Heart Transplant Rejection

Heart transplant rejection is immune-mediated injury to the donor heart. The recipient’s immune system recognizes donor antigens as foreign despite immunosuppressive therapy, and the resulting inflammation can impair myocardial contraction, relaxation, electrical conduction, or coronary blood flow. Acute cellular rejection (ACR) is driven mainly by T lymphocytes. These cells infiltrate the myocardial interstitium and spaces around vessels, then injure cardiac myocytes. Antibody-mediated rejection (AMR) is different: recipient antibodies, usually donor-specific antibodies against human leukocyte antigens, bind to the graft’s capillary endothelium and activate complement. ACR and AMR can coexist, but they are not interchangeable diagnoses; their biopsy findings, laboratory correlations, and treatments differ. The clinical consequence is often a fall in effective cardiac output. That explains fatigue, reduced exercise tolerance, dizziness, hypotension, and sometimes syncope. The kidneys interpret reduced perfusion as inadequate circulating volume, while the failing ventricle raises filling pressures; fluid retention then produces weight gain, peripheral edema, orthopnea, or dyspnea. Inflammation can also disturb conduction and trigger atrial or other new arrhythmias. The transplanted heart is denervated. A patient may therefore have no typical anginal warning even when...