Research agenda for cardiovascular aging: Humans to molecules

Research output: Contribution to journalArticle

Abstract

Clinical manifestations of specific cardiovascular diseases, e.g., atherosclerosis and hypertension, that lead to heart failure and stroke likely become altered in older persons of advanced age because interactions occur between age-associated cardiovascular changes in health and specific pathophysiologic mechanisms that underlie cardiovascular diseases. The interactions result in a lower threshold for clinical symptoms, and greater severity and poorer prognosis of these diseases in older vs. younger persons. In this regard, cardiovascular changes that occur during aging in health ought not to be considered to reflect a "normal process"; rather these specific age-associated changes must be construed as specific "risk factors" for the aforementioned cardiovascular diseases and ought to become targets of interventions designed to prevent the epidemic of cardiovascular disease in later life. Such a strategy would thus advocate preventive treatment for what is now considered to be "normal cardiovascular aging." Effective and efficient prevention of the "risks" associated with cardiovascular aging in apparent health requires a fundamental understanding of these changes ranging in scope from humans to molecules. An opinion regarding specific directions for research aimed toward the achievement of this understanding is provided.

Original languageEnglish (US)
Pages (from-to)251-262
Number of pages12
JournalAmerican Journal of Geriatric Cardiology
Volume9
Issue number5
StatePublished - 2000
Externally publishedYes

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Cardiovascular Diseases
Research
Health
Atherosclerosis
Heart Failure
Stroke
Hypertension

ASJC Scopus subject areas

  • Gerontology
  • Health Policy
  • Geriatrics and Gerontology
  • Cardiology and Cardiovascular Medicine

Cite this

Research agenda for cardiovascular aging : Humans to molecules. / Lakatta, Edward.

In: American Journal of Geriatric Cardiology, Vol. 9, No. 5, 2000, p. 251-262.

Research output: Contribution to journalArticle

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