Key result
HFrEF in stable CAD links to blunted systolic BP and adverse outcomes during mental stress.
Why the study?
Does the presence of HFrEF alter the cardiovascular, hemodynamic, and immune responses to acute mental stress in patients with stable CAD?
Cross-Sectional (n=313)
Does the presence of HFrEF alter the cardiovascular, hemodynamic, and immune responses to acute mental stress in patients with stable CAD?
In patients with stable CAD, the presence of HFrEF is associated with maladaptive hemodynamic and inflammatory responses to acute mental stress.
Answers are grounded in this paper and cite their sources.
HFrEF may mark heightened vulnerability to mental stress in stable CAD; leaves open whether stress reduction improves outcomes.
OBJECTIVE: We studied responses to acute mental stress in individuals with stable coronary artery disease (CAD) with and without heart failure with reduced ejection fraction (HFrEF). METHODS: Individuals with stable CAD ( N = 313, 45 with HFrEF) underwent a laboratory-based mental stress. HFrEF was defined as an ejection fraction of <40%. Hemodynamic reactivity and vasoconstriction during mental stress were evaluated using changes in systolic blood pressure and peripheral arterial tonometry, respectively. Immune function was assessed by measuring changes in interleukin-6 (IL-6) and circulating progenitor cell counts enumerated using flow cytometry of CD34-expressing mononuclear cells before and 90 minutes after mental stress. RESULTS: During the mental stress testing, patients in the HFrEF exhibited a smaller (blunted) increase in systolic blood pressure compared with the non HFrEF group (30.4 ± 14.1 vs 41.9 ± 16.1 mm Hg, p < .001), greater vasoconstriction (PAT ratio 0.69 ± 0.30 vs 0.83 ± 0.40, p = .02), a larger increase in IL-6 levels (0.91 ± 0.11 vs 0.42 ± 0.14 pg/mL, p = .01), and larger increases in circulating progenitor cell counts (0.68 ± 0.12 vs 0.22 ± 0.11 cell/L, p = .009). After adjustment for demographic and traditional risk factors, each of these 4 maladaptive stress responses remained independently associated with the presence of HFrEF. CONCLUSIONS: Among individuals with stable CAD, the presence of HFrEF was independently associated with a blunted systolic blood pressure response, greater vasoconstriction, increased inflammation, and enhanced progenitor cell mobilization with mental stress, a response that is associated with adverse long-term outcomes.
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Moazzami et al. (2026) conducted a cross-sectional in Stable coronary artery disease (CAD) (n=313). Heart failure with reduced ejection fraction (HFrEF) vs. Stable CAD without HFrEF was evaluated on Increase in systolic blood pressure during mental stress (p=< .001). Among individuals with stable CAD, HFrEF was associated with a blunted systolic blood pressure response to mental stress compared to those without HFrEF (30.4 vs 41.9 mm Hg, p<.001).
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