Stress-related neurohormonal profiles across variant angina, stress-induced cardiomyopathy, and acute coronary syndromes

Abstract Background and Aims Stress-induced cardiomyopathy (SICMP), or Takotsubo syndrome, is characterized by transient left ventricular dysfunction precipitated by acute emotional or physical stress. Excessive activation of the sympathetic-adrenal-medullary and hypothalamic-pituitary-adrenal (HPA) axes has been proposed as a central mechanism, yet quantitative comparisons of stress-related hormones between SICMP and ischemic acute coronary syndromes (ACS) remain limited. This study aimed to delineate the neurohormonal profile of SICMP compared with UA/NSTEMI and STEMI. Methods In this prospective, single-center study, 211 patients who underwent coronary angiography for suspected ischemic chest pain between October 2022 and August 2023 were enrolled. Patients were categorized into four groups: stress-induced cardiomyopathy (SICMP, n = 15), UA/NSTEMI (n = 123), STEMI (n = 50), and variant angina (n = 23). Serum norepinephrine, adrenocorticotropic hormone (ACTH), and cortisol levels were measured at admission, one day post-angiography, and after discharge. Clinical and laboratory characteristics were compared across groups using analysis of variance and χ² tests. Results SICMP patients exhibited the highest acute-phase elevations of norepinephrine and cortisol. Mean cortisol levels in SICMP were 14.2 ± 4.8 µg/dL on admission and 13.8 ± 4.6 µg/dL on day 1, significantly exceeding those in UA/NSTEMI (8.2 ± 4.2 µg/dL and 8.7 ± 4.0 µg/dL) and STEMI (8.6 ± 4.0 µg/dL and 8.1 ± 4.2 µg/dL; p 0.01). Norepinephrine concentrations were also markedly elevated in SICMP (610 ± 340 pg/mL) compared with ischemic ACS subtypes (p = 0.03). ACTH levels showed modest, non-significant increases. Baseline demographics were comparable, except for markedly reduced left-ventricular ejection fraction in SICMP (38.5 ± 6.2%). Conclusions SICMP demonstrates a distinct endocrine pattern characterized by concurrent cortisol and catecholamine elevation. In clinical settings where electrocardiographic findings and cardiac biomarkers alone do not clearly differentiate SICMP from ischemic ACS, stress-related hormone profiling—particularly cortisol measurement—may serve as a useful adjunctive diagnostic marker.