Search

Mortality related to heart rate (HR) increase in the elderly has not yet been well established. To ascertain the relationships among cognitive impairment (CI), mortality, and HR increase, the authors prospectively studied a random sample of elderly subjects stratified according to presence or absence of CI. Elderly subjects randomly selected in 1991 (n = 1332) were followed up for 12 years. Mortality was established in 98.1% of the subjects. When HR was stratified in quartiles (< 69, 70-75, 76-80, and > 80 bpm), mortality was linearly associated with increased HR in all (from 47.7 to 57.0; r2 = .43, p = .019) and in subjects without (from 41.7 to 51.1%; r2 = .50, p = .043) but not in those with CI (from 57.5 to 66.1; r2 = .20, p = .363). Cox regression analysis, adjusted for several variables, shows that HR doesn't predict mortality in all subjects (RR 0.69; 95% CI = 0.27-1.73) or in those with CI (RR 0.91; 95% CI = 0.81-1.02). In contrast, HR predicts mortality in subjects without CI (RR 1.10; 95% CI = 1.00-1.22). Hence, HR increase is a predictor of mortality in elderly subjects without CI. However, when considering all elderly subjects and those with CI, HR increase seems to have no effect on mortality. Thus, CI should be considered when focusing on HR increase as risk factor for mortality in the elderly.

Background: The aging heart is characterized by structural changes, which are implicated in the development of left ventricular diastolic dysfunction. However, important changes in systolic function may also occur. Left ventricular end-systolic elastance (E(es)) is a major determinant of cardiac systolic function and ventricular-arterial interaction., Aim: To evaluate left-ventricular E(es) in elderly subjects compared with adult control subjects., Methods: We studied dilated (DA, n=14) and hypertensive (HA, n=21) cardiomyopathy patients, and both adult control (A, n=25; age 55.6+/-6.6 years) and elderly (E, n=25; age 76.3+/-7.1 years) subjects without clinical-instrumental evidence of cardiovascular disease. M-mode, two-dimensional, and pulsed Doppler echocardiogram were performed. Doppler-derived indices of diastolic function were assessed and E(es) was calculated by a modified single-beat method., Results: E(es) was reduced in dilated cardiomyopathy (1.32+/-0.10 mm Hg/ml) and increased in hypertensive cardiomyopathy (3.12+/-0.33 mm Hg/ml) patients compared to age-matched control subjects (1.96+/-0.26 mm Hg/ml; p<0.01 and p<0.05, respectively). More importantly, E(es) was higher in the elderly (2.52+/-0.70 mm Hg/ml) than in the adult control group (p<0.05) and was linearly correlated with age (r2=0.639; p<0.0001)., Conclusion: Age-related increase in E(es), together with diastolic dysfunction, may lead to aging heart decompensation.

Background and Aims: We investigated the prevalence of visual impairment (VI), its determinants and its association with Activities of Daily Living (ADL), Instrumental Activities of Daily Living (IADL), Gross Mobility (GM) and 6-year mortality in elderly subjects. A cross-sectional survey in a large population randomly selected in 1992 with a 6-year mortality evaluation in Campania, a region in southern Italy., Methods: A random sample of 1332 elderly subjects aged 65 to 95 years (mean age 74.2 +/- 6.4), selected from the electoral rolls, was interviewed by trained physicians. Self-reported visual function, socio-demographic and clinical characteristics were recorded. Disability was assessed by measuring ability in ADL, IADL and GM., Results: VI was found to affect 34% of this population, with an age-related increase of mild and severe VI. VI affects ADL, IADL and GM disability. Age, diabetes and low educational level, but not comorbidity or hypertension, proved to be predictors of VI. Mortality increased with severity of VI in 38.1% of subjects with severe functional impairment (p < 0.001). The presence of VI was seen to increase the risk of mortality by 1.40 (95% CI 1.07-1.84), independently of age, sex, comorbidity, diabetes, hypertension or disability., Conclusions: This study demonstrates an association between visual impairment and disability in an elderly population, and the predictive effect of visual impairment on mortality independently of comorbidity. These results illustrate the need to eradicate avoidable blindness, in order to improve the quality of life and to prolong survival of the elderly.

Ischemic preconditioning (PC) has been proposed as an endogenous form of protection against-ischemia reperfusion injury. We have shown that PC does not prevent postischemic dysfunction in the aging heart. This phenomenon could be due to the reduction of cardiac norepinephrine release, and it has also been previously demonstrated that age-related decrease of norepinephrine release from cardiac adrenergic nerves may be restored by caloric restriction. We investigated the effects on mechanical parameters of PC against 20 min of global ischemia followed by 40 min of reperfusion in isolated hearts from adult (6 mo) and "ad libitum"-fed and food-restricted senescent (24 mo) rats. Norepinephrine release in coronary effluent was determined by high-performance liquid chromatography. Final recovery of percent developed pressure was significantly improved after PC in adult hearts versus unconditioned controls (85.2 +/- 19% vs. 51.5 +/- 10%, P < 0.01). The effect of PC on developed pressure recovery was absent in ad libitum-fed rats, but it was restored in food-restricted senescent hearts (66.6 +/- 13% vs. 38.3 +/- 11%, P < 0.05). Accordingly, norepinephrine release significantly increased after PC in both adult and in food-restricted senescent hearts, and depletion of myocardial norepinephrine stores by reserpine abolished the PC effect in both adult and in food-restricted senescent hearts. We conclude that PC reduces postischemic dysfunction in the hearts from adult and food-restricted but not in ad libitum-fed senescent rats. Despite the possibility of multiple age-related mechanisms, the protection afforded by PC was correlated with increased norepinephrine release, and it was blocked by reserpine in both adult and food-restricted senescent hearts. Thus caloric restriction may restore PC in the aging heart probably via increased norepinephrine release.