Acute Psychological Stress and Pulse Wave Velocity: Meta-Analysis and Recommendations for Future Research

Abstract

Repeated exposures to acute psychological stress may be associated with cardiovascular disease (CVD) risk, but the mechanisms underlying this relationship are not fully understood. The objective of this meta-analysis was to determine the effect of acute psychological stress on central pulse wave velocity (PWV) compared to pre-stress (baseline) levels in adults free of overt CVD. Electronic databases (PubMed, SPORTDiscus, and Google Scholar) were queried from inception to July 2024. Reference lists of eligible studies and previous relevant reviews were also screened. Studies were included if: (i) a noninvasive measure of PWV was used that included a central (aortic) arterial segment; (ii) participants were adults (≥ 18 years) free of overt CVD; and (iii) the acute stressor was purely psychological in nature. Appraisal and Synthesis Methods: Effect sizes were calculated as standardized mean differences (SMD) and pooled using a random-effects model. The magnitude of effect was adjudicated as trivial (< 0.2), small (0.2), moderate (0.5), or large (0.8). A total of 11,689 studies were identified, from which 7 studies (11 effects, N = 162 participants) were eligible for inclusion. Moderate Acute psychological stress induced a moderate (SMD: 0.51, p < 0.0001; 95% CI: 0.34, 0.68) increase (detrimental) in central PWV, and there was insubstantial heterogeneity between studies (Cochran's Q (10) = 2.62 (p = 0.99)). The small overall number of studies as well as key differences in study methodologies limit the ability to elucidate the magnitude and consistency of stress-induced increases in PWV. Nonetheless, the present findings suggest that acute psychological stress induces significant increases in central PWV among adults free of overt CVD. The acute PWV response to psychological stress likely contributes to elevated CVD risk over time.

FIGURE 1

Preferred reporting items for systematic reviews and meta‐analyses (PRISMA) flowchart of study selection. Flowchart of study exclusions and selections. *This study (Ellins et al. 2008) was a longitudinal study in which acute stress and PWV were administered and measured 3 years apart, respectively. Abbreviations: n, number of articles; PWV, pulse wave velocity.

FIGURE 2

Forest plot showing the observed outcomes and the estimate of the random‐effects model. Lower‐case letters following study years indicate different trials within a given study (e.g., for differing arterial pathlengths). The random‐effects model produced a moderate effect size SMD (0.51 [95% CI: 0.34, 0.68, p < 0.0001]), indicating a substantial and significant increase in pulse wave velocity. Based on the Q‐test, there was no evidence of significant heterogeneity: (Q(10) = 2.62, p = 0.99, τ ² = 0.00, I ² = 0.00%). Abbreviations: 95% CI, 95% confidence interval; RE, random effects; SMD, standardized mean difference.

FIGURE 3

Funnel plot for studies assessing the acute effects of psychological stress on pulse wave velocity. Visual inspection of the funnel plot indicates no evidence of publication bias.

FIGURE 4

Infographic summarizing meta‐analysis: (A) question, (B) methods, (C) potential mechanisms, and (D) results. (A) This meta‐analysis investigated the effect of acute psychological stress on central (containing an aortic segment) PWV in disease‐free adults. (B) PWV reflects arterial structure (i.e., stiffness) and function and is an established biomarker for CVD risk. PWV is the speed at which the forward pressure waveform is transmitted between a proximal (e.g., carotid) and distal (e.g., femoral) arterial segment, with faster PWV reflecting increased arterial stiffness. (C) Stress‐induced increases in PWV may manifest through several pathways. (i) The ANS directly increases sympathetic activity to the arterial system, the myocardium, and the adrenal glands. (ii) Heightened sympathetic activity stimulates SMCs, leading to vasoconstriction. (iii) Increased sympathetic activity at the level of the SA node increases cardiac output, which together with increased SMC tone, raises BP. The hashed red line indicates that increases in PWV also result in quickening and amplification of reflected pressure waves, which increases myocardial burden. (iv) The adrenal glands respond to sympathetic signaling by releasing the primary stress hormones (catecholamines, cortisol) and aldosterone into the bloodstream. The catecholamines promote further increase in SMC tone and cardiac output and promote the release of pro‐inflammatory cytokines into the bloodstream. Cortisol has been reported to compromise endothelial function and elevate BP by decreasing baroreflex sensitivity. Aldosterone may further increase BP by increasing sodium and water reabsorption. (D) The literature search identified 7 studies [11 (k) effects], with a total of n = 162 participants (mean age: 24 ± 3 years). Acute psychological stress led to a moderate (SMD: 0.51 [0.34, 0.68]) increase in PWV. Abbreviations: ANS, autonomic nervous system; BP, blood pressure; CI, confidence interval; CVD, cardiovascular disease; D, distance; HPA, hypothalamic–pituitary–adrenal; n, total sample size; PTT, pulse‐transit time; PWV, pulse wave velocity; SA, sinoatrial; SMC, smooth muscle cell; SMD, standardized mean difference.