: Central Hemodynamics and Brainmentioning

confidence: 99%

Central Hemodynamics and Target Organ Damage in Hypertension

Hashimoto

2014

Tohoku J. Exp. Med.

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Recent advances in technology have enabled the noninvasive evaluation of pulsatile hemodynamics in the central aorta; namely, central pressure and flow measurements. The central blood pressure represents the true load imposed on the heart, kidney and brain, and the central blood flow influences the local flow into these vital organs. An elevation of the central blood pressure has a direct, adverse impact on the target organ and, thus, the cardiovascular prognosis in patients with hypertension. A decrease in the central blood flow can cause organ dysfunction and failure. The central pressure and flow dynamics were conventionally regarded as unidirectional from the heart to the periphery. However, current evidence suggests that it should be recognized as a bidirectional interplay between the central and peripheral arteries. Specifically, the pressure pulse wave is not only transmitted forward to the periphery but also reflected backward to the central aorta. The flow pulse wave is also composed of the forward and reverse components. Aortic stiffening and arteriolar remodeling due to hypertension not only augment the central pressure by increasing the wave reflection but also may alter the central bidirectional flow, inducing hemodynamic damage/dysfunction in susceptible organs. Therefore, central hemodynamic monitoring has the potential to provide a diagnostic and therapeutic basis for preventing systemic target organ damage and for offering personalized therapy suitable for the arterial properties in each patient with hypertension. This brief review will summarize hypothetical mechanisms for the association between the central hemodynamics and hypertensive organ damage in the heart, kidney and brain.

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Association of Central Systolic Blood Pressure With Intracerebral Small Vessel Disease in Japanese

Abstract: These findings indicate that the SBP2, an estimate of central SBP, is significantly associated with the presence of SVD in an apparently healthy general population.

Cited by 53 publications

References 29 publications

Large-vessel correlates of cerebral small-vessel disease

Large-vessel correlates of cerebral small-vessel disease

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

Central Hemodynamics and Target Organ Damage in Hypertension

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