Looking beyond the mean: Are racial differences in beat‐to‐beat blood pressure variability among young men a harbinger for future cardiovascular risk?

Blood pressure (BP) is a leading modifiable risk factor for early death, with both higher resting and ambulatory BP being associated with a greater risk of mortality and cardiovascular outcomes (Yang et al., 2019). However, serial measurements of BP taken across multiple time scales (beat-to-beat, minutes, hours, days, months and years) demonstrate clearly that BP is not a static value but rather a continuous variable that can be influenced by diurnal, postural, environmental, emotional and physical factors. Although the best index for quantification of BP variability (e.g. standard deviation, coefficient of variation, average real variability, variation independent of the mean) remains to be established (Parati, Stergiou, Dolan, & Bilo, 2018), a growing number of studies have reported independent associations with subclinical organ damage and clinical endpoints, such as all-cause mortality and cardiovascular events (Mena, Felix, Melgarejo, & Maestre, 2017; Stevens et al., 2016). In this issue of Experimental Physiology, Young et al. (2020) investigated racial differences in resting beat-to-beat BP variability in young healthy non-Hispanic Black versus White men. They found that Black men had greater BP variability despite similar time-averaged values of resting BP. These results were accompanied by larger variability in beat-to-beat total peripheral resistance in Black men, illustrated nicely by histogram plots showing a greater percentage of cardiac cycles with changes in BP and total peripheral resistance further away from time-averaged mean values. A subset of participants also underwent microneurography to measure muscle sympathetic nerve activity (which was similar between groups) and calculate the sympathetic baroreflex operating point gain, which was lower in Black men (i.e. a smaller change in muscle sympathetic nerve activity for a given change in diastolic pressure). Across the entire cohort, sympathetic baroreflex gain was negatively correlated with mean arterial pressure variability, demonstrating that those with the greatest muscle sympathetic baroreflex sensitivity had the lowest BP variability. The findings of greater beat-to-beat BP variability in Black men confirm prior reports calculated from 24 h ambulatory or visit-to-visit recordings (e.g. Chen, Srinivasan, Ruan, Mei, & Berenson, 2011; Li et al., 2010). As discussed by the authors, the arterial baroreflex is crucial in regulating beat-to-beat BP through reflex changes in peripheral vasoconstrictor drive. It is intriguing to speculate whether a lower sympathetic baroreflex gain contributes to the increased BP variability in Black men, but it is important to consider that this measure is related to the discharge of efferent postganglionic muscle sympathetic fibres and not necessarily the quanta of neurotransmitter release. Previously, this group has found increased neurovascular transduction in Black men (Vranish et al., 2018), suggesting that a smaller change in muscle sympathetic nerve activity might be necessary to evoke a similar haemodynamic response. Whether reductions in sympathetic baroreflex gain represent a compensatory change to attenuate the end-organ effects of greater neurovascular transduction has not been tested. To provide additional support for a neural mechanism, one future direction could be to calculate the spectral coherence between BP or total peripheral resistance and muscle sympathetic nerve activity. Young et al. (2020) also reported that cardiac baroreflex gain (a measure of reflex parasympathetic control) was unrelated to BP variability. This contrasts with prior work showing a negative correlation with ambulatory BP variability in unmedicated hypertensive patients (Floras et al., 1988). It is important to emphasize that the mechanisms responsible for BP variability might differ depending on the measurement time scale or the population studied. Nonetheless, the observed correlation between sympathetic baroreflex gain and mean arterial pressure variability provides an important first step in elucidating the causative mechanisms responsible for greater BP and total peripheral resistance variability in Black men. With respect to the clinical implications of the study by Young et al. (2020), three important considerations are worthy of further discussion. First, variability was calculated from beat-to-beat BP recordings (i.e. very short time scale) common to the laboratory setting, whereas most population-level studies have derived BP variability from ambulatory or visit-to-visit office BP measurements (Parati et al., 2018). Which time scale yields the highest prognostic benefit remains a key unanswered question. Beat-to-beat BP variability was superior to ambulatory and day-to-day BP variability in predicting organ damage (Wei et al., 2014), but these findings have not been confirmed with hard clinical outcomes. Second, the prognostic significance of BP variability has been determined largely in middle- or older-aged participants with cardiovascular risk factors, such as hypertension (Mena et al., 2017; Stevens et al., 2016). It remains unclear whether BP variability offers similar value in young, healthy, normotensive populations, such as the cohort examined by Young et al. (2020), and what magnitude of differences are predictive of risk. For example, visit-to-visit childhood BP variability was a predictor of adult hypertension, with greater childhood BP variability and adult hypertension in Black participants (Chen et al., 2011), whereas 24 h ambulatory BP variability in middle-aged participants was associated with 20 year cardiovascular mortality in untreated hypertensive but not normotensive participants (Hsu et al., 2016). Third, it is important to consider that several measures of BP variability (e.g. standard deviation, average real variability) can be positively correlated with the mean level of BP and thus require statistical adjustment to determine their independent effects (Parati et al., 2018). Despite the considerable work needed to resolve these outstanding clinical questions, laboratory-based studies are also crucially needed to provide insight into the mechanisms responsible for BP variability. Better understanding of these mechanisms might help to determine more efficacious treatment strategies to reduce BP and its variability concomitantly. Collectively, the findings by Young et al. (2020) remind us to look beyond time-averaged values of resting BP and raise stimulating questions regarding racial differences in neurovascular control and the regulation of BP. Future work is needed to confirm that higher beat-to-beat BP variability in otherwise healthy, young Black adults confers increased clinical risk independent of resting or ambulatory BP. None declared. PJM is supported by a Natural Science and Engineering Research Council of Canada (NSERC) Discovery Grant (#04287), the Canada Foundation for Innovation (#34379), the Ontario Ministry of Research, Innovation and Science (#34379), and an Ontario Early Researcher Award (18-14-288).

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