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• W2040243018 abstract "Heart rate has been implicated as a risk factor in cardiovascular disease [1,2], and sudden death in middle-aged men [3,4]. Furthermore, elevated heart rate has been shown to be an independent predictor of cardiovascular disease [5]. Previously, there was controversy and inconsistency regarding the association between heart rate and hypertension [6–8]. Some studies could not maintain significance for the heart–hypertension association after adjustment for confounders. Therefore, the HARVEST Study [9] published in this issue of the journal should be considered as a landmark study to provide evidence-based medicine data regarding the question of whether the resting heart rate and heart rate changes during follow-up predict the development of sustained hypertension in individuals screened for stage 1 hypertension [9]. Moreover, this study questions whether ambulatory heart rate may improve the predictive value of clinical heart rate for outcome. The main results reveal that clinical heart rate and heart rate changes during the first 6 months of follow-up were independent predictors of subsequent systolic and diastolic blood pressure, regardless of the initial blood pressure level and other confounders. A persistent high heart rate was an independent predictor of future sustained hypertension, regardless of the initial blood pressure and other confounders. These are very important findings because the study population in the HARVEST Study comprised young individuals at low cardiovascular risk who were screened for stage 1 hypertension. Cardiovascular prevention screening should start at a younger age than has previously been the case, starting at age 40 years or older. Measuring heart rate has been the subject of debate in recent years. Heart rate is a highly variable physiologic phenomenon and can be influenced by a large variety of environmental stimuli. In particular, the alerting reaction caused by a medical visit could falsely increase resting heart rate [10]. From a theoretical point of view, it is possible that the association between heart rate and hypertension would be stronger if heart rate could be measured out-of-office; especially considering that the reproducibility of heart rate is better for ambulatory than for office heart rate. However, the HARVEST Study showed that ambulatory heart rate was not an independent predictor of blood pressure after 6 years of follow-up. There is no available evidence to demonstrate the advantage of measuring heart rate out-of-office over clinical heart rate in the prediction of hypertension and, thus, more research is needed. To provide reliable and comparable results, the measurement of a clinical variable should be strictly standardized to minimize methodological bias. A recent analysis of 56 studies published in leading cardiovascular journals showed that, in almost all of the studies, the methods of heart rate measurement were not reported in a scientifically acceptable manner [11]. These methodological problems may have led to an underestimation of the magnitude of the association of heart rate with mortality and emphasize, rather than detract from, the importance of resting heart rate. Recently, the European Society of Hypertension Consensus Meeting [12] regarding the identification and management of hypertensive patients with an elevated heart rate recommended providing the following information in studies reporting heart rate data: (i) resting period before measurement; (ii) environmental conditions; (iii) method of measurement; (iv) number of measurements; (v) duration of measurement; (vi) body position; and (vii) nature of the observer. Whereas blood pressure is usually measured in the sitting position, there is no general agreement on the body position for heart rate measurement in the literature, with one-half of studies using sitting heart rate, and the other half using supine heart rate. A 1–2 beats/min higher heart rate is to be expected in the sitting posture. A period of 30 s appears to be sufficient to obtain a reliable estimate of heart rate because the duration of 30–40 cardiac cycles can be averaged out. This represents a fairly good number of readings considering that no more than two to three heart beats are taken into account for systolic blood pressure and diastolic blood pressure measurement using standard sphygmomanometry. The pathogenic mechanisms that might explain the connection between elevated heart rate, hypertension, atherosclerosis and cardiovascular events are not completely unraveled. Heart rate may be an integrated index of the influence of the autonomic nervous system on the heart, and it is known that increased sympathetic activity can favour the development of hypertension and atherosclerosis in a variety of ways. Studies have demonstrated that individuals with high heart rates have increased blood pressure readings and that this association is stronger in individuals with elevated sympathetic activity [13]. Animal studies indicate that an elevated heart rate can also be an independent factor in the induction of risk because it may intensify the pulsatile nature of the arterial blood flow and increase changes in shear stress direction [14]. Mangoni et al. [15] demonstrated that artery compliance and distensibility are markedly impaired by a progressive increase in heart rate caused by pacing. An association between fast heart rate (> 80 beats/min) and arterial stiffness has been found also in cross-sectional and longitudinal studies performed in human beings [16,17]. Singh et al. [18] reported data from the Framingham Heart Study showing that, among normotensive men, lower heart rate variability was associated with a greater risk for developing hypertension. These findings are consistent with the hypothesis that autonomic dysregulation is present in the early stage of hypertension. Another hallmark in arterial hypertension is the alteration of the renin–angiotensin II–aldosterone system (RAAS). Duprez et al. [19] demonstrated that, during postural maneuvers in stage I hypertension, there is a significant correlation between RAAS and the sympathetic and vagal modulations of heart rate and blood pressure oscillations, expressed as spectral indices of their power spectrum. Particularly, renin release from supine to standing position is correlated with the decrease of vagal modulation of the RR interval. The extent to which resting heart rate is genetically determined has recently become a subject of major interest. Previous family studies have shown a significant heritable component for heart rate, with several groups conducting genomic linkage scans to identify quantitative trait loci. Due to its importance in predicting cardiovascular and all-cause mortality, Laramie et al. [20] used data from Caucasians and African-Americans enrolled in the NHLBI Family Blood Pressure Program to evaluate genetic factors associated with resting heart rate. They performed a genome-wide linkage scan to identify quantitative trait loci influencing resting heart rate among 3282 Caucasians and 3989 African-Americans in three independent networks comprising the Family Blood Pressure Program using 368 microsatellite markers. They found replication between ethnic groups and between study networks with low heterogeneity on chromosome 5p13-14, suggesting that a gene in this region influences resting heart rate, although no genes have been found that contribute to variation in resting heart rate. Because signaling through the β1-adrenergic receptor is a key determinant of cardiac function, Ranade et al. [21] tested whether polymorphisms in this receptor were associated with resting heart rate. A cohort of more than 1000 individuals of Chinese and Japanese descent from nuclear families was genotyped for two polymorphisms resulting in a serine/glycine substitution at amino acid 49 (Ser49Gly) and an arginine/glycine substitution at residue 389 (Arg389Gly) in the β1-adrenergic receptor. The data support an additive model in which individuals heterozygous for the Ser49Gly polymorphism had mean heart rates intermediate to those of either type of homozygote, with Ser homozygotes having the highest mean heart rate and Gly homozygotes having the lowest. Considerable progress has been made in our understanding of the role of high heart rate in determining cardiovascular morbidity and mortality. However, whether the association between fast heart rate and cardiovascular disease is equally strong in males and females remains a matter for debate. In most studies, the predictive value of tachycardia for all-cause mortality has been found to be weaker in women than in men and, in some studies, no association between heart rate and cardiovascular mortality has been observed. In particular, a high heart rate appeared to be a weak predictor of death from coronary heart disease in females [22]. There is an urgent need to explore the gender difference with respect to heart rate as a cardiovascular risk factor, as well as predictor for hypertension, in future studies. Atrial fibrillation and hypertension are two prevalent and often coexistent conditions. Therefore, we need to know whether increased resting heart rate is not only associated with a higher risk of developing hypertension, but also auricular fibrillation [23]. The diagnosis and management strategy of cardiovascular disease in the twenty-first century is characterized by a swift transition from diagnosis and treatment of disease to early detection of cardiovascular functional and structural abnormalities. This evolution is not only driven by the medical world, but also by healthcare authorities because of the economic healthcare burden. The HARVEST Study [9] emphasizes that, in a world overwhelmed by modern technology, carefully measuring vital signs such as heart rate is a very important predictor not only in the development of arterial hypertension, but also in relation to cardiovascular risk. The HARVEST Study once more underlines the importance of choosing global risk assessment and not focusing on either systolic and or diastolic blood pressure. The challenge for the next decade is to investigate whether non-medical and medical regimens to lower heart rate could also prevent or delay the development of hypertension." @default.
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• W2040243018 title "Heart rate: an independent predictor for hypertension?" @default.
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