Silent cerebral infarction as a form of hypertensive target organ damage in the brain.

Abstract

The incidence, number, size, and location of silent cerebral infarction on 0.1 T magnetic resonance imaging was investigated in 66 hypertensive patients (63±9 years old; mean±SD) and 42 age-matched normotensive subjects (61 ±9 years old) to determine the clinical significance of hypertension in silent cerebral infarction. Cerebrovascular risk factors and the severity of hypertensive changes in other major target organs were also investigated. The incidence of silent infarction in hypertensive patients (47%) tended to be higher than that of normotensive subjects (33%) and increased significantly with advancing age. In hypertensive patients, a significantly higher incidence of silent lesions was noted in patients with hypertensive changes in major target organs (72-73% in patients with organ involvement versus 33-39% in those without). The average number of lesions in hypertensive patients was significantly higher than that in normotensive subjects (6.0 versus 2.1), and the lesions in the hypertensive patients were more frequently detected in the brain areas supplied by perforating arteries than those in normotensive subjects (47% versus 24%). These results clearly demonstrate that silent cerebral infarction is frequently seen in Older hypertensive patients, especially when moderate hypertensive changes are noted in major target organs, and suggest that hypertensive arterial changes play a crucial role in the occurrence of silent infarction. {Hypertension 1992^0:816-820)

Associated risk factors for silent cerebral infarcts in sickle cell anemia: low baseline hemoglobin, sex, and relative high systolic blood pressure

“…There was biologic plausibility that relative high SBP was associated with end-organ disease in SCA, including the brain, based on the work of Rodgers et al 14 and others. 13,17 These findings, coupled with strong evidence that elevated SBP measurement was associated with SCI in older adults without SCA, 18,19 provide support for the biologic basis and generalizability of our results.…”

“…There was biologic plausibility that relative high SBP was associated with end-organ disease in SCA, including the brain, based on the work of Rodgers et al 14 and others. 13,17 These findings, coupled with strong evidence that elevated SBP measurement was associated with SCI in older adults without SCA, 18,19 provide support for the biologic basis and generalizability of our results.Our results are different from the largest study to date evaluating risk factors for SCI among participants with SCA. 12 In the CSSCD study, several variables, including seizure history, pain event rate, lower hemoglobin, high WBC, elevated pocked red blood cell counts, and SEN ␤-S globin gene haplotype (a measure of reduced splenic function), were associated in univariate analysis; however, only seizure history, low pain rate, higher WBC, and the presence of a SEN ␤-S globin gene haplotype were associated with risk of SCI in the final multivariable analysis.…”

Low-Density Lipoprotein Subfractions and the Prevalence of Silent Lacunar Infarction in Subjects with Essential Hypertension

“…Toru KATO 1) , Teruo INOUE 1) , Sho-ichi YAMAGISHI 2) , Toshifumi MOROOKA 1) , Takao OKIMOTO 3) , and Koichi NODE 1)…”

Changes in mitochondrial functionality and calcium uptake in hypertensive rats as a function of age

“…A mechanism contributing to maintain high blood pressure during acute hypertension is the increased generation of superoxide (O 2 •− ) in the vessel wall, which leads to vascular injury (Hougaku et al, 1992;Ohtsuki et al, 1995;Halliwell and Gutteridge, 1999). The chronic hypertension selectively causes cell damage and injury in hypertensive-vulnerable organs like brain.…”