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Age-related changes in cardiac physiology. Can they be postponed or treated by drugs?
1Section of Geriatric Medicine, University of Illinois at Chicago, USA.
Insights
Aging causes heart stiffening and reduced filling, with no current drugs directly reversing these effects. Lifestyle changes are more promising for postponing cardiac aging than direct pharmaceutical interventions.
Area of Science:
- Cardiology
- Gerontology
- Physiology
Background:
- The fundamental mechanisms driving the aging process remain largely unknown.
- Longitudinal population studies utilizing noninvasive methods enhance the distinction between aging and disease.
- This review focuses on clinically relevant morphological and functional changes in the aging heart.
Purpose of the Study:
- To review age-related cardiac changes and evaluate potential drug treatments for aging manifestations.
- To explore the efficacy of current medications in addressing cardiac aging.
- To discuss the role of exogenous factors in managing cardiac aging.
Main Methods:
- Review of existing literature on cardiac aging.
- Analysis of morphological and functional changes associated with aging.
- Evaluation of pharmacological interventions for cardiac aging.
Main Results:
- Aging leads to heart tissue stiffening and impaired diastolic filling, impacting function at higher heart rates.
- Drugs like digitalis have not demonstrated efficacy in improving age-related declines in myocardial strength or contractility.
- While some drugs may indirectly improve heart function (e.g., by lowering vascular resistance), none directly enhance myocardial strength or reduce tissue stiffness.
- Morphological changes include left ventricular hypertrophy and atrial/ventricular dilation; angiotensin II may promote hypertrophy, suggesting potential roles for ACE inhibitors.
Conclusions:
- No current drug effectively reverses myocardial aging; digitalis is ineffective for age-related decline.
- Calcium antagonists may offer some benefit for diastolic filling, but direct cardiac effects are unproven.
- Lifestyle modifications and improved external factors (healthcare, living conditions) present the most viable strategies for delaying cardiac aging.
Abstract:
The basic mechanisms that cause aging are still poorly understood. Longitudinal prospective population studies using noninvasive examination techniques have improved our ability to differentiate between aging and disease. This review describes some general morphological and functional aging-related changes of the heart that have clinical relevance, and considers the possibility of drug treatment for the manifestations of aging per se. Digitalis has not been shown to improve the aging-related decline in myocardial strength and contractility. During aging, heart tissue stiffens and the speed and extent of diastolic filling decline. The latter is a limiting functional factor, particularly during increases in heart rate. Lowering peripheral vascular resistance, which is often increased in older people, might indirectly improve heart function. However, no drug has been shown to improve myocardial strength or lower tissue stiffness via a direct effect on the heart. It has been claimed, however, that calcium antagonists might improve diastolic filling. Morphological changes during aging are dominated by some left ventricular wall and septal hypertrophy, and left atrial and ventricular widening. Recent findings have suggested that angiotensin II might act as a growth stimulating factor, promoting cardiac hypertrophy. This has led to speculation that ACE inhibitors might contribute to the restructuring of the heart, not only in hypertension but also in patients with the common combination of slightly elevated blood pressure and aging-related myocardial hypertrophy. At present, it appears that improving exogenous factors (e.g. lifestyle, living circumstances and access to adequate medical care) offers greater opportunities for postponing cardiac aging than drugs that directly interfere with the physiological aging of the heart.