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Published on: February 10, 2013
Association of stress-induced autonomic dysfunction with heart failure in individuals with stable coronary artery
Maggie Wang1, Chang Liu2, Anish Shah1
1Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA.
Insights
Psychological stress can worsen heart failure (HF) risk in coronary artery disease (CAD) patients. Reduced heart rate variability (HRV) during stress indicates autonomic dysfunction and predicts future HF events.
Area of Science:
- Cardiology
- Autonomic Nervous System Research
- Psychophysiology
Background:
- Heart failure (HF) is a common complication in patients with coronary artery disease (CAD).
- Psychological stress and its effects on the autonomic nervous system may contribute to HF development in CAD patients.
- Autonomic dysfunction during stress is an under-recognized factor in the relationship between CAD and HF.
Purpose of the Study:
- To investigate the association between stress-induced autonomic dysfunction, measured by changes in low-frequency heart rate variability (HRV), and the risk of future HF events in individuals with stable CAD.
- To determine if stress-induced HRV changes are a stronger predictor of HF risk than resting HRV.
Main Methods:
- 662 participants with stable CAD and no HF diagnosis underwent a mental stress challenge (speaking task) with Holter monitoring.
- Heart rate variability (HRV) was analyzed in 5-minute windows, focusing on the change from rest to stress.
- Repeated events Cox proportional hazard models were used to assess incident and recurrent acute HF over a median follow-up of 5.7 years.
Main Results:
- A decrease in low-frequency HRV during mental stress was associated with an increased risk of incident and recurrent acute HF (HR 1.39 [95% CI 1.02-1.90], p=0.035).
- This association remained significant after adjusting for clinical factors, ejection fraction, and resting HRV.
- The predictive value of stress-induced HRV changes for HF risk was greater than that of resting HRV alone.
Conclusions:
- Greater reductions in low-frequency HRV during acute mental stress independently predict higher risks of future HF in stable CAD patients.
- Stress-induced autonomic pathways play a significant role in the pathogenesis of HF.
- Assessing autonomic response to stress via HRV offers valuable prognostic information for HF risk stratification in CAD.
Background:
Heart failure (HF) is a common complication in individuals with coronary artery disease (CAD). Autonomic effects of psychological stress may play an important, under-recognized role in this relationship. We hypothesized that stress-induced autonomic dysfunction, measured by change in low-frequency heart rate variability (HRV) during mental stress challenge, associates with increased HF risk.
Methods:
We examined 662 participants with stable CAD and no known diagnosis of HF who underwent mental stress challenge via a standardized speaking task in conjunction with Holter monitoring. We evaluated HRV in 5-minute windows and examined its change from rest to stress as our primary exposure. Repeated events Cox proportional hazard models were used to examine incident and recurrent acute HF in the outpatient and inpatient setting.
Results:
The mean age was 58 years, 35 % were women, and 43 % self-identified as Black. In models adjusted for age, sex, race, comorbidities, ejection fraction, and resting low-frequency HRV, each standard deviation decrease (negative change) in low-frequency HRV change from rest to stress was associated with an increased risk of incident and recurrent acute HF (HR 1.39 [95 % CI 1.02-1.90], p = 0.035) over a median follow-up of 5.7 years. These estimates for HF risk were higher than those of resting HRV.
Conclusion:
Greater decreases in low-frequency HRV change during acute mental stress challenge independently associate with higher risks of future HF development in individuals with stable CAD and had stronger effect sizes than resting HRV alone, highlighting an important role of stress autonomic pathways in the pathogenesis of HF.
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