Importance of appropriate spectral methodology to assess heart rate variability in the frequency domain.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Pagani.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
OBJECTIVE: This study addresses the long term and short term effects of heavy dynamic exercise on neural control of heart rate. METHODS: A group of healthy controls was compared with (1) a group of trained athletes during a period of yearly rest (detrained) and (2) a group of trained athletes at the peak of their training routine. Additionally, a group of 10 controls was studied 1, 24, and 48 h after a single bout of maximal dynamic exercise. Spectral analysis of RR interval variability provided markers of sympathetic (low frequency, LF, 0.10 Hz) and vagal (high frequency, HF, 0.25 Hz) modulation of the sinoatrial node. RESULTS: (1) In detrained athletes resting bradycardia was accompanied by a predominant HF rhythmic component suggestive of a prevailing vagal tone. (2) Trained athletes showed a resting bradycardia together with high LF values, thus suggesting a more complex neural interaction modulating heart rate. An additional longitudinal part of the study, performed on a group of detrained athletes who were examined for the second time after resuming training, confirmed the finding of a prevailing LF component in resting conditions. (3) In the 10 control subjects maximal dynamic exercise induced an increase in LF which outlasted the cessation of exercise up to 24 h, suggesting a persistent sympathetic activation. (4) Passive tilt, a manoeuvre which enhances sympathetic drive, produced a greater enhancement of the LF component in trained athletes than in control subjects. CONCLUSIONS: The cardiac sympathetic excitation outlasting heavy dynamic exercise may explain the coexistence of training bradycardia with signs of enhanced sympathetic activity in trained champion athletes.
The aim of this study was to assess whether age-related changes in thoracic shape modify patterns of thoracoabdominal asynchrony (TAA) or applicability of phase angle analysis during sleep in young children with increased respiratory loads. We assessed TAA during polysomnographic monitoring in 14 young children (mean age 32 months, range 19 to 46; mean weight 12.5 kg, range 9.3 to 17) with severe bronchopulmonary dysplasia (BPD). Of the patients 10 were severely enough affected to require tracheostomy. We measured asynchrony of rib cage (RC) and abdominal (AB) movements at midinspiration and the corresponding phase angle from oscillographic recordings during both non-REM and REM sleep. We measured the amplitude of "paradoxical" displacement of either RC or AB during inspiration and expressed this as a percentage of the total displacement of the compartment. Of 9 children who manifested early inspiratory AB paradox during non-REM sleep, 7 showed a figure eight on the Konno-Mead diagram. The magnitude of abdominal paradox during non-REM sleep was significantly positively correlated with age (n = 14, r = 0.68; p < 0.01). Phase angle was significantly negatively correlated with dynamic lung compliance (n = 14, r = -0.66; p < 0.01). During REM sleep, expiratory abdominal muscle activity was abolished and all patients with abdominal paradox "converted" to an open loop with RC paradox during inspiration. Graphic assessment of the Lissajous figure on the Konno-Mead diagram indicated when midinspiratory phase angle analysis did not reflect the severity of TAA and can be used to infer patterns of respiratory muscle recruitment. We conclude that young children manifest patterns of TAA that differ from the early inspiratory RC paradox commonly observed in infants. Comparison of RC-AB loops between non-REM and REM sleep in the same child can assess increased thoracic inspiratory efforts and expiratory muscle activity as potential mechanisms for abdominal paradox, as distinct from diaphragm ineffectiveness.
There is strong circumstantial evidence supporting the hypothesis that essential arterial hypertension is associated at least initially, with an augmented sympathetic activity. The link between the sympathetic nervous system and the hypertensive state is further supported by the clinical evidence furnished by the efficacy of drugs interfering with sympathetic control. In this lecture we address the role of behavioral and mental factors, globally indicated with the word "stress", that may contribute to the initiation and maintenance of the hypertensive condition. At the core of this approach, there is the view that, operationally, mental stress could be conveniently substituted by some quantification of the sympathetic activity (in its continuous balance with vagal modulation). In our laboratory we employ the normalized power of the low frequency (LF, 0.1 Hz) component of the autospectra of RR interval variability as an index of sympathetic drive. In hypertensives at rest there is a prevalence of LF (as compared to the HF, high frequency, component, which is a marker of vagal activity). Additionally the responsiveness to both physical and mental stimuli is diminished. After chronic beta-adrenergic blockade, the spectral profile, and its responsiveness, returns toward normal. Furthermore the gain of baroreflex mechanisms (obtained with cross spectral analysis of RR interval and systolic arterial pressure variability) is also increased by atenolol treatment. We conclude that this approach may permit a better quantification of the role played by behavioral and mental factors in essential hypertension, and help to define individualized treatments.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Animal experiments suggest that an important component of the antihypertensive effects of ACE inhibitors might derive from an inhibition of the sympathetic vasomotor tone. We addressed this problem on 22 mildly hypertensive subjects (48 +/- 2 years; arterial pressure 151 +/- 3/95 +/- 1 mmHg), in whom sympathetic vasomotor tone was non invasively inferred by the power of the low frequency component (0.1 Hz) of the spontaneous oscillations of systolic arterial pressure (LFSAP), during placebo and after 4 weeks of treatment with a new ACE inhibitor, cilazapril, 5 mg per os oid. LFSAP was computed at rest and during physical (active orthostatism) and mental (computerized attentional test and mental arithmetic) stimuli capable of enhancing sympathetic drive. Cilazapril treatment reduced resting arterial pressure to 128 +/- 3/80 +/- 2 mmHg, without affecting heart rate (78 +/- 2 and 74 +/- 2 b/min, respectively). The increases in LFSAP produced by standing were significantly greater during placebo than during active treatment (delta LFSAP = 10 +/- 3 and 5 +/- 2 mmHg2, respectively). These data suggest that an important reduction of sympathetic vasomotor tone accompanies the antihypertensive effects of chronic ACE-inhibitor treatment.
Explore the source record for details and available documents.
In 11 subjects with mild hypertension (sitting arterial pressure of 146 +/- 5/97 +/- 2 mm Hg), the effects of chronic angiotensin-converting enzyme (ACE) inhibition (cilazapril, 5 mg p.o. once daily for 4 weeks) were studied at rest and during active standing by means of spectral analysis. Sympathetic vascular control was inferred from the power of the low-frequency (LF) component of the systolic arterial pressure (SAP) variability, assessed noninvasively with a plethysmographic technique. Simultaneously, quantitative indices of neural control of the sinoatrial (SA) node were obtained with the power of the LF and of the high-frequency (respiration linked) component of R-R variability. Before treatment, active standing produced a clear increase in the LF components of R-R and SAP variabilities. At the end of the 4 weeks of cilazapril treatment, the LF component of SAP variability during standing was significantly lower than prior to treatment, while the increase in the LF component of R-R variability was left unchanged. These findings suggest an inhibitory effect of chronic ACE inhibition upon vasomotor sympathetic control, as assessed non-invasively by this technique.
The neural mechanisms accompanying dynamic exercise of different intensities were analyzed in dogs and human subjects by means of autoregressive spectral analysis of heart period and arterial pressure variabilities. In the animal experiments, 8 conscious dogs were examined after implanting a solid state pressure gauge in the left ventricle. Animals were examined at rest and during a treadmill run, at 4 km/h, and 0 degrees incline. The experiments were repeated after chronic alpha 1-adrenoreceptor blockade. During the treadmill run, heart rate and systolic left ventricular pressure increased significantly. Simultaneously, the low frequency (LF, 0.1 Hz) component of pulse interval and of systolic pressure variabilities, ie, markers, respectively, of sympathetic modulation of the SA node and of vasomotor activity, increased significantly (evaluated respectively, in normalized and absolute units). After chronic alpha 1-adrenoreceptor blockade, the increase in LF component of systolic pressure variability was prevented, while that observed in R-R interval variability was maintained. Human studies were carried out with either invasive or noninvasive techniques. In the former approach already described, performed in young hypertensive subjects, arterial pressure was recorded with a high fidelity technique. In the second approach applied to young champion swimmers, only the variability of the R-R interval was examined. In both studies, moderate levels of exercise were accompanied by an increase in the LF component of the spectrum: in the case of arterial pressure variability, this increase was detectable both in absolute and normalized units; vice versa, in the case of R-R variability, since physical exercise is accompanied by a marked abatement of the variance, normalized units had to be used in order to evaluate the shift of the sympathovagal balance in favor of sympathetic overactivity.
In this study we addressed the problem of the noninvasive evaluation of the overall gain of baroreceptor control of heart period. We studied a population of healthy controls (n = 49, age 30 +/- 2 years, systolic arterial pressure [by Finapres] 114 +/- 1 mmHg) and a group of mild hypertensive subjects (n = 14, age 51 +/- 2 years, systolic arterial pressure 151 +/- 5 mmHg). Subjects were studied at rest both in absence and in presence of chronic beta-adrenergic receptor blockade (atenolol: controls 50 mg po oid x 4 days; hypertensives 100 mg po oid x 2 weeks). Spectral analysis of RR interval and of systolic arterial pressure variabilities provided noninvasive markers of autonomic control of the SA node and of the vasculature. The index alpha, obtained from bivariate cross spectral and spectral analysis provided a quantitative assessment of the closed loop gain of baroreceptor control of the heart period. The index alpha resulted more elevated in the normotensive than in the hypertensive group. Additionally it appeared significantly increased at the end of the treatment with the beta-adrenergic blocking drug atenolol. Furthermore, alpha appeared significantly and negatively correlated with age, systolic arterial pressure and, although weakly, with low frequency; it was positively correlated with the average RR interval. In conclusion, this study suggested an important link between the average level of sympathetic activity and baroreceptor control of heart rate in normotensive and mild hypertensive subjects. The clinical importance of this sympathetic modulation of the gain of the heart period/arterial pressure relationship can now be assessed with this noninvasive approach.
The Authors have analyzed all different methods for the treatment of gallbladder stones which are performed today: the non invasive treatment of the gallstones (oral dissolution therapy and the extracorporeal shockwave lithotripsy), the minimally invasive procedures (contact dissolution therapy and the cholecystolithotomy) and at the end the new surgical techniques (the "minicholecystectomy" and the laparoscopic cholecystectomy). From this study and their experience, based upon 1346 standard cholecystectomy, the Authors have reached the following conclusions: 1) the cholecystectomy remains the only definitive therapy for the gallbladder stones and it is the gold standard to which must be compared the other alternative therapies; 2) the laparoscopic cholecystectomy, even though introduced recently, would become the only method used for cholecystectomy.
In this study, we used spectral analysis of short-term R-R and systolic arterial pressure (SAP) variabilities to estimate the changes in neural control of the circulation produced by psychological stress. The 0.1 Hz low-frequency (LF) component of R-R and SAP variabilities provided a quantitative index of the sympathetic activity controlling heart rate and vasomotion. Conversely the high-frequency (HF) respiratory component of R-R variability provided an index of vagal tone. In conscious dogs we used the seemingly stressful situation of being accompanied for the first time to the experimental laboratory as a stimulus. In human subjects we used mental arithmetic. In both cases LF of R-R and SAP variabilities increased significantly suggesting enhanced sympathetic activity both to the SA node and the vasculature. In man, the index alpha, a measure of the overall gain of baroreceptor mechanisms, was found to be reduced during mental arithmetic. Spectral analysis of cardiovascular variabilities thus suggests that in man and in conscious dogs psychological challenges induce a profound re-arrangement of neural control of the circulation, which appears to be characterised by sympathetic predominance and which can be monitored by this technique.
Explore the source record for details and available documents.
Transcranial Doppler sonography (TCD) was used in 33 patients undergoing carotid endarterectomy (CEA). Mean flow velocity (MCA MV) and the pulsatility index in the middle cerebral artery (MCA PI) were measured pre- and on six occasions postoperatively. The MCA MV was reduced by anaesthesia but was increased postoperatively (+43%, p less than 0.001) compared to the preoperative value and was still increased at late follow-up after several months. The MCA PI, which was lower preoperatively than normally reported in this age group, was not changed by anaesthesia but then rose and remained elevated, i.e. within normal limits 72 h postoperatively (+30%, p less than 0.01) as well as at late follow-up. No significant changes in MCA MV or MCA PI were noted on the contralateral side. The results from this study support earlier findings from invasive studies showing that CEA results in an increased flow in the middle cerebral artery on the operated side and an increased MCA PI suggests an increased resistance on the operated side. The findings are compatible with an increased cerebral blood flow during the first days after CEA and with the operated side supplying a greater part of the cerebral blood flow even several months after surgery.