Stress-induced inflammation is a critical pathway through which chronic stress contributes to cardiovascular disorders. When the body is under stress, it releases pro-inflammatory cytokines, which are signalling proteins that promote inflammation. This chronic low-grade inflammation can damage the inner walls of the arteries, leading to the development of atherosclerosis, a condition characterized by the buildup of plaque within the arterial walls. Plaque consists of fat, cholesterol, calcium, and other substances found in the blood. Over time, the plaque hardens and narrows the arteries, limiting the flow of oxygen-rich blood to the heart and other parts of the body. This can result in angina (chest pain), coronary artery disease, heart attacks, or strokes. Furthermore, the inflammatory response can make existing plaques unstable, increasing the risk of plaque rupture and leading to acute cardiovascular events. Therefore, managing stress and reducing inflammation are key strategies in preventing and treating cardiovascular diseases.

While psychological stress is a significant risk factor for cardiovascular disorders, it typically interacts with other factors to contribute to the development of these conditions. Stress alone can increase physiological responses, such as elevated blood pressure and heart rate, which over time can harm cardiovascular health. However, the impact of stress is often exacerbated by associated behaviours and conditions, such as unhealthy eating habits, physical inactivity, smoking, and excessive alcohol consumption. Additionally, genetic predisposition, age, and pre-existing health conditions, such as diabetes or obesity, also play crucial roles in the development of cardiovascular diseases. Therefore, while stress is a key player in the pathway to cardiovascular disorders, it is the combination of psychological, behavioural, and physiological factors that ultimately determines the risk and severity of these conditions.

The body's response to acute stress (short-term stress) is significantly different from its response to chronic stress (long-term stress), particularly in terms of cardiovascular health. Acute stress activates the body's "fight or flight" response, leading to a temporary increase in heart rate and blood pressure. This response is mediated by the release of adrenaline, which prepares the body to face or escape the perceived threat. Typically, once the stressor is removed, the body's physiological parameters return to baseline levels, with no long-lasting adverse effects on cardiovascular health.

In contrast, chronic stress results in prolonged activation of the stress response, with continuous release of stress hormones like cortisol. This persistent state can lead to sustained high blood pressure, inflammation, and changes in blood lipid profiles, all of which are risk factors for atherosclerosis and other cardiovascular diseases. Chronic stress can also exacerbate unhealthy behaviours, such as poor diet, physical inactivity, and substance abuse, further increasing the risk of cardiovascular disorders. Thus, while acute stress may have negligible long-term effects on heart health, chronic stress poses a significant threat to cardiovascular well-being.

The hypothalamic-pituitary-adrenal (HPA) axis plays a central role in the body's response to stress and its relationship with cardiovascular disease. When an individual perceives stress, the hypothalamus releases corticotropin-releasing hormone (CRH), which signals the pituitary gland to secrete adrenocorticotropic hormone (ACTH). ACTH then prompts the adrenal glands to produce cortisol, a key stress hormone. Cortisol has various effects on the body, including increasing blood sugar levels and suppressing the immune system, which can be beneficial in the short term.

However, chronic activation of the HPA axis and prolonged cortisol release can lead to adverse cardiovascular outcomes. High levels of cortisol contribute to hypertension, dyslipidemia (abnormal levels of lipids in the blood), and obesity, all of which are risk factors for cardiovascular disease. Cortisol also enhances the accumulation of abdominal fat, which is closely linked to metabolic syndrome, a cluster of conditions that increases the risk of heart disease. Additionally, chronic HPA axis activation can lead to insulin resistance, further exacerbating cardiovascular risk. Therefore, the HPA axis is a critical mediator of the relationship between stress and cardiovascular health, highlighting the importance of managing stress to prevent heart disease.

Social support and coping strategies play significant roles in moderating the impact of stress on cardiovascular health. Social support from family, friends, and communities can buffer the effects of stress by providing emotional, informational, and practical assistance, which can reduce perceptions of stress and its physiological consequences. Individuals with strong social networks tend to report lower levels of stress and are more likely to engage in healthy behaviours, such as regular physical activity and balanced nutrition, which are protective against cardiovascular disease.

Effective coping strategies, such as problem-solving, positive reappraisal, and stress management techniques (e.g., relaxation training, mindfulness meditation), can also mitigate the harmful effects of stress on the heart. These strategies help individuals manage their stress more effectively, reducing the activation of the sympathetic nervous system and the HPA axis, and thereby decreasing the risk of hypertension, inflammation, and other stress-related cardiovascular risks. In contrast, maladaptive coping strategies, such as denial, substance abuse, and disengagement, can exacerbate stress and its negative impact on cardiovascular health. Therefore, fostering social support and teaching effective coping mechanisms are crucial for protecting cardiovascular health in the face of stress.