Purpose Many patients who develop severe cardiac allograft vasculopathy (CAV) after heart transplant demonstrate restrictive cardiac physiology. We hypothesized that this phenomenon is related to fibrosis of myocardial and adjacent myocardial tissue (often observed at the time of redo transplant) resulting from CAV and inflammation. We reviewed our redo heart transplant patients to assess for fibrosis in the explanted donor heart and adjacent tissues in patients who demonstrated restrictive cardiac physiology.
Methods In our program 28 patients underwent redo heart transplants, all on triple-drug immunosuppression. We reviewed all pathology reports of the explanted donor heart and hemodynamic and echocardiographic data for the presence of restrictive cardiac physiology in the 3 months prior to the redo heart transplantation. Restrictive cardiac physiology was defined as symptomatic heart failure (documented dyspnea, edema, or increase in diuretic dose) with echocardiographic E to A velocity ratio > 2, shortened isovolumetric relaxation time (< 60 msec), shortened deceleration time (< 150 msec), or restrictive hemodynamic values (RA > 12, PCW > 25, CI < 2.0). Patients were divided into those who had fibrosis noted in the myocardium and/or adjacent tissues (n = 15) and those who did not (n = 13).
Results The fibrosis group had significantly more patients exhibiting restrictive cardiac physiology in the period preceding the redo heart transplant (83.5% patients vs 16.7% patients, p < .001). In the fibrosis group, seven patients (47%) had severe fibrosis and scarring in the tissues surrounding the donor heart. There was no difference in immunosuppression regimen between the two study groups.
Conclusions Restrictive cardiac physiology appears to correlate with the presence of significant fibrosis in the myocardium of the donor heart. Severe fibrosis of adjacent myocardial tissue may also be contributing toward this restrictive cardiac physiology. The mechanism of fibrosis development warrants further investigation.
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