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Stroke. 1997;28:1671-1676

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(Stroke. 1997;28:1671-1676.)
© 1997 American Heart Association, Inc.

Articles

Cardiac Baroreceptor Sensitivity Is Impaired After Acute Stroke

Thompson G. Robinson, MRCP(UK); Martin James, MD; Jane Youde, MRCP(UK); Ronney Panerai, PhD; John Potter, DM

From the University Division of Medicine for the Elderly, The Glenfield Hospital, and the University Division of Medical Physics, Leicester Royal Infirmary (R.P.), Leicester, UK.

Correspondence to Dr T.G. Robinson, Department of Medicine, Leicester General Hospital, Gwendolen Rd, Leicester LE5 4PW, UK.


*    Abstract
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 *Abstract
down arrowIntroduction
 down arrowSubjects and Methods
 down arrowResults
 down arrowDiscussion
 down arrowReferences
 
Background and Purpose The blood pressure (BP) fall and increased BP variability after acute stroke have been previously described. The underlying pathophysiological mechanisms producing these findings are unclear but may include abnormalities of cardiac baroreceptor reflex arc and/or changes in sympathetic nervous system activity. To date, evidence of impaired cardiac baroreceptor sensitivity (BRS) after stroke is limited to patients with chronic disease as determined by invasive methodology. Therefore, it was proposed to assess cardiac BRS and sympathovagal balance with the use of novel noninvasive techniques after acute stroke.

Methods Thirty-seven acute stroke patients underwent simultaneous surface electrocardiographic and noninvasive beat-to-beat BP recording. Cardiac BRS was assessed by power spectral analysis techniques, and sympathovagal balance was determined from the ratio of the low- to high-frequency powers for pulse interval variability. The responses were compared with a control group matched for age, sex, and BP.

Results Median cardiac BRS was significantly lower in stroke patients than in control subjects (high-frequency {alpha}-index, 4.89 versus 6.50 ms/mm Hg; P=.007; combined {alpha}-index, 4.65 versus 5.46 ms/mm Hg; P=.02). Median normalized high- but not low-frequency power of systolic BP variability was significantly greater in stroke patients (11.0 versus 6.7 normalized units; P<.001), probably reflecting differences in the mechanical effects of respiration on BP in stroke patients. No significant differences were observed in the power spectrum of pulse interval variability between stroke patients and control subjects. Patients with right hemisphere strokes, however, had a significant reduction in median high-frequency pulse interval power compared with patients with left hemisphere strokes (8 versus 20 normalized units; P=.03), which may reflect a change in sympathovagal balance in favor of increased sympathetic tone in this group.

Conclusions The impairment of cardiac BRS may be important in explaining the increased BP variability after stroke. There was no significant difference in surrogate measures of sympathovagal activity between acute stroke patients and control subjects, but right hemisphere stroke patients had a significant alteration in the sympathovagal balance of pulse interval variability compared with left hemisphere stroke patients. This sympathetic predominance in right hemisphere strokes may be important in the development of cardiac arrhythmias after stroke. The prognostic implications of these findings need to be further explored.


Key Words: baroreflex • blood pressure • stroke, acute


*    Introduction
up arrowTop
 up arrowAbstract
 *Introduction
down arrowSubjects and Methods
 down arrowResults
 down arrowDiscussion
 down arrowReferences
 
Blood pressure levels are elevated within the first 24 hours of acute stroke and decrease spontaneously within 3 to 10 days in most patients.1 2 3 The underlying pathophysiological mechanisms producing such changes are debated but may be related to changes in sympathetic nervous system activity, as reflected by increases in catecholamine and corticosteroid levels.4 5 6 7 However, the baroreceptor reflex arc, which includes peripheral afferent (aortic and carotid baroreceptors) and efferent (vagal and sympathetic tone) as well as central mechanisms (brain stem and higher cerebral centers), may also play an important role in these BP changes after acute stroke.

To date, evidence of impaired cardiac BRS in stroke is limited to animal models8 9 and to patients with chronic disease as determined by invasive methodology.10 11 However, previous work in our department has shown an increase in short-term (beat-to-beat) systolic BP variability independent of the underlying BP level in acute stroke patients compared with control subjects matched with respect to age and sex.12 This may reflect impaired cardiac BRS, since BP variability is inversely related to BRS,13 14 15 or may be related to alterations in the vascular-baroreceptor reflex mediated by centrally induced changes in sympathetic nervous system activity.

The advent of newer, reliable, noninvasive techniques of beat-to-beat BP measurement16 17 18 19 together with the increased availability of powerful microcomputers and appropriate analysis techniques has made possible the calculation of cardiac BRS from the assessment of continuous BP and PI recordings taken at rest. BP and PI variability can be described in terms of the underlying rhythmic factors affecting the cardiovascular system, including the cardiac cycle, the respiratory cycle, and vasomotor activity.20 The technique of PSA with the use of FFT can be used to detect such underlying rhythmicity by assessing the number, frequency, and amplitude of the oscillatory components.21 Cardiac BRS can be estimated by calculation of the square root of the ratio of the powers of PI to SBP, the {alpha}-index, which has been shown to correlate well with cardiac BRS calculated by means of the "gold standard" pharmacological techniques.22 23 Furthermore, the powers of various components of the decomposed spectra of BP and PI variability can be compared and allow an assessment of the integrity of the underlying sympathovagal balance of autonomic cardiovascular system control.20 24 25

The aim of this study was to use these novel noninvasive techniques to assess the effects of acute stroke on cardiac BRS compared with an appropriately matched control population. In addition, it was proposed to indirectly assess the potential integrity of underlying parasympathetic and sympathetic neural cardiovascular control with the use of PSA techniques after acute stroke, and in particular to compare patients with right and left hemisphere strokes given reports of the laterality of cardiovascular control.26 27 28 29


*    Subjects and Methods
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 up arrowAbstract
 up arrowIntroduction
 *Subjects and Methods
down arrowResults
 down arrowDiscussion
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Subjects
Thirty-seven consecutive acute stroke patients (17 men; mean age, 69.4 years; range, 45 to 89 years) admitted to the medical wards of the Leicester Teaching Hospitals within 24 hours of ictus were studied. Head CT scanning was performed in 29 patients (24 with infarctions, 5 with hemorrhages). In addition, patients were classified by reference to the site of the neurological lesion (18 right hemisphere, 17 left hemisphere, and 2 cerebellar/brain stem). Of the 37 subjects, 14 had a history of hypertension, defined as a past medical history of SBP >=160 mm Hg and/or DBP >=90 mm Hg before stroke onset or history of antihypertensive therapy. However, those patients requiring the continuation of antihypertensive therapy or any treatment with effects on cardiovascular or autonomic function were excluded. Unconscious patients and those with atrial fibrillation or neurological signs lasting <24 hours were also excluded, as were patients with a past medical history or evidence at the time of study of diabetes mellitus, impaired renal function (creatinine >200 µmol/L), ischemic heart disease, or other conditions associated with autonomic dysfunction.

Thirty-seven control subjects matched with respect to age and sex (18 men; mean age, 67.5 years; range, 45 to 82 years) were also studied. These subjects were recruited from among respondents to a local newspaper advertisement, as well as elective orthopedic admissions before major joint replacement surgery. However, to ensure that the study groups would also be matched for BP, a proportion of untreated hypertensive control subjects (n=11) were recruited from among outpatient subjects at two of the Leicester Teaching Hospitals and through a liaison with several large local general practices. Control subjects with known diagnoses of ischemic heart disease, cerebrovascular disease, atrial fibrillation, diabetes mellitus, impaired renal function (creatinine >200 µmol/L), or other conditions associated with autonomic dysfunction were excluded. No subject received antihypertensive therapy or medication known to affect cardiovascular or autonomic responses.

Protocol
All stroke patients were assessed within 24 hours of stroke onset by one of us (T.G.R.). Height (or arm span), weight, and body mass index (weight [kilograms] divided by height [meters] squared) were recorded. After it was determined that there was no interarm difference in BP >10 mm Hg, casual supine BP was measured in the hemiparetic arm on three occasions with a standard mercury sphygmomanometer and cuff of appropriate size (diastolic phase V), and the mean value was taken in subsequent analysis. Control subjects were also assessed with casual BP recorded in the nondominant arm.

Noninvasive assessments of the cardiac BRS were thereafter performed in the cardiovascular laboratory. Stroke patients were assessed within 72 hours of ictus and at the time of study were hemodynamically stable, did not require intravenous or subcutaneous fluid administration, and were not clinically or biochemically dehydrated. Control subjects were assessed on one occasion, either on the day before surgery for elective orthopedic admissions or within 2 weeks of the last assessment visit for all other control subjects.

All subjects attended the cardiovascular laboratory at least 2 hours after a light meal and had abstained from smoking, alcohol, and all caffeinated products for at least 12 hours. The investigations took place in a quiet room (ambient temperature, 20°C to 24°C), and the subjects were asked to micturate before the study. The subject was fitted with chest leads for continuous electrocardiographic recording (model CR7, Cardiac Recorders Limited) and the appropriately sized cuff of the 2300 Finapres noninvasive BP monitor (Ohmeda). This is a fully automated instrument that allows continuous noninvasive assessment of finger arterial pressure. It uses the arterial clamp technique of Penaz30 and is well validated against intra-arterial BP measurements in all age groups.16 17 18 19 The cuff was fitted to the middle finger or thumb of the hemiparetic hand in stroke patients and the nondominant hand in control subjects and was maintained at heart level by resting on an adjustable support throughout.

After a period of at least 15 minutes of rest and after achievement of a satisfactory BP signal from the monitor and stabilization of BP at the same level (mean 2-minute BP levels not varying by >10 mm Hg over >=10 minutes), recordings were performed for three sequential periods of 10 minutes each. The Finapres device has a built-in system (Physio-Cal) that briefly interrupts the BP recording automatically to keep the finger arteries fully unloaded and the transmural pressure equal to zero (usually for 2 to 3 beats every 70 beats). This was switched off during the recording period but applied at 10-minute intervals during the monitoring period. Subjects were asked to maintain a respiratory rate >15 breaths per minute, although respiratory rate and tidal volume were not formally measured. No patients clinically exhibited Cheyne-Stokes respiration. The analog outputs from the Finapres and simultaneous surface electrocardiographic recordings underwent analog-to-digital conversion at a rate of 200 samples per second and were downloaded to a dedicated personal computer for subsequent analysis and noninvasive estimation of BRS.

Data Analysis
Software specially written by Leicester University Division of Medical Physics (R.P.), and which is in routine use in the department at which these studies were undertaken,31 32 was used in the off-line analysis of the beat-to-beat BP and PI recordings. The derived PI and SBP series were analyzed by means of PSA with FFT with 512 samples. The data segments used were extracted under visual inspection from the most stable (ie, stationary) segment of each 10-minute recording. The beat-to-beat series of PI and SBP were interpolated with a third-order polynomial and resampled with an interval of 0.5 second to produce signals with a uniform time axis. The power spectra were obtained as the average of three recordings for each patient and were smoothed with a 13-point triangular window. This produced estimates of power spectra of PI and SBP, coherence function, and frequency response between PI and SBP with 58 df. Coherence between BP and PI variability reflects the amount of linear coupling between the two spectra and is therefore comparable to the correlation coefficient in regression analysis. A coherence value >0.40 was considered significant.33 Recordings with an ectopy rate >2% were rejected. Spikes on the resampled tracings of the PI and SBP recordings were manually removed, and a straight line was interpolated by the computer, although resampled tracings with >4 spikes were excluded from subsequent analysis to avoid bias.

PSA estimates of cardiac BRS were obtained by calculation of the {alpha}-index (square root of the ratio of the powers of PI to BP) for the LF band (0.05 to 0.15 Hz), for the HF band (0.20 to 0.35 Hz), and for the combined {alpha}-index (0.5x[LF cardiac BRS+HF cardiac BRS]). To correct for variability in total and VLF powers (0.02 to 0.05 Hz), the powers of the LF and HF spectra for PI and for SBP were calculated in normalized units20 34 :



Statistical Methods
Normality of the data was determined by construction of a normal probability plot with the use of the Minitab statistical package (Minitab 10 for Windows, Minitab Inc). If a value of P<.05 was obtained with the Ryan-Joiner test, then the data were not considered normally distributed. For normally distributed data the results are presented as mean (SD), and statistical comparisons between stroke and control groups were made with the use of the Student's unpaired t test. For nonnormally distributed data, results are presented as median (range), and statistical comparisons between stroke and control groups were made with the Mann-Whitney test. Significance was taken at the 5% level.

Ethical Considerations
Subjects or their caregivers (when appropriate) gave their informed consent, and the study was approved by the Leicestershire Hospitals Ethical Committee.


*    Results
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 up arrowAbstract
 up arrowIntroduction
 up arrowSubjects and Methods
 *Results
down arrowDiscussion
 down arrowReferences
 
Stroke patients and control subjects were matched with respect to age, sex, and similar mean casual SBP and DBP levels (Table 1Down). However, baseline PI was significantly lower in the stroke patients (Table 1Down). Cardiac BRS was significantly reduced in acute stroke patients compared with control subjects matched with respect to age, sex, and BP as assessed in the HF band and by the combined {alpha}-index, although the difference in the LF band did not reach statistical significance (Table 2Down). In control subjects there was a negative correlation between cardiac BRS as assessed by the combined {alpha}-index and increasing SBP (r=-.40, P<.02), although the negative relationship with age was not significant (r=-.27, P=.11). Neither of these correlation coefficients was significant in acute stroke patients (age, r=-.25, P=.19; SBP, r=-.13, P=.51). Cardiac BRS and PI were positively correlated in the whole study group (r=.51, P<.001).


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  		Table 1. Baseline Characteristics of Stroke Patients and Control Subjects


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  		Table 2. Cardiac BRS Values in Acute Stroke Patients and Control Subjects Assessed by PSA Techniques Using FFT

No difference in the mean coherence between the SBP and PI spectra (reflecting the relationship between changes in PI and SBP) was seen for control subjects and acute stroke patients (LF band, 0.47 versus 0.47; HF band, 0.52 versus 0.45). The phase difference between PI and SBP was approximately 0° at HF but at LF was negative, implying that the SBP was leading the PI change, and therefore was consistent with a baroreceptor-derived response.

The analyses of cardiac BRS were repeated to compare the 24 acute stroke patients with a CT diagnosis of cerebral infarction and confirmed the results of the whole group. The HF BRS (4.75 [2.00 to 14.62] versus 6.50 [2.31 to 21.49] ms/mm Hg; P=.03) and combined {alpha}-indices(4.75 [1.86 to 13.31] versus 5.46 [2.82 to 16.83] ms/mm Hg; P=.05) were significantly lower in stroke patients than in control subjects, although differences in LF BRS did not reach statistical significance (4.51 [1.43 to 12.00] versus 5.08 [1.56 to 20.67] ms/mm Hg; P=.4).

The normalized values of the LF and HF components of the PI and SBP spectra were calculated. No significant differences were observed in the LF component of either PI or SBP spectra between acute stroke patients and control subjects (Table 3Down). However, the normalized power of the HF component of the SBP spectrum was significantly greater in acute stroke patients, with a significant reduction in the normalized ratio of LF to HF (Table 3Down). There was no significant difference in the ratio of LF to HF for PI between stroke patients and control subjects. The power spectra for PI (Fig 1Down) and SBP (Fig 2Down) are shown. The LF and HF components of the PI and SBP spectra were also compared in the 18 right and 17 left hemisphere stroke patients; the 2 patients with signs of cerebellar/brain stem stroke were excluded. Right hemisphere stroke patients showed a significant reduction in the normalized HF component of PI variability, with an associated increase in the ratio of LF to HF (Table 4Down).


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  		Table 3. PI and SBP Powers in Acute Stroke Patients and Control Subjects



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  		Figure 1. Power spectrum using the FFT for PI variability over frequency range 0 to 0.5 Hz in acute stroke patients and control subjects.



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  		Figure 2. Power spectrum using the FFT for SBP variability over frequency range 0 to 0.5 Hz in acute stroke patients and control subjects. Inset shows the differences between acute stroke patients and control subjects in the power spectrum for SBP variability in the HF range (0.20 to 0.35 Hz).


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  		Table 4. Absolute and Normalized Spectral Powers of PI and SBP Variability in Right Compared With Left Hemisphere Stroke Patients

SBP variability, as assessed by the SD of beat-to-beat BP recordings, was significantly increased in acute stroke patients compared with control subjects (14.7 [6.9] versus 10.9 [3.5] mm Hg; P=.008), although no significant difference was observed in PI variability (59.8 [36.7] versus 46.5 [22.5]; P=.09). Cardiac BRS, assessed by the combined {alpha}-index, was negatively correlated with SBP variability (r=-.11, P=.36) and positively correlated with PI variability (r=.36, P=.003).


*    Discussion
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowSubjects and Methods
 up arrowResults
 *Discussion
down arrowReferences
 
Cardiac BRS has been assessed with novel noninvasive techniques in stroke patients studied within 72 hours of ictus and control subjects matched with respect to age, sex, and BP. The present study demonstrated a significant reduction in cardiac BRS after acute stroke as assessed by PSA techniques with the use of FFT. These findings were confirmed when only patients with CT-diagnosed cerebral infarcts were included in the analysis. The ratio of LF to HF of PI variability, which has been shown to be a good surrogate marker of sympathovagal balance,20 24 25 was similar in stroke patients and control subjects. However, the HF component of SBP was significantly increased in the acute stroke patients.

The traditional pharmacological vasopressor (with the use of angiotensin or phenylephrine) and vasodepressor (with the use of nitroglycerin or sodium nitroprusside) stimuli are usually considered the gold standard techniques of cardiac BRS estimation. The development of alternative analyses for the assessment of cardiac BRS, including PSA techniques, has obviated the need for drug-induced BP disturbances and their potential shortcomings, and these techniques were used in the present study. The present study has demonstrated a significant reduction in cardiac BRS in patients studied within 72 hours of acute stroke and to our knowledge is the first study assessing cardiac BRS changes in the acute stroke period.

Impaired cardiac BRS may not be a benign phenomenon; it is now well recognized as a useful prognostic indicator after acute myocardial infarction.35 36 37 38 Odemuyiwa and colleagues38 observed that early markedly depressed cardiac BRS (<3 ms/mm Hg) predicted markedly depressed cardiac BRS at 3 months. This may explain the observation that impaired cardiac BRS after acute myocardial infarction identifies a group of patients at high risk of serious ventricular arrhythmias and sudden death not only acutely but for several months after myocardial infarction.39 40 Indeed, the importance of impaired cardiac BRS in the risk assessment of patients after acute myocardial infarction is currently being assessed in an ongoing multicenter trial, Autonomic Tone and Reflexes After Myocardial Infarction.41

Total SBP power reflecting beat-to-beat variability in SBP was increased in acute stroke patients compared with control subjects, although the difference was not statistically significant. However, SBP variability assessed by the SD of beat-to-beat BP recordings was significantly increased after acute stroke, in keeping with our previous findings.12 The possible explanations of this can now be considered in more detail. The short-term increase in BP variability may be inversely related to cardiac BRS,13 14 15 ie, the greater the BP variability, the less sensitive the baroreceptor. The present study has clearly demonstrated impaired cardiac BRS sensitivity in acute stroke patients compared with control subjects matched with respect to age, sex, and BP. However, baroreceptor-derived responses to BP variability are mediated by changes in PI or vasomotor tone, and no significant difference in PI variability in stroke patients compared with control subjects was observed, as we have previously reported.12 Issues related to vasomotor tone may also be important, and factors involved in vasomotor tone are understood to influence the VLF component of the power spectrum of BP variability,42 although influences on VLF power are imprecise and speculative25 and cannot be commented on in this study because of the short recording periods.

In addition to impaired cardiac BRS, increased short-term BP variability after acute stroke may be related to changes in sympathetic tone, although this was not reflected by an increase in SBP LF power, which may be a surrogate marker of sympathetic vasomotor tone.25 The increase in SBP HF power probably simply reflects the mechanical effects of respiration on BP,43 44 45 46 although formal measurements of respiratory rate or tidal volume were not made in the present study; this is a limitation of this study, particularly given the changes that may occur in the frequency and amplitude of respiration after stroke.

The present study found no significant difference in the power spectra for PI variability during supine rest between acute stroke patients and control subjects (Fig 1Up). Barron and colleagues47 have recently reported the results of the PSA of PI variability in 40 patients studied 4 to 11 days after ictus compared with age- and sex-matched control subjects. In contrast to the present study, they found a significant reduction in respiratory-related activity (frequency range not stated) in stroke patients. However, the results are expressed in absolute units despite a significant reduction in total power in the stroke patients. More importantly, the respiratory pattern of both groups is not clearly stated, despite the differing effects of spontaneous respiration and respiration controlled at different rates on the HF peak.48 Barron and colleagues also reported further differences in the PI variability power spectra between the 20 right and 20 left hemisphere strokes and found that respiratory-related activity was further reduced in right compared with left hemisphere stroke patients.47 Naver and colleagues49 also assessed PI changes, expressed by the ratio of maximum to minimum PI during a 1-minute cycle of 6 breaths per minute, and found evidence of selective parasympathetic dysfunction in right hemisphere stroke. The present study identified a significant reduction in normalized HF power in the 18 right hemisphere compared with the 17 left hemisphere patients. This resulted in a change in the sympathovagal balance, as evidenced by a significant increase in the normalized ratio of LF to HF in right hemisphere strokes and a resulting sympathetic predominance. Such a change in sympathetic tone may be important in explaining the increased risk of abnormalities of heart rate control after stroke.50 51 Lane and colleagues52 observed a significant increase in supraventricular arrhythmias after right hemisphere stroke and suggested that this may be related to an alteration in parasympathetic/sympathetic tone.

In summary, the present study, in which novel noninvasive techniques were used as an alternative to traditional pharmacological vasopressor and depressor methods, found that cardiac BRS was significantly reduced in acute stroke patients compared with age-, sex-, and BP-matched control subjects. The HF variability in SBP was significantly greater after acute stroke, probably reflecting differences in respiratory rate as well as volume on the mechanical effects of respiration on BP. No significant differences were found in PI variability between stroke patients and control subjects, suggesting that sympathovagal balance is not altered in the acute poststroke period. However, the increase in BP variability in the acute stroke period may have prognostic implications that require further study.


*    Selected Abbreviations and Acronyms
 
BP = blood pressure
BRS = baroreceptor sensitivity
DBP = diastolic blood pressure
FFT = fast Fourier transform
HF = high frequency (0.20 to 0.35 Hz)
LF = low frequency (0.05 to 0.15 Hz)
PI = pulse interval
PSA = power spectral analysis
SBP = systolic blood pressure
VLF = very low frequency (0.02 to 0.05 Hz)


*    Acknowledgments
 
This study was supported by a grant from the Stroke Association of the United Kingdom (Dr Robinson).

Received January 7, 1997; revision received April 18, 1997; accepted May 16, 1997.


*    References
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowSubjects and Methods
 up arrowResults
 up arrowDiscussion
 *References
 

  1. Britton M, Carlsson A, de Faire U. Blood pressure course in patients with acute stroke and matched controls. Stroke. 1986;17:861-864.[Abstract/Free Full Text]
  2. Jansen P, Schulte B, Poels E, Gribnau F. Course of blood pressure after cerebral infarction and transient ischaemic attack. Clin Neurol Neurosurg. 1987;89:243-246.[Medline] [Order article via Infotrieve]
  3. Harper G, Castleden C, Potter J. When can we diagnose hypertension after stroke? Age Ageing. 1991;20(suppl 1):P23. Abstract.
  4. Meyer J, Stoica E, Pascu I, Shimazu K, Hartmann A. Catecholamine concentrations in CSF and plasma of patients with cerebral infarction and haemorrhage. Brain. 1973;96:277-288.[Free Full Text]
  5. Feibel J, Baldwin C, Joynt R. Catecholamine-associated refractory hypertension following acute intracranial hemorrhage: control with propranolol. Ann Neurol. 1981;9:340-343.[Medline] [Order article via Infotrieve]
  6. Myers M, Norris J, Hachinski V, Sole M. Plasma norepinephrine in stroke. Stroke. 1981;12:200-204.[Abstract/Free Full Text]
  7. Olsson T. Urinary free cortisol excretion shortly after ischaemic stroke. J Intern Med. 1990;228:177-181.[Medline] [Order article via Infotrieve]
  8. Doba N, Reis D. Role of the cerebellum and the vestibular apparatus in regulation of orthostatic reflexes in the cat. Circ Res. 1974;34:9-18.[Abstract/Free Full Text]
  9. Cechetto D, Wilson J, Smith K, Wolski D, Silver M, Hachinski V. Autonomic and myocardial changes in middle cerebral artery occlusion: stroke models in the rat. Brain Res. 1989;502:296-305.[Medline] [Order article via Infotrieve]
  10. Appenzeller O, Descarries L. Circulatory reflexes in patients with cerebrovascular disease. N Engl J Med. 1964;271:820-823.
  11. Gross M. Circulatory reflexes in cerebral ischaemia involving different vascular territories. Clin Sci. 1970;38:491-502.[Medline] [Order article via Infotrieve]
  12. Robinson T, Ward-Close S, Potter J. A comparison of beat-to-beat blood pressure variability in acute and subacute stroke patients with cerebral infarction. Cerebrovasc Dis. 1997;7:214-219.
  13. Mancia G, Ferrari A, Gregorini L, Parati G, Pomidossi G, Bertinieri G, Grassi G, Zanchetti A. Blood pressure variability in man: its relation to high blood pressure, age and baroreceptor sensitivity. Clin Sci. 1980;59:401S-404S.
  14. Mancia G, Parati G, Pomidossi G, Casadei R, Di Rienzo M, Zanchetti A. Arterial baroreflex and blood pressure and heart rate variabilities in humans. Hypertension. 1986;8:147-153.[Abstract/Free Full Text]
  15. Floras J, Hassan M, Vann Jones J, Osikowska B, Sever P, Sleight P. Factors influencing blood pressure and heart rate variability in hypertensive humans. Hypertension. 1988;11:273-281.[Abstract/Free Full Text]
  16. Imholz B, van Montfrans G, Settels J, van der Hoeven G, Karemaker J, Wieling W. Continuous non-invasive blood pressure monitoring: reliability of Finapres device during Valsalva manoeuvre. Cardiovasc Res. 1988;22:390-397.[Medline] [Order article via Infotrieve]
  17. Parati G, Casadei R, Groppelli A, di Rienzo M, Mancia HG. Comparison of finger and intra-arterial blood pressure monitoring at rest and during laboratory testing. Hypertension. 1989;13:647-655.[Abstract/Free Full Text]
  18. Imholz B, Settels J, van der Meiracker A, Wesseling K, Wieling W. Non-invasive continuous finger blood pressure measurement during orthostatic stress compared to intra-arterial pressure. Cardiovasc Res. 1990;24:214-221.[Abstract/Free Full Text]
  19. Rongen G, Bos W, Lenders J, van Montfrans G, van Lier H, van Goudever J, Wesseling K, Thien T. Comparison of intrabrachial and finger blood pressure in healthy elderly volunteers. Am J Hypertens.. 1995;8:237-248.[Medline] [Order article via Infotrieve]
  20. Malliani A, Pagani M, Lombardi F, Cerutti S. Cardiovascular neural regulation explored in the frequency domain. Circulation. 1991;84:482-491.[Abstract/Free Full Text]
  21. Kay S, Marple S. Spectrum analysis: a modern perspective. Proc IEEE. 1981;69:1380-1419.
  22. Pagani M, Somers V, Furlan R, Dell'Orto S, Conway J, Baselli G, Cerutti S, Sleight P, Malliani A. Changes in autonomic regulation induced by physical training in mild hypertension. Hypertension. 1988;12:600-610.[Abstract/Free Full Text]
  23. James M, Panerai R, Potter J. Spectral and sequence analysis in the assessment of arterial baroreceptor sensitivity in the elderly. J Hypertens. 1996;12:1499. Abstract.
  24. Malliani A, Lombardi F, Pagani M. Power spectrum analysis of heart rate variability: a tool to explore neural regulatory mechanisms. Br Heart J. 1994;71:1-2.[Free Full Text]
  25. Parati G, Saul P, di Rienzo M, Mancia G. Spectral analysis of blood pressure and heart rate variability in evaluating cardiovascular regulation: a critical appraisal. Hypertension. 1995;25:1276-1286.[Abstract/Free Full Text]
  26. Rosen A, Gur R, Sussman N, Gur R, Hurtig H. Hemispheric asymmetry in the control of heart rate. Neurosci Abs. 1982;8:917. Abstract.
  27. Lane R, Novelty R, Cornell C, Zeitlin S, Schwartz G. Asymmetric hemispheric control of heart rate. Psychophysiology. 1988;25:464.
  28. Zamrini E, Meador K, Loring D, Nichols F, Lee G, Figueroa R, Thompson W. Unilateral cerebral inactivation produces differential left/right heart rate responses. Neurology. 1990;40:1408-1411.[Abstract/Free Full Text]
  29. Lane R, Abrams R, Schwartz C, DuBois M, Van A. Differential effects of right and left unilateral electroconvulsive therapy on heart rate. Psychophysiology. 1991;28:S36.
  30. Penaz J. Photoelectric measurement of blood pressure, volume and flow in the finger. In: Digest of the International Conference on Medicine and Biological Engineering, Conference Committee of the 10th International Conference on Medicine and Biological Engineering; Dresden, Germany; 1973:104.
  31. James M, Panerai R, Potter J. Comparison of spontaneous sequence analysis and pharmacological methods in assessment of the arterial baroreflex in the elderly. In: Proceedings of the 7th European Meeting on Hypertension; June 9-12, 1995; 86.
  32. Panerai R, James M, Potter J, Fan L, Evans D. Baroreceptor sensitivity in human subjects: sequence or spectral analysis? Comput Cardiol.. 1995;305-308.
  33. Panerai R, James M, Potter J. Impulse response analysis of baroreceptor sensitivity. Am J Physiol. 1997;272:H1866-H1875.[Abstract/Free Full Text]
  34. Montano N, Ruscone T, Porta A, Lombardi F, Pagani M, Malliani A. Power spectrum analysis of heart rate variability to assess the changes in sympathovagal balance during graded orthostatic tilt. Circulation. 1994;90:1826-1831.[Abstract/Free Full Text]
  35. Schwartz P, Zoza A, Pala M, Locati E, Beria G, Zanchetti A. Baroreflex sensitivity and its evaluation during the first year after myocardial infarction. J Am Coll Cardiol. 1988;12:629-636.[Abstract]
  36. Osculati G, Grassi G, Giannattasio C, Seravalle G, Valagussa F, Zanchetti A, Mancia G. Early alterations of the baroreceptor control of heart rate in patients with acute myocardial infarction. Circulation. 1990;81:939-948.[Abstract/Free Full Text]
  37. Grassi G, Giannattasio C, Seravalle G, Osculati G, Valagussa F, Zanchetti A, Mancia G. Cardiopulmonary receptor and arterial baroreceptor after acute myocardial infarction. Am J Cardiol. 1992;69:873-878.[Medline] [Order article via Infotrieve]
  38. Odemuyiwa O, Farrell T, Staunton A, Sneddon J, Poloniecki J, Bennett D, Malik M, Camm J. Influence of thrombolytic therapy on the evaluation of baroreceptor sensitivity after myocardial infarction. Am Heart J. 1993;125:285-291.[Medline] [Order article via Infotrieve]
  39. La Rovere M, Specchia G, Montana A, Schwartz P. Baroreflex sensitivity, clinical correlates, and cardiovascular mortality among patients with a first myocardial infarction: a prospective study. Circulation. 1988;78:816-824.[Abstract/Free Full Text]
  40. Farrell T, Odemuyiwa O, Bashir Y, Cripps T, Malik M, Ward D, Camm A. Prognostic value of baroreceptor sensitivity testing after acute myocardial infarction. Br Heart J. 1992;67:129-137.[Abstract/Free Full Text]
  41. Maggioni A, Zuanetti G. Arrhythmias and the autonomic nervous system. J Cardiovasc Risk. 1994;1:322-331.[Medline] [Order article via Infotrieve]
  42. Akselrod S, Gordon D, Madwed J, Snidman N, Shannon D, Cohen R. Hemodynamic regulation: investigation by spectral analysis. Am J Physiol. 1985;249:867-875.
  43. DeBoer R, Karemaker J, Strackee J. Hemodynamic fluctuations and baroreflex sensitivity in humans: a beat-to-beat model. Am J Physiol. 1987;253:H1680-H1689.
  44. Peters J, Kindred M, Robotham J. Transient analysis of cardiopulmonary interactions, I: diastolic events. J Appl Physiol. 1988;64:1506-1517.[Abstract/Free Full Text]
  45. Peters J, Kindred M, Robotham J. Transient analysis of cardiopulmonary interactions, II: systolic events. J Appl Physiol. 1988;64:1518-1526.[Abstract/Free Full Text]
  46. Saul J, Berger R, Albrecht P, Stein S, Chen M, Cohen R. Transfer function analysis of the circulation: unique insights into cardiovascular regulation. Am J Physiol. 1991;261:H1231-H1245.[Abstract/Free Full Text]
  47. Barron S, Rogovski Z, Hemli J. Autonomic consequences of cerebral hemisphere infarction. Stroke. 1994;25:113-116.[Abstract]
  48. Sanderson J, Yeung L, Yeung D, Kay R, Tomlinson B, Critchley J, Woo K, Bernardi L. Impact of changes in respiratory frequency and posture on power spectral analysis of heart rate and systolic blood pressure variability in normal subjects and patients with heart failure. Clin Sci. 1996;91:35-63.[Medline] [Order article via Infotrieve]
  49. Naver H, Blomstrand C, Wallin B. Reduced heart rate variability after right-sided stroke. Stroke. 1996;27:247-251.[Abstract/Free Full Text]
  50. Natelson B. Neurocardiology: an interdisciplinary area for the 80s. Arch Neurol. 1985;42:178-184.[Abstract]
  51. Talman W. Cardiovascular regulation and lesions of the central nervous system. Ann Neurol. 1985;18:1-12.[Medline] [Order article via Infotrieve]
  52. Lane R, Wallace J, Petrosky P, Schwartz G, Gradman A. Supraventricular tachycardia in patients with right hemisphere strokes. Stroke. 1992;23:362-366.[Abstract/Free Full Text]



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