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ABSTRACT: In patients with refractory neurally mediated syncope, tilt training--standing motionless against a wall for increased periods of time per day over one month--can often eliminate recurrent episodes and reduce presyncopal symptoms. We designed dual retrospective and prospective studies to assess cardiovascular autonomic function in subjects with recurrent syncope and identify the most effective length of tilt training between one and three months.
In the retrospective study, before tilt training, and in the prospective study, before and after training, all subjects underwent a recording for short-term spectral analysis of heart rate and systolic blood pressure variability. Before tilt-training, autonomic nervous system function differs in patients with recurrent neurally mediated syncope who respond to tilt training for one month and those who do not. "Responders", patients experiencing no episodes of syncope during the 12-month follow-up, had higher low-frequency power of RR (LF(RR)) (p < 0.05) and LF(RR) in normalized units (NU) (p < 0.001) and lower high-frequency power (HF(RR)) (p < 0.05) and HF(RR)NU (p < 0.001) than "non-responders", patients reporting at least one syncopal episode during the 12-month follow-up. In the retrospective study, no difference was found between spectral data for "non-responders" with positive responses to tilt test with and without nitro derivatives. Prolonging tilt-training to three months increased the number of responders (late-responders) by 80% (p < 0.001) and power spectral analysis of heart rate variability (HRV) before tilt training can identify late-responders by their low LF(RR)NUs (<40) and high HF(RR)Nus (>60). Furthermore in late-responders, tilt training brings about a change in cardiovascular autonomic function: at 3 months, LF(RR)NUs increase and HF(RR)NU diminish.
Power spectral analysis of HRV seems to be a useful tool to preselect patients who are most likely to benefit from prolonged therapy, thus increasing compliance.
International Journal of Cardiology 08/2006; 111(1):59-66. · 7.08 Impact Factor
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ABSTRACT: 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 alpha 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.
Clinical Science 07/2004; 107(1):55-61. · 4.61 Impact Factor
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ABSTRACT: In this study, we used spectral analysis to assess changes in respiratory recording variability during infusion of L-arginine and vitamin C, individually or together, in patients with chronic heart failure. We found that healthy subjects have a substantial ability to modulate sympathetic-mediated peripheral vascular resistance through endothelial synthesis of nitric oxide. Patients with chronic heart failure lose this ability.
The American Journal of Cardiology 04/2004; 93(5):650-4. · 3.37 Impact Factor
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ABSTRACT: Chronic heart failure (CHF) reduces baroreflex sensitivity. Low baroreflex sensitivity, a risk factor for sudden death, could arise partly from CHF-dependent endothelial dysfunction. Vitamin C at high doses has a protective role against CHF-related endothelial damage. This study was conducted to investigate the effect of vitamin C on baroreflex sensitivity in CHF. A study group of 33 subjects with CHF secondary to postischemic dilated cardiomyopathy with an ejection fraction </=35% and a control group (11 subjects) underwent assessment of baroreflex sensitivity by the phenylephrine method and an autonomic nervous system study by power spectral analysis. Variables were assessed after infusion of placebo and high doses of vitamin C (2.5 mg). In subjects with CHF, baroreflex sensitivity was significantly higher after vitamin C than after placebo infusion (placebo: 4.1+/-0.4 versus vitamin C: 5.3+/-0.5 ms/mm Hg, P<0.001). Low-frequency of R-R (LFRR), expressed in normalized units (NU) (P<0.05); LF/high-frequency (HF) ratio (P<0.05), and LF of SBP (LFSBP) decreased significantly; HF power (P<0.05), and alpha-HF (P<0.001) increased. Conversely, in the control group, baroreflex sensitivity and other spectral variables measured at baseline, after placebo, and after vitamin C infusion remained statistically unchanged (placebo: 10.2+/-0.1 versus vitamin C: 10.0+/-0.2 ms/mm Hg, NS). Acute administration of vitamin C at high doses improves baroreflex sensitivity and vagal sinus modulation in patients with CHF. This finding could have notable clinical and therapeutic implications. Key issues to understand are whether the beneficial effect persists during chronic administration and whether it helps to improve survival.
Hypertension 06/2003; 41(6):1240-5. · 6.21 Impact Factor
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ABSTRACT: Am J Hypertens (2003) 16, 89A–89A; doi:10.1016/S0895-7061(03)00304-2
P-139: Influence of long-term of carvedilol and metoprolol therapy on cardiovascular autonomic control and QT variability in patients with heart failure
Gianfranco Piccirillo1, Marialuce Nocco1, Camilla Naso1, Antonio Moisè1, Marco Lionetti1, Damiano Magrì1, Tiziana De Laurentis1, Sabrina Matera1 and Vincenzo Marigliano11Dipartimento di Scienze dell’Invecchiamento, Università La Sapienza, Rome, Italy
American Journal of Hypertension 04/2003; · 3.18 Impact Factor
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ABSTRACT: Chronic heart failure (CHF) is a risk factor for sudden death. Temporal and spatial changes in repolarization are among the most studied mechanisms for inducing fatal ventricular arrhythmias. Beta blockers effectively reduce the risk of sudden death in CHF. Our aim in this study was to investigate changes induced by metoprolol and carvedilol on the QT variability index (QTVI), a new measure reflecting the temporal heterogeneity of cardiac repolarization. A total of 82 subjects, who were in New York Heart Association functional class II or III, underwent short-term spectral analysis of RR and QT variability before and after a 1-year course of high-dose metoprolol (40 subjects) or carvedilol (42 subjects) at baseline (rest) and after sympathetic stress (head-up tilt). At rest, both drug-treated groups had lower QTVI (p <0.001) than after placebo, but during tilt patients treated with carvedilol had a lower QTVI than those treated with metoprolol (p <0.05). Although both beta-blocker treatments helped to normalize the QTVI measured in normal subjects at rest, they each differentially altered the index after tilt. Carvedilol seemed to improve the QTVI more than metoprolol.
The American Journal of Cardiology 12/2002; 90(10):1113-7. · 3.37 Impact Factor
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ABSTRACT: 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; chi(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.
Clinical Science 04/2002; 102(3):363-71. · 4.61 Impact Factor
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ABSTRACT: Cases of sudden death associated with sildenafil citrate use have been reported in men with coronary artery disease. The aim of this study was to investigate the drug's effect on cardiac repolarization and sinus autonomic and vascular control in men with mild chronic heart failure (CHF; New York Heart Association classification II). Changes in these variables could predispose patients to malignant ventricular arrhythmias.
We measured QT dispersion, the QT-RR slope, and the index of QT variability (QTVI) and analyzed spectral power of RR and systolic blood pressure variability in 10 men with dilated cardiomyopathy and in 10 control subjects after administration of a single 50-mg oral dose of sildenafil citrate or placebo at rest (not followed with any attempt at intercourse).
In both groups, oral sildenafil citrate decreased the systolic blood pressure (P <.05) and increased the heart rate (P <.05). In subjects with CHF, it also increased the QT-RR (P <.001) and QTVI (from -0.45 +/- 0.07 to -0.27 +/- 0.07; P <.001), but in controls, it increased the QTVI (from -1.20 +/- 0.08 to -0.78 +/-.014; P <.001). In these subjects and controls, oral sildenafil citrate induced a significant reduction in high frequency, expressed in absolute power (subjects with CHF: from 4.04 +/- 0.14 to 3.43 +/- 0.16 natural logarithm ms2; P <.001; controls: from 5.61 +/- 0.44 to 4.98 +/- 0.32 natural logarithm ms2; P <.05) and in normalized units (P <.05). In subjects with CHF but not in controls, it also significantly increased the low frequency to high frequency ratio (from 1.3 +/- 0.12 to 1.89 +/- 0.16; P <.001) and low frequency expressed in normalized units (P <.05). Sildenafil citrate caused no significant changes in the QT interval or dispersion.
These findings indicate that, in men with heart failure, sildenafil citrate reduces vagal modulation and increases sympathetic modulation, probably through its reflex vasodilatory action. The autonomic system changes induced with sildenafil citrate could alter QT dynamics. Both changes could favor the onset of lethal ventricular arrhythmias. At the dose usually taken for erectile dysfunction, sildenafil citrate has no direct effect on cardiac repolarization (QT interval or dispersion).
American heart journal 04/2002; 143(4):703-10. · 4.65 Impact Factor
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ABSTRACT: 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 ( index).RESULTS: The population, subdivided into tertiles for each variable studied, had lower BSphe values and lower indexes as a function of age, plasma low-density lipoprotein (LDL) cholesterol, and systolic blood pressure. The 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 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.
Journal of the American Geriatrics Society 12/2001; 49(8):1059 - 1065. · 3.74 Impact Factor
