Cardiovascular diseases increase dramatically with age in both men and women. While it is clear that advanced age allows more time for individuals to be exposed to risk factors in general, there is strong evidence that age itself is a major independent risk factor for cardiovascular disease. Indeed, there are distinct age-dependent cellular, structural, and functional changes in both the heart and blood vessels, even in individuals with no clinical evidence of cardiovascular disease. Studies in older humans and in animal models of aging indicate that this age-related remodeling is maladaptive. An emerging view is that the heart and blood vessels accumulate cellular and subcellular deficits with age and these deficits increase susceptibility to disease in older individuals. Aspects of this age-dependent remodeling of the heart and blood vessels differ between the sexes. There is also new evidence that these maladaptive changes are more prominent in older animals and humans with a high degree of frailty. These observations may help explain why men and women are susceptible to different cardiovascular diseases as they age and why frail older adults are most often affected by these diseases.
Keywords: Age; Aging; Animal models; Cardiovascular disease; Female; Fibrosis; Frailty; Frailty index; Gender; Heart; Heart failure; Hypertrophy; Male; Myocytes; Pathology; Physiology; Sex differences.