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Hypertension and age-related changes in the heart. Implications for drug therapy
1First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Insights
Aging hearts struggle to adapt to stress, with hypertension worsening this decline. Understanding these changes is key to improving cardiovascular health in older adults.
Area of Science:
- Cardiology
- Gerontology
- Molecular Biology
Background:
- Heart disease in the elderly stems from hypertension and atherosclerosis, leading to heart failure.
- Aging hearts exhibit molecular, cellular, and organ-level changes, reducing adaptive capacity.
- Proto-oncogene induction (e.g., c-fos, c-myc, c-jun) diminishes in aged hearts, impairing hypertrophic responses.
Purpose of the Study:
- To investigate age-related changes in the heart's response to hypertension.
- To explore the impact of hypertension onset age on coronary vascularity and cardiac adaptation.
- To clarify the mechanisms of regression for hypertension-induced cardiac and vascular changes in aged hearts.
Main Methods:
- Comparative analysis of hypertrophic responses in infant versus aged hearts under mechanical load.
- Assessment of coronary angiogenesis and dilator reserve in relation to hypertension onset.
- Review of existing literature on the effects of antihypertensive treatments on aged hearts.
Main Results:
- Aged hearts have a limited hypertrophic response to mechanical load, linked to reduced proto-oncogene induction.
- Late-onset hypertension impairs coronary dilator reserve without causing hypertrophy, unlike early-onset hypertension.
- Hypertension normalization can regress hypertrophy but may decrease coronary dilator reserve; regression mechanisms in aged hearts are unclear.
Conclusions:
- The aging process inherently limits cardiac adaptation, particularly in response to hypertension.
- The timing of hypertension onset significantly influences cardiac and vascular remodeling in aging.
- Further research is needed to elucidate how antihypertensive treatments reverse hypertension-induced cardiac alterations in the elderly.
Abstract:
Heart disease in older individuals can be characterised as the result of 2 processes, hypertension and atherosclerosis, which are the major causes of heart failure in the elderly population. The aging heart undergoes changes at the molecular, cellular and organ levels. These age-related changes may then be modulated by pathological conditions, such as hypertension, and by the reduction of blood pressure. One characteristic of the aged heart is a limited capacity for adaptation, by hypertrophy, to increased mechanical load. This age-related attenuation of the hypertrophic response may be attributed to the diminished induction of proto-oncogenes such as c-fos, c-myc and c-jun. This diminution results from aging of the heart per se and may be modulated by extracardiac factors. With regard to the coronary vasculature, the age at which hypertension develops seems to be an important factor for determining the vascularity of hypertrophied hearts. Late-onset hypertension is not accompanied by coronary angiogenesis, and it decreases dilator reserve in spite of the absence of myocardial hypertrophy. In contrast, mechanical overload in infant hearts is accompanied by angiogenesis and normal dilator reserve. In principle, the normalisation of hypertension results in the regression of myocardial hypertrophy and decreased coronary dilator reserve. In aged hearts, it is not clear how hypertension-induced myocardial hypertrophy or coronary vascular changes regress. Although antihypertensive treatment is clearly associated with an improvement of cardiovascular mortality and morbidity in hypertensive elderly individuals, it remains unclear how treatments ameliorate the hypertension-induced alterations.