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Coronary artery disease in cardiac transplant recipients is the main cause of mortality after the first postoperative year. This atheroma has unique anatomical features with widespread infiltration of the intima by inflammatory cells. The different physiopathological hypotheses are analysed. Immunological processes are probably responsible, suggesting chronic rejection. The cytomegalovirus could be an inductive mechanism. The classical vascular risk factors probably play a role but their action is not as clear as that of immunological and viral factors. Hyperlipidaemia is a causative mechanism and the predisposing role of steroid therapy is also recognised. From the practical point of view, correction of the classical risk factors is the only available therapeutic possibility at present.
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PMID:[Coronary disease of transplanted heart. Physiopathology, prevention]. 133 27

Since the time that coronary artery disease was first described in the transplanted human heart, attempts have been made to define risk factors for its development. Although recent reports have emphasized immunologic and infectious (i.e., cytomegalovirus) mechanisms in the development of transplant coronary disease, the influence of several nonimmunologic risk factors has also been studied. Some of the nonimmunologic risk factors that have been evaluated include recipient characteristics (age, sex, obesity, hyperlipidemia, hypertension, smoking, diabetes mellitus, pretransplantation heart disease), donor characteristics (age, sex), immunosuppressive agents/protocols, and nonimmune mechanisms of endothelial injury (cyclosporine, ischemic time). Studies evaluating the role of these risk factors have produced variable results. One or more studies, however, have suggested an effect of recipient age and sex, donor age and sex, obesity, hyperlipidemia, pretransplantation diagnosis, and ischemic time on the development of transplant coronary disease. The most consistently described relationship has been between hyperlipidemia and transplant coronary disease. Hyperlipidemia is common after heart transplantation, with elevations noted in total cholesterol, low-density lipoprotein cholesterol, and triglycerides. The cause of posttransplantation hyperlipidemia is not well defined, but obesity and the immunosuppressive agents prednisone and cyclosporine play a role. Treatment of posttransplantation hyperlipidemia can be difficult because commonly used lipid-lowering agents have side effects and interactions with immunosuppressive drugs that necessitate caution in their use in the posttransplantation population. Transplant coronary disease almost certainly has a multifactorial cause, with endothelial injury and nonimmunologic risk factors, particularly hyperlipidemia, playing contributory roles. Because hyperlipidemia and the obesity that commonly accompany it are modifiable risk factors, weight loss and treatment of hyperlipidemia are recommended.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transplant coronary disease: nonimmunologic risk factors. 162 91

Because coronary atherosclerosis after heart transplantation has been a limiting problem in long-term survival of adults, we reviewed the coronary angiograms, and autopsy data when available, from 21 of 30 children who underwent orthotopic heart transplantation and survived the perioperative period. Six patients had coronary atherosclerosis, and five of these patients died 6 months to 3 years after heart transplantation. The late deaths were sudden and unexpected. Coronary angiography demonstrated several types of lesions, including concentric narrowing, tubular segmental lesions, and abrupt obliteration of major coronary vessels. Risk factors assessed included hypertension, hyperlipidemia, cytomegalovirus infection, type of immunosuppressive regimen, number of rejection episodes, and major histocompatibility antigen mismatches. Only the frequency and duration of rejection episodes seemed to be more prevalent in the patients in whom coronary atherosclerosis developed. Despite the benefits of heart transplantation in treating children with end-stage heart disease, coronary atherosclerosis may limit long-term survival. We suggest that these children should undergo serial coronary angiography to identify those at risk for subsequent events related to coronary artery disease.
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PMID:Coronary arteriosclerosis in pediatric heart transplant survivors: limitation of long-term survival. 229 87

Allograft coronary artery disease (CAD) is the major determinant of long-term survival following heart transplantation (HTx). In a group of 210 heart transplant recipients, we diagnosed CAD in 54 (27.1%) by coronary angiography, postmortem examination or examination of the transplanted heart at the time of retransplantation. Retrospective analysis of potential risk factors for the development of CAD was performed for both immunological (rejection pattern, immunosuppressive therapy, cytomegalovirus [CMV] infection), and nonimmunological (hyperlipidemia, smoking, hypertension, diabetes mellitus, obesity) risk factors. The total number of rejection episodes correlated significantly with the occurrence of CAD (P less than 0.05), showing that patients who experienced two or more rejection episodes had an incidence of CAD of 40%, as opposed to a 23% incidence in patients who experienced no rejection. A composite rejection score derived from multivariate regression analysis of the severity, frequency, and timing of acute cardiac rejection episodes was found to correlate with the development of CAD (P less than 0.05). Postoperative arterial hypertension also correlated significantly with the onset of CAD (P less than 0.01), with a 92.6% incidence of hypertension in the group with CAD versus 76.3% in the group without CAD. Smoking after transplantation correlated significantly with the occurrence of CAD (P less than 0.05). There was no significant correlation with other analyzed factors in this group of patients. In this review, the development of CAD after heart transplantation correlated with treated allograft rejection. Aggressive treatment of hypertension and cessation of smoking may contribute to alleviation of this serious complication.
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PMID:Risk factors for development of accelerated coronary artery disease in cardiac transplant recipients. 236 Oct 19

The development of post-transplantation coronary graft disease (CGD) is a major cause of late morbidity and mortality. Recent reports have suggested that CGD is a type of chronic vascular rejection, possibly enhanced by cofactors such as concurrent CMV infection and hyperlipidemia. It remains controversial whether established CGD can be improved by modifications in immunosuppressive therapy. The purpose of this study was to examine whether CsA could reverse or halt the progression of CGD after it was already established. Lewis to Fisher (F-344) heterotopic heart allografts develop CGD resembling human disease. Group 1 (n = 29) had no CsA therapy for chronic rat CMV (RCMV) infection in recipients for 8 weeks before transplant. Group 2 (n = 17) had chronic RCMV infection along with CsA therapy from days 15 to 28 post-transplant. Allografts were killed at 2 and 4 weeks and 90 days post-transplantation. In group 1, leukocyte adhesion to arterial endothelium and intimal hyperplasia were well established at 2 weeks and progressed to stenotic, proliferative arterial lesions at 4 weeks. In group 2, CsA therapy was effective in significantly reversing histologic parameters of vascular rejection such as leukocyte adhesion, intimal proliferation, and periarterial edema at 4 weeks. By 90 days, however, arterial pathology was as severe as in group 1. In conclusion, these results support the hypothesis that CGD is a form of chronic vascular rejection, and once established, can be significantly modified by CsA therapy. These effects are not permanent, and progressive CGD recurs after CsA therapy is discontinued.
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PMID:Late cyclosporine treatment ameliorates established coronary graft disease in rat allografts. 821 46

Liver transplantation poses enormous and complex medical problems. Of the infective complications, bacterial infections are the commonest overall, but the single commonest is cytomegalovirus and the most deadly are the fungal infections. Therapeutic options and possibilities for prophylaxis are improving. Rejection, both acute and chronic, is the other major cause of mortality, and the balance between immunosuppression and infection is difficult. Cyclosporin treatment contributes to renal impairment, hypertension, and multitudinous potential neurological problems. The risk of long-term neoplasia is unclear. Relatively more minor is the potential for osteoporosis and metabolic complications, such as diabetes and hyperlipidaemia. Hepatitis B disease has a sizable risk of recurrence, but the most recent prophylaxis regimes have improved relapse rates. Having survived the physical problems following transplantation, most of which occur in the first 6 months, there are considerable psychosocial adjustments to be made particularly in the case of children where growth and development may have been delayed. Despite all these difficulties, liver transplantation is an expanding and optimistic area with enormous potential.
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PMID:Medical complications of liver transplantation. 833 63

A 22-year-old female with diffuse mixed T cell lymphoma in second complete remission underwent allogeneic BMT from her HLA-compatible brother. Transplantation was complicated by acute graft-versus-host disease (GVHD), cytomegalovirus (CMV) infection, and combined hepatotoxic/cholestatic liver disease 45 days post-BMT. Cholesterol levels reached 65 mmol/l, and high density lipoprotein (HDL) cholesterol decreased to 0.23 mmol/l. She developed skin xanthelasmas, lipemia retinalis, and a solitary lung lesion, which was clinically diagnosed as pulmonary cholesteroloma. All these complications resolved following plasmapheresis and hypolipidemic treatment with lovastatin and cholesterol levels normalized.
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PMID:Solitary pulmonary cholesteroloma, multiple xanthelasmas and lipemia retinalis complicating hypercholesterolemia after bone marrow transplantation. 886 64

The incidence of atherosclerosis of the heart transplant in long term survivors is 38% at 5 years. In the present work, myocardial perfusion 201Tl-SPET was assessed as a non-invasive diagnostic method for the detection of postransplant coronary artery disease, as well as its efficiency with regard to other techniques. Twenty patients, aged (47 +/- 9) years old, who underwent heart transplantation at least 3 years earlier, were studied by 201Tl-SPET. Qualitative and quantitative analysis of the images were performed. It was found ischemia in 6 patients, 4 of them asymptomatics. In 5 of the 6 positive cases by SPET coronary stenosis was found by angiography. Kappa coefficient and percent of agreement were k = 0. 76 and Pe = 90%, respectively. There were no relationships among rejection crisis, sepsis by cytomegalovirus and coronary artery disease detected by using 201Tl-SPET (p > 0.05). The most relevant risk factors in the sample were hypertension and hyperlipidemia. Two patients died because of coronary artery disease. It was confirmed by necropsy findings. These results suggest that thallium-201 myocardial perfusion tomography could be useful to detect coronary artery disease in the transplanted heart.
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PMID:[Myocardial perfusion SPET in the detection of coronary artery disease in orthotopic heart transplantation]. 987 29

More than 30 years have passed since the first human heart transplantation was performed. Since then, short-term survival after heart transplantation has been markedly improved, but this development has not been paralleled with a similar improvement in long-term survival. One of the major reasons for this is the subsequent development of heart allograft vascular disease, an obliterative disease in the coronary arteries of the transplanted heart. The dubious effect of re-vascularization in this disease, the less favorable outcome after repeat heart transplantation, and the low donor supply have called for intensified research for new and efficient prophylactic therapies against heart allograft vascular disease. This research has lead to improved knowledge about diagnosis, etiology, pathogenesis, prophylaxis, and treatment possibilities. The most important among these seem to be: (i) the introduction of intravascular ultrasound for early detection of the disease; (ii) evidence to suggest that hyperlipidemia, insufficient immunosuppressive therapy, human leukocyte antigen (HLA)-mismatch, and infection with cytomegalovirus (CMV) all may promote allografts vascular disease; and (iii) the introduction of at least two promising prophylactic therapies in humans namely 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and calcium entry blockers, and others potentially promising e.g. angiotensin-converting enzyme-inhibitors, angiopeptin, mycophenolate mofetil and rapamycin. This review summarizes present knowledge on the possibilities of inhibiting or treating heart allograft vascular disease incorporating evidence from both human and experimental studies.
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PMID:Heart allograft vascular disease: an obliterative vascular disease in transplanted hearts. 1003 Mar 75

On a variety of fronts, chronic infection has been found to be significantly associated with the development of atherosclerosis and the clinical complications of unstable angina, myocardial infarction, and stroke. For the most part, these are still just associations. Specific causative relationships on par with that determined between H. pylori and peptic ulcer disease have not yet been established. Potential mechanisms whereby chronic infections may play a role in atherogenesis are myriad. In the case of C. pneumoniae, the effect may result from direct vessel wall colonization, which may damage the vessel directly or indirectly by initiating immunologic responses. In other cases, the effect may simply be that of enhancing the preexisting chronic inflammatory response of the body to standard risk factors, such as hyperlipidemia. Even though the infectious agent may not directly infect the vessel wall, it may perform its critical role from afar. Chronic infection might also influence preexisting plaque by enhancing T cell activation or other inflammatory responses that may participate in the destabilization of the intimal cap. Chronic infection may play a role in the initiation, progression, or destabilization of atherosclerotic plaques. The infectious agents with the most evidence to support a causative role in atherosclerosis include C. pneumoniae and cytomegalovirus. Evidence is mounting for a variety of other potential agents, including H. pylori, various periodontal agents, and even hepatitis A. Future studies are expected to elucidate further the pathophysiologic relationship between chronic infection and atherosclerosis and to evaluate the potential of a variety of treatment approaches, including antibiotics.
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PMID:Chronic infection and coronary artery disease. 1068 31


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