Objective: Hypertension is the leading cause of cardiovascular disease and premature death. New methods for early detection of hypertension and its consequences can reduce complications arising from uncontrolled hypertension. Pulse-wave velocity (PWV), a measure of arterial stiffness, has been recognized as a valuable tool in assessing risk for cardiovascular complications, although its use in clinical practice is currently limited. Here we examine whether brachial--ankle PWV (baPWV) and femoral--ankle PWV (faPWV) are elevated in nonhypertensive volunteers, with and without a history of familial hypertension. Methods: Volunteers were recruited and questioned as to their medical background and family history. Participants were divided into two groups based on history of familial hypertension and were measured for baPWV and faPWV. Carotid--femoral PWV was computed from these measurements. Results: A total of 82 healthy nonhypertensive volunteers (mean age 31.4 ± 9.6) were recruited. Among the study cohort, 43.7% had a history of familial hypertension. There were no between-group differences in any other clinical or demographic characteristics. Both baPWV and faPWV were significantly elevated in volunteers with a history of familial hypertension (10.86 ± 1.69 vs. 9.68 ± 1.52 m/s, P < 0.004, and 7.01 ± 1.65 vs. 6.28 ± 1.26 m/s, P < 0.028, respectively). Conclusion: Volunteers with a history of familial hypertension present with elevated baPWV and faPWV. This is suggestive of increased central and peripheral arterial stiffness in susceptible individuals before the onset of hypertension. Routine measurement of these parameters may allow for early intervention and risk stratification, especially in persons with a history of familial hypertension.

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It has been suggested that some of the adverse, long-term cardiovascular outcomes of smoking are mediated by impaired autonomic nervous system (ANS) activity. Yet, this association is currently inconclusive. Heart rate variability (HRV) and the deep breathing test (DBT) represent common quantitative markers of ANS activity due to their simplicity and reliability. This large cross-sectional study was designed to assess the effect of active smoking on ANS function as manifested by HRV or DBT abnormalities. Electrocardiograms were recorded at rest for 5 min and during forced metronomic breathing. HRV and DBT were calculated according to accepted standards. Participants were divided into two groups based on current smoking status. The study included 242 healthy volunteers (196 nonsmokers and 46 smokers). There were no significant differences in age, sex, and BMI between groups. Cumulative smoking exposure burden (CSEB) for the study group was 5.3 ± 1.3 pack-years. Comparative analysis of HRV and DBT parameters according to smoking status revealed no significant differences between groups. Significant (p < 0.05), yet weak or moderate correlations (r < 0.7) were found between CSEB and abnormal change in HRV parameters consistent with sympathetic overactivity and decreased parasympathetic tone. In conclusion, smoking for a relatively short period in healthy adults does not seem to lead to significant impairment in ANS function. Yet, the consequences of smoking seem to be amplified when cumulative exposure burden increases.

Background Autonomic nervous system (ANS) dysfunction has been implicated with cardiovascular diseases, sudden‐cardiac‐death, and aging. The pupillary light reflex (PLR) and heart rate variability (HRV) are noninvasive tools of autonomic evaluation. However, the former remains underutilized in clinical practice. Purpose We investigated the relationship between PLR, HRV, and aging to determine the normal distribution of age‐adjusted PLR and HRV measurements and to determine which method is best correlated with age. Methods Healthy participants aged 18–65 years were recruited. Following a dark adaptation period, pupillary reactivity parameters were collected using an automated, commercial pupillometer. HRV measurements were derived using a high‐resolution electrocardiogram. Correlations of PLR and HRV parameters to age were computed using linear‐regression analysis. Results A total of 111 healthy participants were included. Older age was correlated with lower maximum and minimum pupillary diameters following dark adaptation and illumination (R = −0.51, p < 0.001 and R = −0.47, p < 0.001, respectively). Average constriction and dilatation velocity were correlated with age (R = 0.33, p < 0.001 and R = −0.21, p = 0.025, respectively). HRV parameters were also associated inversely with age (SDNN; R = −0.31, p < 0.001 and RMSSD; R = −0.33, p < 0.001). Other parameters showed lower significance levels. Conclusion Pupillary light reflex measurements demonstrated stronger age correlation than short‐term HRV time‐domain indices. Due to its merit in depicting normal age‐related ANS changes, PLR can be utilized to differentiate between pathological and physiological deviations from age‐adjusted norms, seemingly better than HRV. Further research is warranted on incorporating PLR‐based ANS dysfunction evaluation and monitoring the increasingly aging population.

Vasovagal syncope (VVS) has a high prevalence in the general population and is associated with potential complications. There is limited information on the possible association between venous capacitance (VC) and venous return (VR), important determinants of preload and VVS. Since the tilt test was reported to yield a high rate of false positive results, the aim of this study was to evaluate whether abnormal VC and VR at baseline could predispose individuals to VVS.To this end, 88 young, healthy volunteers were recruited and classified to 26 (29.5%) who experienced typical VVS and 62 (70.5%) who did not. VC and VR were evaluated with a commercial device and plethysmography applied to the elevated legs. Maximum venous outflow (MVO), segmental venous capacitance (SVC) and MVO/SVC ratio were calculated and averaged.No significant differences between MVO (5.0±0.5 vs 5.6±0.8, p>0.05), SVC (6.0±0.5 vs 6.3±0.8, p>0.05) or MVO/SVC ratio (0.83±0.02 vs 0.86±0.03, p>0.05) were observed for the non-VVS and VVS volunteers, respectively. There was a significant association between a higher MVO and SVC values and a larger decrease in diastolic blood pressure with standing, although correlations were weak (R2=0.0582 and 0.0681, respectively).In conclusion, at baseline, VC and VR are not impaired in healthy volunteers with a history of VVS. It remains unknown if similar results would be found in patients with cardiovascular comorbidities. Also, the sensitivity of VC and VR evaluations to identify a predisposition for VVS following physiological provocations merits further study.