Blunted Heart Rate Response Research Articles

Blunted heart rate response to upright tilt in people with Down syndrome

Fernhall B, Figueroa A, Collier S, Baynard T, Giannopoulou I, Goulopoulou S. Blunted heart rate response to upright tilt in people with Down syndrome. Arch Phys Med Rehabil 2005;86:813–8. Objectives To determine whether heart rate and blood pressure responses to upright tilt would be lower in subjects with Down syndrome (DS) than in control subjects with no disabilities. Design Comparative study. Setting University research laboratory. Participants Nineteen people with DS (mean age, 25.1±7.3y) and 17 control subjects without disabilities (mean age, 28.4±5.6y). Interventions Not applicable. Main outcome measures Heart rate and blood pressure recordings were obtained at rest and during a 2-minute period of passive head up tilt to 80°. Results Heart rate and blood pressure increased significantly during the first 30 seconds of upright tilt in both groups ( P<.05) and then stabilized for the remainder of the test. The initial heart rate response to head up tilt (first 30s) was significantly higher in controls compared with subjects with DS ( P<.05), whereas the blood pressure response did not differ between groups ( P>.05). Controlling for heart rate reserve showed a blunted heart rate response through the tilt period in subjects with DS. Conclusions These data show a blunted heart rate response to upright tilt in people with DS, despite similar changes in blood pressure, consistent with reduced sympathoexcitation and possibly altered baroreceptor function in these people with DS.

Abnormal heart rate response to adenosine infusion is associated with silent myocardial ischemia in asymptomatic patients with diabetes mellitus

Background: Many patients with type 2 Diabetes Mellitus (T2DM) have cardiac autonomic neuropathy (CAN), which has been associated with poor outcome. CAN is also associated with blunted heart rate response (HRR) to dipyridamole infusion. Furthermore in the Detection of Ischemia in Asymptomatic Diabetics (DIAD) study CAN was associated with moderate and large myocardial perfusion defects. Therefore, we hypothesized that blunted HRR during adenosine infusion is associated with myocardial perfusion abnormalities and silent myocardial ischemia. Methods: 442 asymptomatic patients with T2DM, without known coronary artery disease who were enrolled in DIAD study, had quantitative adenosine-Tc-99m-Sestamibi SPECT imaging. Heart rate response to adenosine infusion was assessed as the ratio between baseline HR and HR at end of adenosine infusion. Myocardial perfusion defects were quantified and categorized as small, moderate and large. Results: Mean age of patients was 60.5± 6.8 years; females 47%; males 53%; T2DM duration 8.1 ± 7.1 years. 7% of the patients had either moderate or large perfusion abnormalities. Patients in the lowest decile of HRR (< 1.10), the cut point used to define an abnormal response, were more likely to have moderate or large perfusion abnormalities (OR=3.0, 95% CI 1.2, 7.0; p = .01). The sensitivity of lower HRR to predict moderate to large myocardial perfusion defects was 24% and specificity was 90%. The negative predictive value was 94%. Conclusion: In asymptomatic patients with T2DM a blunted HRR to adenosine infusion is a simple marker with high negative predictive value and high specificity for moderate and large silent myocardial ischemia.

PC47 IMPACT OF MATERNAL UNDERNUTRITION DURING EARLY-MID GESTATION ON RESULTING ADULT OFFSPRING IN SHEEP

Introduction: Suboptimal maternal nutrition during pregnancy is associated with increased risk of diseases in resulting adult offspring. Maternal undernutrition during placental growth produced a longer fetus at term with a disproportionately larger placenta and increased fat deposition. This study aimed to determine the long term consequences of early-mid gestation maternal undernutrition on blood pressure and plasma leptin concentration in young adult offspring. Methods: Seventeen male singleton bearing Scottish Black-face ewes of similar liveweight and body condition were individually housed from day of mating. Nine ewes were nutrient restricted (NR) consuming 4.0 MJ of metabolisable energy (ME) per day (50% ME requirements for maintenance and growth of conceptus) until 95 days gestation with 8 controls (C) consuming 8.0 MJ/day. After 95 days gestation until term (147 days) all ewes consumed 100% of requirements. At term lambs were delivered spontaneously and at 3 years old, the jugular vein and carotid artery were surgically catheterised for blood pressure (BP) measurement and blood sampling. Plasma was collected before and after a noradrenaline (NA) infusion with dose increases (2–48 ng/kg/min) at 10-minute intervals, and leptin concentration analysed. Animals were then humanely euthanased by barbiturate overdose to allow tissue sampling. Results are presented as mean ± standard error. Results: Between groups offspring body weight was similar at birth and 3 years of age but the NR group had larger fat (omental, perirenal and subcutaneous) deposits compared to controls. Basal BP prior to feeding was significantly higher in the NR offspring compared to controls (eg. diastolic 65 ± 3; NR 74 ± 2 mmHg (P<0.05)). Following NA infusion BP was similar between groups and rose with increasing NA concentration. With controls heart rate simultaneously decreased but this response was blunted in the NR group. The NR but not C offspring exhibited a significant increase in plasma leptin following NA infusion (C pre NA 3.22 ± 1.9; Post NA 3.16 ± 1.7; NR pre NA 3.47 ± 0.9; Post NA 4.5 ± 1.3 ng/ml (P<0.05)). Conclusion: Nutrient restriction between early-mid gestation produced hypertensive offspring with a blunted heart rate response to a vasoconstrictor challenge, with more fat and higher plasma leptin levels. Altering maternal nutrition during gestation may contribute to reprogramming of adult blood pressure and fat deposition contributing to hypertension and obesity in later life.

Cardiovascular Adaptations To Pregnancy Are Still Evident In The Early Postpartum Period

1464 Cardiovascular adaptations occur early in pregnancy and persist throughout gestation. Some of these changes may still be apparent in postpartum women for an unknown period of time. To date there is a paucity of research aimed at the postpartum period regarding the duration and magnitude of these cardiovascular changes. PURPOSE: To investigate cardiovascular responses to peak treadmill exercise in active postpartum women. METHODS: We evaluated cardiovascular responses to a peak treadmill exercise test in active 2 months postpartum women (PP; N = 20). Comparisons were made to active non-pregnant women (NP; N = 20). RESULTS: Pre-exercise heart rate (PrHR) was significantly lower in the PP group (77 ± 2 vs 84 ± 2 bpm; means ± SE; p < .05). There were no significant differences between groups in the pre-exercise VO2, VCO2, VE and oxygen pulse. Peak exercise heart rate (PHR) was significantly lower in the PP group (171 ± 3 vs 180 ± 2bpm; p < .05), with no differences between groups in time to peak, VO2, VCO2, and VE at peak. Recovery heart rate (RHR) remained significantly elevated over baseline values for both groups (PP; 112 ± 2.5 vs NP; 108 ± 3 bpm; p < .01). However heart rate recovery (RHR-PrHR) was significantly less in the PP vs. NP groups (34 ± 2 vs 24 ± 3 bpm; p < .01). Values for recovery VO2, VCO2, VE and oxygen pulse were not significantly different between groups. CONCLUSION: PrHR and PHR were lower in PP women. Since peak VO2 was not different between groups, a higher stroke volume in the PP group may explain the blunted heart rate response. PP heart rate recovery was reduced, however the significance of this is unclear. Cardiovascular adaptations to pregnancy are still evident in the early postpartum period and should caution future pregnancy study designs from including postpartum women as non-pregnant controls. Supported by the Canadian Forces Personnel Support Agency

Cardiovascular Adaptations To Pregnancy Are Still Evident In The Early Postpartum Period

1464 Cardiovascular adaptations occur early in pregnancy and persist throughout gestation. Some of these changes may still be apparent in postpartum women for an unknown period of time. To date there is a paucity of research aimed at the postpartum period regarding the duration and magnitude of these cardiovascular changes. PURPOSE: To investigate cardiovascular responses to peak treadmill exercise in active postpartum women. METHODS: We evaluated cardiovascular responses to a peak treadmill exercise test in active 2 months postpartum women (PP; N = 20). Comparisons were made to active non-pregnant women (NP; N = 20). RESULTS: Pre-exercise heart rate (PrHR) was significantly lower in the PP group (77 ± 2 vs 84 ± 2 bpm; means ± SE; p < .05). There were no significant differences between groups in the pre-exercise VO2, VCO2, VE and oxygen pulse. Peak exercise heart rate (PHR) was significantly lower in the PP group (171 ± 3 vs 180 ± 2bpm; p < .05), with no differences between groups in time to peak, VO2, VCO2, and VE at peak. Recovery heart rate (RHR) remained significantly elevated over baseline values for both groups (PP; 112 ± 2.5 vs NP; 108 ± 3 bpm; p < .01). However heart rate recovery (RHR-PrHR) was significantly less in the PP vs. NP groups (34 ± 2 vs 24 ± 3 bpm; p < .01). Values for recovery VO2, VCO2, VE and oxygen pulse were not significantly different between groups. CONCLUSION: PrHR and PHR were lower in PP women. Since peak VO2 was not different between groups, a higher stroke volume in the PP group may explain the blunted heart rate response. PP heart rate recovery was reduced, however the significance of this is unclear. Cardiovascular adaptations to pregnancy are still evident in the early postpartum period and should caution future pregnancy study designs from including postpartum women as non-pregnant controls. Supported by the Canadian Forces Personnel Support Agency

Slow Kinetics of Oxygen Uptake in Patients with a Fontan-Type Circulation

Peak oxygen consumption and anaerobic threshold are both decreased in patients with a Fontan-type circulation. This study wanted to evaluate oxygen uptake kinetics at the onset and at the end of of a steady-state low-level exercise. The delay in cardiorespiratory response was evaluated by calculating the oxygen deficit at the onset of exercise and the recovery half-time at the end. Twelve patients with Fontan circulation (aged 11.4 − SD 5.1 year; 5.2 − 1.9 year after surgery) and 26 normal controls of comparable age (11.3 − 2.2 year) were submitted to a constant-load exercise test of six minutes on a treadmill (speed 5 km/h, inclination 4%). Gas exchange was measured using a breath-by-breath technique. The normalized oxygen deficit was calculated by subtracting the oxygen uptake (VO2) values measured at the onset of exercise from the steady-state VO2 obtained at the end of exercise. These differences were cumulated and expressed as a percentage of the cumulated oxygen cost for the 6 min exercise test. The half-time recovery time was defined as the time to reach 50% of the end exercise VO2 value. The normalized oxygen deficit was significantly higher in Fontan-patients compared to the control group (10.2 − 4.6% vs. 6.1 − 1.3%; p &lt; .001). Also the recovery half-time was significantly higher in the patient group compared to the control group (74.2 − 25.6 s vs. 51.2 − 10.8 s; p &lt; .05). A blunted heart rate response was present in the patients during the first two minutes of exercise, indicating that a slowed cardiac output response could explain the decreased oxygen kinetics in Fontan-patients.

Use of atropine in patients with submaximal heart rate during exercise myocardial perfusion SPECT

Background. Failure to reach 85% of maximal predicted heart rate (MPHR) during exercise may render a myocardial perfusion single photon emission computed tomography (MPS) study nondiagnostic for ischemia detection. Although commonly used to increase heart rate (HR) during dobutamine stress, the administration of atropine for patients failing to achieve 85% of MPHR during exercise performed for MPS is still infrequent. Methods and Results. Patients undergoing dual-isotope MPS were considered candidates for the study when, during exercise treadmill testing, they had less than 85% of MPHR and were unable to continue because of fatigue, without an ischemic response. Forty-seven patients (aged 65.3 ± 12.5 years, 78.7% men) received atropine (0.6-1.2 mg). Maximal HR achieved before and after atropine was 118.0 ± 14.8 beats/min (76.3% ± 6.2% of MPHR) and 146.4 ± 12.6 beats/min (94.4% ± 8.1% of MPHR), respectively (P < .001). Of patients, 44 (93.6%) reached at least 85% of MPHR after atropine and had diagnostic MPS studies. After atropine, arrhythmias occurred in 14 patients (29.8%) and other minor side effects in 1 (2.1%). Conclusions. Atropine allows patients initially failing to achieve 85% of MPHR during exercise to increase HR and have a diagnostic MPS study, without major complications. It may provide an alternative to pharmacologic stress for patients with a blunted HR response to exercise. (J Nucl Cardiol 2003;10:51-5)

Prediction of the haemodynamic response to tracheal intubation: comparison of laser-Doppler skin vasomotor reflex and pulse wave reflex

The laser-Doppler skin vasomotor reflex (SVmR) caused by tetanic stimulation of the ulnar nerve may be a test that can predict the haemodynamic response to tracheal intubation. A decrease in pulse wave amplitude (pulse wave reflex, PWR) may be an alternative index of this response. We compared the abilities of PWR and SVmR to predict the haemodynamic response to tracheal intubation and studied how alfentanil, muscle relaxation, stimulation site and stimulation pattern affected the two reflexes. Anaesthesia was induced and maintained with 2% sevoflurane and 50% nitrous oxide in two groups of 10 ASA status 1 patients. Tetanic stimuli were applied to the flexor muscles of the forearm and the ulnar nerve before and after administration of vecuronium. The change in skin blood flow (laser-Doppler) and pulse wave amplitude (pulse oximetry) after a 5 and 10 s stimulation was measured on the opposite hand. If skin blood flow (laser-Doppler) decreased by more than 10%, a computer-controlled infusion of alfentanil was started and the target plasma concentration was increased in steps until this response was suppressed (< 10%). The trachea was intubated and arterial pressure and heart rate responses were recorded. Plasma alfentanil concentration was measured. When PWR and SVmR were suppressed, the haemodynamic response to tracheal intubation was reduced in 100 and 53% of patients respectively. PWR and SVmR responses decreased with increasing plasma alfentanil concentration. The SVmR response to muscle stimulation was reduced by muscle relaxants. The pulse wave response to both muscle and neural stimulation was reduced by relaxants. The responses to 5 and 10 s stimulations were similar. An absent SVmR does not predict a blunted arterial pressure or heart rate response to tracheal intubation. The PWR may be a better predictor.

Attenuated Heart Rate Responses to Public Speaking in Individuals With Alcohol Dependence

Because individuals with alcohol dependence (AD) have shown blunted cortisol responses to psychological stress, we assessed whether they also show attenuated cardiovascular responses. This study examined the cardiovascular responses of people meeting DSM-IV criteria for AD to orthostasis and public speaking. Heart rate (HR), stroke volume, cardiac output, total peripheral resistance, mean arterial pressure, systolic blood pressure, and diastolic blood pressure during orthostasis and public speaking were assessed by use of impedance cardiography and Dinamap blood pressure monitoring in 20 AD subjects abstinent for 21 to 28 days and in 10 age-matched controls. Orthostasis consisted of standing, whereas public speaking involved preparing and presenting two speeches. Self-reported mood state was also assessed during the tasks. AD subjects had significantly lower resting BP compared with controls. Cardiovascular responses to orthostasis were similar between groups. AD subjects had attenuated HR during public speaking but reported similar anxiety responses to controls. Comparable cardiovascular responses to orthostasis in controls and AD subjects suggest intact reflex control of circulation. AD subjects had blunted HR responses to public speaking; this is consistent with the attenuated cortisol responses observed in this sample and in previous studies. This suggests a possible alteration in limbic system regulation of hypothalamic and brainstem responses to psychological stress. Cardiovascular responses of AD subjects that are inconsistent with subjective accounts of tension and anxiety suggest a disconnection between perception of threat and resulting physiologic responses in AD subjects.

Attenuated Heart Rate Responses to Public Speaking in Individuals With Alcohol Dependence

Background: Because individuals with alcohol dependence (AD) have shown blunted cortisol responses to psychological stress, we assessed whether they also show attenuated cardiovascular responses. This study examined the cardiovascular responses of people meeting DSM-IV criteria for AD to orthostasis and public speaking. Methods: Heart rate (HR), stroke volume, cardiac output, total peripheral resistance, mean arterial pressure, systolic blood pressure, and diastolic blood pressure during orthostasis and public speaking were assessed by use of impedance cardiography and Dinamap blood pressure monitoring in 20 AD subjects abstinent for 21 to 28 days and in 10 age-matched controls. Orthostasis consisted of standing, whereas public speaking involved preparing and presenting two speeches. Self-reported mood state was also assessed during the tasks. Results: AD subjects had significantly lower resting BP compared with controls. Cardiovascular responses to orthostasis were similar between groups. AD subjects had attenuated HR during public speaking but reported similar anxiety responses to controls. Conclusions: Comparable cardiovascular responses to orthostasis in controls and AD subjects suggest intact reflex control of circulation. AD subjects had blunted HR responses to public speaking; this is consistent with the attenuated cortisol responses observed in this sample and in previous studies. This suggests a possible alteration in limbic system regulation of hypothalamic and brainstem responses to psychological stress. Cardiovascular responses of AD subjects that are inconsistent with subjective accounts of tension and anxiety suggest a disconnection between perception of threat and resulting physiologic responses in AD subjects.

Peak and kinetic cardiorespiratory responses during arm and leg exercise in patients with spinal cord injury.

A paired comparison of the peak and submaximal responses of oxygen uptake and heart rate in patients with spinal cord injury (SCI) performing voluntary arm cycle exercise and functional electrical stimulation (FES) leg cycling exercise. To test if the blunted heart rate response and slower rate of adjustment of oxygen uptake seen in patients with SCI performing FES leg cycle exercise are also characteristic of arm exercise in these patients. Eight paraplegics performed incremental and constant work rate (CWR) exercise with the legs and arms. Mean response times (MRT) for Vo2 during exercise (on) and in recovery (off) were calculated from the breath-by-breath Vo2 profile. Peak heart rate was higher during incremental arm exercise, and uncorrelated with that observed during incremental FES leg cycling. For the same increase in Vo2, constant work rate arm exercise was associated with faster (and normal) Vo2 kinetics, greater increase in heart rate, and lower end-exercise blood lactate, compared to FES leg cycling. The consistently higher peak heart rate and Vo2, and faster Vo2 kinetics, for voluntary arm compared to FES leg cycle exercise suggest no intrinsic dysfunction of heart rate control in these paraplegics. Rather, these data suggest that during FES leg cycling the changes seen are due to some characteristic specific to the injury, such as reduced muscle mass and/or deconditioning of the remaining muscle. This research was supported by The Department of Veterans Affairs, Rehabilitation Research and Development Project #B603-RA. Spinal Cord (2000) 38, 340 - 345.

Effects of FK506 in rat and human resistance arteries

FK506 is widely used in organ transplantation and causes hypertension. However, little is known about the impact of the drug on the cardiovascular system. We therefore investigated the effect of FK506 on resistance artery and blood pressure responsiveness to vasoconstrictors and vasodilators. Studies were conducted in vitro using human and murine resistance artery, ex vivo in resistance artery isolated from rats treated with FK506 (6 mg/kg/day), and in vivo in conscious, treated animals. In vitro exposure (24 hr) of human and rat resistance artery to FK506 (1000 ng/ml) increased the sensitivity to norepinephrine (NE) and impaired the response to acetylcholine (Ach) and sodium nitroprusside (SNp). In contrast, arteries isolated from rats given FK506 for eight days showed a reduced sensitivity to NE (P < 0.05) and a normal endothelium-dependent relaxation. Their incubation with L-arginine caused a significant reduction in Ach sensitivity in the FK506 group (P < 0.05) but not in controls, suggesting enhancement of nitric oxide production by the drug. The sensitivity to SNp was reduced, as in the in vitro experiments (P < 0.05). Rats given FK506 for eight days presented blood pressure similar to that in controls but also presented signs of a compensatory response to excess vasodilation: tachycardia (P < 0.01), reduced blood pressure sensitivity to NE and Ach, blunted heart rate response to both agonists, and exaggerated hypotension at high doses of Ach. After 21 days of treatment, blood pressure remained similar to that in controls, but resistance artery showed further functional deterioration, with significant impairment of the maximum responses to Ach and to SNp. FK506 presents significant vascular toxicity affecting mainly smooth muscle relaxation and alters vascular hemodynamics. The data suggest that similar cardiovascular changes may occur in transplant patients and represent the forerunner of hypertension often seen with more prolonged use of the drug.

Exercise studies in patients with transposition of the great arteries after atrial repair operations (Mustard/Senning): a review.

Exercise evaluation studies of patients after atrial repair surgery for transposition of the great arteries, as in tetralogy of Fallot, represent only a small fraction of the 3970 Medline references (1966 to mid-1997) concerning this congenital heart lesion. We have abstracted data from 27 studies from 20 institutions reporting on measurements during exercise on work capacity, heart rate response, respiratory gas exchange, or radionuclide/radiographic systemic ventricular ejection fraction measurements in addition to resting pulmonary function measurements. These studies provide almost uniform general conclusions that even after 20 or more years of follow-up (1) most patients "report" that they are asymptomatic in performing usual levels of physical activities; (2) significant abnormalities are present, often in more than half of the patients studied, in one or more of the exercise measurements when compared to control subjects; and (3) the diminished exercise performance is related to a diminished cardiac output, results from diminished stroke volume but is also related to a blunted heart rate response.

Acute and long-term effects of the angiotensin-converting enzyme inhibitor, enalapril, on adrenergic activity and sensitivity during exercise in patients with left ventricular systolic dysfunction

Patients with heart failure and left ventricular systolic dysfunction exhibit increased adrenergic activity but blunted adrenergic responsiveness. We studied patients enrolled in the Studies of Left Ventricular Dysfunction, examining exercise responses of heart rate (HR) and plasma norepinephrine (PNE). Eighty-seven patients were studied before randomization; 65 of these were examined 1 year after randomization to placebo or enalapril. Compared with prevention trial (asymptomatic) patients, patients in the treatment trial (symptomatic) had higher resting HR and PNE levels and less increase in HR with a greater increase in PNE with exercise. Acute administration of enalapril increased the resting HR in patients in the prevention trial only but had no significant effect on PNE. After 1 year of therapy, patients in the prevention trial exhibited no change. Within the treatment trial, the placebo group displayed both a higher peak PNE and increase in PNE with exercise than did the enalapril group, whose HR response was maintained in spite of a reduction of exercise PNE. We conclude that (1) compared with asymptomatic patients, symptomatic patients with reduced left ventricular ejection fraction manifest greater resting and exercise adrenergic activity, with blunted HR response; and (2) in symptomatic patients, 1 year of enalapril treatment effected an augmented HR response to adrenergic stimulation, supporting an interaction between the renin/angiotensin and adrenergic nervous systems. Normalization of adrenergic tone and response likely contributes to the benefits of long-term angiotensin-converting enzyme inhibitor therapy. (Am Heart J 1997;134: 37-43.)

ATTENUATED HR AND BLOOD PRESSURE RESPONSE TO ISOMETRIC EXERCISE IN MULTIPLE SCLEROSIS (MS) 472

Our previous investigation of 104 MS patients revealed an attenuated pressor response to isometric handgrip exercise at 30% of maximal voluntary contraction (MVC) sustained to fatigue (IHE). Increase in heart rate (HR) was identical to control subjects, and clinical indices of symptom severity (EDSS and ISS scores) did not predict abnormal pressor response in regression analysis. The distribution of the pressor response, however, showed a wide range and was distinctly bimodal, suggesting two subgroups within the cohort. Therefore we retrospectively compared patients with attenuated pressor responses (A) to similar patients with nonattenuated responses (NA). A patients (n = 27), defined by an increase in mean arterial pressure (MAP) of< 20mmHg at end-IHE, were matched with NA patients (n = 22) (peak MAP = 46± 6mmHg). Groups were similar in MVC (37.3 ± 2.6 vs. 38.5± 3.1N, mean ± SEM), time to fatigue (206.8 ± 11.7 vs. 232.0 ± 15.3s) and resting MAP (94.3 ± 2.5 vs. 97.6 ± 2.2mmHg). By definition, change in MAP was lower in A at all time points during IHE (peak Δ: 12.8 ± 1.1 vs. 44.2 ± 1.1 mmHg; P<.0001). Resting HR was higher in A (79.6 ± 2.1 vs. 71.7 ± 2.4 bpm; P =.015) and the change in HR was less in A at all time points during IHE (peak Δ: 14.4 ± 2.3 vs. 26.7 ± 2.3 bpm; P =.0005). Indices of MS-related neurologic symptoms were higher in A (EDSS: 4.5 ± 0.4 vs. 3.1 ± 0.3; P=.009; ISS: 14.9 ± 1.4 vs. 9.5 ± 1.0; P =.003). These data suggest that, contrary to previous reports, certain MS patients have a blunted heart rate response to IHE which may in part underlie the attenuated pressor response seen in these individuals. Moreover, greater overall symptom severity may increase the likelihood of cardiovascular/autonomic involvement in MS patients.

Changes in the Cardiopulmonary Response to Exercise after Cardiac Transplantation in Patients Enrolled in an Early Rehabilitation Program

OBJECTIVE: To evaluate the changes in the cardiopulmonary response to exercise in the first year after cardiac transplantation in patients enrolled in a rehabilitation program in the first three months post-transplantation.METHODS: A graded cycle exercise test with mixed expired gas analysis was performed on patients with end-stage cardiac failure before and serially after cardiac transplantation at one, three and 12 months.RESULTS: Before cardiac transplantation, seven patients were fit enough to be tested. They had a low peak oxygen uptake (VO2 max) and a blunted heart rate and blood pressure response to exercise. They also displayed a restrictive pattern of ventilation during exercise. At three months following transplantation, patients (n=19) had a significantly higher VO2 max(19.9±5.3 versus 9.8±1.4 mL/kg/min, P&lt;0.05), higher peak systolic blood pressure (177±22 versus 94±18 mmHg, P&lt;0.05), greater peak minute ventilation (70±23 versus 34±5 L/min, P&lt;0.05) and lower slope of minute ventilation to carbon dioxide output (35.4±6.2 versus 45.1±6.7, P&lt;0.05) than before transplantation. The VO2 maxmeasured at 12 months post-transplant was similar to the three month value and was on average equal to 59% of the predicted value.CONCLUSIONS: These results indicate that there is a rapid and marked improvement in exercise capacity in patients following cardiac transplantation. These changes are associated with significant respiratory and cardiovascular adaptations. However, despite the marked improvement in exercise capacity, the VO2 maxof cardiac transplant recipients enrolled in an early rehabilitation program did not return to normal at 12 months after surgery.

Hemodynamic responses to upright exercise of adolescent cardiac transplant recipients

To characterize the hemodynamic response to exercise after cardiac transplantation, we asked seven adolescent transplant patients (aged 15.1 +/- 0.7 years; mean +/- SE) to perform upright discontinuous exercise to volitional exhaustion on a mechanically braked cycle ergometer. Data were compared with those of seven control subjects matched for age, gender, body mass, percentage of fat, and body surface area. The transplant group had lower peak power output values (92 +/- 13 vs 146 +/- 30 watts; p less than or equal to 0.001) and maximum oxygen consumption values (22 +/- 8 vs 32 +/- 8 ml/kg per minute; p less than or equal to 0.03), despite achieving the same peak venous lactic acid concentration (6.2 +/- 3 vs 5.9 +/- 3 mEq/L; p = not significant). The transplant group had a diminished heart rate in response to exercise--44% lower than the control group had (delta = 49 +/- 6.4 vs 87 +/- 9.1 beats/min; p = 0.005). The cardiac output response to exercise was maintained in the transplant group (delta = 6.5 +/- 1.5 vs 4.6 +/- 0.8 L/min; p = not significant) by an augmented stroke volume response (delta = 31 +/- 10 vs -4 +/- 3.4 ml; p = 0.01), which may relate to a greater decrease in systemic vascular resistance during exercise (delta = -13.7 +/- 2.2 vs -6.3 +/- 1.2 Wood units; p = 0.02). Thus adolescents who have undergone cardiac transplantation have a normal cardiac output response to upright exercise. This is accomplished, despite a blunted heart rate response, by an augmented stroke volume that may relate to the greater decrease in systemic resistance during exercise.

PR Interval Behavior During Exercise: Implications for Physiological Pacemakers

The relationship between heart rate response and the dynamic changes in the PR interval was assessed in 631 patients undergoing routine cardiac exercise tests for a variety of clinical indications. Patients were stratified into four subsets: nonmedicated normals (n = 437), patients on beta-antagonist agents (n = 118), those on antiarrhythmic agents alone (n = 61) and those with a clinical diagnosis of advanced (New York Heart Association [NYHA] Class III or IV) congestive heart failure. All patients were in stable sinus rhythm throughout the test. PR intervals were measured at rest, at mid-exercise and at peak exercise. Mean PR intervals shortened to a statistically significant degree in most subgroups. This effect was predominantly observed in the earlier stages of exercise. In patients with advanced heart failure, there was no statistically significant shortening of exercise PR intervals later in exercise, demonstrating a parallel with their relatively blunted heart rate response. These changes in exercise PR intervals suggest that implanted pacemaker algorithms may be constructed to maximize hemodynamic benefit in patients requiring physiological pacemakers.

The beat-to-beat blood pressure response to postural change in young and elderly healthy adult males

Heart rate and blood pressure were studied with the beat-to-beat tracking cuff system in two groups (n = 20 per group) of healthy, unmedicated males, one between 60 and 75 years of age and the second between 18 and 29 years of age. The study confirms the previously reported blunted heart rate response to standing and the fact that, when blood pressure is recorded by conventional means, the response exhibited during orthostasis does not differ in healthy groups of young and elderly subjects. With the tracking cuff system, however, the elderly exhibited a smaller immediate systolic and diastolic drop in response to the change to upright posture and less variability in beat-to-beat blood pressure changes. The results have implications for cardiovascular studies, where age and posture can influence both blood pressure and heart rate.

Regulation of blood pressure in pregnancy: pressor system blockade and stimulation

Contributions of the autonomic nervous system (ANS), renin-angiotensin system (RAS), and arginine vasopressin (AVP) to basal mean arterial pressure (MAP) were evaluated in near-term pregnant and virgin rats as follows. MAP and heart rate (HR) were measured before and after ganglionic, alpha-adrenoreceptor, RAS, and/or AVP blockade. In addition, pressor responses to angiotensin II (ANG II), norepinephrine, phenylephrine, or AVP were determined in ganglionic-blocked animals. In both groups decrements in MAP were greatest after ganglionic or alpha-blockade, intermediate after RAS blockade, and negligible after AVP-V1 antagonism ([d(CH2)5Tyr(Me)]AVP). Recovery of MAP was also similar in the two groups except after phentolamine when MAP and HR remained lower in gravid rats. Superimposition of RAS or AVP blockade during phentolamine infusion suggested that ANG II and AVP were less effective in supporting MAP during alpha-blockade in pregnancy. Pressor responses to ANG II and norepinephrine during ganglionic blockade were markedly blunted during pregnancy; however, those to phenylephrine and AVP were unchanged. We conclude that contributions of ANS, RAS, and AVP to basal MAP are similar in pregnant and virgin rats; neural mechanisms dominating in both groups. However, recovery during alpha-blockade is impaired during gestation, apparently due to blunted HR responses and decreased pressor contributions of ANG II and AVP. This may be explained, in part, by decreased vascular reactivity to ANG II, although a similar mechanism cannot be invoked for AVP.