Abstract
Objective: Psychological factors have been related to poor outcome in patients with heart failure. Pathophysiological mechanisms explaining this link may include the cardiovascular response to acute mental stress. The current study examined whether heart rate and blood pressure responses to acute mental stress predicted mortality in patients with chronic heart failure. Methods: Patients with HF (N=100, 26% female, mean age 65±12 years) underwent a public speech task, during which heart rate (HR) and blood pressure (BP) were recorded. Their all cause mortality status was assessed 4.8 years thereafter. Heart rate reactivity was recoded into high, low, and negative responsiveness based on the 25th (bpm ≤0) and 75th (>6 bpm) percentile. Blood pressure reactivity was recoded in high (>12.1 mmHg), medium (2.3-12.1 mmHg) and low (<2.3 mmHg) responsiveness based on the 25th and 75th percentile. The following covariates were added to the Cox proportional hazards regression: gender, left ventricular ejection fraction, use of beta blocking agents (HR), use of ACEi/ARB medication (BP), and presence of implanted devices. A p value of <.10 was considered of interest, due to the limited sample size. Results: At follow-up, 31 patients had died (31%), of whom 15 from cardiac causes. Results from the Cox proportional hazards regression showed that blunted HR reactivity (between 0.5-6 bpm; HR=2.3, 95% CI=0.9-6.2, p=.09) and low diastolic BP reactivity (HR=3.1, 95% CI=1.3-7.9, p=.02) were significantly associated with an increased risk of mortality in HF independent of included covariates (all ns, except ACEi/ARB use (HR=0.3, 95% CI=0.1-0.8, p=.02)). SBP reactivity was not significantly related to future mortality risk. Conclusion: In this preliminary study, low heart rate and diastolic blood pressure reactivity to acute mental stress were independent associates of all cause mortality in patients with chronic heart failure. The observed blunted autonomic and hemodynamic response to mental stress is in accordance with physical stress reactivity. These findings call for replication by larger studies that also should examine whether mental stress reactivity is a mediator in the relation between psychological risk factors and adverse cardiac outcomes.
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