Molecular and cellular changes in vein grafts: influence of pulsatile stretch

Sudden cardiac death is frequent in patients with dilated cardiomyopathy. To assess the risk of an arrhythmic event is still difficult. Here the analysis of the heart rate variability offers new possibilities. METHOD: 25 patients (18 males, 7 females, age 53 +/- 9 yrs) with dilated cardiomyopathy were included in the study. Analysis of heart rate variability assessed by time- and frequency-domain measures was determined from Holter recording. The mean follow-up was 18 +/- 5 months. RESULTS: 6 patients died (5 of sudden cardiac death, 1 of heart failure), 1 patient with an implanted defibrillator received an adequate shock. Parameters influenced by low- and mid-frequent oscillations of the heart rate were significantly lower in patients who died suddenly or had adequate shocks. The best predictive parameter was the s.d.RR: all patients with an s.d.RR < 50 ms had lethal arrhythmias whereas the s.d.RR of the surviving patients was > or = 50 ms. No significant difference was found or high frequency parameters, which are mainly influenced by parasympathetic activity. CONCLUSION: The analysis of heart rate variability is of prognostic relevance in patients with dilated cardiomyopathy. Especially the s.d.RR is able to identify patients with a high risk of a sudden cardiac death.     

Circadian rhythm of heart rate variability is reversibly abolished in ischemic stroke

BACKGROUND AND PURPOSE: Acute brain infarction significantly decreases heart rate variability as a result of cardiovascular autonomic dysregulation. However, information regarding circadian rhythms of heart rate and heart rate variability is limited. METHODS: In this prospective study, we analyzed 24-hour circadian rhythm of heart rate and the time and frequency domain measures of heart rate variability in 24 patients with hemispheric brain infarction, 8 patients with medullary brainstem infarction, and 32 age- and sex-matched healthy control subjects. ECG data were obtained from the patients in the acute phase and at 6 months after the infarction. RESULTS: In the acute phase of stroke, all the components of heart rate variability, ie, standard deviation of RR intervals, total power, high-frequency power, low-frequency power, and very-low-frequency power, were similar at night (from midnight to 6 AM) and during the day (from 9 AM to 9 PM), indicating that the circadian oscillation of heart rate variability had been abolished. At 6 months after brain infarction, the circadian rhythm had returned and, as in the control subjects, the values at night were significantly higher than those in the daytime. The values in hemispheric and in brainstem infarction did not differ significantly from each other. CONCLUSIONS: These results suggest that circadian fluctuation of heart rate variability is reversibly abolished in the acute phase of ischemic stroke and that it returns during the subsequent 6 months. The loss of the relative vagal nocturnal dominance may contribute to the incidence of cardiac arrhythmias and other cardiovascular complications after acute stroke.     

Is there increased sympathetic activity in patients with hypertrophic cardiomyopathy?

OBJECTIVES: This study aimed to assess autonomic nervous system activity in patients with hypertrophic cardiomyopathy. BACKGROUND: Patients with hypertrophic cardiomyopathy are traditionally thought to have increased sympathetic activity. However, convincing evidence is lacking. METHODS: Heart rate variability was assessed from 24-h ambulatory electrocardiographic (Holter) recordings in 31 patients with hypertrophic cardiomyopathy and 31 age- and gender-matched normal control subjects in a drug-free state. Spectral heart rate variability was calculated as total (0.01 to 1.00 Hz), low (0.04 to 0.15 Hz) and high (0.15 to 0.40 Hz) frequency components using fast Fourier transformation analysis. RESULTS: There was a nonsignificant decrease in the total frequency component of heart rate variability in patients with hypertrophic cardiomyopathy compared with that of normal subjects (mean +/- SD 7.24 +/- 0.88 versus 7.59 +/- 0.57 ln[ms2], p = 0.072). Although there was no significant difference in the high frequency component (5.31 +/- 1.14 versus 5.40 +/- 0.91 ln[ms2], p = 0.730), the low frequency component was significantly lower in patients than in normal subjects (6.25 +/- 1.00 versus 6.72 +/- 0.61 ln[ms2], p = 0.026). After normalization (i.e., division by the total frequency component values), the low frequency component was significantly decreased (38 +/- 8% versus 43 +/- 8%, p = 0.018) and the high frequency component significantly increased (16 +/- 6% versus 12 +/- 6%, p = 0.030) in patients with hypertrophic cardiomyopathy. The low/high frequency component ratio was significantly lower in these patients (0.94 +/- 0.64 versus 1.33 +/- 0.55, p = 0.013). In patients with hypertrophic cardiomyopathy, heart rate variability was significantly related to left ventricular end-systolic dimension and left atrial dimension but not to maximal left ventricular wall thickness. No significant difference in heart rate variability was found between 14 victims of sudden cardiac death and 10 age- and gender-matched low risk patients. CONCLUSIONS: Our observations suggest that during normal daily activities, patients with hypertrophic cardiomyopathy experience a significant autonomic alteration with decreased sympathetic tone.     

Nonsustained ventricular tachycardia in severe heart failure. Independent marker of increased mortality due to sudden death. GESICA-GEMA Investigators

BACKGROUND: The goal of the study was to determine the prognostic value of nonsustained ventricular tachycardia (NSVT) in total mortality in severe congestive heart failure (CHF) and in death modes. NSVT is associated with an increased mortality in CHF. However, the predictive value of NSVT as a marker for sudden death or death due to progressive heart failure has not been determined. METHODS AND RESULTS: Five hundred sixteen patients from the GESICA trial (33.4% with NSVT) were initially studied with the results of 24-hour Holter and 2 years of follow-up. Within 2 years, 87 of 173 patients (50.3%) with NSVT and 106 of 343 patients (30.9%) without NSVT died. Relative risk (RR) was 1.69 (95% confidence interval [CI], 1.27 to 2.24; P < .0002), and Cox proportional hazard analysis was 1.62 (95% CI, 1.22 to 2.16; P < .001). Sudden death increased from 8.7% (30 of 343) to 23.7% (41 of 173) in patients with NSVT (RR, 2.77; 95% CI, 1.78 to 4.44; P < .001). Progressive heart failure death was also increased from 17.5% (60 of 343) to 20.8% (36 of 173) (P = .22). Quantitative analysis of 24-hour Holter (first 295 patients) demonstrated that couplets had a similar RR to that of NSVT for both total mortality (RR, 1.81; 95% CI, 1.22 to 2.66; P < .002) and sudden death (RR, 3.37; 95% CI, 1.57 to 7.25; P < .0005). Couplets and/or NSVT (ventricular repetitive beats) were even more predictive for sudden death (RR, 10.1; 95% CI, 1.91 to 52.7; P < .01). CONCLUSIONS: In patients with CHF, NSVT is an independent marker for increased overall mortality rate and sudden death. The absence of NSVT and ventricular repetitive beats in a 24-hour Holter indicates a low probability of sudden death.     

Circadian activity of the endogenous fibrinolytic system in stable coronary artery disease: effects of beta-adrenoreceptor blockers and angiotensin-converting enzyme inhibitors

OBJECTIVES: To examine circadian changes in the sympathovagal balance, the activity of the renin-angiotensin system and hemostatic variables in patients with stable coronary artery disease, and the effects of beta-adrenoceptor blockade and angiotensin-converting enzyme inhibition. BACKGROUND: Sympathovagal balance and key components of the fibrinolytic system show circadian variability. The effects of beta-adrenergic blocking agents and angiotensin-converting enzyme inhibitors on these autonomic and hemostatic rhythms are not well defined. METHODS: Twenty patients with coronary artery disease underwent 24-h Holter monitoring for heart rate variability and blood sampling (6 hourly for 24 hours) after three consecutive treatment phases, (firstly with placebo, then bisoprolol, and finally quinapril). The effects on sympathovagal balance, hemostatic variables and the renin-angiotensin system activity were measured. RESULTS: The fibrinolytic capacity showed marked circadian variation at the end of the placebo phase (p = 0.002), plasminogen activator inhibitor-1 (PAI-1) activity peaking at 06.00 AM when tissue plasminogen activator (tPA) activity was at its nadir. Sympathovagal balance showed a sharp increase at approximately the same time but plasma renin activity did not rise until later in the day. Inspection of the 24-h profiles suggested that bisoprolol reduced sympathovagal balance and the morning peak of PAI-1 activity and antigen, with a small increase in tPA activity, although these changes were not significant. Quinapril produced a substantial rise in renin (p = 0.01) but did not significantly affect either PAI-1 or tPA. Sympathovagal balance was unaffected by quinapril. CONCLUSIONS: In patients with stable coronary artery disease, angiotensin-converting enzyme inhibition with quinapril does not affect either sympathovagal balance or the endogenous fibrinolytic system. Our data suggest that the sympathoadrenal system may modify fibrinolytic activity, judged by the response to beta-adrenoreceptor blockade with bisoprolol.     

Subject''s perceptions of the crew interaction dynamics under prolonged isolation

BACKGROUND: Short-term variability of RR interval and blood pressure occurs predominantly at low frequency (LF; approximately 0.1 Hz) and high frequency (approximately 0.25 Hz). The arterial baroreflex is thought to be the predominant determinant of the LF component of RR variability. Patients with severe congestive heart failure (CHF) have an attenuated or absent LF oscillation in RR variability. The left ventricular assist device (LVAD) offers a unique possibility for analysis of spectral oscillations in RR interval independent of any effects of blood pressure that influence these oscillations via the baroreflex. METHODS AND RESULTS: We performed spectral analysis of RR, blood pressure, and respiration in 2 patients with CHF before and after LVAD implantation. LF components of the RR-interval and blood pressure variability were absent in both CHF patients before LVAD implantation. After LVAD implantation, spectral analysis of the RR interval showed restoration of a clear and predominant LF oscillation in the native hearts of both patients, with no such oscillation evident in the blood pressure profile. CONCLUSIONS: During total circulatory support with the LVAD, the LF oscillation in RR interval of the native heart, absent in CHF, is restored. This LF oscillation in RR interval occurs in the absence of LF oscillations in blood pressure and thus is unlikely to be explained by baroreflex mechanisms. Hence, the absence of LF oscillation in the RR interval in CHF is functional and is reversible by LVAD circulation. The presence of a predominant LF oscillation in RR interval independent of any oscillation in blood pressure suggests that the LF oscillation is a fundamental property of central autonomic outflow.     

Twenty-four-hour rhythms in immune responses in rat submaxillary lymph nodes and spleen: effect of cyclosporine

Twenty-four-hour variations in cellularity, lipopolysaccharide (LPS)- and concanavalin A (Con A)-induced cell proliferation, and natural killer (NK) activity were examined in submaxillary lymph nodes and spleen of rats injected with Freund's complete adjuvant or its vehicle and kept under light from 08:00 to 20:00 h daily. A significant daily variation in cellularity was detected, exhibiting maxima at 09:00 h in submaxillary lymph nodes (nonimmunized and immunized rats) and at 13:00 h in spleen (immunized rats only). Submaxillary lymph node LPS- and Con A-mitogenic effect displayed maximal activity during daytime (peak at 13:00-17:00 h). In spleen, the maxima for 24-h rhythm in LPS-induced cell proliferation and NK activity occurred at midnight and at early morning (09:00 h), respectively. Con A-induced spleen cell proliferation peaked at midday in nonimmunized rats only. Injection of the immunosuppressive drug cyclosporine decreased Freund's adjuvant-induced augmentation of LPS and Con A mitogenic effect in both tissues and diminished spleen cell number. Cyclosporine blunted circadian rhythms in submaxillary lymph node Con A response and cell number, while it shifted the maximum in LPS effect to peak at 01:00 h. Cyclosporine also suppressed the circadian changes in LPS- and Con A-induced spleen cell proliferation, but not those found in NK activity. The results indicate the existence of 24-h rhythms in immune responses of rat submaxillary lymph nodes and spleen with maxima at different times of the day and that were significantly affected by cyclosporine injection.     

Change of circadian pattern of arterial pressure in patients with congestive heart failure treated with perindopril, an inhibitor of angiotensin-converting enzyme (ACE)

The 24-h profile of blood pressure (BP) was studied in 28 patients (21 males and 7 females) with congenital heart failure (CHF) of NYHA class II-III (ejection fraction < 45%). The patients were 46 to 76 years of age and had postinfarction cardiosclerosis. They had not received ACE inhibitors before. Two groups were formed basing on the presence of hypertension. Perindopril was administered in a single daily dose of 2 mg or higher if demanded to reduce symptoms of CHF and/or to normalize BP. The treatment continued for 3 months. The 24-h BP profile was assessed using portable device SpaceLabs 90207 (USA). In CHF patients with hypertension perindopril significantly lowered mean 24-h, day and night BP and its loads, reestablished two-phase circadian rhythm of AP and corrected BP variability. In CHF patients free of hypertension significant changes of the profile were not registered. It is evident that unwanted changes in the BP 24-h profile due to perindopril were absent in CHF normotensives.     

Circadian variation of ventricular arrhythmia recurrences after cardioverter-defibrillator implantation in patients with healed myocardial infarcts

Past studies using Holter monitoring and retrospective reviews of death certificates have documented peak occurrence of sudden death and nonsustained ventricular tachycardia (VT) in the morning hours. We used the Ventritex Cadence device (Ventritex, Sunnyvale, California) which documents the date and time of all stored arrhythmias leading to device therapy to evaluate the circadian pattern of sustained ventricular arrhythmia recurrence. Mean follow-up after defibrillator implantation was 628 +/- 285 days. All 390 patients had at least 1 episode (range 1 to 43) of sustained VT documented from analysis of the stored electrograms associated with an arrhythmia event. Stored electrograms were available for review and analysis in 3,041 device detections; 349 stored events were excluded because they did not fulfill the diagnostic criteria for VT or failed to document the onset of the ventricular arrhythmia at the beginning of the recorded event of the arrhythmia episode. Criteria for the diagnosis of VT or ventricular fibrillation were met in 2,692 arrhythmia episodes occurring in 390 patients. There was circadian variation for ventricular arrhythmia recurrence for the whole patient group with the data fit to the sinusoidal density function: f(t) = 126 - 51 x cos (-57 + 2 pi t/24) - 25 x sin (63 + 2 pi t/12) (p < 0.0001). Ventricular arrhythmia occurrence rate was lowest between 2:00 and 3:00 A.M., and highest between 10:00 and 11:00 A.M. In addition, the same circadian pattern was demonstrated regardless of patient age, gender, left ventricular ejection fraction (< 35% or > or = 35%), and VT cycle length (< 300 or > or = 300 ms).(ABSTRACT TRUNCATED AT 250 WORDS)     

QT interval as a cardiac risk factor in a middle aged population

OBJECTIVE: To evaluate the value of QT interval as a cardiac risk factor in middle aged people. METHODS: The association between QT interval and cardiac risk factors and mortality in a middle aged Finnish population of 5598 men and 5119 women was evaluated over a 23 year follow up. To adjust the QT interval confidently for heart rate, a nomogram was constructed from the baseline electrocardiograms separately for men and women. RESULTS: Nomogram-corrected QT interval (QTNc) prolongation was associated with elevated blood pressure and signs of cardiovascular disease; QTNc shortening was associated with smoking. Over 10% prolongation of QTNc predicted death in men with heart disease: adjusted relative risk (RR) was 2.17 (95% confidence interval 0.67-7.45) for sudden death; 2.12 (1.25-3.59) for total cardiovascular mortality; and 1.92 (1.23-3.00) for all cause mortality. In healthy men the increase in RR was not significant: sudden death, 1.48 (0.67-3.25); total cardiovascular mortality, 1.25 (0.92-1.70); all cause mortality, 1.21 (0.96-1.53). However, healthy men with long QTNc in the lowest heart rate quartile exhibited an RR of 2.75 (1.00-7.40) for sudden death. Over 10% shortened QTNc predicted cardiovascular death in men with heart disease who smoked; RR 3.72 (1.45-9.54). Non-smoking men with short QTNc had low mortality risks irrespective of possible signs of cardiovascular disease. The trends in mortality risks were similar but weaker for women. CONCLUSIONS: In a middle aged population, prolonged QT interval predicts cardiac mortality in men with signs of cardiovascular disease. In women and healthy men this risk is weak and may reflect subclinical heart disease. A shortened QT interval predicts death in men with heart disease who smoke.     

Postinfarction use of beta-blockers in elderly patients

beta-Adrenoceptor antagonists (beta-blockers) reduce mortality and recurrent myocardial infarction (MI) in older patients after both Q-wave MI and non-Q-wave MI. The effects of beta-blockers are to: (i) reduce complex ventricular arrhythmias, including ventricular tachycardia; (ii) increase the ventricular fibrillation threshold; (iii) reduce myocardial ischaemia; (iv) decrease sympathetic tone; (v) markedly attenuate the circadian variation of complex ventricular arrhythmias: (vi) abolish the circadian variation of myocardial ischaemia; and (vii) abolish the circadian variation of sudden cardiac death or MI. beta-Blockers reduce mortality in patients with MI and complex ventricular arrhythmias. In addition, they are excellent antianginal agents. Older persons with hypertension who have had an MI should be treated initially with a beta-blocker. beta-Blockers reduce mortality in patients with: (i) diabetes mellitus who have had an MI; (ii) MI and congestive heart failure with an abnormal or normal left ventricular ejection fraction; and (iii) MI and an asymptomatic abnormal left ventricular ejection fraction. Severe congestive heart failure, severe peripheral arterial disease with threatening gangrene, greater than first degree atrioventricular block, hypotension, bradycardia, lung disease with bronchospasm, and bronchial asthma are contraindications to treatment with beta-blockers.     

Influence of heart rate on stroke volume variability in atrial fibrillation in patients with normal and impaired left ventricular function

Both resting tachycardia and irregular ventricular rhythm may contribute to impaired cardiac performance in atrial fibrillation (AF). This study assesses the relation between resting heart rate and beat-to-beat changes in left ventricular (LV) ejection and filling in patients with normal and impaired LV systolic function. Beat-to-beat variation in LV outflow and inflow velocity-time integral was measured using pulsed Doppler ultrasound in 39 patients with chronic AF and normal (n=22) or impaired (n=17) LV systolic function. Aortic velocity-time integral variability increased with mean heart rate (p=0.003) even though RR interval variability decreased (p <0.001). Aortic velocity-time integral was more sensitive to the duration of both the preceding (p <0.001) and prepreceding (p <0.001) RR intervals at higher heart rates. These relations were similar for patients with normal and impaired LV systolic function. The sensitivity of the filling velocity-time integral to RR interval variability also increased with heart rate (p <0.001). However, at higher heart rates the filling velocity-time integral (p=0.009) and filling time (p=0.005) were less sensitive to change in RR intervals in patients with impaired LV function. We conclude that beat-to-beat stroke volume variability in AF increases with heart rate. Stroke volume variability was not influenced by LV systolic function.     

Heart rate variability index in congestive heart failure: relation to clinical variables and prognosis

AIM: To evaluate the clinical and prognostic value of the heart rate variability index in patients with congestive heart failure. METHODS: Sixty-four patients with chronic congestive heart failure and sinus rhythm underwent clinical assessment, 24-h ambulatory electrocardiography and echocardiography. Patients were followed for 6 to 30 months. Cardiac death or heart transplantation constituted the primary end-point of the study. RESULTS: The heart rate variability index was related to left ventricular ejection fraction (r=0.29, P=0.02) and New York Heart Association class (P=0.01). Patients with a restrictive left ventricular filling pattern had a lower heart rate variability index compared to patients with a non-restrictive pattern (26+/-11 vs 33+/-9 units, P=0.01). Patients who died (n=11) or underwent heart transplantation (n=4) had a lower heart rate variability index compared to survivors (21+/-10 vs 33+/-9 units, P<0.0001). In multivariate survival analysis, a reduced heart rate variability index was related to survival independent of parameters of left ventricular function. CONCLUSION: The heart rate variability index provides independent information on clinical status and prognosis in patients with chronic congestive heart failure.     

Breathing measurement reduces false-negative classification of tachypneic preextubation trial failures

A method using a parameter from the field of nonlinear dynamics to quantify the variability of ventricular premature complexes (VPCs) is presented. One hundred patients with coronary artery disease and > or = 10 VPCs/hour were included in the study. The RR intervals were plotted in a three-dimensional artificial phase space, and the structures in phase space were quantified by the local scaling indices, alpha. In the frequency distribution histogram, n(alpha), for each patient, the maximum of the ventricular ectopies alpha VPC, adjusted to the VPC frequency, was assessed; alpha VPC was used as the risk indicator. Endpoints were total mortality and sudden cardiac death. During follow-up (mean 3.1 years), 28 out of 100 patients died, 16 suddenly; alpha VPC had a significant prognostic impact and was independent from other risk indicators, such as left ventricular ejection fraction (LVEF). Patients who died during follow-up were characterized by a high alpha VPC. The optimal discrimination of high risk patients and low risk patients occurred at alpha VPC = 3.0. After 4 years, the survival rate of patients with a alpha VPC > 3.0 was 59%, in contrast to 97% in patients with alpha VPC < or = 0.3. As to the sudden death mortality, the survival rates were 74% and 97%, respectively. The difference between the groups were significant for both endpoints. Patients with an increased VPC variability (i.e., alpha VPC > 3.0) were at enhanced risk of sudden death and total mortality risk; alpha VPC was independent from other risk indicators such as the LVEF or heart rate variability parameters.     

Evidence that platelets promote tube formation by endothelial cells on matrigel

OBJECTIVES: This study sought to evaluate long-term predictors of coronary events in men and women with arteriographically defined coronary artery disease (CAD). BACKGROUND: There is conflicting evidence of the role of triglycerides (TGs) as a prognosticator of CAD, and no studies have examined the long-term outcome of "normal" levels in predicting new coronary events. METHODS: This was a retrospective cohort study that evaluated 740 consecutive patients presenting for diagnostic coronary arteriography between 1977 and 1978. Beginning in 1988, patients with arteriographic CAD (n=350) were recontacted and asked to complete detailed medical questionnaires. Case and control patients were stratified by development of new coronary events, including death from ischemic heart disease, nonfatal myocardial infarction and revascularization. RESULTS: There were 199 events during the 18-year follow-up period. The mean high density lipoprotein cholesterol (HDL-C) was significantly lower (35 vs. 39 mg/dl; p=0.002) and TGs higher (160 vs. 137 mg/dl; p=0.03) in case patients than in control patients; After adjusting for age, gender and beta-adrenergic blocking agent use, multiple logistic regression analysis revealed the following independent predictors of CAD events: diabetes mellitus (relative risk [RR] 2.1, 95% confidence interval [CI] 1.4% to 3.1%), HDL-C <35 mg/dl (RR 1.5, 95% CI 1.1% to 2.00) and TGs >100 mg/dl (RR 1.5, 95% CI 1.1% to 2.1%). A Kaplan-Meier analysis revealed significantly reduced survival from CAD events in patients with baseline TG levels > or = 100 mg/dl compared with TG levels <100 mg/dl (p=0.008). CONCLUSIONS: TG levels previously considered "normal" are predictive of new CAD events. The cutpoints established by the National Cholesterol Education Program for elevated TGs (>200 mg/dl) may need to be refined.     

Solitary fibrous tumour: clinicopathological, immunohistochemical, and ultrastructural analysis of 12 cases arising in soft tissues, nasal cavity and nasopharynx, urinary bladder and prostate

Heart-rate variability (HRV), a measure of fluctuation around the mean heart rate, reflects the sympathetic and parasympathetic balance of the autonomic nervous system, and is an excellent technique to study cardiovascular tone in patients with neurological injuries. The purpose of this study was to determine whether abnormal HRV is present in patients with traumatic brain injury (TBI) during the post-acute recovery phase. Using a prospective, case/control design, we performed 24-h ambulatory ECG monitoring in seven TBI patients and in seven controls (C). There was a significant difference in root mean squared successive difference of RR intervals (C 40.4 +/- 10.3, TBI 23.3 +/- 16.5, p = 0.04) between TBI and C. Four patients with TBI (compared to one control) had abnormal standard deviation of the RR interval. When these four patients were compared to their matched controls, significant differences were found in frequency domain measure (In total power: TBI 4.4 +/- 0.9 ms2, C 7.1 +/- 1.4 ms2, In low frequency: TBI 3.3 +/- 1.1 ms2, C 6.4 +/- 1.4 ms2; In high frequency TBI 2.0 +/- 1.0 ms2, C 4.8 +/- 1.3 ms2, all p < 0.05). Thus, abnormalities in both time and frequency domains of HRV are present in TBI during the post-acute recovery phase.     

Circadian pattern of heart rate variability in chronic heart failure patients. Effects of physical training

The effect of physical training on the circadian pattern of heart rate variability (recorded over 24 h in relation to both time and frequency) was assessed in 12 chronic heart failure patients randomized, in a cross-over design, to 8 weeks training or detraining, and compared with 12 age-matched normals. Training improved heart rate variability indices: all R-R interval 5 min standard deviations increased by 17.6%, the root mean square of the differences of successive R-R intervals by 34.9%, the percentage difference between adjacent normal R-R intervals > 50 ms by 112.5%, total power by 58.3%, high frequency by 128.5% and low frequency by 65.0%. Compared with controls, circadian variations in autonomic parameters were maintained in chronic heart failure. Training-induced changes were observed at different time intervals throughout the day: the highest values were at 0100 h-0700 h (detraining: low frequency 361 +/- 83 ms2, high frequency 126 +/- 47 ms2; training: low frequency 535 +/- 202 ms2, high frequency 227 +/- 115 ms2, P < 0.01) and the lowest at 1300 h-1900 h (detraining: low frequency 91 +/- 23 ms2, high frequency 39 +/- 14 ms2; training: low frequency 154 +/- 42 ms2, high frequency 133 +/- 67 ms2, P < 0.05). In chronic heart failure, training maintains and improves circadian variations in heart rate variability measures.     

Treatment acute myocardial infarct in the pre-hospital phase

OBJECTIVE: To examine the circadian variation in the signal averaged electrocardiogram (saECG) and heart rate variability and investigate their relations in healthy subjects. METHODS: 24 hour ECGs were obtained with a three channel recorder using bipolar X, Y, and Z leads in 20 healthy subjects. The following variables were determined hourly: heart rate, filtered QRS (f-QRS) duration, low and high frequency components of heart rate variability (LF and HF), and the LF/HF ratio. RESULTS: Heart rate, f-QRS duration, HF, and the LF/HF ratio showed significant circadian rhythms, as determined by the single cosinor method. Heart rate and the LF/HF ratio increased during daytime, and f-QRS duration and HF increased at night. f-QRS duration was negatively correlated with heart rate (r = 0.95, p < 0.001) and the LF/HF ratio (r = 0.94, p < 0.001) and positively with HF (r = 0.93, p < 0.001). CONCLUSIONS: f-QRS duration has a significant circadian rhythm in healthy subjects and is closely related to the circadian rhythm of autonomic tone.     

Circadian and ultradian rhythms of drinking behavior of albino rats maintained in constant darkness

The objective of the present study was to investigate the circadian and the ultradian rhythms of drinking behavior in Wistar rats maintained under conditions of constant darkness. Six mature male rats (weighing 270-350 g) were exposed to light-dark 12:12-h cycles (LD 12:12, light on at 12:00 h) for 35 days and then switched to constant darkness (DD) conditions for at least 2 weeks. Drinking behavior was monitored continuously with a standard drinkometer circuit and the data was stored in 5-min bins. A modification of Enright's periodogram technique was used to evaluate the free-running drinking behavior circadian rhythm. Ultradian rhythms in drinking behavior were estimated by the Fast Fourier Transform (FFT) technique. Two of the animals (rats 4 and 6) showed no statistically significant circadian or ultradian rhythms and the other four showed free-running drinking circadian rhythm behavior shorter than 24 h (ranging from 23.333 to 23.967 h). Ultradian rhythms of drinking behavior of 12- and 8-h periods were detected in 4 (rats 1, 2, 3 and 5) and 2 (rats 1 and 5) animals, respectively. The relation of the compound structure of the circadian and ultradian rhythms is discussed demonstrating that drinking behavior is a good marker for studies of physiology of temporal organization.     

Systematic analytic procedure for identification of unknown medicaments in biological material

Increase in blood pressure and its circadian alterations in Type 1 diabetes are usually associated with diabetic nephropathy. To evaluate if diabetes itself could be responsible for the observed increase in blood pressure levels, we studied a group of 17 normotensive, normoalbuminuric Type 1 diabetic patients with a disease duration more than 15 years, with no clinical evidence of autonomic neuropathy or ischaemic heart disease, and without any known determinant of hypertension, and a control group of 17 normal subjects, normotensive, each matched for sex, age, BMI, albumin excretion rate, and clinical blood pressure to a diabetic subject. In both groups an ambulatory blood pressure monitoring was performed through an oscillometric recorder. The mean systolic and diastolic ambulatory blood pressure values were significantly higher in diabetic patients (p < 0.001) in the 24-h analysis and during waking and sleeping periods. The night/day ratio of systolic and diastolic blood pressure were not significantly different in patients and controls, as well as heart rate values and heart rate variability. We conclude that mechanism(s) inherent to the diabetic condition other than diabetic nephropathy or autonomic neuropathy could be responsible for blood pressure evaluation in normotensive Type 1 diabetes with normoalbuminuria.