Abstract
ALTHOUGH coronary artery disease develops within three years of heart transplantation in up to 40 percent of transplant recipients,1,2 chest pain late after cardiac transplantation is usually dismissed as being “noncardiac” because it has been assumed that the transplanted heart is permanently denervated. The presumption that the donor heart remains denervated in humans is based primarily on the lack of appropriate neural reflex—mediated changes in the heart rate.3, 4 That reinnervation would not occur is surprising, because there is extensive evidence of sympathetic reinnervation after cardiac transplantation in nearly all animal models.5 6 7 8 In the transplanted heart, sympathetic nerves are severed from.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1791-1794 |
| Number of pages | 4 |
| Journal | New England Journal of Medicine |
| Volume | 324 |
| Issue number | 25 |
| DOIs | |
| State | Published - Jun 20 1991 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
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