Circadian heart rate and blood pressure variability considered for research and patient care
Introduction
The (single or a 1-min or even a 24-h) measurement of heart rate and blood pressure can be taken to ascertain whether a patient is dead or alive. In all other cases the clinician may gain from assessing chronobiologically the variability of these and other vital signs [1], [2], [3] that undergo a broad spectrum of rhythmic and other changes. Circadians account for the difference between life and death, along the scale of a day, e.g. in response to ouabain [4]. These circadian rhythms, reflected also in mortality and morbidity patterns, are modulated by rhythms with yet longer periods, e.g. of a decade, that are beyond our scope, even if they also are reflected in morbidity and mortality [5].
A circadian cell cycle resides in every cell (Fig. 1) [6], [7] and peripheral timing mechanisms are being documented in molecular biologic terms at about 24-h (circadian) [8], [9] and higher (ultradian) [10] frequencies, with coordination, in mammals, by the adrenal and the pineal–hypothalamic–pituitary network (Fig. 1). The suprachiasmatic nuclei (SCN) contribute to the coordination of the circadian rhythms’ phase and amplitude, in everyday life [11]. The SCN are influenced by the daily alternation between light and darkness directly via the eyes and by plasma melatonin concentrations secreted by the pineal gland, which is a window to both light and geomagnetics (Fig. 1) [5]. A clinical event occurs when our neuroendocrine time structures (chronomes) are not able to cope with the adverse effects of stimuli from within or from without, acting, e.g., via the sympathetic nervous system [1], [2], [3]. Triggering of the neuroendocrines by environmental factors may activate the pineal gland, pituitary functions and adrenal secretions, resulting in adverse effects on circadian variations, heart rate variability (HRV) and blood pressure variability (BPV) [1], [2], [3], [12], [13]. The role of time-adjusted drug intake, especially in the early morning, was also known to ancient Indian physicians [13], [14], [15]. In Ayurveda, drinking of large amounts of water in the early morning is advised, which appears to be in an attempt to increase vagal tone due to gastric distention [16]. Frey [17] considered the mean distribution of deaths along the scales of the day and the year. In one industrial population, Pell and D’Allonzo [18] discussed time-macroscopically the occurrence of a peak in the morning hours in a study of acute myocardial infarction (AMI), a proposition also ascertained and extended to the yearly pattern time-microscopically [19], [20]. The subsequent reports from other countries, the Soviet Union and the extensive data by WHO in the report of myocardial infarction Community Registers [19], [20], [21], [22] from 19 European centers demonstrated a peak incidence of onset of chest pain due to AMI from 08:00 to 11:00 h with a ratio of ∼2:1. In one study from India [13], in 605 AMI patients, 39% of those who had Q wave infarction (n=174) had the onset between 06:00 h and 12:00 noon. In a more recent study [1], among 202 AMI patients, the incidence of onset of chest pain was highest in the second quarter of the day (41.0%), mainly between 04:00 and 08:00 h, followed by the 4th quarter, usually after large meals (28.2%). Emotion was the second most common trigger (43.5%), which was commonest in the patients with onset of chest pain in the second quarter of the day (51.8%). Cold weather was a predisposing factor in 29.2% and hot temperature (>40 °C) was common in 24.7% of the patients. Blood pressure is usually lower during the night, starts increasing before awakening, and remains high during the daytime. Various triggers responsible for circadian rhythms and cardiovascular events are given in Table 1.
In a recent study [21], 65 angina pectoris patients, free from other diseases and drug-free, were monitored by ECG for 24 h. A total of 30 patients were also monitored on isosorbide-5-mononitrate (IS-5-MN) and on metoprolol, respectively. Matched healthy subjects served as controls. Spectral components of HRV were analyzed hourly, with special reference to the rapid changes of autonomic tone during the night and early morning hours. During the night/morning hours, healthy controls demonstrated faster high frequency maximal velocity and higher high frequency gradient than angina patients. Metoprolol and IS-5-MN increased the high frequency gradient and metoprolol tended to increase the maximal velocity. Metoprolol substantially decreased the low frequency/high frequency gradient, velocity and maximal velocity. Rapid vagal withdrawal seemed to be a sign of a healthy autonomic nervous system in the control group of healthy subjects. It was significantly lower in angina patients, however. Both drugs tended to normalize vagal withdrawal, and metoprolol slowed down the rapid increase in sympathetic predominance in the morning in angina patients.
Section snippets
Variations in blood pressure and heart rhythm
HRV results from the cyclic and other, e.g., chaotic, interplay with the sino-atrial node, the main natural pacemaker of the heart, of sympathetic and parasympathetic branches of the autonomic nervous system and/or other local or systemic humoral factors. It is possible that beat-to-beat fluctuations in the cardiac rhythm provide us with a measure of heart health, as defined by the interactions of humoral and sympathetic and vagus nerve activity. BPV and HRV may be quantified by around the
Protective factors, risk factors, and variability
There is substantial evidence that HRV as well as BPV appear to be influenced by age, health status, lifestyle and nutritional factors. Christensen et al. [58] were the first to investigate the effect of dietary supplementation with n-3 fatty acids on HRV. Dietary n-3 fatty acids in a randomized controlled trial in 81 patients with post-myocardial infarction significantly increased HRV, compared with controls, indicating that an increased vagal cardiac tone may be beneficial in these patients.
Risk factors
Age, sedentary habits, coronary artery disease, hypertension, diabetes, obesity, insulin resistance, pollution, hyperlipidemia, hyperglycemia, head injury and anesthesia, are risk factors of decreased HRV [75], [76], [77], [78], [79]. Increased plasma fatty acids can stimulate an animal’s sympathetic nervous system. In a recent study [75] in healthy subjects, 20 experimentals and 10 controls were randomly assigned to receive an infusion of lipid emulsion or saline. The infusion of a lipid
Rhythm disturbances and sudden cardiac death (SCD)
An acute precipitating trigger present in the brain’s suprachiasmatic nucleus, and a chronic electrical instability of the myocardium reportedly contribute to the pathogenesis of SCD. Sudden death has been commonly attributed to arrhythmias, but recent data based on stored electrocardiograms (ECGs) of patients with implantable cardioverter-defibrillators indicate that more than half of the deaths defined as sudden were not arrhythmic [84], [85], [86]. The incidence of both non-sudden and sudden
Cardiovascular events and variability
Early detection of cardiac autonomic neuropathy permits individual risk stratification. HRV and baroreflex sensitivity are suggested to be superior to classic autonomic testing in that they detect neuropathy earlier with greater reliability. A low SDNN has been demonstrated to be a predictor of death in the elderly in the Framingham study [107]. Data in younger subgroups from the same cohort revealed that low HRV indicates the occurrence of adverse cardiac events [108]. In another study,
Progression of hypertrophy and heart failure
The syndrome of congestive heart failure (CHF) entails complex autonomic and hormonal responses. Profound abnormalities in autonomic function, characterized by sympathetic over-activity and parasympathetic withdrawal, exert direct deleterious effects on the heart and contribute to progressive circulatory failure. In a recent study by Burger and Aronson [115], in 64 patients with decompensated CHF, time and frequency domain HRV indices were obtained from 24-h Holter recording. Neurohormonal
Variability and progression of atherosclerosis
There is recent evidence in humans that decreased HRV and elevated 24-h heart rate predict the progression of coronary atherosclerosis [122], as assessed in serial quantitative coronary angiograms. Rapid heart rate has been reported to predispose to the rapid progression of atherosclerosis in several animal models [123], [124], [125]. It seems that adverse effects on hemodynamic factors due to low HRV and increased heart rate may be responsible for greater risk of atheroma development.
Mechanisms
It is tempting to suggest that neurohumoral activation and altered sympathovagal interaction are the most common mechanisms of abnormal HRV in patients with heart disease. The suprachiasmatic nuclei influenced by the daily alternation between light and darkness and by plasma melatonin concentrations secreted by the pineal gland, can be considered as mechanisms contributing to the timing of hard vascular events. Melatonin secretion, increasing with darkness during the night, may be beneficial to
Methodology for measurement of heart rate variability
There is no consensus about the best available index of HRV for clinical use. The Task Force of the North American Society of Pacing and Electrophysiology and the European Society of Cardiology have unified and standardized the methodology of HRV [135]. Noisy data, artifacts, trends and ectopic beats are the major practical problems encountered in HRV measurements. A single HRV index would be an ideal method for clinical work that could be calculated reliably based on a simple, widely available
Management
There is no definite management of circadian rhythms in HRV and BPV. One study by Watanabe et al. [45], however, showed that relaxation (autogenic training) may have a beneficial effect on BPV. Exercise training, breathing exercises, trimetazidine, β-blockers, ACE-inhibitors, n-3 fatty acids, estrogens, ubiquinone, spironolactone have been observed to have beneficial effects on HRV and BPV [58], [59], [60], [61], [62], [63], [64], [65], [68], [71], [73], [74]. Experimental evidence suggests
Summary
Blood pressure and heart rate variabilities undergo a very broad spectrum of rhythms, have important chaotic aspects, some of them resolvable by methods of deterministic chaos [44], and certainly undergo trends with age. Rhythms, chaos and trends constitute time structures, chronomes, which can be resolved by tools reviewed elsewhere [45].
With exceptions, the majority of the literature reviewed herein with focus literally upon circadian variability, is unaware of the fact that from the
Epilogue
For the collection of desirable reference values by 7-day/24-h monitoring at the University of Minnesota (contact Germaine Cornélissen at [email protected]), ambulatory monitors are available from their manufacturer with a 90% reduction in price [161].
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