title: Age-related changes in cardiac physiology. Can they be postponed or treated by drugs?
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.
authors.affiliation: Section of Geriatric Medicine, University of Illinois at Chicago, USA.
authors.forename: A
authors.initials: A
authors.lastname: Svanborg
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000368:Aged; D000375:Aging / Q000473:pathology / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use; D004232:Diuretics / Q000494:pharmacology / Q000627:therapeutic use; D005260:Female; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006331:Heart Diseases / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D009206:Myocardium / Q000166:cytology / Q000473:pathology*
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002121:Calcium Channel Blockers; D004232:Diuretics