Review Calls Chronic Stress Before Surgery a Possible Modifiable Heart Risk

The paper appeared in Biomolecules in 2026. It is a narrative review, not an experiment. The authors, led by Jancic and colleagues, gathered and summarised existing research. They searched PubMed/MEDLINE, Embase and Cochrane through 31 May 2026. They did not formally assess the quality of each study. The review does not report its own participant numbers.

The setting is large. According to the review, an estimated 313 million surgical procedures are performed worldwide each year. In the United States, death, heart attack or stroke around the time of surgery occurs in about 1 in 33 hospital admissions among patients over 45. That adds up to more than 150,000 cardiovascular events a year.

The authors say current risk models do not include psychosocial stress. They write that no major guideline recommends screening for chronic psychological stress before surgery.

The review lays out a biological case. Long-term stress keeps the body's main stresshormone system, the HPA axis, switched on. Over time, cells can become less responsive to cortisol, the hormone that normally helps calm inflammation. The review calls this glucocorticoid resistance. It describes a further chain of effects: inflammation, damage to the lining of blood vessels, a greater tendency for blood to clot, and activation of the sympathetic (fight-or-flight) nervous system.

According to the authors, these pathways overlap with the ways surgery can injure the heart, trigger irregular heart rhythms and cause blood clots in the veins.

The human evidence they cite is observational. Prospective data showed that psychological distress before noncardiac surgery independently predicted cardiovascular complications within 30 days and death within one year. Studies of allostatic load, a measure of wear across body systems, linked high preoperative burden to up to twice the risk of death after surgery. They also linked it to higher rates of heart attack and venous blood clots. Broader research, the authors add, finds that anxiety and depression independently raise cardiovascular risk.

These findings show links, not cause and effect. The authors stress that the measures differ. Questionnaires such as the PHQ-9 and GAD-7 capture recent symptoms at one point in time. They are only proxies for long-term stress. Allostatic load also reflects ageing, other illness and social circumstances. Some of the biological evidence comes from cardiac surgery, the general population, steroid-drug exposure and animal models, not from noncardiac surgery patients.

The most important gap is that no randomized controlled trial has tested whether reducing stress before surgery lowers postoperative cardiovascular events. So the review cannot say that easing stress will protect the heart. It calls chronic stress a potentially modifiable risk factor, and the word "potentially" matters.

For people facing planned surgery, the practical point is modest. The review offers no patient advice and does not show that stress reduction or mental health support will cut heart complications.

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The authors call for prospective trials of preoperative stress reduction, and those results would show whether this risk can actually be changed.

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