Stress and cardiovascular disease

  title={Stress and cardiovascular disease},
  author={Andrew Steptoe and Mika Kivim{\"a}ki},
  journal={Nature Reviews Cardiology},
The physiological reaction to psychological stress, involving the hypothalamic–pituitary–adrenocortical and sympatho–adrenomedullary axes, is well characterized, but its link to cardiovascular disease risk is not well understood. Epidemiological data show that chronic stress predicts the occurrence of coronary heart disease (CHD). Employees who experience work-related stress and individuals who are socially isolated or lonely have an increased risk of a first CHD event. In addition, short-term… 
Mental Stress and Cardiovascular Disease
Evidence exists that the association between mental stress and CV morbidity and mortality may in part be mediated by increased exposure to organic risk factors.
Stress and cardiovascular disease: an update on current knowledge.
A major challenge over the next decade is to incorporate stress processes into the mainstream of cardiovascular pathophysiological research and understanding.
Effects of stress on the development and progression of cardiovascular disease
In real-life settings, mechanistic studies have corroborated earlier laboratory-based observations on stress-related pathophysiological changes that underlie triggering, such as lowered arrhythmic threshold and increased sympathetic activation with related increases in blood pressure, as well as pro-inflammatory and procoagulant responses.
The Role of Mental Stress in Ischaemia with No Obstructive Coronary Artery Disease and Coronary Vasomotor Disorders
Overall, many studies demonstrate an association between mental stress, coronary microvascular dysfunction and coronary vasospasm in patients with INOCA – especially women, and future research on stress-reducing therapies that target coronary vasomotor disorders in Patients with InOCA is needed.
Stress and sleep disturbance—a connection in CVD
These studies provide robust evidence supporting the pronounced impact of sleep disorders on the incidence of CVD, and the underlying mechanisms for the association between stress and cardiovascular risk have not been fully elucidated.
Psychosocial Risk Factors and Coronary Artery Disease
Stress-related psychiatric disorders, especially depression and post-traumatic stress disorder (PTSD), are increasingly recognized as risk factors for CAD and the extent to which interventions targeting psychosocial risk factors reduce coronary risk remains an area of active investigation.
Work-related stress and cardiovascular effects
The cardiovascular alterations induced by work-related stress seem to be triggered by neuroendocrine mechanisms (increase in cortisol and catecholamines), hemodynamic (abnormal coronary circulation) and aptitudinal (wrong life styles).
Fatigue Is Associated With Diminished Cardiovascular Response to Anticipatory Stress in Patients With Coronary Artery Disease
Investigating the links between cardiovascular response to mental stress and fatigue in CAD patients after acute coronary syndrome found fatigue was linked with diminished cardiovascular function during anticipation of a mental stress challenge, even after inclusion of possible confounders.
Stress and hemostasis: an update.
Randomized placebo-controlled trials suggest that several cardiovascular drugs attenuate the acute prothrombotic stress response and Behavioral interventions and psychotropic medications might mitigate chronic low-grade hypercoagulability in stressed individuals, but further studies are clearly needed.


Emotional triggering of cardiac events
Salivary cortisol responses to mental stress are associated with coronary artery calcification in healthy men and women.
In healthy, older participants without history or objective signs of CHD, heightened cortisol reactivity is associated with a greater extent of CAC, and data support the notion that heightened hypothalamic pituitary adrenal activity is a risk factor for CHD.
Work stress and coronary heart disease: what are the mechanisms?
Work stress may be an important determinant of CHD among working-age populations, which is mediated through indirect effects on health behaviours and direct effects on neuroendocrine stress pathways.
Social Isolation and Stress-related Cardiovascular, Lipid, and Cortisol Responses
  • N. Grant, M. Hamer, A. Steptoe
  • Medicine, Biology
    Annals of behavioral medicine : a publication of the Society of Behavioral Medicine
  • 2009
The impact of social isolation on cardiovascular disease risk may be mediated through stress-related dysregulation of cardiovascular, metabolic, and neuroendocrine processes.
Physical, psychological and chemical triggers of acute cardiovascular events: preventive strategies.
The purpose of this review is to bring together the evidence of the association between several triggers and cardiovascular outcomes and to discuss the common underlying pathophysiology of these triggers.
Ischemic, hemodynamic, and neurohormonal responses to mental and exercise stress. Experience from the Psychophysiological Investigations of Myocardial Ischemia Study (PIMI).
Mental stress-induced myocardial ischemia is associated with a significant increase in systemic vascular resistance and a relatively minor increase in heart rate and rate-pressure product compared with ischemIA induced by exercise.
Pathophysiological processes underlying emotional triggering of acute cardiac events.
The results suggest that some patients with coronary artery disease may be particularly susceptible to emotional triggering of ACS because of heightened platelet activation in response to psychological stress, coupled with impaired hemodynamic poststress recovery.
Neurohumoral features of myocardial stunning due to sudden emotional stress.
Emotional stress can precipitate severe, reversible left ventricular dysfunction in patients without coronary disease andaggerated sympathetic stimulation is probably central to the cause of this syndrome.
Triggering of Acute Cardiovascular Disease and Potential Preventive Strategies
The aim of the present review is to update current knowledge about triggering of acute cardiovascular disease (CVD), place it in the context of advances in understanding of the mechanisms of onset, and suggest a 5-faceted strategy to protect against the pathophysiological effects of triggering.