Sustained psychological stress is shown to accelerate the progression of atherosclerosis. The most plausible biological explanations involve the effects of stress on (a) the immune system, resulting in raised inflammatory signaling, and on (b) blood pressure. Raised blood pressure can accelerate atherosclerosis, as well as raise the risk of rupture of atherosclerotic lesions. The relationship between stress and atherosclerosis may well have as much to do with the lifestyle effects of stress and their downstream effects on cardiovascular health over the long term, however.
Although the specific biological mechanisms by which chronic stress increases cardiovascular disease risk remain unclear, chronic low-grade inflammatory load appears as a possible link. Chronic stress exacerbates this load and leads to early progression of atherosclerosis and thrombotic complications. Inflammation plays a key role in the overall atherosclerotic step, involving the accumulation of foam cells, the formation of fatty stripe tissue and fibrous plaques, the rupture of acute plaques, and the formation of thrombus. Persistence of inflammation is necessary for plaque development and instability, and plays a decisive role in the pathogenesis and progression of coronary artery disease.
Studies have shown that chronic stress-induced hyperlipidemia and oxidative damage can contribute to the development of atherosclerosis. Although atherosclerosis is a chronic inflammatory disease, hyperlipidemia is a major risk factor for changes in intimal and media thickness during atherosclerosis. Experiments have found that compared with the control group, the high concentrations of serum total cholesterol, triglyceride, low density lipoprotein cholesterol (LDLC), and very low density lipoprotein cholesterol (VLDLC) could increase the atherosclerosis index in the chronic stress group, while the concentration of high density lipoprotein cholesterol did not change significantly.
Chronic stress plays a very important role in the development of hypertension, and its mechanisms are known to involve long-term abnormal neurological and endocrine activity, such as significantly elevated levels of corticosteroids, cortisol, epinephrine, norepinephrine, and angiotensin. Initially, the sympathetic nerve-adrenal medulla system is an important factor in the development of hypertension. Under chronic stress, plasma adrenaline, norepinephrine, and dopamine increase rapidly. It is now clear that in hypertension, the sympathetic nervous system activity is increased, and sympathetic excitation causes small arteriovenous contractions, leading to an increase in diastolic/systolic blood pressure.