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Lifetime Data and Concepts
Published in Prabhanjan Narayanachar Tattar, H. J. Vaman, Survival Analysis, 2022
Prabhanjan Narayanachar Tattar, H. J. Vaman
Sharples, et al. (2003)[105] collected data related to analyze the diagnostic accuracy of coronary angiopathy and risk factors for post-heart-transplant cardiac allograft vasculopathy. The heart transplant monitoring dataset consists of a series of approximately yearly angiographic examinations of heart transplant recipients. Here, the state at each time is a grade of cardiac allograft vasculopathy (CAV), a deterioration of the arterial walls. The dataset has 622 unique patients and 2846 measurements among them.
Haemodynamic evaluation of the heart transplant patient
Published in John Edward Boland, David W. M. Muller, Interventional Cardiology and Cardiac Catheterisation, 2019
Kavitha Muthiah, Christopher S. Hayward, Andrew Jabbour, Peter Macdonald
Cardiac allograft vasculopathy contributes to a significant proportion of deaths after cardiac transplantation, and its contribution to mortality increases with time from transplant. The prevalence is high – 20% at 3 years, 30% at 5 years and 45% at 8 years post-transplant.16 Classical angina may be experienced in up to 50% of patients as the transplanted heart reinnervates. The characteristics that affect the risk of CAV development include: (i) donor characteristics: higher age, male sex, higher body surface area, history of hypertension, history of infection, and (ii) recipient characteristics such as history of ischemic heart disease, LVAD implant before transplant, and history of infection. In addition, medication use such as azathioprine rather than mycophenolate mofetil, use of cyclosporine rather than tacrolimus, and use of OKT3 for induction therapy have been implicated as risk factors.16
Complications of Cardiac and Lung Transplantation
Published in Stephen M. Cohn, Matthew O. Dolich, Complications in Surgery and Trauma, 2014
Jay D. Pal, Daniel T. DeArmond, Hao Pan, Scott B. Johnson
Chronic rejection presents in the transplanted heart as cardiac allograft vasculopathy. The disease process results in interstitial fibrosis and diffuse atherosclerotic changes of coronary arteries and small vessels. This accelerated form of coronary artery disease is manifested by concentric fibrous neointimal hyperplasia [28]. This intimal hyperplasia is due to a proliferation of smooth muscle cells into the media in response to immune-mediated and alloantigenic-independent processes. In addition, graft ischemic time, ischemia–reperfusion injury, CMV infection, hyperlipidemia, and diabetes mellitus have also been implicated in the pathogenesis of CAV. The clinical presentation of CAV can involve dysrhythmias, myocardial infarction, or heart failure. Typical anginal symptoms are uncommon. The aggressive management of risk factors and CMV prophylaxis is protective; diltiazem and statin medications have been shown to reduce the incidence of CAV [29]. Treatment options for extensive CAV are limited, as the diffuse nature of the disease usually precludes percutaneous intervention or coronary artery bypass grafting. In appropriate patients, re-transplantation is the only effective treatment.
Percutaneous coronary intervention in patients with cardiac allograft vasculopathy: a Nationwide Inpatient Sample (NIS) database analysis
Published in Expert Review of Cardiovascular Therapy, 2021
Waqas Ullah, Nishant Thalambedu, Salman Zahid, Muhammad Zia Khan, Tanveer Mir, Sohaib Roomi, David L. Fischman, Salim S. Virani, Mahboob Alam
Cardiac allograft vasculopathy (CAV) is an inflammatory condition usually involving intramyocardial vessels characterized by diffuse concentric proliferation of intima [1]. It can have focal proximal or mid-coronary involvement or widespread, ‘pruning’ of the distal vessels [1]. Its incidence ranges from 40% to 50% with only half of the population surviving at the end of 5 years [2,3]. As per the registry of the International Society for Heart and Lung transplants (ISHLT) CAV is among the top three causes of death in post-heart transplant patients [3]. Patients with CAV usually lack the classic anginal symptoms due to afferent denervation aiding for the silent progression of vasculopathy delaying the diagnosis and limiting the success of the HT [4]. This can partly explain the higher associated mortality and poor prognosis of these patients.
Impact of low tacrolimus exposure and high tacrolimus intra-patient variability on the development of de novo anti-HLA donor-specific antibodies in kidney transplant recipients
Published in Expert Review of Clinical Immunology, 2019
Aleixandra Mendoza Rojas, Dennis A. Hesselink, Nicole M. van Besouw, Carla C. Baan, Teun van Gelder
Steroid-free maintenance therapy may also be a risk factor for the development of dnDSA. Pizzo et al. found that a high tacrolimus IPV (CV >31%) was weakly correlated with a high sirolimus IPV (CV >25%) [62], suggesting that the deleterious effects of under-immunosuppression due to a high tacrolimus IPV might be offset by other immunosuppressive medication. This may be especially relevant in the case of patients treated with standard triple immunosuppression therapy with high levels of prednisone and/or MPA. Recently, Shuker et al. found that a high tacrolimus IPV was not associated with the incidence and progression of cardiac allograft vasculopathy in heart transplant recipients [89]. The authors hypothesized that the effect of tacrolimus IPV on heart allograft outcomes may be considerably less than on kidney allograft outcomes due to the continuous use of prednisone and a higher number of immunosuppressive drugs after heart transplantation [89]. In 2019, the results from the TRANSFORM study demonstrated that the use of reduced tacrolimus + everolimus versus tacrolimus + MPA resulted in comparable two-year outcomes and dnDSA incidence (22% versus 18%, respectively) [90]. So, while reduced tacrolimus in combination with MPA seems to be associated with higher dnDSA development [64], it seems that everolimus is better able to protect against the deleterious effects of a lower tacrolimus exposure. Based on these studies, we think that the type of induction therapy, co-medication, and overall immunosuppressive load may need to be considered when assessing the risk of tacrolimus underexposure in the development of dnDSA.
Recommendations and guidance on the diagnosis and management of Danon disease
Published in Expert Opinion on Orphan Drugs, 2021
Kimberly N. Hong, Michela Brambatti, Sonya John, Quan M. Bui, Marzia Rigolli, Matthew Taylor, Eric D. Adler
Cardiomyopathy in DD can either progress to or present as a dilated cardiomyopathy [4]. Guideline directed medical therapy for heart failure with reduced ejection fraction is informed by ACC/AHA heart failure guidelines. Further studies are needed to establish efficacy within the DD population [64,65]. Given rapid progression to end-stage cardiomyopathy, early referral, and evaluation for ICD and resynchronization devices, due to high risk for malignant arrhythmias, as well as cardiac transplantation is recommended [25]. In a study of 82 patients with DD, 18 patients received transplants while 36 died of sudden cardiac death or complications of heart failure while awaiting transplantation [4]. Because cardiac transplantation only modifies the cardiac risks in DD, involvement of other organs may limit patient selection. There are, however, multiple case reports and series that describe successful cardiac transplantation in DD, although variable outcomes are reported. In a study of 16 individuals with DD who underwent cardiac transplant with median follow-up time of 2.35 years, there was 1 death in the entire cohort (occurred 5 days post-transplant) and no re-transplants [66]. At 1 year, there were no episodes of AMR, and five episodes of ACR (33%) in those who survived to discharge after transplantation. This is discrepant from data from the European multicenter registry that reported five of eight heart transplant/assist device male recipients (62%) dying within 1 year from the index procedure [67]. It has also been postulated that patients with DD, because they undergo transplant at younger ages, are at higher risk for cardiac allograft vasculopathy and re-transplantation [67,68].