Gender difference in autonomic and hemodynamic reactions to abrupt coronary occlusion.

OBJECTIVES: We sought to determine whether there are gender-related differences in autonomic and hemodynamic responses to abrupt coronary occlusion. BACKGROUND: The risk of sudden death before hospital admission is higher in men with an acute myocardial infarction. The reasons for this gender-related difference are not well understood. Cardiovascular autonomic regulation modifies the outcome of acute coronary events, and there are gender differences in the autonomic regulation of heart rate (HR) in normal physiologic circumstances. METHODS: We analyzed the changes in HR, HR variability and blood pressure and the occurrence of ventricular ectopic beats during a 2-min coronary occlusion in 140 men and 65 women referred for single-vessel coronary angioplasty. The ranges of nonspecific responses were determined by analyzing a control group of 19 patients with no ischemia during a 2-min balloon inflation in a totally occluded coronary artery. RESULTS: Women more often had ST segment changes (p < 0.01) and chest pain (p < 0.05) during the occlusion. Significant bradycardia or increase in HR variability as a sign of vagal activation occurred more often in women than in men (31% vs. 13%, p < 0.01 and 25% vs. 11%, p < 0.05, respectively). Coronary occlusion also more often caused (28% vs. 11%, p < 0.01) a decrease in blood pressure in women. The most pronounced female preponderance was in the incidence of Bezold-Jarisch-type reaction (i.e., simultaneous bradycardia and decrease in blood pressure [16% vs. 0.7%, p < 0.0001]). Logistic regression models developed to analyze the significance of gender while controlling for baseline variables and signs of ischemia identified female gender to be an independent predictor of bradycardic reactions (odds ratio [OR] 3.2, 95% confidence interval [CI] 1.4 to 7.7, p < 0.01), hypotensive reactions (OR 2.6, 95% CI 1.1 to 6.0, p < 0.05) and Bezold-Jarisch-type response (OR 22.2, 95% CI 2.5 to 200, p < 0.01). Significance of female gender as a protector against early coronary occlusion-induced ventricular ectopic beats emerged as having borderline significance (OR 0.4, CI 0.1 to 1.1, p = 0.07). CONCLUSIONS: Vagal activation is more common in women than in men during abrupt coronary occlusion and may have beneficial antiarrhythmic effects, modifying the outcome of acute coronary events.

Arterial baroreflex impairment in patients during acute coronary occlusion.

OBJECTIVES: We tested whether acute coronary occlusion interferes with arterial baroreceptor control of heart rate in humans. BACKGROUND: Subnormal baroreflex sensitivity (BRS) is an important risk indicator for sudden death. Animal research indicates that both chronic myocardial infarction and acute coronary occlusion impair baroreflex modulation of heart rate. METHODS: We measured RR interval prolongation after phenylephrine-induced systolic pressure increases before and during 2-min coronary occlusions in 47 patients (27 men) undergoing clinically indicated single-vessel coronary angioplasty for stenoses in the proximal or midportion of the vessel causing >50% reduction in the arterial diameter, with normal antegrade flow (33 anterior descending, 10 circumflex, 4 right coronary artery). A control group of 11 patients treated for chronic total occlusion of a coronary artery was assessed to evaluate nonspecific changes in baroreflex function during a 2-min balloon inflation in the occluded artery. RESULTS: The BRS decreased from 5.2+/-3.8 (mean+/-SD) to 4.1+/-3.5 ms x mm Hg(-1) (p=0.01) during the coronary occlusion in the 28 patients with preserved arterial baroreceptor control of heart rate-that is, adequate blood pressure responses and correlation coefficients of the slopes both in baseline and during coronary occlusion. The same phenylephrine dose increased systolic pressure less during than before coronary artery occlusion (21+/-21 versus 36+/-16 mm Hg, p < 0.0001), and in 6 patients it failed to prevent systolic pressure reduction during occlusion. Correlation coefficients of the baroreflex regressions decreased from 0.81+/-0.27 to 0.47+/-0.44 (p < 0.0001) during coronary artery occlusion in the 41 patients with adequate systolic pressure rises in both phenylephrine tests, and the association between RR intervals and rising systolic pressures was lost in 13 patients during coronary occlusion. Balloon inflation in a chronic total occlusion of a coronary artery did not cause significant changes in BRS (from 5.3+/-4.0 to 5.2+/-3.7 ms x mm Hg(-1)), correlation coefficient of the slope or phenylephrine-induced pressure rise. CONCLUSIONS: Our study shows that abrupt coronary occlusion impairs baroreflex modulation of vagal and sympathetic nervous outflow in humans.

Low-dose transdermal scopolamine decreases blood pressure in mild essential hypertension.

BACKGROUND: Increasing cardiovascular parasympathetic nervous activity could have antihypertensive effects. Low-dose transdermal scopolamine increases vagal-cardiac modulation of sinus node and baroreflex sensitivity in healthy subjects and in cardiac patients. OBJECTIVE: To study the short-term effects of transdermal scopolamine on blood pressure and cardiovascular autonomic control in patients with mild essential hypertension. DESIGN: A randomized, double-blind, placebo-controlled crossover trial with 12 untreated middle-aged [aged 39+/-5 years (mean+/-SD)] patients with mild essential hypertension. METHODS: We recorded the electrocardiogram, auscultatory sphygmomanometric and continuous photoplethysmographic finger arterial pressure, and spirometry signals with patients supine and 70 degrees tilted during controlled (0.25 Hz) breathing. Cardiovascular autonomic regulation was analyzed with power spectrum analysis of R-R interval and arterial pressure variability and a spontaneous sequence method for baroreflex sensitivity. In addition, a deep-breathing test was performed to assess maximal breathing-related sinus arrhythmia. RESULTS: Transdermal scopolamine treatment significantly decreased blood pressure both when patients lay supine and when they were in the 70 degrees tilted position. Scopolamine also slowed heart rate and increased baroreflex sensitivity and R-R interval high-frequency variability for both body positionings. In addition, scopolamine accentuated respiratory sinus arrhythmia during deep breathing and blunted the tilt-induced increase in heart rate. Scopolamine did not affect blood pressure variability. CONCLUSIONS: Transdermal scopolamine decreases arterial pressure, increases baroreflex sensitivity and accentuates vagal-cardiac modulation of sinus node in patients with mild hypertension. Our study supports the hypothesis that increasing cardiovascular parasympathetic activity could have antihypertensive effects in essential hypertension.

Heart rate variability and occurrence of ventricular arrhythmias during balloon occlusion of a major coronary artery.

Experimental studies suggest that autonomic mechanisms are important in the genesis of ischemia-induced malignant ventricular arrhythmias, but the role of the autonomic nervous system in human arrhythmogenesis is not well known. To assess whether heart rate variability (HRV) predicts the occurrence of ventricular arrhythmias during acute coronary artery occlusion, we performed continuous electrocardiographic, heart rate, and blood pressure recordings before and during a 2-minute balloon occlusion of a stenotic coronary artery in 252 patients with no baseline ventricular premature complexes (VPCs). The ranges of nonspecific responses in heart rate and blood pressure were determined by analyzing a control group of 19 patients with no ischemia during a 2-minute balloon inflation in a totally occluded coronary artery. Balloon occlusion of a coronary artery was stopped because of complex, i.e., bigeminal or repetitive, VPCs in 14 patients, and solitary (<5) VPCs were observed in an additional 19 patients. During coronary occlusion, HRV increased (p <0.001) and heart rate decreased (p <0.05) in patients with no VPCs, whereas an opposite tendency to reduction in HRV (p = 0.08) was observed in patients with complex VPCs. Complex VPCs were observed in 5 (42%) of the 12 patients with a significant coronary occlusion-induced decrease in HRV, in 7 (3.5%) of 200 patients with no change in HRV, but in none of the 40 patients with a significant increase in HRV (p <0.001). Baseline HRV did not predict the occurrence of VPCs during coronary occlusion. Logistic regression analysis identified the decrease in HRV (p <0.001) to be the only independent predictor of complex VPCs. In conclusion, coronary occlusion-induced increase in HRV seems to protect against occurrence of complex ventricular arrhythmias during the early phase of abrupt coronary occlusion, suggesting that vagal activation may modify the outcome of acute coronary events in patients with coronary artery disease.

Baroreflex sensitivity in drug-treated systemic hypertension.

Baroreflex sensitivity is impaired in patients with systemic hypertension. The persistence of abnormal baroreflex sensitivity despite adequate blood pressure control may be one of the reasons why the effect of antihypertensive therapy on coronary artery disease mortality has been less than expected on the basis of the achieved blood pressure levels.

Cardiac positron emission tomography imaging with [11C]hydroxyephedrine, a specific tracer for sympathetic nerve endings, and its functional correlates in congestive heart failure.

The integrative mechanisms of autonomic dysfunction in congestive heart failure (CHF) remain poorly understood. We sought to study cardiac retention of [11C]hydroxyephedrine (HED), a specific tracer for sympathetic presynaptic innervation, and its functional correlates in CHF. Thirty patients with mild to moderate heart failure underwent resting cardiac HED positron emission tomography imaging, spectrum analysis testing of systolic pressure and heart rate variability in the resting supine and 70 degrees head-up tilt positions, and testing of baroreflex sensitivity. Compared with control subjects, global myocardial HED retention index was reduced by 30% (p <0.01) in patients with CHF. The HED retention index did not correlate significantly with heart rate variability. However, it correlated with baroreflex sensitivity at rest (r = 0.43, p = 0.05) and with systolic pressure low-frequency (0.03 to 0.15 Hz) variability at head-up tilt (r = 0.76, p <0.01), as well as with low-frequency systolic pressure variability response from baseline to tilt (r = 0.75, p <0.01). We conclude that cardiac HED retention is reduced in patients with CHF. This correlates with blunted vascular sympathetic effector responses during posture-induced reflex activation and baroreflex control of heart rate, suggesting an interdependence between cardiac presynaptic innervation abnormalities and neural mechanisms important to blood pressure maintenance in CHF.

Vagal cardiac activity in essential hypertension: the effects of metoprolol and ramipril.

Cardiovascular parasympathetic activity is attenuated in essential hypertension. Both beta-adrenoceptor antagonists and angiotensin converting enzyme inhibitors have been reported to increase vagal modulation of heart rate and baroreflex sensitivity, but the relations between the antihypertensive and vagal cardiac effects of these drugs have remained unclear in essential hypertension. In the present study we evaluated the effects of a 4-week crossover monotherapy with metoprolol and ramipril on spectrum analysis indices of heart rate variability in the supine rest and head-up tilted positions, baroreflex sensitivity (phenylephrine method), and 24-h ambulatory blood pressure (BP) in 12 formerly untreated stage 1-2 essential hypertensive patients. Compared to the pretreatment values, both drugs decreased BP similarly and significantly. However, the drugs showed different effects on cardiac vagal activity: metoprolol increased significantly mean R-R interval, R-R interval total, and high-frequency variability at supine rest and baroreflex sensitivity, but ramipril did not significantly affect these variables. The metoprolol-induced decrease in ambulatory BP correlated with the prolongation of the R-R interval and the increase of high-frequency variability at supine rest. The present data show that 4-week treatment with metoprolol increases tonic and reflex vagal cardiac activity, whereas ramipril does not affect vagal cardiac control in essential hypertension. Increase in vagal activity may contribute to the BP-lowering effect of metoprolol in hypertensive patients.

Nine months in space: effects on human autonomic cardiovascular regulation.

We studied three Russian cosmonauts to better understand how long-term exposure to microgravity affects autonomic cardiovascular control. We recorded the electrocardiogram, finger photoplethysmographic pressure, and respiratory flow before, during, and after two 9-mo missions to the Russian space station Mir. Measurements were made during four modes of breathing: 1) uncontrolled spontaneous breathing; 2) stepwise breathing at six different frequencies; 3) fixed-frequency breathing; and 4) random-frequency breathing. R wave-to-R wave (R-R) interval standard deviations decreased in all and respiratory frequency R-R interval spectral power decreased in two cosmonauts in space. Two weeks after the cosmonauts returned to Earth, R-R interval spectral power was decreased, and systolic pressure spectral power was increased in all. The transfer function between systolic pressures and R-R intervals was reduced in-flight, was reduced further the day after landing, and had not returned to preflight levels by 14 days after landing. Our results suggest that long-duration spaceflight reduces vagal-cardiac nerve traffic and decreases vagal baroreflex gain and that these changes may persist as long as 2 wk after return to Earth.

Valsalva manoeuvre can be used to study baroreflex sensitivity in pregnancy.

OBJECTIVE: The aim of this study was to assess whether baroreflex sensitivity can be measured in a non-invasive manner with the Valsalva manoeuvre in pregnancy. STUDY DESIGN: Baroreflex sensitivity was measured from the reflex response to phenylephrine injection and phase four of the Valsalva manoeuvre in nine pregnant women at 27 (range 24-33) gestational weeks. RESULTS: Both the phenylephrine test and the Valsalva manoeuvre yielded similar estimates of baroreflex sensitivity (9.3 (4.1) ms/mmHg vs. 8.0 (5.2) ms/mmHg, Pearson's correlation coefficient r = 0.81, P < 0.008, linear regression BRSValsalva (ms/mmHg) = 1.03 x BRSPhenylephrine + 1.59). Comparable changes in heart rate and blood pressure were obtained with the phenylephrine test and the Valsalva manoeuvre. CONCLUSION: The physiological challenge caused by the Valsalva manoeuvre can be used to measure baroreflex sensitivity in pregnancy. A possibility to study baroreflex function non-invasively, without pharmacological intervention, benefits future research of blood pressure regulation in pregnancy.

Human baroreflex rhythms persist during handgrip and muscle ischaemia.

AIM: To determine whether physiological, rhythmic fluctuations of vagal baroreflex gain persist during exercise, post-exercise ischaemia and recovery. METHODS: We studied responses of six supine healthy men and one woman to a stereotyped protocol comprising rest, handgrip exercise at 40% maximum capacity to exhaustion, post-exercise forearm ischaemia and recovery. We measured electrocardiographic R-R intervals, photoplethysmographic finger arterial pressures and peroneal nerve muscle sympathetic activity. We derived vagal baroreflex gains from a sliding (25-s window moved by 2-s steps) systolic pressure-R-R interval transfer function at 0.04-0.15 Hz. RESULTS: Vagal baroreflex gain oscillated at low, nearly constant frequencies throughout the protocol (at approx. 0.06 Hz - a period of about 18 s); however, during exercise, most oscillations were at low-gain levels, and during ischaemia and recovery, most oscillations were at high-gain levels. CONCLUSIONS: Vagal baroreflex rhythms are not abolished by exercise, and they are not overwhelmed after exercise during ischaemia and recovery.

Heart rate and blood pressure variabilities are increased in pregnancy-induced hypertension.

OBJECTIVE: Our purpose was to study whether cardiovascular changes in pregnancy-induced hypertension are associated with the increase in sympathetic control of hemodynamics and change in sympathovagal balance. STUDY DESIGN: Fourteen women with pregnancy-induced hypertension and 16 women with uncomplicated pregnancies of similar duration were studied. Electrocardiographic signals and arterial blood pressure (Finapres monitor, Ohmeda) were continuously measured noninvasively throughout the study. Heart rate and blood pressure were measured while the subject was breathing (1) with her normal tidal volume at a frequency of 15 breaths per minute and (2) as deeply as possible at a frequency of six breaths per minute. Heart rate and systolic blood pressure variability were calculated with use of the autoregressive model of spectral analysis. RESULTS: Heart rate and systolic blood pressure variabilities were significantly increased in women with pregnancy-induced hypertension compared with normotensive pregnant women. This increase was greatest in the high frequency component of heart rate variability (p = 0.02) while the women were breathing with a normal tidal volume. Further, the medium frequency (p = 0.03) and high-frequency variabilities (p = 0.03) of systolic blood pressure were significantly increased in women with preeclampsia compared with normotensive pregnant subjects. CONCLUSIONS: Neural control of the heart rate and blood pressure are disturbed in pregnancy-induced hypertension, as shown by increased heart rate and blood pressure variability. Both the sympathetic and parasympathetic control of the heart rate and blood pressure appear to be increased. The maladaptation of the cardiovascular system in women with pregnancy-induced hypertension is manifested as a lack of the physiologic decline in cardiovascular oscillations.

Power spectral analysis of heart rate and blood pressure variability in anaesthetized dogs.

Short-term oscillation of heart rate and blood pressure are mainly regulated by the automatic nervous system. It has been proposed that non-neural factors, such as changes in intrathoracic pressure, can strongly modulate this rhythmicity. Our aim was to evaluate the effect of changing intrathoracic pressure and central autonomic nervous activity on heart rate and blood pressure variability. Evaluation was performed by using spectral analysis techniques with autoregressive modelling. The variability in heart rate and blood pressure remained in animals with open chest or paralysed respiratory muscles. After vagotomy, the variability in heart rate decreased, but not that of blood pressure. Total spinal anaesthesia elicited a decrease in the variability in blood pressure. The pharmacological blockade of alpha- and beta-receptors further decreased both variabilities. It was concluded that in anaesthetized dogs heart rate and blood pressure variability are mainly of central origin and non-neural factors have only minor effect on these central rhythms. High (> 0.15 Hz), medium (0.07-0.15 Hz) and, obviously low (0.00-0.07 Hz) frequency variations in heart rate are mostly mediated vagally. In blood pressure, medium and obviously low frequency variations are modulated by sympathetic nervous system, whereas high frequency variations are secondary to the heart rate variation.

The high frequency component of heart rate variability reflects cardiac parasympathetic modulation rather than parasympathetic 'tone'.

This study was designed to evaluate the effect of modulating cardiac parasympathetic input on the high frequency component of heart rate variability. We stimulated the right vagus nerve with three different stimulation patterns in anaesthetized, vagotomized and spinal anaesthetized dogs. We kept the mean stimulation frequency constant; controlled the amplitude of modulation with programmed stimulation patterns, and analysed the resulting heart rate variability by power spectral analysis. Constant frequency vagal stimulation increased the cardiac interval, but did not change heart rate variability markedly. There was a slight increase, from 11 +/- 2 to 27 +/- 11 ms2, in the high frequency component. However, when the instantaneous stimulation frequency oscillated between 4 and 17 Hz during 5 s period, we could produce a marked heart rate variation, with 91 +/- 9% of the variation corresponding to the frequency of the modulation (0.20 Hz). The high frequency component was 12932 +/- 7701 ms2. With an increased magnitude of modulation, i.e. the difference between minimum and maximum instantaneous frequency, the high frequency component increased to 32711 +/- 17943 ms2. Thus, the high frequency component of heart rate variability reflects the magnitude of fluctuation in the cardiac parasympathetic input rather than parasympathetic 'tone'.

Effect of sympathetic modulation and sympatho-vagal interaction on heart rate variability in anaesthetized dogs.

Changes in the function of the autonomic nervous system underlying changes in heart rate variability are not fully understood. Furthermore, decreased heart rate variability has been found to be related to poor prognosis, for example, in patients with coronary artery disease. Our aim was to study how modulation in sympathetic stimulation at various frequencies is transferred into heart rate variation, and how the interaction between sympathetic and parasympathetic inputs can affect the high-frequency component of heart rate variability. We stimulated electrically cardiac sympathetic and vagal nerves in anaesthetized, vagotomized, spinal anaesthetized dogs. We controlled the frequency and magnitude of the modulation in programmed stimulation patterns and analysed the resulting changes in heart rate variability by power spectral analysis. We found that modulations in sympathetic stimulation were reflected in the high-frequency component of heart rate variability, as well as in the low- and medium-frequency components. In addition, a novel finding was that sympathetic stimulation reduced the magnitude of the high-frequency variations caused by vagal stimulation. This suggests that, although the high-frequency component of heart rate variability is mainly under parasympathetic regulation, it may also be influenced by the sympathetic nervous system.

Non-invasive evaluation of sympathovagal balance in athletes by time and frequency domain analyses of heart rate and blood pressure variability.

We examined how the time and frequency domain measures of heart rate and blood pressure variability at supine rest reflect the sympathovagal balance of 23 female and male endurance athletes. Pharmacological blocking by atropine and propranolol was used as a standard for defining autonomic control of the heart. The Rosenblueth and Simeone model for neural control of heart rate was used to calculate the sympathovagal balance index (Abal). Atropinization significantly decreased all time and frequency domain measures of heart rate and blood pressure variability. beta-Blockade significantly decreased further the low- (< 0.07 Hz) and medium-frequency power (0.07-0.15 Hz) variability of R-R intervals (RRI) and SD of RRI. Abal was 0.629 +/- 0.019, indicating that parasympathetic activity predominated in the athletes. Basal heart rate (r = 0.519, P < 0.01), SD of RRI (r = -0.533, P < 0.01), root-mean-square of successive RRIs (RRI RMSSD) (r = -0.579, P < 0.05), RRI total (r = -0.557, P < 0.01) and RRI high-frequency (HF) power (r = -0.582, P < 0.01) correlated significantly with Abal and parasympathetic activity index. We concluded that the best non-invasive method of evaluating the sympathovagal balance of athletes at supine rest is to measure SD of RRI, RRI RMSSD, HF and total power of RRI variability. All heart rate variability measures were mainly parasympathetically modulated. The nature of blood pressure variability measures remained unclear and they could not be used to evaluate the sympathovagal balance among athletes.

Comparison of vagal baroreflex function in nonpregnant women and in women with normal pregnancy, preeclampsia, or gestational hypertension.

OBJECTIVE: Our aim was to compare baroreflex function among nonpregnant women and among women with normal pregnancy, preeclampsia, or gestational hypertension. STUDY DESIGN: Baroreflex function was tested in 20 women with preeclampsia, in 20 age- and gestational age-matched normotensive gravid women, in 20 age-matched nonpregnant women, and in 20 nonmatched women with gestational hypertension. The baroreflex was measured by several modalities. RESULTS: Vagal baroreflex gain measured by cross-spectral analysis of parallel spontaneous heart rate and blood pressure changes is significantly decreased in normal pregnancy (15.8 +/- 7.2 vs 10.8 +/- 4.1 ms/mm Hg; P = 0.001), in comparison with vagal baroreflex gain in nonpregnant women. Baroreflex gain is further reduced in preeclamptic pregnancy (10.8 +/- 4.1 vs 7.2 +/- 2.6 ms/mm Hg; P = 0.003) and in gestational hypertension (10.8 +/- 4.1 vs 6.5 +/- 2.7 ms/mm Hg; P = 0.001), compared with that in normal pregnancy. Similar differences were seen with other baroreflex testing modalities. CONCLUSIONS: The normal reduction of baroreflex gain in pregnancy is further depressed in subjects with hypertensive disorders of pregnancy.

Valsalva manoeuvre in the assessment of baroreflex sensitivity in patients with coronary artery disease.

The overshoot rise in arterial pressure after release of Valsalva strain is a natural challenge for baroreflex regulation of heart rate. To assess the feasibility of the Valsalva manoeuvre in the determination of baroreflex sensitivity (BRS), we measured the slope of the linear relationship between the length of the RR interval and preceding systolic blood pressure value during the overshoot phase after the strain and compared this index of BRS to a standard phenylephrine test in 64 subjects, of whom 58 had coronary artery disease. The BRS slopes obtained with the Valsalva manoeuvre showed a good linear correlation with the phenylephrine test (r = 0.77 in the 27 patients with two Valsalva and phenylephrine tests and r = 0.56 in the whole cohort). The correlation coefficients of the BRS slopes were better than in the phenylephrine test (r = 0.89 vs r = 0.85, P < 0.05). The rise in systolic blood pressure in the slope calculation area was higher than with phenylephrine (41 +/- 18 vs 30 +/- 10 mmHg, P < 0.01). The reproducibility of BRS slopes in successive tests was comparable with both methods. These results suggest that non-invasive assessment of BRS using Valsalva strain to induce blood pressure rise is possible in patients with coronary artery disease.

Simultaneous invasive and noninvasive evaluations of baroreflex sensitivity with bolus phenylephrine technique.

Estimation of baroreflex sensitivity (BRS) is receiving increasing attention in clinical and experimental cardiology. Until recently, in most studies BRS has been assessed on the basis of invasive blood pressure measurement, which limits its use in large-scale studies and in clinical practice. The development of continuous noninvasive blood pressure monitoring has made it possible to assess BRS noninvasively. We compared central invasive and peripheral noninvasive techniques in the assessment of BRS during cardiac catheterization in 40 patients with possible coronary artery disease. The correlation between noninvasive and invasive BRS was high (r = 0.92; p < 0.001). However, the noninvasive method resulted in significantly higher BRS values than did the invasive method (7.1 +/- 6.5 msec/mm Hg vs 5.1 +/- 4.3 msec/mm Hg, respectively; p < 0.001) because of the smaller increase in systolic blood pressure after phenylephrine injection by the noninvasive technique than by the invasive technique (18.9 +/- 6.8 mm Hg vs 25.2 +/- 7.8 mm Hg, respectively; p < 0.01). The difference between noninvasive and invasive BRS correlated positively with invasive BRS (r = 0.54; p < 0.001) and inversely with age (r = -0.39; p < 0.01) and resting systolic blood pressure (r = -0.30, p < 0.05). A noninvasive BRS value of < 4.0 ms/mm Hg showed a sensitivity of 94%, a specificity of 91%, and an accuracy of 93% in identifying cases of reduced invasive BRS (< 3.0 msec/mm Hg). Our findings encourage the use of finger-cuff method in the assessment of BRS. However, noninvasive BRS values were slightly but significantly higher than invasive BRS values, a difference that should be taken into account when BRS is measured by the noninvasive approach.

Effect of coronary artery bypass grafting on cardiac parasympathetic nervous function.

Low heart rate variability (HRV) is a predictor of a poor outcome after myocardial infarction. To determine whether coronary artery bypass grafting (CABG) has any effect on HRV, the power spectrum components of HRV were measured in 35 patients before, and 1 week after, CABG. Significant attenuation of all spectral components of HRV were found after CABG (P less than 0.001). High frequency (HF) power decreased to one third of the preoperative level, mid-frequency (MF) power to as little as one fifteenth and low frequency (LF) power to one seventh of the preoperative level. No significant restoration in MF or HF powers occurred during the 6-week follow-up period. The results suggest that CABG causes a marked attenuation of HRV. The prognostic significance of this attenuation is not known.