Cardiac autonomic control and hostility in healthy subjects

doi:10.1016/0002-9149(94)90382-4

The American Journal of Cardiology

Volume 74, Issue 3, 1 August 1994, Pages 298-300

https://doi.org/10.1016/0002-9149(94)90382-4 Get rights and content

Abstract

Disordered autonomic regulation of the cardiovascular system has been implicated in sudden cardiac death and coronary artery disease in numerous studies. Bigger et al¹ showed that survival after myocardial infarction was predicted by high-frequency (HF) power of the heart period power spectrum, a measure of vagal modulation of RR intervals,² by power in other frequency bands, and by the low-frequency (LF) to HF power ratio, a measure that has been used to estimate sympathovagal balance. Increased heart rate, reflecting global cardiac autonomic control, is associated with development of atherosclerosis in animal models³ and age-adjusted levels of atherogenic lipoproteins in humans.⁴ Heart rate-lowering interventions such as surgical ablation of the sinoatrial node and β-adrenergic antagonists have antiatherogenic effects.³

Cardiovascular regulation by the autonomic nervous system may link negative personality characteristics, e.g., hostility, with increased risk of coronary artery disease, an association generally supported by available data.^5,6 Two views about the nature of the link, the constitutional and the transactional theories, specify different mechanisms. The constitutional theory holds that the autonomie activity associated with risk of coronary artery disease is caused by a constitutional characteristic which also accounts for hostility.⁵ In this view, hostility is a marker of factors that influence brainstem cardioregulatory centers. The transactional theory holds that hostile persons interact with their environment in a way that creates interpersonal conflict and reduces social support.⁵ Since in laboratory experiments, psychological Stressors decrease HF power in the heart period power spectrum,⁷ the stressfulness of the transactions that persons high in hostility have with their interpersonal environments suggests an inverse relation between hostility and HF power, which in turn may increase risk of coronary artery disease.

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Conclusion: The result indicated that the increased parasympathetic modulation concurred with the decreased expressive hostility (anger-out) behavior after the compassion-based CBGT. This effect might be helpful to the disease prognosis.
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Citation Excerpt :
To meet the increased demand for oxygen distribution to the body HR would need increase. Heart rate variability has been used extensively in humans to assess the shift in balance of the autonomic nervous system in response to stress (Rechlin, 1994; Sloan et al., 1994; McCraty et al., 1995; Thayer et al., 1996; Liao et al., 1997; Bernardi et al., 2000) and in recent years has shown use as a barometer for the stress response in horses (Schmidt et al., 2010a,b; Visser et al., 2002; Werhahn et al., 2012; von Lewinski et al., 2013; von Borell et al., 2007). Decreased values of the HRV variable SDNN appear in horses exposed to stressful situations.
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: This study was supported in part by Grant MH-43977, Research Scientist Development Award MH-00416 (Dr. Gorman), and Scientist Development Award MH-01035 (Dr. Sloan) from the National Institute of Mental Health, Rockville, Maryland; Grant M01-RR00645 from the General Clinical Research Centers Program of the National Institutes of Health, Bethesda, Maryland; an Irving Assistant Professorship (Dr. Shapiro); and the Nathaniel Wharton Fund.

¹: Dr. Sloan's address is: Behavioral Medicine Program, Box 427, Columbia-Presbyterian Medical Center, 622 West 168th Street, New York, New York 10032.

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Cardiac autonomic control and hostility in healthy subjects

Abstract

Physiol Behav

Am J Cardiol

J Am Coll Cardiol

Frequency domain measures of heart period variability and mortality after myocardial infarction

Circulation

Transfer function analysis of the circulation: unique insights into cardiovascular regulation

Am J Physiol

Role of sympathoadrenal medullary activation in the initiation and progression of atherosclerosis

Circulation