Influence of aging and other cardiovascular risk factors on baroreflex sensitivity.

OBJECTIVES: To examine the influence of known cardiovascular risk factors (cholesterol, blood glucose levels, arterial pressures, heart rate, and aging) on baroreflex sensitivity. DESIGN: An observational epidemiological study. SETTING: Geriatric Division at the Policlinico Umberto Primo, University of Rome La Sapienza. PARTICIPANTS: Two hundred three subjects whose ages ranged from 9 to 94 years, apparently healthy and free of detectable clinical evidence of atherosclerosis. MEASUREMENTS: All subjects underwent determination of baroreflex sensitivity by phenylephrine infusion (BSphe), and by a noninvasive method derived from spectral analysis of R-R interval and arterial pressure variabilities (alpha index). RESULTS: The population, subdivided into tertiles for each variable studied, had lower BSphe values and lower alpha indexes as a function of age, plasma low-density lipoprotein (LDL) cholesterol, and systolic blood pressure. The alpha index was significantly lower in both groups with elevated LDL cholesterol levels than in those with lower levels (II and III vs I tertile, P <.001), whereas BSphe differed significantly only in the two groups who had extreme levels of LDL (I vs III tertile, P <.001). Multiple regression analysis identified a negative association of the alpha index with age (P <.001), heart rate (P <.01), area under the glucose-response curve (P <.001), and LDL cholesterol (P <.01), but of BSphe only with age (P <.001) and heart rate (P <.01). CONCLUSION: These findings indicate that some risk factors for coronary heart disease adversely influence baroreflex sensitivity.

Influence of age, the autonomic nervous system and anxiety on QT-interval variability.

As QT variability increases and heart rate variability diminishes, the QT variability index (QTVI) - a non-invasive measure of beat-to-beat fluctuations in QT interval on a single ECG lead - shows a trend towards positive values. Increased QT variability is a risk factor for sudden death. Aging lengthens the QT interval and reduces RR-interval variability. In the present study we investigated the influence of aging and the autonomic nervous system on QT-interval variability in healthy subjects. We studied 143 healthy subjects, and divided them into two age ranges (younger and older than 65 years). For each subject we measured two QTVIs: from the q wave to the end of the T wave (QTeVI) and to the apex of the T wave (QTaVI). Both indexes were calculated at baseline and after sympathetic stress. In 10 non-elderly subjects, both QTVIs were determined after beta-adrenoreceptor blockade induced by intravenous infusion of propranolol or sotalol. The QTVI was higher in elderly than in younger subjects (P<0.001). QTVIs obtained during sympathetic stress remained unchanged in the elderly, but became more negative in the younger group (P<0.05). QTeVI and QTaVI at baseline were correlated positively with age (P<0.01) and anxiety scores (P<0.05), but inversely with the low-frequency spectral power of RR-interval variability (P<0.001). QTVIs were higher in subjects with higher anxiety scores. In younger subjects, sotalol infusion increased both QTVIs significantly, whereas propranolol infusion did not. In conclusion, aging increases QT-interval variability. Whether this change is associated with an increased risk of sudden death remains unclear. The association of abnormal QT-interval variability with anxiety and with reduced low-frequency spectral power of heart rate variability merits specific investigation. In healthy non-elderly subjects, acute sympathetic stress (tilt) decreases the QTVI. beta-Adrenoreceptor blockade inhibits this negative trend, thus showing its sympathetic origin. Because a negative trend in QTVI induced by sympathetic stress increases only in younger subjects, it could represent a protective mechanism that is lost with aging.

Influence of aging on cardiac baroreflex sensitivity determined non-invasively by power spectral analysis.

Aging reduces cardiac baroreflex sensitivity. Our primary aim in the present study was to assess the effects of aging on cardiac baroreflex sensitivity, as determined by power spectral analysis (alpha index), in a large population of healthy subjects. We also compared the alpha indexes determined by power spectral analysis with cardiac baroreflex sensitivity measured by the phenylephrine method (BS(phen)). We studied 142 subjects (79 males/63 females; age range 9-94 years), who were subdivided into five groups according to percentiles of age (25, 50, 75 and 95). Power spectral analysis yields three alpha indexes: an alpha low-frequency (LF) index of cardiac baroreflex sensitivity that ranges around 0.1 Hz; an alpha high-frequency (HF) index reflecting cardiac baroreflex sensitivity corresponding to the respiratory rate; and alpha total frequency (alpha TF), a new index whose spectral window includes all power in the range 0.03-0.42 Hz. Spectra were recorded during controlled and uncontrolled respiration. Under both conditions, all three alpha indexes were higher in the youngest age group (< or =34 years old) than in the three oldest groups. Notably, alpha TF was significantly higher in younger subjects than in the three oldest groups [14+/-1 ms/mmHg compared with 9+/-1 (P<0.05), 8.1+/-1 (P<0.001) and 8.1+/-1 (P<0.05) ms/mmHg respectively]. BS(phen) showed a similar pattern [12+/-1 ms/mmHg compared with 8+/-0.5 (P<0.001), 6+/-0.5 (P<0.05) and 6+/-1 (P<0.05) ms/mmHg respectively]. No significant differences were found for cardiac baroreflex sensitivity among the three oldest groups. All alpha indexes were correlated inversely with age. The index yielding the closest correlation with BS(phen) was alpha TF (r=0.81, P<0.001). Cardiac baroreflex sensitivity in normotensive individuals declines with age. It falls predominantly in middle age (from approx. 48 years onwards) and remains substantially unchanged thereafter. The elderly subjects we selected for this study probably had greater resistance to cardiovascular disease that is manifested clinically, with preserved cardiac baroreceptor sensitivity.

Autonomic modulation of heart rate and blood pressure in normotensive offspring of hypertensive subjects.

Predominant sympathetic cardiovascular modulation in the hyperkinetic phase of arterial hypertension has been well described. Less information is available on autonomic control in persons with a family history of arterial hypertension. To investigate this question, we selected 61 normotensive subjects (mean age 30.9 +/- 1.8 years) whose mother or father or both had arterial hypertension and 30 normotensive patients (mean age 30.1 +/- 1.4 years) whose parents had not had arterial hypertension (neither mother nor father) to undergo short-term power spectral analysis of RR interval and arterial pressure variabilities. The same recordings were used to determine baroreflex sensitivity or the alpha index by means of the transfer function. Normotensive offspring of hypertensive subjects had higher diastolic blood pressures (P < .05) and left ventricular mass index (P < .05) than did normotensive offspring of non-hypertensive subjects. They also had higher spectral densities of low frequency expressed in normalized units, both for R-R intervals (P < .05) and systolic pressure variabilities (P < .05); they also had a greater ratio of low-frequency to high-frequency powers of R-R interval variability (P < .05). No difference was observed between the two normotensive groups for baroreflex sensitivity. Our spectral data indicate that normotensive persons with a positive family history of arterial hypertension have lower parasympathetic modulation than those with a negative history. In normotensive persons with a family history of arterial hypertension, normal baroreflex sensitivity could be the mechanism that buffers the tendency for pressures to increase. The gradual loss of this regulatory mechanism may favor rising arterial pressures.

Autonomic modulation and QT interval dispersion in hypertensive subjects with anxiety.

Anxiety is associated with an increased risk of sudden death. QT dispersion is a marker of cardiac repolarization instability and is seen in conditions of high risk of sudden death. The purpose of this study was to evaluate autonomic nervous system control and QT dispersion in hypertensive subjects with anxiety symptoms. In a recent preliminary study, we observed that hypertensive individuals reporting high scores on a self-assessment anxiety scale had more marked left ventricular hypertrophy. In 105 hypertensive subjects divided into 3 groups according to severity of anxiety, we evaluated autonomic control by short-term power spectral analysis of RR and arterial pressure variability at rest (baseline) and during sympathetic stress (tilt test), left ventricular mass index, and heart rate-corrected QT (QTc) dispersion. At baseline, hypertensive subjects with higher anxiety symptom scores had significantly lower high-frequency RR values expressed in absolute terms (P<0.05) and in normalized units (P<0.05) than their counterparts without anxiety symptoms. Hypertensive subjects with anxiety also had a higher mean left ventricular mass index (P<0.001) and greater QTc dispersion (P<0.001). Both indexes and high frequency (P<0.05) correlated with severity of anxiety. These findings suggest that anxiety is associated with autonomic imbalance. This condition could favor an increase in left ventricular mass. Myocardial hypertrophy alone or combined with neuroautonomic imbalance may lead to QT dispersion.

QT interval dispersion and autonomic modulation in subjects with anxiety.

This study was designed to assess Q-T interval dispersion as a marker of electrical instability in subjects with anxiety. Recent observations have shown that the presence of anxiety symptoms increases the risk of sudden death. The Kawachi anxiety questionnaire identified 29 subjects (male/female ratio 13:16) who scored 0, 22 subjects (male/female ratio 14:8) who scored 1, and 37 subjects (male/female ratio 13:24) who scored 2 or more. In all subjects we measured electrocardiographic interlead QT dispersion and autonomic function through spectral analysis of R-R interval and blood pressure variabilities and left ventricular mass. Compared with subjects who scored 0, those reporting 2 or more symptoms showed increased heart rate-corrected QT dispersion (54.9+/-1.7 ms vs. 34.9+/-3.2 ms, P<.001), sympathetic modulation (normal logarithm low-frequency power/high-frequency power 0.59+/-0.1 vs. 0.12+/-0.04, P<.05), and left ventricular mass (120.7+/-3.5 g/m2 vs. 97.9+/-2.8 g/m2, P<.001). Probably because it augments sympathetic activity, anxiety causes left ventricular mass to increase and, like hypertension, increases heart rate-corrected Q-T interval dispersion. The consequent electrical instability could be the substrate responsible for inducing fatal ventricular arrhythmias.

Sex differences in correlates of steady state and pulsatile component of blood pressure.

1. The aim of the present study was to evaluate whether metabolic factors are linked to the steady component and the pulsatile component of blood pressure, evaluated as mean arterial pressure and pulse pressure respectively, in a sex-specific manner. 2. A cohort of 299 subjects (152 males, 147 females; 25-80 years of age) was studied. Patients presenting congestive heart failure, coronary insufficiency, severe valvular heart disease, neurological accident in the last 6 months, renal or respiratory failure, cancer, diabetes mellitus or acute infectious disease were excluded. None of the women was taking oral contraceptives or oestrogen supplementation. All cardioactive drugs were withdrawn at least 2 weeks before the subjects entered the study. 3. Men presented higher mean arterial pressure (120 +/- 15 compared with 115 +/- 16 mmHg, P < 0.01) and lower pulse pressure values (63 +/- 16 compared with 67 +/- 18 mmHg, P < 0.05) than women. In men, no significant relation between mean arterial pressure and the tested variables was detected; multiple regression analysis demonstrated that age contributed independently to the model for pulse pressure with a multiple r2 of 0.10 (P < 0.01). In women, body mass index contributed independently to the model for mean arterial pressure, with a multiple of 0.12 (P < 0.005); age and, to a lesser extent, body mass index, glycaemia and triglyceridaemia persisted as independent determinants of pulse pressure at the multiple regression analysis, with a multiple r2 of 0.20 (P < 0.001). 4. Our findings suggest that metabolic risk factors are associated differently with pulse pressure and mean arterial pressure values in the two sexes.

[Pathology of bus drivers. I]. / La patologia degli autoferrotramvieri. I.

A short synthesis of data available on bus-drivers' pathology has been made and several features, related to work conditions, have been discussed taking in account their influence on health.