HeartMend scores acute cellular rejection risk from a locked 5-gene expression panel — CD7, DEF6, UBE2L6, PSMB9, STAT1 — measured directly from the same endomyocardial biopsy tissue your pathology team already collects.
Histologic grading of rejection severity varies meaningfully between experienced cardiac pathologists, particularly at borderline grades.
Rejection can be patchy. A biopsy forceps samples a small fraction of the myocardium, and a normal read doesn't rule out disease elsewhere.
Treatment decisions for suspected rejection often can't wait for a second opinion or repeat biopsy — a molecular read runs alongside routine histology.
The gene panel was fixed before this pipeline ever ran — there's no feature selection happening at read time, only measurement and scoring.
A portion of the same endomyocardial biopsy core collected for routine histology is submitted for expression profiling — no additional procedure required.
Expression levels for the five locked genes — CD7, DEF6, UBE2L6, PSMB9, STAT1 — are measured and normalized against reference values.
An L2-regularized logistic regression model, trained once and never re-fit to new cohorts, converts the five values into a rejection probability.
No per-patient retraining · same model weights every timeA molecular rejection score is delivered to the transplant team as a second, independent data point — to be read together with, not in place of, histologic grading.
The classifier was fit once on the training cohort, then applied without any re-fitting to a fully independent external cohort — the strictest available test of whether the panel generalizes.
External test cohort: 25 biopsies (12 rejection / 13 non-rejection), evaluated against a model trained on a separate 43-sample cohort with no shared patients. Significance assessed by permutation testing (n = 2,000 label shuffles) against the fixed model outputs.
Marks infiltrating T-lymphocytes, the primary effector cells in acute cellular rejection.
Regulates T-cell receptor signaling and activation within infiltrating lymphocyte populations.
Interferon-stimulated gene involved in the ISGylation response seen during active graft inflammation.
Immunoproteasome subunit upregulated during interferon-driven antigen presentation in rejecting tissue.
Core transcription factor downstream of interferon-gamma signaling, elevated across rejection episodes.
HeartMend doesn't replace histologic grading or your pathology team's read. It's designed to run in parallel, using tissue you're already collecting.
We're currently working with a small number of transplant centers on pilot evaluations.