Fortunato Marciano

Intensive training and cardiac autonomic control in high level athletes

PURPOSE We aimed to evaluate in a longitudinal study the effect of intensive training on cardiac autonomic control in athletes using 24-h heart rate variability analysis. METHODS Time and frequency domain measures of heart rate variability were calculated from 24-h Holter monitoring in 15 high level bicyclists (mean age 21 +/- 4 yr) after 1 month of detraining and after 5 months of vigorous training. At the same times echocardiographic left ventricular mass and dimensions and maximal oxygen consumption (VO2max) were assessed. RESULTS In detrained athletes, VO2max values, left ventricular mass and dimensions, and time and frequency domain measures of vagal modulation of heart rate were higher than in a group of untrained subjects of similar age while heart rate and the low-to-high frequency ratio were lower, indicating an enhanced vagal modulation of heart rate in athletes as compared with that in control subjects. After 5 months of vigorous training, left ventricular mass and dimensions and VO2max increased in athletes, while heart rate decreased further. In contrast, no changes were detectable in time and frequency domain measures of heart rate variability over the entire 24-h and in both waking and sleeping hours. CONCLUSIONS This study demonstrates that an increased cardiac vagal control is detectable in detrained athletes; however, after intensive training, despite a significant decrease in heart rate, time and frequency domain measures of heart rate variability reflecting cardiac vagal control remain unchanged. Thus, other mechanisms than changes in cardiac autonomic control could be involved in determining the profound bradycardia of athletes.

Independent and incremental prognostic value of heart rate variability in patients with chronic heart failure

BACKGROUND Decreased heart rate variability (HRV), indicating derangement in cardiac autonomic control, has been reported in patients with chronic heart failure. However, the independent and incremental prognostic value of HRV over clinical data and measures of left ventricular dysfunction has been less thoroughly investigated. This study was designed to evaluate the predictive value of HRV and Poincaré plots as assessed by 24-hour Holter recording in patients with chronic heart failure. METHODS Ninety-seven patients, mean age 55 +/- 13 years, with radionuclide left ventricular ejection fraction </=40% underwent echocardiographic examination and 24-hour Holter recording. Heart failure was caused by coronary artery disease in 57 patients (59%) and idiopathic dilated cardiomyopathy in 40 (41%). RESULTS During follow-up (39 +/- 18 months), 32 cardiac deaths occurred. By Cox multivariate analysis, significant predictors of death were left ventricular end-systolic volume (hazard ratio 1.04), low- to high-frequency ratio (hazard ratio 0.09), percentage of differences between successive normal R-R intervals >50 ms (hazard ratio 0.93), and age (hazard ratio 1.06). Furthermore, HRV analysis improved (P <. 001) the prognostic power of a model including clinical and echocardiographic data, left ventricular ejection fraction, and ventricular arrhythmias at Holter recording, whereas the inclusion of Poincaré plots did not add further predictive value. CONCLUSIONS Our investigation demonstrated that HRV has independent and incremental prognostic value in patients with chronic heart failure and seems useful to stratify patients at high risk of cardiac death.

Power spectral analysis of heart period variability in hypertensive patients with left ventricular hypertrophy.

This study aimed to characterize sympathovagal balance by heart period power spectrum analysis in hypertensive patients with echocardiographic evidence of left ventricular hypertrophy. Twenty ambulatory patients (11 men and 9 women), aged 50 +/- 10 years, with established essential hypertension and echocardiographic left ventricular hypertrophy, performed 24-h blood pressure monitoring and electrocardiogram Holter recording on 2 consecutive days. Twenty age- and sex-matched normal subjects comprised the control group. Power spectrum analysis, performed using the fast Fourier transform algorithm, demonstrated lower values of low and high frequency power in hypertensives than in controls, while ultralow and very low frequency power were similar in the two groups. Very low frequency, low frequency, and high frequency power increased during the night in both groups, showing a similar circadian pattern. We found a direct correlation between daytime systolic (r = 0.51; P < .05) and diastolic (r = 0.52; P < .05) blood pressure and left ventricular mass index. Moreover, negative correlations were found between left ventricular mass index and low frequency (r = -0.47; P < .05) and high frequency power (r = -0.47; P < .05). There was a direct correlation between nighttime decrease in systolic blood pressure and nighttime increase in high frequency power (r = 0.45; P < .05). As 24-h low frequency and high frequency power, obtained using the Fourier transform algorithm, both reflect the parasympathetic modulation of heart rate, our results demonstrate that hypertensive patients with left ventricular hypertrophy are characterized by a sympathovagal imbalance with a reduction of vagal tone that is more evident with increasing severity of hypertension.

Cardiac autonomic responses to volume overload in normal subjects and in patients with dilated cardiomyopathy.

This study evaluated the effects of acute isotonic volume expansion on heart rate variability (HRV) in 10 patients with dilated cardiomyopathy (DCM) and in 10 age- and sex-matched normal volunteers. Echocardiographic left ventricular volumes and HRV measurements by continuous Holter recording were assessed at baseline, at 60 and 120 min during intravenous saline load (0.9% NaCl, 0.25 ml. kg(-1). min(-1)), and 60 min after infusion was terminated. Data analysis was performed by repeated-measures ANOVA. After volume expansion, left ventricular ejection fraction increased (F = 9.8; P < 0.001) in normal subjects and decreased (F = 8.7; P < 0.001) in DCM patients. During volume expansion a significant difference was also detectable between the two groups in root-mean-square successive difference (F = 25.2; P < 0.001), percentage of differences between successive normal R-R intervals >50 ms (F = 97.6; P < 0.001), high-frequency power (F = 50.1; P < 0.001), and low-frequency power (F = 41.6; P < 0.001), all of which reflect parasympathetic modulation of heart rate; in fact, these measurements increased in normal subjects and decreased in DCM patients. In normal subjects, the increase in HRV measurements during volume expansion suggests a parasympathetic activation, mediated by stimulation of cardiopulmonary and arterial mechanoreceptors. On the contrary, in DCM patients the parasympathetic withdrawal, already detectable at baseline, increases during volume expansion.This study evaluated the effects of acute isotonic volume expansion on heart rate variability (HRV) in 10 patients with dilated cardiomyopathy (DCM) and in 10 age- and sex-matched normal volunteers. Echocardiographic left ventricular volumes and HRV measurements by continuous Holter recording were assessed at baseline, at 60 and 120 min during intravenous saline load (0.9% NaCl, 0.25 ml ⋅ kg-1 ⋅ min-1), and 60 min after infusion was terminated. Data analysis was performed by repeated-measures ANOVA. After volume expansion, left ventricular ejection fraction increased ( F = 9.8; P < 0.001) in normal subjects and decreased ( F = 8.7; P < 0.001) in DCM patients. During volume expansion a significant difference was also detectable between the two groups in root-mean-square successive difference ( F = 25.2; P < 0.001), percentage of differences between successive normal R-R intervals >50 ms ( F = 97.6; P < 0.001), high-frequency power ( F = 50.1; P < 0.001), and low-frequency power ( F = 41.6; P < 0.001), all of which reflect parasympathetic modulation of heart rate; in fact, these measurements increased in normal subjects and decreased in DCM patients. In normal subjects, the increase in HRV measurements during volume expansion suggests a parasympathetic activation, mediated by stimulation of cardiopulmonary and arterial mechanoreceptors. On the contrary, in DCM patients the parasympathetic withdrawal, already detectable at baseline, increases during volume expansion.

Heart rate variability in patients with hypertrophic cardiomyopathy: Association with clinical and echocardiographic features

Autonomic dysfunction has been reported in patients with hypertrophic cardiomyopathy. To evaluate the influence of different clinical and echocardiographic features of the disease on sympathovagal balance, as assessed by heart rate variability, 33 patients with hypertrophic cardiomyopathy and 33 healthy volunteers underwent echocardiographic examination and 24-hour electrocardiogram Holter recording. Measures of vagal modulation of heart rate were lower in patients with hypertrophic cardiomyopathy than in controls, particularly in those exhibiting syncope, exertional chest pain, dyspnea, or moderate or severe mitral regurgitation. Furthermore, the age-corrected multiple regression analysis showed that the parasympathetic cardiac control was inversely related to left atrial dimension and directly related to left ventricular end-systolic dimension. Therefore in hypertrophic cardiomyopathy the parasympathetic withdrawal is more evident in patients with symptoms than in those without; the reduction in left ventricular end-systolic dimension and the increase in left atrial size are the echocardiographic features that most influence the sympathovagal balance.

Influence of reversible segmental left ventricular dysfunction on heart period variability in patients with one-vessel coronary aetery disease

OBJECTIVES This study evaluated the relation between reversible segmental left ventricular dysfunction and frequency domain measures of heart period variability in patients with coronary artery disease. BACKGROUND Heart period variability is frequently reduced in patients with coronary artery disease. However, the mechanisms of this reduction are still unclear. METHODS Echocardiographic left ventricular wall motion and frequency domain measures of heart period variability were evaluated in 32 patients with one-vessel coronary artery disease before and 16 to 24 days after successful percutaneous transluminal coronary angioplasty. Of these, 12 patients (Group A) had normal and 20 patients (Group B) had abnormal regional wall motion. A control group of 15 healthy subjects (Group C) underwent 24-h Holter recording twice at 2-week intervals to check for spontaneous variations. RESULTS At baseline, low and high frequency power were lower in Group B than in Groups A and C, whereas no difference was detectable in ultra low and very low frequency and total power. After coronary angioplasty, regional wall motion and frequency domain measures of heart period variability were unchanged in Group A. In Group B the mean (+/- SD) summed segment score improved from 17.1 +/- 3.6 to 12.8 +/- 2.0 (p < 0.01), and mean low and high frequency power (logarithmic units) increased from 6.14 +/- 0.23 to 6.35 +/- 0.34 (p < 0.01) and from 5.43 +/- 0.32 to 5.68 +/- 0.52 (p < 0.01), respectively. Furthermore, low and high frequency power, lower at baseline in Group B than in the other two groups, were comparable in the three groups after coronary angioplasty. CONCLUSIONS This study demonstrates that segmental left ventricular dysfunction is involved in determining sympathovagal imbalance in patients with one-vessel coronary artery disease; the reversal of left ventricular dysfunction by successful coronary angioplasty improves the heart period power spectrum. Thus, alterations in cardiac geometry influence the discharge of afferent sympathetic mechanoreceptors, contributing to the derangement in autonomic control of heart rate.

Comparison of Verapamil Versus Felodipine on Heart Rate Variability After Acute Myocardial Infarction

A depressed heart rate variability (HRV) is a powerful predictor of poor outcome in myocardial infarction patients. The beneficial effect of specific interventions on its recovery has been reported, but data concerning calcium antagonists are scarce. We evaluated the effect of a phenylalkylamine derivative, verapamil, and a dihydropyridine derivative, felodipine, on time- and frequency-domain measurements of HRV by 24-hour Holter monitoring in 60 patients with acute myocardial infarction (AMI). After a first Holter recording (65 +/- 8 hours from the onset of symptoms), patients were randomly assigned to continue standard treatment or to also receive verapamil retard (120 mg 3 times daily) or felodipine extended-release (10 mg/day). Holter recording was repeated after 7 days. After verapamil, mean RR interval increased from 823 +/- 92 to 907 +/- 95 ms and the SD of all normal RR (NN) intervals (SDNN) from 99 +/- 24 to 120 +/- 30 ms (p < 0.01); the root mean square successive difference (r-MSSD) and the percent of differences between adjacent NN intervals > 50 ms (pNN50) also increased (p < 0.01). After felodipine, only SDNN increased (p < 0.01). Regarding frequency-domain measurements, after receiving verapamil, very low frequency, low- and high-frequency powers increased (p < 0.01), whereas the low- to high-frequency ratio decreased (p < 0.01). After receiving felodipine, very low-frequency power increased (p < 0.01), whereas low- and high-frequency powers and the low- to high-frequency ratio remained unchanged. This study demonstrates that verapamil, but not felodipine, improves HRV in the early phase after AMI.

Comparison of verapamil versus felodipine on heart rate variability in hypertensive patients.

OBJECTIVE We evaluated the effect of two calcium channel blockers, verapamil and felodipine, on heart rate variability in hypertensive patients. DESIGN Time and frequency domain measures of heart rate variability were obtained from 24 h Holter recording in 25 previously untreated hypertensive patients without left ventricular hypertrophy, before and after 3 months of verapamil slow-release treatment (240 mg once daily) or felodipine extended-release treatment (10 mg once daily). RESULTS Blood pressure values decreased with both drugs. Measures of heart rate variability, comparable at baseline in the two groups, were unchanged after felodipine. After verapamil, the average RR interval, the square root of the mean of the squared differences between all adjacent normal RR intervals (r-MSSD) and the percentage of differences between all adjacent normal RR intervals > 50 ms (pNN50), measures of vagal modulation of heart rate, increased (from 735 +/- 67 to 827 +/- 84 ms, P < 0.001; from 30 +/- 10 to 44 +/- 15 ms, P < 0.001; and from 3 +/- 2 to 7 +/- 6%, P < 0.01, respectively) and were higher than after felodipine. The coefficient of variation, a measure that compensates for heart rate effects, increased only after verapamil (from 5.8 +/- 1.3% to 6.6 +/- 1.0%; P < 0.05). High frequency power and its coefficient of component variance, both representing the vagal modulation of heart rate, increased after verapamil (from 5.33 +/- 0.29 to 5.80 +/- 0.27 In units, P < 0.001 and from 1.9 +/- 0.3 to 2.2 +/- 0.25%; P < 0.05). Finally, the low to high frequency power ratio, an indicator of sympathovagal balance, with a high value suggesting a sympathetic predominance, decreased after verapamil (from 2.16 +/- 0.41 to 1.36 +/- 0.35; P < 0.001), confirming the improvement in vagal modulation of heart rate. CONCLUSION In hypertensive patients, despite a comparable anti-hypertensive effect, verapamil, but not felodipine, has favourable effect on cardiac autonomic control.

Assessment of dynamic relationship between QT dispersion and RR interval in normal subjects

Little is known to what extent heart rate and its circadian variations can influence QT dispersion (QTd). Thus we studied the relationship between RR and QTd in 10 healthy subjects (6 M, 4 F mean age 32/spl plusmn/11 years). Beat-to-beat automated measurement of RR and QT was performed on a home-made analyzer. QTd was automatically measured for each beat on X, Y and Z leads. Mean hourly RR and QTd values were calculated for each 60 min period of 24-hour Holter recordings. A significant linear relationship was found between mean hourly RR and QTd values (r=.47; p=0.02). Hourly median RR values showed the expected circadian variation, with a nocturnal peak between 3 and 6 A.M. Similarly, there was a circadian rhythm in hourly median QTd values, with a prominent peak between the hours 2 and 3 A.M. In conclusion, in healthy subjects QTd is weakly correlated to RR and shows a circadian variation.

Relation of the total ejection isovolume index to symptoms in aortic stenosis

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