High Heart Rate and Hypertension: Two Intertwined Cardiovascular Risk Factors

Abstract

A large number of studies have shown that high heart rate (HR) is correlated with many risk factors for atherosclerosis and cardiovascular events, including high blood pressure, dyslipidemia, hyperinsulinemia, hyperglycemia, and obesity [1-3]. These associations have been observed in general populations as well as in patients with hypertension, diabetes, coronary artery disease, and heart failure, indicating that measurement of HR should be an important component of cardiovascular risk assessment. Although many prospective studies performed in general populations showed significant associations between the baseline office HR and subsequent blood pressure or hypertension, in only a few studies did the predictive power of HR remain significant after controlling for the baseline blood pressure level [4, 5]. Furthermore, the confounding effect of physical fitness was considered only in the CARDIA study [6] in the United States, in people aged 18 to 30 years. These results were later confirmed by the Kailuan prospective study [7], which included a large number of participants aged 38 to 54 years, and by a prospective cohort study carried out in rural China in 39- to 59-year-old subjects [8]. Finally, in a meta-analysis of 9 cohort studies encompassing 79 399 individuals, Shen et al. found a linear dose–response association between HR and incident hypertension in adults [9]. All these studies were carried out in young or middle-aged people while little information was available for older individuals.

This knowledge gap was addressed by Lou and colleagues in an article published in this issue of Journal of Clinical Hypertension [10]. These investigators showed that high HR was associated with an increased risk of developing hypertension also in older individuals, with a 6% increase in risk for every 10 beats/min increment in HR. This association may explain at least in part the higher risk of mortality found in elderly subjects with fast HR [11].

As hypothesized by Lou and colleagues, a heightened sympathetic activity may explain why subjects with high HR tend to develop sustained hypertension in later years [10]. A high sympathetic activity causes an increase in cardiac output, peripheral vascular resistance, and sodium reabsorption in the kidney, which leads to an

Elevation of blood pressure [12]. However, whether tachycardia in these individuals reflects a temporary reaction to the medical environment or is the consequence of a stable sympathetic activation is still a matter of debate. Results of the HARVEST Study showed that in most subjects with elevated HR at the initial visit, HR tends to return to normal values after baseline assessment, and that these subjects are not at increased risk of future hypertension [5]. This suggests that a transient increase in sympathetic activity on a background of normal autonomic nervous system tone does not seem to have a detrimental effect and that only a sustained elevation of the sympathetic tone can affect future blood pressure levels. Whether HR has a direct effect on the arterial wall or is only a marker of autonomic nervous system dysfunction is still an unresolved issue.

Another interesting finding of Lou and colleagues study is that the longitudinal association between baseline HR and future hypertension was present in the sedentary subjects, with a hazard ratio of 1.09 (95% CI, 1.02–1.17), but not in the participants performing regular physical activity (1.02; 0.94–1.11) [10]. The favorable effect of exercise for the prevention or treatment of hypertension has been well documented [13]. In addition, physical activity has a beneficial effect also on lipids and other metabolic factors [13], and on the hemodynamic responsiveness to stressors by attenuating or even abolishing the detrimental effects of these risk factors [14]. In the HARVEST study, we showed that the risk of hypertension associated with high uric acid was present only among the sedentary participants and not among those engaging in endurance sports [15].

A reduction of blood pressure responsiveness to stressors has been described in physically active individuals [16]. In the HARVEST, people who performed regular physical activity had a blunted blood pressure response to public speaking, a powerful psychological stressor, and a lower risk of future hypertension compared to subjects with sedentary habits [14]. As mentioned above, high HR is often a marker of increased sympathetic activity. Physical activity has a favorable action on the sympathovagal balance, which can result in decreased cardiac–sympathetic drive, in part by enhancing baroreceptor sensitivity [17]. In addition, exercise decreases the activity of the renin–angiotensin system [18]. These mechanisms may account for the beneficial effect of exercise training on blood pressure, which may have contributed to the prevention of hypertension in Lou and colleagues active participants. Central autonomic adaptations in response to regular physical activity would be responsible for the reduced blood pressure responsiveness to stressors [17] and might represent an additional mechanistic pathway for the decreased tendency to develop hypertension in physically active individuals [19]. Overall, these findings suggest that regular exercise may counteract many pathophysiological mechanisms involved in the development of hypertension.

A limitation of Lou and colleagues study is that HR was measured only at baseline, and thus information on HR during the follow-up was not available. HR changes during the first months or years of follow-up may add important prognostic information to that provided by the baseline HR because they allow to distinguish people with transiently elevated HR from those with sustained tachycardia [20]. In the HARVEST study, the participants with high HR throughout the follow-up had a doubled risk of developing hypertension compared with those with a high HR only at the initial visit, in whom the HR elevation was probably caused by a marked alarm reaction that attenuated during subsequent visits [5].

The results of Lou and colleagues study have implications for the management of elderly people with elevated HR. Up to now, no human study has demonstrated the efficacy and the risk–benefit ratio of cardiac slowing drugs in patients without cardiac diseases. Pharmacological treatment of high HR in noncardiac subjects thus appears at the very least to be premature. The pathogenetic considerations discussed above suggest that in people with tachycardia, rather than merely reduce the elevated HR, it would be rationale to use a treatment that also corrects the underlying pathogenetic mechanism, restoring a normal sympathovagal balance. One such goal can be achieved with the improvement of an unhealthy lifestyle. Besides reducing the consumption of tobacco, alcohol, and caffeinated beverages, a program of regular physical activity should be implemented. Exercise causes a reduction of HR by decreasing sympathetic activity and increasing vagal tone. Regular endurance exercise has not only a beneficial effect on HR but also a favorable impact on all factors of the insulin resistance syndrome: overweight, serum insulin, blood pressure, and plasma lipids [13].

Paolo Palatini is the sole author of this article and took care of implementing and writing the article.

The author declares no conflicts of interest.