Possible Complications

Rejection

Acute rejection of the transplanted heart is a T-cell mediated process that is diagnosed on endomyocardial biopsy. The degree of rejection is graded according to amount of lymphocytic infiltration, edema and myocyte injury. Clinical presentation may include GI complaints, right heart failure symptoms, fatigue, dyspnea, arrhythmias, tachycardia or low-grade fever. Patients will undergo routine endomyocardial biopsies for surveillance of acute rejection. If detected, it can most often be treated as an outpatient without any effect on graft function.

Infection

All infections identified in the immunosuppressed transplant recipient should be treated expeditiously to limit sequelae. Patients with persistent low-grade fevers or acute “spiking” fevers (greater than 101?F) should be admitted to the hospital for stabilization and infectious work-up.The transplant center would like to be informed of any hospitalizations that a recipient requires. We would also appreciate a copy of the discharge summary from each admission.

Hypertension

Greater than 75% of heart transplant recipients develop systemic hypertension as an adverse effect when using cyclosporine or Prograf in addition to maintenance steroid therapy. Many patients respond to single antihypertensive therapy but a number of them require multiple agents for adequate control. Immunosuppression doses are also decreased, if possible, to improve renal artery perfusion, thus lowering rennin production. Certain calcium channel blockers (diltiazem, verapamil) increase cyclosporine levels- discuss with transplant center.

Renal Dysfunction

Calcineurin inhibitors (cyclosporine, Prograf) are moderately potent nephrotoxins and frequently cause dose-related renal dysfunction. This is caused by vasoconstriction of the afferent renal arterioles, thereby decreasing the glomerular filtration rate. Patients should not be treated with drugs that increase the nephrotoxicity effect of their immunosuppression. These drugs include NSAIDS, indocin, erythromycin or medications that may increase calcineurin inhibitor levels (see “Medications to Avoid” table).

Hyperlipidemia

Hyperlipidemia can occur early post-transplant and affects 60-80% of heart transplant recipients due to the effects of cyclosporine and Prograf. HMG-CoA reductase inhibitors are used with care in these patients because of risk of myositis when used in conjunction with calcineurin inhibitors. Patients are placed on Pravachol immediately following transplant for lipid control and it’s beneficial effects on lowering the risk of coronary vasculopathy. Pravachol has been shown to have the lowest incidence of myositis in this population as it is not metabolized through the same pathway as calcineurin inhibitors.
Malignancy

Transplant recipients are at increased risk for developing malignancies due to immunosuppressants necessary to maintain allograft function. Skin cancers (basal cell and squamous cell carcinomas) are the most commonly encountered. The treatment of skin cancers can include cryotherapy, excision and reduction in immunosuppression, if possible.

Transplant Vasculopathy (Graft CAD)

Transplant vasculopathy is an obstructive, proliferative process that causes the formation of lesions in the coronary arteries of the transplanted graft. It can occur within months but is more typically seen 3-5 years after transplant surgery. It is characterized by diffuse, concentric lesions in the small tributaries of epicardial vessels and their branches that involve the entire length of the artery and appear to abruptly cut off or obliterate the distal vessels. Proximal, focal blockages can also be found which are more typical of stenosis seen in native coronary disease.

Transplant Center