Natriuretic peptide and echocardiography after operation of atrial septal defect.

Patients benefit from surgical seclusion of atrial septal defect but have excessive cardiovascular morbidity after the operation. We evaluated haemodynamics and looked for abnormalities of cardiac structures and function late after surgical seclusion of the defect. Serum N-terminal natriuretic peptide measurement and transthoracic and transoesophageal echocardiography were performed in 61 patients aged 43+/-15 years (mean+/-standard deviation) 21+/-5 years after surgery. The findings were compared with 67 control subjects. The patients had higher serum N-terminal atrial natriuretic peptide concentration than the control subjects (0.40+/-0.32 vs. 0.24+/-0.12 nmol/l, P=0.0001). Peptide levels correlated with current age (P=0.0001) and age at operation (P=0.0014), but not with age in the control subjects. In the patients, echocardiography measurements of cardiac dimensions correlated with hormone levels (atrial natriuretic peptide concentration with left atrial end-systolic diameter (P=0.042), left ventricular end-diastolic (P=0.021) and end-systolic diameter (P=0.042). There were only 10 patients (16%) without any abnormality in echocardiography. Their peptide concentration was 0.25+/-0.18 nmol/l (P=not significant compared to the control subjects). The association between increasing N-terminal atrial peptide levels and operation age together with echocardiography findings support the clinical consensus of treating atrial septal defect patients in their childhood and adolescence.

Heart rate and blood pressure variability during heavy training and overtraining in the female athlete.

We investigated heavy training- and overtraining-induced changes in heart rate and blood pressure variability during supine rest and in response to head-up tilt in female endurance athletes. Nine young female experimental athletes (ETG) increased their training volume at the intensity of 70-90% of maximal oxygen uptake (VO2max) by 125% and training volume at the intensity of < 70% of VO2max by 100% during 6-9 weeks. The corresponding increases in 6 female control athletes were 5% and 10%. The VO2max of the ETG and the control athletes did not change, but it decreased from 53.0 +/- 2.2 ml x kg(-1) x min(-1) to 50.2 +/- 2.3 ml x kg(-1) x min(-1) (mean+/-SEM, p < 0.01) in five overtrained experimental athletes. In the ETG, low-frequency power of R-R interval (RRI) variability during supine rest increased from 6 +/- 1 ms2 x 10(2) to 9 +/- 2 ms2 x 10(2) (p < 0.05). The 30/15 index (= RRI(max 30)/RRI(min 15), where RRI(max 30) denotes the longest RRI close to the 30th RRI and RRI(min 15) denotes the shortest RRI close to the 15th RRI after assuming upright position in the head-up tilt test), decreased as a result of training (analysis of variance, p = 0.05). In the ETG, changes in VO2max were related to the changes in total power of RRI variability during standing (r = 0.74, p < 0.05). Heart rate response to prolonged standing after head-up tilt was either accentuated or attenuated in the overtrained athletes as compared to the normal training state. We conclude that heavy training could increase cardiac sympathetic modulation during supine rest and attenuated biphasic baroreflex-mediated response appearing just after shifting to an upright position. Heavy-training-/overtraining-induced decrease in maximal aerobic power was related to decreased heart rate variability during standing. Physiological responses to overtraining were individual.

Endurance training, overtraining and baroreflex sensitivity in female athletes.

We examined heavy training-induced changes in baroreflex sensitivity, plasma volume and resting heart rate and blood pressure variability in female endurance athletes. Nine athletes (experimental training group, ETG) increased intense training (70-90% VO2max) volume by 130% and low-intensity training (< 70% Vo2max) volume by 100% during 6-9 weeks, whereas the corresponding increases in six control athletes (CG) were 5% and 10% respectively. Maximal oxygen uptake (VO2max) in the ETG and CG did not change, but in five ETG athletes VO2max decreased from 53.0 +/- 2.2 (mean +/- SEM) (CI 46.8-59.2) ml kg-1 min-1 to 50.2 +/- 2.3 (43.8-56.6) ml kg-1 min-1 (P < 0.01), indicating overtraining. Baroreflex sensitivity (BRS) measured using the phenylephrine technique and blood pressure variability (BPV) did not change, but the low-frequency power of the R-R interval variability increased in the ETG (P < 0.05). The relative change in plasma volume was 7% in the ETG and 3% in the CG. The changes in BRS did not correlate with the changes in plasma volume, heart rate variability and BPV. We conclude that heavy endurance training and overtraining did not change baroreflex sensitivity or BPV but significantly increased the low-frequency power of the R-R interval variability during supine rest in female athletes as a marker of increased cardiac sympathetic modulation.

Hormonal responses to endurance training and overtraining in female athletes.

OBJECTIVE: To examine different hormonal responses to heavy endurance training and overtraining in female athletes. DESIGN: Submaximal and maximal treadmill tests, self-report mood measures, and stress hormone analyses were repeated at baseline, after 4 weeks and at the end of 6 to 9 weeks of experimental intensive training and after 4 to 6 weeks of recovery. SUBJECTS: Fifteen healthy female endurance athletes increased their intensive training volume by 130% and base training volume by 100% (ETG, n = 9) or served as controls (CG, n = 6). MAIN OUTCOME MEASURES: Maximal oxygen uptake (VO2max), mood dynamics, blood catecholamines, cortisol and testosterone at rest and after submaximal and maximal exercise, and nocturnal urine catecholamines. RESULTS: Five females from the ETG demonstrated an over-training state (OA subgroup) at the end of the training period. Their VO2max decreased (mean +/- SEM) from 53.0 +/- 2.2 ml.kg-1.min-1 (range, 46.8-59.2) to 50.2 +/- 2.3 ml.kg-1.min-1 (range, 43.8-56.6) (p < 0.01). Maximal treadmill performance expressed as oxygen demand decreased (mean +/- SEM) from 56.0 +/- 1.6 ml.kg-1.min-1 (range, 51.5-60.5) to 52.2 +/- 1.1 ml kg-1.min-1 (range, 49.1-55.3) (p < 0.01). Maximal heart rate also decreased (mean +/- SEM) from 190 +/- 1 bpm (range, 185-197) to 186 +/- 2 bpm (range, 184-193) (p < 0.05), and the athletes experienced mood disturbances. Plasma adrenaline levels at maximal and noradrenaline at submaximal work rate decreased during the last 2 to 5 training weeks (p < 0.05), and serum cortisol levels at maximal work rate decreased during the first 4 training weeks (p < 0.05) in the ETG. Plasma adrenaline at maximal work rate decreased during the first 4 training weeks (p < 0.05) in the OA subgroup. There were no changes in the CG. Individual hormonal response types to heavy training and overtraining were found. CONCLUSIONS: Hormone responses to exercise load are superior in indicating heavy training-induced stress when compared with resting hormone levels. These responses indicated decreased sympathoadrenal and/or adrenocortical activity (or exhaustion of the adrenal gland or the central nervous system). Individual hormonal profiles are needed to follow up training effects. Marked individual differences were found in training- and overtraining-induced hormonal changes.

Exhaustive endurance training for 6-9 weeks did not induce changes in intrinsic heart rate and cardiac autonomic modulation in female athletes.

We investigated the effects of progressively increased training load and overtraining on resting and intrinsic heart rate (IHR) and cardiac autonomic modulation (CAM), and their relationships to performance variables. Nine athletes (ETG) increased training volume at 70-90% of maximal oxygen uptake (VO2max) by 130% (p<0.01) and training volume at <70% VO2max by 100% (p < 0.01) during 6-9 weeks. The corresponding increases in six female control athletes (CG) were 5 and 10%. Pharmacological blocking through atropine and propranolol and the Rosenblueth and Simeone model were used to calculate the sympathovagal balance index (Abal) and to measure IHR. The results were analysed using two-way analysis of variance. VO2max, IHR and Abal did not change. Resting heart rate had a tendency to decrease in the ETG and increase in the CG during the training period (interaction p < 0.01). Five ETG athletes demonstrated overtraining state (OA subgroup). Their VO2max (mean+/-SEM) decreased from 53.0+/-2.2 ml x kg(-1) x min(-1) to 50.2+/-2.3 ml x kg(-1) x min(-1) (p < 0.01), but no changes in resting HR, IHR and Abal were found. A significant correlation between the baseline values of VO2max and the parasympathetic activity index was found (r=-0.59, p < 0.05). In conclusion, progressively increased training load and overtraining did not induce significant changes in intrinsic heart rate or cardiac autonomic modulation in female endurance athletes. Resting heart rate rather decreased with heavy endurance training and overtraining. High maximal oxygen uptake was correlated with high cardiac parasympathetic modulation.

Whole-body impedance cardiography in the measurement of cardiac output.

OBJECTIVE: To evaluate the reliability of whole-body impedance cardiography with electrodes on wrists and ankles in the measurement of cardiac output compared with the thermodilution method. DESIGN: Prospective, clinical investigation. SETTING: Surgical intensive care unit and operating room at a university hospital. PATIENTS: Simultaneous cardiac output measurements by thermodilution and whole-body impedance cardiography were performed in 74 patients undergoing a coronary artery bypass grafting operation. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: A total of 97 triplicate, simultaneous cardiac output measurements were carried out with thermodilution and whole-body impedance cardiography: 74 measurements were conducted in patients who were awake and 23 measurements were conducted during anesthesia but before the commencement of surgery. The mean cardiac output difference (bias) between the two methods was 0.25 +/- 0.81 (SD) L/min; the limits of agreement (2 SD) were-1.37 and 1.87 L/min, respectively. The repeatability value (rv = 2.83 x SD) for whole-body impedance cardiography (rv = 0.46 L/min) was considerably better than for the thermodilution method (rv = 1.05 L/min). Whole-body impedance cardiography reliably detected cardiac output changes induced by head-up tilt before anesthesia, by anesthesia induction, and by intubation. Two factors predicted the between-methods stroke volume difference: hematocrit (correlation coefficient r = -.36, r2 = .13; p < .001); and body mass index (r = .29, r2 = .08; p < .01). Using the multiple linear regression equation for correcting the stroke volume by hematocrit and body mass index, the limits of agreement (2 SD) between the methods studied were reduced to +/-1.28 L/min for cardiac output and +/-0.72 L/min/m2 for cardiac index. CONCLUSIONS: There was close agreement between whole-body impedance cardiography and thermodilution in the measurement of cardiac output in patients with coronary artery disease without cardiac shunts and valvular lesions. The repeatability of the impedance method was significantly better than the repeatability of thermodilution. Whole-body impedance cardiography can be recommended for the assessment of cardiac output and its changes in the resting state. Whole-body impedance cardiography is a feasible and handy method for noninvasive and continuous measurement of cardiac output.

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.

Blood pressure level changes caused by posture change and physical exercise: can they be determined accurately using a standard cuff method?

The accuracy of the indirect standard cuff method of measurement was tested against intra-arterial blood pressure readings (Oxford method) in a series of simple clinical tests: in the sitting, supine and standing positions, during bicycle ergometer test and during recovery. The mean discrepancy between methods varied in tests from -2.3 to 12.9 mmHg for systolic blood pressure level and from -4.3 to 18.2 mmHg for diastolic blood pressure level. Blood pressure responses to other tests were analysed using the value measured in the sitting position as the reference. The mean discrepancy between the methods in test responses varied from -6.3 to 8.9 mmHg for systolic responses and from -2.3 to 20.3 mmHg for diastolic responses. The data analysis indicates that the accuracy of the indirect method varies considerably between tests and also between subjects. We conclude that at present the standard cuff method cannot replace the direct method for determining blood pressure responses and reactivity.

Slow-release metoprolol in angina pectoris. A comparative study of a cardioselective beta-blocking drug, metoprolol, in ordinary and slow-release tablets (Durules) in the treatment of angina pectoris.

A double-blind cross-over study was undertaken to compare the effects of ordinary metoprolol tablets (tablets) 0.1 g b.i.d. and metoprolol slow-release tablets (Durules) 0.2 g once daily in 16 patients with angina pectoris. Initially, the patients were treated with placebo for 2 weeks, and then during the cross-over periods with either 1 tablet morning and evening or 1 Durules in the morning and 1 placebo in the evening. Standardized bicycle ergometer exercise tests with heart rate and blood pressure measurements were performed 2 hours after placebo, 2 hours after tablets and Durules, 12 hours after tablets and 24 hours after Durules. The patients kept diaries of their anginal attacks throughout the study. There were no statistically significant differences in total work between tablets and Durules when the values at 12 hours and 24 hours were compared. However, total work was significantly greater at 2 hours and at 12 hours after tablets and 24 hours after Durules than after placebo. Heart rate and systolic blood pressure during exercise were significantly decreased 24 hours after Durules compared to placebo. The heart rate was, however, lower 12 hours after tablets than 24 hours after Durules (p less than 0.05), although this slight difference in the degree of beta-blockade did not seem to be of clinical importance in these patients.

Carboxyhaemoglobin saturation in relation to smoking and various occupational conditions.

The effects of smoking and occupational conditions on COHb saturation were studied among employees on traffic duty, in restaurants, in iron foundries, and in an office. The subjects were 139 smokers and 152 nonsmokers working in the same environments. Changes in COHb saturation were observed in samples of blood obtained before and after the working period. Samples of air were collected during the working hours in restaurants, in foundries and in office, 190 samples in all, for the determination of content of CO. Among the nonsmokers there was no change in COHb saturation in restaurants and in office work. On traffic duty and in iron foundries the increase was significant, but the values after work were less than half the permitted occupational threshold limit value (TLV) level of 6 per cent units. In the smoking group the mean values of COHb saturation before work were about twice the mean COHb saturation in the nonsmokers after work. In office work and in foundries the mean COHb saturations after the work exceeded the permitted TLV.