Arrhythmias in the Heart Transplant Patient

Abstract

Orthotopic heart transplantation (OHT) is the most effective long-term therapy for end-stage heart disease, with implanted left ventricular assist devices ('destination therapy') as an alternative for selected patients. The denervation of the transplanted heart with complete loss of autonomic nervous system modulation, the use of immunosuppressant drugs, as well as the risk of allograft rejection (AR) and vasculopathy, all change the incidence, prognosis and treatment of tachyarrhythmias and bradyarrhythmias, as well as the mechanisms of sudden cardiac death (SCD).Arrhythmias post-OHT can be classified according to their underlying mechanisms (see Table 1). Tachyarrhythmias and bradyarrythmias can come from the transplanted heart, be due to the surgery itself or result from AR or vasculopathy. In addition, bradyarrhythmias may be caused by drugs taken by the recipient patient before surgery. This review aims to present the most common causes of arrhythmias in OHT patients, and to highlight the importance of ruling out and treating AR and vasculopathy -transplant coronary artery disease (TCAD), which should always be the first concern. The causative mechanisms represent different risk factors, and overlap is possible, which may increase the occurrence of such arrhythmias.With the increasing success of radiofrequency (RF) ablation techniques, it is important that cardiologists are familiar with tachycardias and bradycardias in this context, which may benefit from a multidisciplinary approach in the management of the patient starting with the underlying mechanisms. Tachyarrhythmias Supraventricular TachycardiaThe most common atrial arrhythmia in OHT patients is atrial flutter AbstractOrthotopic heart transplantation (OHT) is currently the most effective long-term therapy for patients with end-stage cardiac disease, even as left ventricular devices show markedly improved outcomes. As surgical techniques and immunosuppressive regimens have been refined, short-term mortality caused by sepsis has decreased, while morbidity caused by repeated rejection episodes and vasculopathy has increased, and is often manifested by arrhythmias. These chronic transplant complications require early and aggressive multidisciplinary treatment. Understanding the relationship between arrhythmias and these complications in the acute and chronic stages following OHT is critical in improving patient prognosis, as arrhythmias may be the earliest or sole presentation. Finally, decentralised/ denervated hearts represent a unique opportunity to investigate the underlying mechanisms of arrhythmias.

Atrial fibrillation after heart transplantation

“…Частота возникновения послеоперационной фибрилляции предсердий после трансплантации ниже по сравнению с дру-гими кардиохирургическими вмешательствами. Денервация органа и изоляция легочных вен с исходящей из них триггерной активностью [7], способствующей формированию и поддержанию фибрилляции, обусловливают меньший риск развития данной аритмии после трансплантации сердца.…”

“…С учетом прогностической значимости и меха-низмов, лежащих в основе данной аритмии у пациентов после ОТС, фибрилляцию предсердий принято классифицировать на раннюю послеопе-рационную (в течение 1 месяца после операции) и позднюю (через 1 месяц и более после ОТС) [7].…”

“…В настоящее время не суще-ствует единого мнения в отношении выбора и Особенностями больных после пересадки серд-ца являются значительный риск кровотечения в раннем послеоперационном периоде, а также необходимость проведения эндомиокардиальных биопсий. Ряд авторов считают, что всем пациен-там с фибрилляцией предсердий показано назна-чение антикоагулянтной терапии независимо от CHA2DS2-VASc-риска [7]. Предпочтение следу-ет отдавать новым оральным антикоагулянтам или гепаринам.…”

Drug‐Drug Interaction Study of Apixaban with Cyclosporine and Tacrolimus in Healthy Volunteers

“…Similarly, NVAF is common after solid organ transplantation, with a cumulative incidence of 3.6–7.3% at 12 and 36 months post‐kidney transplant . The incidence of NVAF after lung transplantation is 33–39% and between 0.3% and 24% following heart transplant …”

“…12 The incidence of NVAF after lung transplantation is 33-39% 13 and between 0.3% and 24% following heart transplant. 14 Apixaban is a direct oral anticoagulant (DOAC) that inhibits factor Xa. 15 The use of DOACs, including apixaban, has substantially increased due to ease of administration, lack of coagulation monitoring, and fixed dosage schedule in contrast to warfarin.…”