An autonomic phenotype you can build from the notes, before the patient arrives

Design

Single-centre retrospective cohort with 1:1 propensity score matching

Population

612 matched pairs aged 65 and over undergoing major non-cardiac surgery with perioperative hs-cTnT surveillance, from 2,184 eligible

Primary outcome

Adjudicated ischaemic myocardial injury after non-cardiac surgery

Effect

MINS 14.2% versus 8.7% (OR 1.75, 95% CI 1.23-2.49); 30-day MACE HR 1.68 (1.12-2.51); 1-year mortality HR 1.54 (1.07-2.22); highest hypotension quartile OR 2.84 (1.62-4.97)

Myocardial injury after non-cardiac surgery is common, mostly silent, and carries real mortality. The patients who get it are disproportionately older with diabetes or hypertension — but those conditions are so common that they do not stratify anyone.

This single-centre retrospective cohort tried a sharper phenotype, built entirely from what is already in the electronic record: diabetes and/or hypertension plus at least one of documented neuropathy, orthostatic hypotension or syncope/presyncope, or unexplained resting bradycardia or chronotropic incompetence. Patients aged 65 and over having major non-cardiac surgery with high-sensitivity troponin T surveillance were propensity-matched 1:1, giving 612 pairs from 2,184 eligible.

Adjudicated ischaemic MINS occurred in 87 of 612 (14.2%) with the phenotype against 53 of 612 (8.7%) without (OR 1.75, 95% CI 1.23-2.49, P=.002). Troponin elevation was more frequent (27.1% versus 18.5%), 30-day major adverse cardiac events higher (HR 1.68, 95% CI 1.12-2.51) and one-year mortality higher (HR 1.54, 95% CI 1.07-2.22).

The part that changes intraoperative conduct is the interaction. Hypotension burden modified the association (P for interaction = .018), and the excess risk concentrated in the highest hypotension quartile (OR 2.84, 95% CI 1.62-4.97). These patients cannot compensate, so the hypotension you would tolerate in someone else is the hypotension that injures them.

• Look for neuropathy, orthostatic symptoms or unexplained bradycardia in the diabetic or hypertensive patient over 65
• The phenotype needs no new test — it is assembled from what is already recorded
• Set a tighter pressure target for these patients rather than the unit default
• The interaction with hypotension burden is the actionable finding, not the phenotype alone
• Postoperative troponin surveillance is worth more in this group than in unselected older patients

Why it matters

It turns two conditions too common to stratify anyone into a phenotype that does.

Don't overread it

Retrospective, single-centre, and the phenotype was defined from record documentation rather than autonomic testing — the authors ask for external validation.

The statistics, in plain English

Propensity matching balances the confounders that were measured, which here means the phenotype and the outcome could still share an unmeasured cause — severity of vascular disease, most obviously. The interaction P value of .018 is the statistically interesting part: it says the phenotype's effect genuinely differed across hypotension quartiles, rather than being the same risk at every level. The authors call the whole thing hypothesis-generating and ask for validation with formal autonomic testing.

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