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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rate response to arm movements of the respiratory dependent rate responsive pacemaker (RDP3, Biotec) was assessed in four patients implanted with this pacemaker. The pacemaker was implanted in the left prepectoral region and the auxiliary impedance measuring electrode positioned subcutaneously over the right second intercostal space with its tip lateral to the mid-clavicular line. The lower rate of the pacemaker was programmed to 75 bpm. While holding the breath, swinging arm movements (30 times) resulted in rate acceleration. The peak rate was faster when the arm on the side of the auxiliary electrode was swung (mean +/- SEM, 117 +/- 8 compared to 130 +/- 5 bpm, P less than 0.5). The mean rate response of the subjects to brief treadmill exercise (Bruce stage I) performed with both hands holding the support rails, swinging the right arm only, swinging left arm only and swinging both arms were 108, 140, 135 and 128 bpm respectively. Impedance measurement confirmed the significant influence of arm movements on thoracic "impedance" changes, which was mainly caused by electrode motion artifacts affecting the two electrode measuring system. This effect was dependent on the relative positions of the impedance measuring electrodes (i.e., between the pacemaker casing the auxiliary lead). Subsequently the auxiliary lead of the respiratory pacemaker (MB-1, and Biorate) was implanted in the lower part of the chest on the right sternal edge in another patient. Rate acceleration was only observed when the arm on the side of the pacemaker was swung. As arm movements often accompany physical activities, pacing rate can be affected and should be considered when programming this pacemaker.
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PMID:Rate modulation by arm movements of the respiratory dependent rate responsive pacemaker. 245 55

Sensolog 703 is a new activity sensing rate responsive pacemaker which detects body vibration during physical exercise and uses the vibration as an indicator of the physiological need for a rate increase. This pacemaker was implanted in 11 patients with complete heart block and atrial arrhythmias. Their mean age was 58 (range 39-72) years. With appropriate rate response, exercise capacity, as assessed by the duration of graded treadmill exercise using the Bruce protocol, was significantly improved over the VVI pacing mode (mean +/- SEM, 462 +/- 52 s in the rate responsive mode and 368 +/- 34 s in the VVI mode, P less than 0.02). Cardiac output at peak exercise, as assessed by continuous wave Doppler sampling of aortic root blood flow, was also significantly increased compared to the resting value in both piecing modes. However, the increase was more marked when exercise was performed in the rate response mode (93 +/- 22% increase over resting cardiac output in the rate responsive mode and 57 +/- 13% increase in the VVI mode, P less than 0.05). The rate responses of this pacemaker were compared with those of a Medtronic Activitrax pacemaker. Although both pacemakers responded to an increase in walking speed, neither responded appropriately to walking up different gradients, In both cases, ascending and descending four flights of stairs resulted in similar pacing rates. There was no response to physiological activities with minimal body movements such as isometric exercise and the Valsalva maneuver. Technical problems were encountered in two implanted Sensolog pacemakers: one had spontaneous rate acceleration at rest immediately following implantation and one showed intermittent rate acceleration while the patient was at rest. Both units were programmed to the VVI mode. In conclusion, satisfactory rate response, improvement in exercise duration and increase in cardiac output were achieved with the Sensolog 703 pacemaker. However, as body vibration is not closely related to physiological needs, it has similar limitations in rate response as the Activitrax pacemaker.
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PMID:Clinical experience with Sensolog 703: a new activity sensing rate responsive pacemaker. 246 22

Sixteen healthy men aged 27.2 +/- 1.2 yr (mean +/- SEM) were tested to volitional exhaustion using the Balke, Bruce, and Ellestad treadmill protocols. Balke resulted in a greater (p less than 0.01) time to exhaustion and total work output, but a lower (p less than 0.05) peak oxygen consumption (ml.kg-1.min-1), and a lower (p less than 0.0001) cumulative net oxygen debt. Oxygen debt, expressed as a percent of total net oxygen cost, was smaller (p less than 0.001) on the Balke than the Bruce and Ellestad protocols (9.9 +/- 0.5, 18.7 +/- 0.6, and 19.3 +/- 0.6%, respectively). The rate of increase in oxygen consumption (p less than 0.0001) and blood lactate concentration (p less than 0.05) were lower on the Balke than on the Bruce and Ellestead protocols. Therefore, the observed differences in oxygen debt and lactate concentrations probably reflect differences in the rate of energy requirement, aerobic and anaerobic metabolism and physiological stress associated with each protocol.
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PMID:Comparison of metabolic responses and oxygen cost during maximal exercise using three treadmill protocols. 263 52

To determine whether endogenous opioids play a role in modulating the appreciation of chest pain in angina pectoris, the specific opioid antagonist, Naloxone, was used. The hypothesis was that the appearance time of ischemic myocardial pain should decrease after Naloxone if centrally mediated pain perception is significantly influenced by the endorphin system in angina pectoris. A randomized double blind clinical trial was conducted in 5 men with effort-induced angina pectoris associated with ST segment changes. Three multi-stage exercise tests, using the Bruce protocol were performed on the same day and time, on three successive weeks. Chest pain was reported 4.3 +/- 0.3 (SEM) minutes after starting exercise on the first or baseline test. On subsequent tests patients received either Naloxone 2 mg IV or a similar volume of saline placebo. Angina pectoris occurred significantly (p. less than 0.05) earlier (1.6 +/- 0.2 minutes) after Naloxone compared to placebo. There were no significant differences in myocardial ischemia indicated by ST segment changes and no significant differences in resting or exercise blood pressure and heart rate between Naloxone and placebo. Thus, these data focus attention on a neglected area of myocardial ischemic pain and suggest that endogenous opioids play a significant role in the recognition of the pain of effort-related angina pectoris.
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PMID:Effect of naloxone on exercise-induced angina pectoris: a randomized double blind crossover trial. 351 46

The efficacy of labetalol, an alpha and beta receptor antagonist, was evaluated in 12 normotensive patients with stable angina pectoris in a single blind dose ranging study. After a two week period of placebo treatment, labetalol was given in doses of 100, 150, 200, and 300 mg twice daily, each for two weeks. Frequency of angina attacks decreased from 9.4 (SEM 2.3)/week in the control period to 7.3 (2.8), 5.2 (2.6), 3.8 (1.8), and 3.3 (1.9)/week in the four successive treatment periods. In the same periods the number of glyceryl trinitrate tablets consumed decreased from 7.0 (2.6)/week to 5.8 (3.3), 3.9 (2.9), 2.7 (1.8), and 2.6 (2.1)/week. Maximal symptom limited treadmill exercise tests were performed three and 12 hours after dosage at each dose. Exercise tolerance (expressed as seconds of the Bruce protocol) increased from 266 (44) with placebo to 306 (44), 369 (50), 396 (48), and 413 (51) in the four treatment periods. This improvement was accompanied by a significant blunting of the heart rate and blood pressure responses to exercise. Trough point exercise tolerance did not differ significantly from that at three hours after dosage. Thus labetalol is effective as an antianginal agent at doses of 150-300 mg twice daily and is well tolerated by the normotensive patient with angina.
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PMID:Oral labetalol in the management of stable angina pectoris in normotensive patients. 391 74

The short-term effect of oral nifedipine on effort tolerance was tested in 10 patients with effort angina pectoris and a positive effort test (GXT). The patients had four symptom-limited GXTs, using the Bruce protocol, on each day of the study at 0800, 1000, 1400, and 1800 hours. They received four doses of 10 mg oral nifedipine on one day and four doses of placebo on the other, each dose given half an hour prior to each GXT. Values with nifedipine were compared to values with placebo at the same time during each day. Nifedipine improved effort tolerance by 0.5 +/- 0.6 min (p = NS) on the first GXT (mean +/- SEM), by 1.2 +/- 0.6 min (p = NS) on the second GXT, by 1.0 +/- 0.3 min (p less than 0.01) on third GXT, and by 1.3 +/- 0.3 min (p less than 0.01) on the fourth GXT. Improvement of effort tolerance was associated with a fall in resting blood pressure and less ST depression; these changes were statistically significant only on the fourth GXT, which may indicate a cumulative effect of subsequent doses of nifedipine.
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PMID:Short-term effect of nifedipine on effort tolerance in patients with angina pectoris. 394 42

The slope of the linear relationship between ventilation (V(E)) and carbon dioxide production (VC0(2)) has been thought to indicate that VC0(2) is one of the major stimuli to V(E). A group of 15 normal subjects undertook different incremental treadmill exercise protocols to explore the relationship between V(E) and VCO(2). An incremental protocol using 1 instead of 3-min stages of exercise resulted in an increase in the V E to VCO(2) ratio [26.84 (SEM 1.23) vs 31.08 (SEM 1.36) (P <0.008) for the first stage, 25.24 (SEM 0.86) vs 27.83 (SEM 0.91) (P <0.005) for the second stage and 23.90 (SEM 0.86) vs 26.34 (SEM 0.81) (P = 0.001) for the third stage]. Voluntary hyperventilation to double the control level of V(E) during exercise resulted in an increase in the V(E) to VCO(2) slope [from 21.3 (SEM 0.71) for the control run to 35.1 (SEM 1.2) for the hyperventilation run (P <0.001)]. Prolonged hyperventilation (5 min) during exercise at stage 2 of the Bruce protocol resulted in a continued elevation of VCO(2) and the V(E)/VCO(2) slope. A steady state of V(E) and metabolic gas exchange can only be said to have been present after at least 3 min of exercise. Voluntary hyperventilation increased the slope of the relationship between V(E) and VCO(2). End-tidal carbon dioxide fell, but remained within the normal range. These results would suggest that a non-carbon dioxide factor may have been responsible for the increase we found in V(E) during exercise, and that factors other than increased dead space ventilation can cause an increased ventilation to VCO(2) slope, such as that seen in some pathophysiological conditions, such as chronic heart failure.
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PMID:Factors which alter the relationship between ventilation and carbon dioxide production during exercise in normal subjects. 886 83

An indirect ELISA was adapted to measure individual classes of anti-phosphatidylcholine (PC) antibodies in patients with brucellosis; a comparison was made with patients with other infectious diseases and healthy human controls. Immunoconjugates of alpha, gamma or mu chain specificity were used. The results were compared with those of conventional tests for brucella antibodies, Rose Bengal, microagglutination (MAT) and Coombs tests, as well as with VDRL. The results indicated that although all sera from patients with brucellosis were VDRL negative, 97% of them (30 of 31) had higher levels of IgA or IgG anti-PC antibodies than the healthy control group. The IgM anti-PC antibodies isotype was not discriminatory between both groups. Seven sera (19%) from patients with other infections had values of IgG anti-PC higher than those of the healthy group; three of them were VDRL positive. The mean ELISA values of IgG and IgA anti-PC (serum diluted 1 in 1600) in the brucellosis and healthy groups were: IgG, 0.80 SEM 0.17 versus 0.23 SEM 0.10; and IgA, 0.86 SEM 0.26 versus 0.35 SEM 0.15. The sensitivity and specificity for the ELISA-PC were: IgG, 96.8% and 96.5%, respectively; IgA, 90.3% and 89.7%, respectively. Only one of 14 individuals clinically cured from brucellosis had significant IgG anti-PC antibodies. In contrast, all of these patients gave positive values in the conventional test for brucellosis. No correlation was found between the serum levels of IgA, IgG anti-PC by ELISA-PC and the results of the MAT or Coombs tests.
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PMID:Anti-phosphatidylcholine antibodies in patients with brucellosis. 944 49

1. There is controversy regarding plasma catecholamine levels in patients with hypertrophic cardiomyopathy (HCM) and few data exist on serial plasma catecholamine measurements during exercise. The present study determined whether cardiovascular and plasma catecholamine responses to exercise were altered in patients with HCM. 2. Plasma noradrenaline (NA) and adrenaline were measured at rest, at the end of each stage during exercise and immediately and 5 min after submaximal treadmill exercise in 15 patients with non-obstructive HCM (13 males, two females; mean (+/- SEM) age 54 +/- 3 years) and in 15 age- and sex-matched controls. The ratio of the increment in heart rate (HR) divided by the increment in plasma NA during exercise (delta HR/delta NA) was used as an index of chronotropic sympathetic responsiveness to exercise. 3. Exercise duration was shorter (11.2 +/- 0.6 vs 8.7 +/- 0.6 min for control vs HCM, respectively; P < 0.01) and diastolic blood pressure was significantly higher at stages I and II of modified Bruce protocol HCM. 4. Resting plasma NA levels (149 +/- 17 vs 167 +/- 28 pg/mL for control vs HCM, respectively; NS) were not different, but plasma NA levels at stages I and II were significantly higher in HCM than in controls (243 +/- 26 vs 399 +/- 69 pg/mL (P < 0.05) and 308 +/- 30 vs 548 +/- 110 pg/mL (P < 0.05), respectively). 5. Peak plasma NA levels were not significantly higher in HCM than in controls (578 +/- 59 vs 918 +/- 184 pg/mL, respectively; NS). 6. The ratio delta HR/delta NA was significantly lower in HCM compared with control at stages I and II (0.49 +/- 0.10 vs 0.21 +/- 0.05 (P < 0.05) and 0.38 +/- 0.06 vs 0.20 +/- 0.05 (P < 0.05), respectively). There were no differences in plasma adrenaline responses during exercise between the two groups. 7. Patients with HCM had augmented plasma NA levels during submaximal exercise with a higher diastolic blood pressure response. Chronotropic sympathetic responsiveness was impaired during the early stages of exercise in patients with HCM.
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PMID:Augmented exercise plasma noradrenaline with impaired chronotropic responsiveness in patients with hypertrophic cardiomyopathy. 988

The present investigation was undertaken to examine whether maximal oxygen uptake (VO2max) and anaerobic threshold (AT) measured during incremental treadmill exercise would be affected by the exercise protocol in trained and untrained individuals. Fifteen untrained men, 10 untrained women, and 12 trained individuals participated in this study. The Astrand, Bruce, and Costill/Fox protocols were selected for comparison. Each subject was tested using all three protocols and the three tests were conducted in a randomized counterbalanced order. During each test, oxygen uptake was measured every 30 s and the test was terminated according to the standard criteria. The VO2max was determined by averaging the two consecutive highest measurements, whereas AT was determined using ventilatory parameters following the V-slope technique. The Astrand, Bruce, and Costill/Fox protocols produced test durations of 9.8 (SEM 0.5), 12.4 (SEM 0.4), and 4.9 (SEM 0.3) min, respectively, in the untrained men, 9.0 (SEM 0.8), 11.0 (SEM 0.6), and 5.3 (SEM 0.6) min, respectively, in the untrained women, and 14.5 (SEM 0.5), 17.0 (SEM 0.5) and 10.4 (SEM 0.4) min, respectively, in the trained men. In the untrained men and women, no differences in VO2max were observed among the three different protocols, but AT was lower when using the Bruce compared to the Astrand protocol. In the trained men, VO2max and AT were lower when using the Bruce protocol than either the Astrand or Costill/Fox protocols. In conclusion, VO2max measured during treadmill exercise is not affected by the protocol of the test and using a running protocol of short duration (i.e. about 5 min) could be a time-efficient way of assessing VO2max in healthy untrained subjects. In trained subjects, however, a protocol consisting of running with small increments in gradient is effective in eliciting a higher VO2max. The lower AT associated with the Bruce protocol seen in both untrained and trained groups suggests this aerobic parameter is protocol dependent and this protocol dependency is not affected by training status.
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PMID:Physiological comparisons among three maximal treadmill exercise protocols in trained and untrained individuals. 1137 12


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