A decreased LFP (low-frequency power) spectral component of HRV [HR (heart rate) variability] is a risk factor for sudden death in patients with CHF (chronic heart failure). In the present study, we evaluated factors (age, arterial pressures and HR) influencing LFP and HFP (high-frequency power) components in short-term recordings during controlled breathing in patients with CHF or hypertension, and healthy normotensive subjects. In patients with CHF, we also compared LFP values with known markers of sudden death [NYHA (New York Heart Association) class, HR and ejection fraction]. All HRV measures were significantly lower in patients with CHF than in hypertensive and normotensive subjects ( P <0.001), and in hypertensive than in normotensive subjects ( P <0.05). Stepwise multiple regression analysis showed that, in patients with CHF, LFP was inversely associated with NYHA class (β=−0.5, P <0.0001) and HR (β=−0.2, P =0.001) and was positively associated with ejection fraction (β=0.28, P <0.0001). In patients with CHF, LFP remained unchanged with age. In normotensive and hypertensive subjects, HFP decreased with age, but in patients with CHF it did not. In the ≥60<70 and ≥70 years of age subgroups, we found no difference between HFP in the three groups studied. Hence, in normotensives and hypertensives, LFP tended to diminish with age (β=−0.4, P <0.0001 in normotensives; β=−0.4, P <0.001 in hypertensives) and was inversely associated with HR (β=−0.2, P =0.002 in normotensives; β=−0.3, P =0.002 in hypertensives). Conversely, in patients with CHF, LFP is predominantly influenced by NYHA class, HR and ejection fraction, but not by age. LFP might therefore increase the sensitivity of factors already used in stratifying the risk of sudden death in patients with CHF.

Autonomic nervous system control in subjects with vasovagal syncope is controversial. In the present study, we used short-term spectral analysis to evaluate autonomic control in subjects with recurrent vasovagal syncope. We assessed the ability of spectral indices of HR (heart rate) variability to predict tilt-test responses. A series of 47 outpatients with recurrent vasovagal syncope and with positive responses to head-up tilt testing underwent a further study of RR variability during controlled breathing at rest and during tilt testing. During controlled breathing, RR interval variability of total power (TP RR ; P <0.001), low-frequency power (LF RR ; P <0.05), high-frequency power (HF RR ; P <0.001) and HF expressed in normalized units (HFnu RR ; P <0.001) were all higher, and LF expressed in normalized units (LFnu RR ) and LF/HF ratio were lower in subjects with vasovagal syncope than in controls ( P <0.001). To assess the ability of spectral components of RR variability to predict tilt-test responses, we prospectively studied 109 subjects with recurrent vasovagal syncope. The two normalized measures, HFnu RR and LFnu RR , determined during controlled breathing alone predicted a positive tilt-test response (sensitivity, 76%; specificity, 99%; positive predictive value, 96%; and negative predictive value, 90%). During tilting, subjects with vasovagal syncope had lower SBP (systolic blood pressure; P <0.05), LF component of peak SBP variability (LF SBP ) and LFnu RR than controls, and higher TP RR , HF RR , HFnu RR and α HF ( P <0.001). These spectral data indicate that vagal sinus modulation is increased at rest in subjects with vasovagal syncope. Spectral analysis of RR variability during controlled breathing, a procedure that predicts tilt-test responses, could be a useful guide in choosing the method of tilt testing.

Left ventricular hypertrophy is a risk factor for sudden death. Malignant ventricular arrhythmias originate from altered cardiac repolarization. Ample data have described spatial abnormalities in cardiac repolarization [QT interval (QT) dispersion] in subjects with hypertension; more data are needed on temporal changes. This study was designed to assess the QT variability index (QTVI), the slope between QT and the RR interval (QT-RR slope ) and spectral QT variability in subjects with arterial hypertension. The results were compared with those from a population at high risk of sudden death, i.e. patients with hypertrophic cardiomyopathy (HCM) who had received an implantable cardioverter/defibrillator (ICD), and those from normotensive control subjects. A total of 44 hypertensive subjects, six patients with HCM and an ICD and 33 control subjects underwent simultaneous short-term recording (256 beats) of QT, RR and systolic blood pressure variability, in the supine position, during controlled breathing. QTVI and spectral components of QT variability in the hypertensive group were significantly higher than in normotensive control subjects ( P < 0.001), but significantly lower than in patients with HCM and an ICD ( P < 0.001). The severity of left ventricular hypertrophy correlated significantly with QTVI and the ratio of low-frequency (LF) to high-frequency (HF) power obtained from the RR variability spectra (RR LF/HF , slope = 0.24, P < 0.05; QTVI, slope = 4.06, P < 0.0001; intercept, slope = 2.40, P < 0.05; χ 2 = 38.8; P < 0.0001). The QT-RR slope was significantly higher only in patients with HCM and an ICD ( P < 0.001). In conclusion, the increased QTVI and the correlation of this index with left ventricular hypertrophy indicates that hypertension increases temporal cardiac repolarization abnormalities. At the level of the cardiac sinus node, this alteration is associated with increased sympathetic and reduced vagal modulation. As already noted in patients with HCM, the increased QTVI could be a factor responsible for triggering malignant ventricular arrhythmias in subjects with hypertension.

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 143healthy 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 β-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. β-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.

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 (α index), in a large population of healthy subjects. We also compared the α 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 α indexes: an α low-frequency (LF) index of cardiac baroreflex sensitivity that ranges around 0.1 Hz; an α high-frequency (HF) index reflecting cardiac baroreflex sensitivity corresponding to the respiratory rate; and α total frequency (α 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 α indexes were higher in the youngest age group (⩽ 34 years old) than in the three oldest groups. Notably, α 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 α indexes were correlated inversely with age. The index yielding the closest correlation with BS phen was α 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.