Stress Hyperglycemia Ratio and Atrial Thrombus After Stroke: Thrombotic Signal or Stress Response?

The stress hyperglycemia ratio (SHR) expresses acute glucose relative to estimated background glycemia. Its association with atrial thrombus after ischemic stroke raises a clinically relevant question. Does it identify a thrombogenic atrial substrate, reflect the response to cerebral injury, or capture both? This critical narrative review compares human studies of glycemic disturbance, inflammatory biomarkers and thrombus-related outcomes. Anatomically detected thrombus, composite echocardiographic findings, coronary thrombus burden and laboratory thrombogenicity are evaluated separately. The identified atrial SHR evidence is observational. Coronary studies provide supporting context but examine a different vascular process. C-reactive protein (CRP) and related inflammatory indices also show associations with atrial thrombus, although discrimination and adjustment vary. Experimental hypoglycemia studies demonstrate changes in platelet activity, fibrin structure and ex vivo thrombus formation. They do not establish hypoglycemia-induced atrial thrombosis. Interpretation is further limited by measurement timing, selected imaging populations, possible cohort overlap and imperfect thrombus classification. Neither an adjusted association nor a high multivariable-model area under the curve establishes a causal pathway or a safe imaging rule. Future studies should test whether SHR adds clinically useful information beyond atrial structure, rhythm, inflammation and stroke severity. Current evidence supports mechanistic investigation and prospective validation rather than biomarker-directed anticoagulation or omission of indicated imaging.