There are number of changes
were occur with time with leads to the cardiac output.
- Structural
changes: Substantial structural change in the heart and
vasculature; e.g. vascular stiffening, increased left ventricular
wall thickness (within normal limits) and fibrosis with aging,
leading to diastolic dysfunction, increased afterload, and HF with
preserved ejection fraction. These are described individually in
the Cardiac structural and Vascular
structuralsections below.
- Functional
changes: There are a number of functional changes and
compensatory responses that the aged heart undergoes that diminish
its ability to respond to increased workload and decrease its
reserve capacity. Changes in maximal heart rate, end-systolic
volume (ESV), end-diastolic volume (EDV), contractility, prolonged
systolic contraction, prolonged diastolic relaxation, sympathetic
signaling, etc. These are described individually in the Cardiac
functional, Vascular functional, and Arterial-Ventricular
interaction sections below.
- Cardioprotection and Repair
Processes: The cardiac mechanisms responsible for
protection from injury and injury repair become increasingly
defective with age, leading to accentuated adverse remodeling and
increased dysfunction.
- Increased cardiovascular
disease incidence and prevalence: There is a progressive
increase in the prevalence of cardiovascular disease (CVD); e.g.
coronary artery disease (CAD), hypertension, and diabetes leading
to the development of ischemic, hypertensive, or diabetic
cardiomyopathy. The reader is referred to any number of
epidemiologic studies for evidence of this fact.
- Systemic disease/Other
organ systems: Aging-associated changes in other organ
systems may affect cardiac structure-function and thereby
contribute to HF development. This facet, however, is beyond the
scope of the current review.