Women and men recover differently after a heart attack, and their blood markers show it

Heart disease looks different in women and men. Women tend to have smaller coronary arteries, more diffuse and less lipid-rich plaque, and develop acute coronary syndrome (ACS) later. Blood biomarkers that track myocardial injury, heart strain and inflammation are used to diagnose and monitor ACS, but reference values are rarely sex-specific. Little is known about how these markers evolve in the months after an ACS.

This analysis used BIOMArCS, a prospective Dutch observational study of ACS patients aged 40 and older with at least one cardiovascular risk factor. Patients who had cardiovascular death or a repeat ACS were excluded to avoid distortion by new events. The full cohort comprised 787 patients (173 women, 22%) with frequent blood sampling for one year, in which hs-troponin T, NT-proBNP, hs-CRP and GDF-15 were measured. A 191-patient subcohort (43 women) had nine further markers measured, including troponin I, sST2, galectin-3, myeloperoxidase, von Willebrand factor, cystatin C and lipids. Linear mixed-effects models adjusted for age, BMI, time since ACS and, in the subcohort, kidney function. Acute (<30 days) and stabilized (30 days to 1 year) phases were analyzed separately.

Women had lower troponin T in both phases: 386 vs 559 pg/mL acutely, and 8.5 vs 10.8 pg/mL at 180 days. Troponin T fell faster in men during stabilization. At six months, 21% of men and 12% of women still exceeded the 14 pg/mL upper reference limit. NT-proBNP was higher in women acutely (70 vs 47 pmol/L) and at 180 days (30 vs 19 pmol/L). Hs-CRP was higher in women in the stabilized phase (1.8 vs 1.5 mg/L at 180 days). GDF-15 did not differ significantly. In the subcohort, women had higher galectin-3 (22.8 vs 18.6 ng/mL) and HDL, and lower sST2 at 180 days. Troponin I, myeloperoxidase, von Willebrand factor, cystatin C and LDL showed no significant sex differences.

The authors suggest lower troponin in women mainly reflects smaller left ventricular mass, with possible contributions from sex-specific coronary pathophysiology and estrogen effects. Higher NT-proBNP may relate to more diastolic dysfunction and comorbidity in older women. The findings support exploring sex-specific thresholds for post-ACS risk assessment and detection of repeat events.

There are important caveats. Confidence intervals overlapped for every biomarker despite significant p-values, so the absolute differences may be small at the individual level. Women made up only 22% of the cohort, and the subcohort was small. Unmeasured factors such as myocardial mass, hormonal status and gender-related behaviors could contribute, and the clinical value of sex-specific cut-offs remains unproven.