Yasser El-Wazir, Suez Canal University, Egypt
It has become a well-documented fact that the normal heart does not beat like a Swiss watch. In other words, the time between successive beats is not exactly equal, but varies slightly from beat-to-beat and this apparent irregularity has turned out to be an indicator of how the healthy heart responds to the normal beat-to-beat sympatho-vagal interplay. Special computer software can provide quantitative indices of the magnitude of this variability. Indicators used can be analysed in either the time-domain such as the variance of the R-R interval in an ECG recording, or analysed in the frequency-domain by extraction of high-frequency and low-frequency components after appropriate processing of the data (e.g. Fourier transformation).
Although still somewhat controversial, absence or reduction of such physiological heart rate variability (HRV) has thus been suggested to indicate compromised or disturbed sympatho-vagal balance, with a greater dominance of the sympathetic component. This has been found to be a risk factor for cardiovascular morbidity, and a strong predictor of cardiac and all-cause mortality (Caetano & Delgado Alves, 2015). Because there are reported differences in the prevalence of cardiovascular diseases and in the number of deaths among various ethnic groups, it was rational to explore whether this was associated with differences in HRV.
Factors known to affect HRV
Many physiological and environmental factors as well as lifestyle habits are reported to affect HRV. Studies consistently agree that HRV exhibits more sympathetic dominance with advancing age and in male subjects as compared to pre-menopausal females of the same age groups (Voss et al., 2015). Regular physical exercise is associated with higher vagal activity and higher HRV. Indeed, regular exercise improves vagal (i.e. parasympathetic) influence in cardiac patients with reduced HRV (Routledge et al., 2010). On the other hand, chronic stress, smoking, obesity and diabetes are all associated with reduced HRV (Aeschbacher et al., 2016).
Possible ethnic differences in HRV
The majority of studies on ethnic differences in HRV investigated the difference between Americans of African versus Caucasian origins, with controversial or inconclusive results. Studies which reported that African Americans have reduced HRV compared to European Americans, presented their findings as a plausible explanation of the epidemiological disparities in cardiovascular morbidity between the two ethnic groups (Choi et al., 2006). In contrast, a recent meta-analysis analysed a total of 11,162 subjects in 17 studies, and reported a higher HRV in Americans of African origin as compared to those of European origin (Hill et al., 2015). One study reported lower HRV in Indian Asians living in the UK as compared to Europeans, but the Indian Asian sample had a higher blood glucose level which could possibly explain the difference (Bathula et al., 2010). Unlike other authors, Bathula et al. (2010) explicitly indicated a potential attribution of ethnic difference in HRV, at least partially, to health conditions and lifestyles that are more prevalent in certain ethnic groups. Something which is not always explored, reported or controlled for in other studies.
Studies on other ethnic groups such as original dwellers of Africa or Africans of European or Indian origins are still largely missing in the literature
Genetic basis of HRV
A large meta-analysis that involved over 70,000 subjects of European, Hispanic and African American descent identified a number of genetic polymorphisms which can affect acetylcholine release from vagal nerve endings in the sinoatrial node as well as the signaling pathways downstream of muscarinic acetylcholine receptors. These differences may partially account for inter-individual, inter-cohort and inter-ethnic HRV (Nolte et al., 2017). Another study investigated HRV in 1,103 adult twins, and reported a high intra-couple correlation ranging from 0.4 to 0.71 in monozygotic twins and much less in dizygotic ones (0.11 to 0.42), which supports a hereditary origin of HRV (Golosheykin et al., 2017). It thus seems that certain genes involved in the control of vagal cardiac function may account for the individual variations in HRV. Some of these genetic variations are more prevalent in certain ethnic groups and thus can partially account for ethnic variability.
Although it is well agreed that increased vagal-originating parasympathetic influence in basal state HRV is associated with better health and less mortality, a few studies challenge this concept, among which is the meta-analysis of Hill et al. in 2015, which showed greater HRV in African Americans despite having greater cardiovascular morbidity and mortality. In another study, Hill et al., showed that HRV was positively associated with left ventricular hypertrophy in African but not in European Americans (Hill et al., 2017). Therefore, the prognostic value of HRV may need to be considered cautiously in some ethnic groups, specifically African Americans.
With respect to therapy, it is acknowledged that the clinical response to some classes of cardiovascular drugs varies among different populations. The most notable example is that African Americans show reduced anti-hypertensive response to beta-blockers compared to European Americans (Johnson, 2008). Taken together with the finding that pharmacological sympathetic inhibition enhances HRV in cardiac patients may highlight the need to investigate the effect of beta-blockers on HRV in African Americans compared to Europeans.
HRV is but one example of the many physiological variables whose interpretation needs to be contextualised according to the physiological, environmental, and disease conditions of the studied subjects.
Large-scale controlled studies that investigate ethnic differences in HRV are quite scarce, and therefore it is still too early to draw a solid conclusion in this field. However, given the reports that HRV is higher in Americans of African than of European descent, despite the former being known to have concurrently higher cardiovascular disease burden, undoubtedly raises questions about the prognostic impact of normal HRV among differing ethnic groups. Without more rigorous study of diverse populations that take these aspects into consideration, we cannot expect to increase the validity of interpretation of HRV for use as a diagnostic and prognostic indicator.
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