Heart Transplantation
Abstract
:1. Introduction
2. Graft Selection
2.1. ABO and HLA Compatibility
2.2. Graft Size
2.3. Ischemic Time
2.4. Age
2.5. Infections
2.6. Cause of Death
2.7. Laboratory-Imaging Tests
3. Allocation System—Graft Distribution
4. Transplantation Techniques
4.1. Orthotopic Transplantation
- (A)
- Bicaval technique: The placement of the graft in the recipient is an anastomosis of the left sinus of the graft with part of the recipient. Initially, suture placement is performed at the left atrial cuff adjacent to the left superior pulmonary vein and passing through the donor’s left atrial cuff adjacent to the left atrial appendage. Then, it is performed sequentially or posteriorly, and the anterior suturing of the sinus with care for the surfaces of the endocardium is sutured to reduce the possibility of thrombus formation. After this, the superior and inferior vena cava are anastomosed, taking care not to injure the coronary sinus, pulmonary artery, and aorta.
- (B)
- Biatrial technique: The anastomosis of the atrium is performed as above, with the sutures ending at the inter-atrial septum. The difference is that part of the recipient’s right sinus is also preserved, and an anastomosis is also performed there. The suture is initiated at the superior end of the atrial incision, and the anastomosis of the diaphragm follows. Then, the great vessels are sutured as before. After the anastomoses, the patient is placed in the Trendelenburg position, the cavities are vented, temporary right atrium and ventricle pacing is instituted, and the patient is weaned from mechanical circulation.
4.2. Heterotopic HTx
5. Transplant Recipients
6. Complications
6.1. Rejection
- Acute cellular rejection: This is the most frequent type of rejection. Pathophysiologically, the major and minor histocompatibility antigens are not uniformly expressed, with the result that they function as allografts and activate T-cytotoxic lymphocytes either indirectly or through antigen presentation. CD-4 and CD-8 positive T lymphocytes with high affinity to interleukin-2 receptors and increased intercellular adhesion molecules with high MHC-II expression on cardiac myocytes produce cytokines. This leads to the accumulation of inflammatory cells, such as macrophages and neutrophils, perivascularly inducing inflammation in the epicardial and endomyocardial arteries. Histopathologically, it is divided into three categories. The first is called low-grade, where inflammation is not observed in the myocardium. The second is the partial degree, where two or more foci are found in the myocardium. Finally, the third one, identified as high grade, shows multiple foci of damage with various types of inflammatory cells and necrotic elements.
- Acute humoral rejection: This shows a more complicated clinical manifestation. It is believed that the production of antibodies against the major and minor histocompatibility complex system is induced due to previous exposure to allogens such as transfusion, transplantation, and long-term circulatory support devices. It is divided into five categories according to antibody-mediated rejection in histopathological and immunopathological studies. The first is pAMR 0 Negative for antibody-mediated rejection with negative histopathological and immunopathological studies. The second is called pAMR 1(H+), with the presence of histopathological findings such as activated immune cells, inflammation, necrosis, etc. The third is pAMR 1(I+) antibody-mediated rejection with immunopathological and not histopathological findings. Next is pAMR 2, combining histopathological and immunopathological findings. Last is pAMR 3, in which severe histopathology (hemorrhage, capillary fragmentation, inflammation, interstitial edema) and immunopathological markers are observed.
- Hyperacute: This is created due to incompatibility with the ABO system, and its manifestations begin early with thrombosis of the vessels of the graft [68].
- Corticosteroids
- 2.
- Calcineurins inhibitors
- 3.
- Anti-proliferative agents
- 4.
- mTOR inhibitors
- 5.
- Induction Therapy
- -
- Monoclonal anti-lymphocyte antibodies;
- -
- Polyclonal anti-lymphocyte antibodies;
- -
- Antibodies against cytokine receptors.
6.2. Graft Angiopathy
6.3. Primary Graft Failure
6.4. Infections
6.5. Neoplasms
6.6. Retransplantations
7. Future Perspectives
8. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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For the left ventricle |
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For the right ventricle |
Either criteria I and II or III alone must be met:
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© 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
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Chrysakis, N.; Magouliotis, D.E.; Spiliopoulos, K.; Athanasiou, T.; Briasoulis, A.; Triposkiadis, F.; Skoularigis, J.; Xanthopoulos, A. Heart Transplantation. J. Clin. Med. 2024, 13, 558. https://doi.org/10.3390/jcm13020558
Chrysakis N, Magouliotis DE, Spiliopoulos K, Athanasiou T, Briasoulis A, Triposkiadis F, Skoularigis J, Xanthopoulos A. Heart Transplantation. Journal of Clinical Medicine. 2024; 13(2):558. https://doi.org/10.3390/jcm13020558
Chicago/Turabian StyleChrysakis, Nikolaos, Dimitrios E. Magouliotis, Kyriakos Spiliopoulos, Thanos Athanasiou, Alexandros Briasoulis, Filippos Triposkiadis, John Skoularigis, and Andrew Xanthopoulos. 2024. "Heart Transplantation" Journal of Clinical Medicine 13, no. 2: 558. https://doi.org/10.3390/jcm13020558