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When Does the Heart Become Larger versus Smaller in Old Age?


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Posted 30 November 2022 - 11:22 AM


As you may know, the aging heart often exhibits ventricular hypertrophy, an enlargement and weakening of the muscle. This appears driven in large part by the increased burden of cellular senescence in later life, given reversal of hypertrophy observed after senolytic treatment in old animals. This hypertrophy can also be thought as a downstream consequence of hypertension, but biology is rarely so simple as to have a single line of cause and effect. As noted in this paper, people lose muscle mass and strength with age, leading to the weakness and frailty of sarcopenia. The heart is a muscle, and a shrinking of that muscle is observed in sarcopenia patients, a condition here termed cardiosarcopenia. So does the heart become larger or smaller with age? That appears to vary from individual to individual, implying interactions between, or common mechanisms affecting, the state of skeletal muscle and heart muscle.

The traditional view of cardiovascular aging is that of age-related adaptations in the heart characterized by increased left ventricular (LV) mass (LVM) and LV hypertrophy (LVH), which are often secondary to increased systolic blood pressure mainly mediated by arterial stiffening. Yet skeletal muscle sarcopenia occurs with aging but may be accelerated in heart failure states. In advanced stages of heart failure, skeletal muscle wasting accompanied by severe exercise intolerance have long been observed in various cohorts.

To date, observations pertaining to the cardiac muscle-skeletal muscle axis among non-heart failure cohorts have provided useful insights. In a population-based cohort of older Asian subjects without clinical cardiovascular disease, skeletal muscle mass was associated with left ventricular mass, independent of age, diabetes mellitus status, and body size. In a selected cohort of frail sarcopenic older European subjects without severe cardiovascular disease (some had mild cardiovascular disease), appendicular lean mass was strongly associated with LVM and cardiac output.

Although advanced age was associated with loss of skeletal muscle mass, the relationship between LVM and skeletal muscle mass appears to be independent of age. Among 228 community adults aged 65-91 years, individuals with low skeletal muscle mass had lower LVM than those without low skeletal mass, without significant interaction between age and LVM. These observations are hypothesis-generating for possible age-related yet age-independent processes that mediate the cardiac and skeletal muscle systems in older persons.

The observations seem to run counter to the dogma of aging-associated LVH, especially in the context of hypertension which dominates aging. Traditionally, cardiac aging has been associated with increased LV wall thickness, with or without myocyte hypertrophy. High LVM, and not low LVM, has been deemed to be clinically unfavorable. The purpose of this perspective is to summarize the background for this syndrome of concern of low LVM, review the body of work generated by various human aging cohorts, and to explore future directions and opportunities for understanding this syndrome.

Link: https://doi.org/10.3...ed.2022.1027466


View the full article at FightAging




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