age-associated changes in cardiovascular function
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Introduction
Cardiovascular function declines with age
Physiology
- decreased inotropic & chronotropic responses
- diminished response to orthostasis
- decreased baroreceptor sensitivity
- diminished beta-adrenergic responsiveness
- stress-induced increase in LV ejection fraction & cardiac index is blunted, but responsive to training
- increased afterload resulting from
- changes in proximal arteries > distal arteries
- elongation & tortuosity of arteries, including aorta
- increased intimal thickening of arteries
- increased fibrosis of media of arteries
- fragmentation of elastin in media
- subendothelial layer thickened with connective tissue
- increased arterial stiffness
- irregularities in endothelial cells
- increased peripheral vascular resistance
- peripheral vasculature constriction is maintained
- diminished peripheral vasculature relaxation
- impaired beta-adenergic mediated vasorelaxation
- vasorelaxation to other vasodilators may be intact
- increased systolic blood pressure
- changes in proximal arteries > distal arteries
- increased afterload results in LV diastolic dysfunction
- increased LV mass
- decreased mycocardial relaxation & compliance
- diminished early diastolic filling
- increased late diastolic filling
- end diastolic volume is decreased
- left atrial hypertrophy
- increased prevalence of S4 reflecting left atrial contraction into a noncompliant left ventricle[7]
- diastolic blood pressure tends to peak in midlife
- increased contraction duration
- reduced myocardial contractility[5]
- decreased heart rate variability
- decreased response to exercise
- decreased maximum heart rate
- refractory to training
- unchanged resting heart rate
- decreased maximum cardiac output
- decreased VO2 max, responsive to training
- diminished coronary blood flow
- diminished peripheral vasodilation
- decreased maximum heart rate
- decreased intrinsic sinus (SA node) rate
- decreased cardiac conduction velocity
- through the AV node
- through the His Bundle & bundle branchers
- increased refractoriness to electrical stimulation
- decreased beta-adrenergic-mediated vasodilation
- alpha-adrenergic-mediated vasoconstriction unchanged
- brain autoregulation of perfusion impaired
- decreased baroreceptor responsiveness
- sclerosis & calcification of heart valves
- increased fibrosis of myocardium
- increased fibrosis of cardiac conduction system
- increased serum ANP
Comparative biology
- GDF11 reverses LV diastolic dysfunction in mice[6]
More general terms
Additional terms
References
- ↑ Essentials of Clinical Geriatrics, 4th ed, Kane RL et al (eds) McGraw Hill, NY, 1999
- ↑ UCLA Intensive Course in Geriatric Medicine & Board Review, Marina Del Ray, CA, Sept 29-Oct 2, 2004
- ↑ The Merck Manual of Geriatrics, 3rdh ed, Merck & Co, Rahway NJ, 2000
- ↑ Taffet GE, Physiology of Aging, In: Geriatric Medicine: An Evidence-Based Approach, 4th ed, Cassel CK et al (eds), Springer-Verlag, New York, 2003
- ↑ 5.0 5.1 Geriatric Review Syllabus, 7th edition Parada JT et al (eds) American Geriatrics Society, 2010
Geriatric Review Syllabus, 8th edition (GRS8) Durso SC and Sullivan GN (eds) American Geriatrics Society, 2013
Geriatric Review Syllabus, 10th edition (GRS10) Harper GM, Lyons WL, Potter JF (eds) American Geriatrics Society, 2019 - ↑ 6.0 6.1 Loffredo FS et al. Growth differentiation factor 11 is a circulating factor that reverses age-related cardiac hypertrophy. Cell 2013 May 9; 153:828 PMID: https://www.ncbi.nlm.nih.gov/pubmed/23663781
- ↑ 7.0 7.1 Kitzman DW, Upadhya B, Taffet GE. Effects of aging on cardiovasculare structure and function: In: Ouslander JG, Studenski S et al eds Hazzard's Geriatric Medicine and Gerontology, 7th ed. McGraw Hill;2017:1129-1144