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[Heart aging and its clinical implications]
P Carbonin1, A Cocchi, G Zuccalà
1Cattedra di Gerontologia, Università Cattolica del Sacro Cuore, Roma.
Insights
The aging heart undergoes structural changes like hypertrophy and fibrosis, maintaining function through compensatory mechanisms. Despite reduced mitochondrial function and altered ionic fluxes, maximal oxygen consumption declines without apparent cardiac impairment.
Area of Science:
- Cardiovascular Physiology
- Gerontology
- Cardiac Pathophysiology
Context:
- Aging leads to significant cardiac structural and functional alterations, often mimicking chronic pathologies.
- Key changes include myocyte hypertrophy, increased collagen, and fat accumulation, increasing heart weight.
- Valvular, arterial, and interstitial cardiac tissues exhibit regressive modifications with age.
Purpose:
- To elucidate the structural and functional adaptations of the aging heart.
- To compare age-related cardiac changes with those seen in chronic diseases.
- To investigate the functional consequences of aging on cardiac performance and oxygen consumption.
Summary:
- The aging heart shows increased weight due to myocyte hypertrophy, fibrosis, and fat accumulation.
- Structural changes affect valves, coronary arteries, and interstitium (lipofuscins, amyloid deposits).
- Functional maintenance during exercise relies on increased end-diastolic volume rather than enhanced chronotropic/inotropic responses, potentially due to damped beta-receptor sensitivity.
Impact:
- Understanding age-related cardiac changes is crucial for differentiating normal aging from disease states.
- Identifies compensatory mechanisms in the aging heart, such as increased end-diastolic volume during exercise.
- Highlights age-related declines in mitochondrial function and altered ionic fluxes, impacting overall cardiovascular health.
Abstract:
Aging-induced cardiac modifications are almost never different--at least qualitatively--from those linked to chronic pathologies that are usually found in advanced age. Due to many factors, as myocyte hypertrophy, increase in the amount of collagen and subepicardial fat accumulation, the aging heart increases its own weight. All cardiac structures undergo regressive modifications: valvular apparatus show fibrosis, collagen fragmentation, lipid accumulation and calcifications, the coronary arteries are characterized by tortuosity, minimal atherosclerotic lesions, calcium precipitates and--at least in animals--by an imbalance between the capillary bed extension and the myocyte hypertrophy. The most peculiar changes of interstitium, aside from fibrosis, are represented by lipofuscins and amyloid deposits. From a functional point of view, the aging heart does not show any substantial difference from the adult one in the basal state. Cardiac output seems to be maintained during exercise in the elderly. Nevertheless, such a result is achieved by an end-diastolic volume increase, instead of positive chronotropic and inotropic response and to the peripheral resistance decrease of the younger. This could be partly due to a damped cardiovascular response to sympathetic beta-receptor stimulation. The diastolic phase undergoes a progressive dysfunction, as its duration increases, the early filling falls and the atrial contribution plays a major role. The reduction of many mitochondrial enzymatic processes--such as fatty acid oxidation and oxidative phosphorylation--has been documented in animals, as well as transmembrane ionic fluxes alteration. The maximal oxygen consumption is progressively reduced, although this does not seem to be due to a cardiac performance impairment.(ABSTRACT TRUNCATED AT 250 WORDS)