How Stress Increases the Risk of Cardiovascular Disease (CVD)
Stress is a physiological response to a stressor that threatens an individual’s internal physiological state or psychological wellbeing. Life is critically dependent on the control of the body’s internal state even when the external environment is constantly changing. This is called homeostasis and when it is threatened, the body undergoes a stress response.
Research shows that acute psychological stress can elicit a cardiovascular response with concomitant increases in heart rate and blood pressure. Epidemiological observations have demonstrated that due to the unpredictable nature of an acute stressor, it can significantly alter cardiac rhythm in susceptible individuals to such an extent so as to trigger an acute coronary event. Many of these studies also report an emotional episode approximately two hours prior to cardiac arrest.
Chronic stress is often the result of an acute stress response becoming maladaptive due to the continuous or prolonged nature of the stressor. Experimental studies show that chronic stress is associated with sustained increases in blood pressure and vascular hypertrophy. There is also an increased risk of developing atherosclerosis with chronic stress resulting in cardiac instability and increased sensitivity to myocardial ischemic injury.
The physiological cardiovascular response to stress involves a cascade of downstream consequences that integrate neuronal and endocrine information in the brain and the periphery. Stress-associated cardiovascular disease (CVD) begins with activation of both the sympathetic nervous system and the hypothalamus-pituitary-adrenal (HPA) axis causing an increase in the secretion of catecholamines, glucocorticoids and inflammatory cytokines. These conditions facilitate increases in heart rate and blood pressure that will eventually contribute to endothelial dysfunction.
Furthermore, research in animal models suggest that psychological stress mobilises the immune system with increased activity of haemopoietic progenitor cells in the bone marrow. The bone marrow derived monocytes that are released in response to stress have been shown to migrate to the arterial wall and cause atherosclerotic inflammation.
However, it is unknown whether these processes occur in humans and whether it is the brain stress-network that begins this pathogenic process. A newly published study in The Lancet would appear to suggest that the amygdala—an almond shaped part of the brain situated in the temporal lobe that is involved in stress and has been previously implicated with post-traumatic stress disorder (PTSD), anxiety and depression—has heightened activity that leads to a greater risk of developing CVD.