title: Pathophysiology and end-organ damage in elderly hypertensives.
abstract: PATHOPHYSIOLOGY OF HYPERTENSION: Blood pressure increases with advancing age in most developed countries. The pathophysiology of elderly hypertension is characterized by changes in the structure and function of the cardiovascular system. Changes in arterial structure lead to a decrease in aortic compliance, which augments the aortic pressure component generated by the wave reflection mechanism. The age-related increase in the reflected-wave component of arterial pressure may contribute, at least in part, to the age-related rise in systolic blood pressure. Disproportionately elevated systolic blood pressure in the elderly may account for the progressive increase in left ventricular mass with advancing age. In addition to the changes in vascular and cardiac structures, the haemodynamic function of elderly hypertensives is characterized by increased peripheral resistance as well as reduced cardiac output, renal blood flow and intravascular volume. In contrast to younger hypertensives, the sympathetic and renin-angiotensin systems may not be major factors in the genesis of high peripheral resistance in this patient group. END-ORGAN DAMAGE: The most important end-organ damage in elderly hypertensives is left ventricular hypertrophy with or without coronary heart disease, cerebrovascular disease or renal impairment. Furthermore, this end-organ damage is frequently asymptomatic (silent). The prevalence of silent cerebrovascular disease in particular is surprisingly high in this elderly population. Asymptomatic cerebrovascular disease has been shown to be associated with various cardiovascular risk factors, and depressed neurobehavioural function. Diurnal blood pressure variations appear to be related to end-organ damage. The presence of occult end-organ damage and co-existing diseases common in elderly hypertensives has important clinical implications in the management of this disorder.
authors.affiliation: Department of Cardiology, Jichi Medical School, Tochigi, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Shimada
authors.forename: H
authors.initials: H
authors.lastname: Miyashita
authors.forename: A
authors.initials: A
authors.lastname: Kawamoto
authors.forename: K
authors.initials: K
authors.lastname: Matsubayashi
authors.forename: M
authors.initials: M
authors.lastname: Nishinaga
authors.forename: S
authors.initials: S
authors.lastname: Kimura
authors.forename: T
authors.initials: T
authors.lastname: Ozawa
mesh_terms: D000368:Aged; D000375:Aging / Q000502:physiology*; D001794:Blood Pressure; D002561:Cerebrovascular Disorders / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D008875:Middle Aged; D011379:Prognosis