Percutaneous coronary intervention versus medical therapy for coronary allograft vasculopathy

Aranda, Juan M.; Pauly, Daniel F.; Kerensky, Richard A.; Cleeton, Timothy S.; Walker, Tracy; Schofield, Richard S.; Leach, Dana; Lin, Lang; Monroe, V.Stephen; Calderón, Rafael; Hill, James A.

doi:10.1016/s1053-2498(02)00413-8

Cited by 46 publications

(38 citation statements)

References 16 publications

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“…Aggressive medical therapy may be a reasonable treatment option for TCAD [11]. However, medical therapy for OHT patients with ULMCA disease is probably not an option, as the only clinical manifestation of ULCMA disease may be sudden death.…”

Section: Discussionmentioning

confidence: 99%

Drug‐eluting stenting of unprotected left main coronary artery stenosis in patients with orthotopic heart transplantation: Initial clinical experience

Lee

Chun

Tobis

2008

Cathet Cardio Intervent

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Section: Discussionmentioning

confidence: 99%

Drug‐eluting stenting of unprotected left main coronary artery stenosis in patients with orthotopic heart transplantation: Initial clinical experience

Lee

Chun

Tobis

2008

Cathet Cardio Intervent

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“…Although a variety of pharmacological interventions has been applied, [7][8][9][10][11] their effects are limited and these agents have not achieved popularity. Catheter-based coronary interventions have been reported, 12 but the results are not satisfactory because the coronary lesions are not segmental; they are diffuse. To save a patient's life, cardiac re-transplantation is sometimes performed, but the survival rate is worse than that for first-time transplantation.…”

Section: Risk Factors For and Treatment Of Graft Vasculopathymentioning

confidence: 99%

T Cell Costimulation in the Development of Cardiac Allograft Vasculopathy

Isobe

Kosuge

Suzuki

2006

ATVB

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Abstract-Cardiac allograft vasculopathy (CAV) is a form of coronary arterial stenosis and a leading cause of death in patients who survive beyond the first year after heart transplantation. Histopathologically, this lesion is concentric diffuse intimal hyperplasia of the arterial wall that is accompanied by extensive infiltration of inflammatory cells, including T cells. Many studies have explored the potential risk factors related to this arterial lesion and its pathogenesis. Continuous minor endothelial cell damage evokes inflammatory processes including T cell activation. Costimulatory molecules play crucial roles in this T cell activation. Many costimulatory pathways have been described, and some are involved in the pathogenesis of CAV, atherogenesis, and subsequent plaque formation. In this review, we summarize the present knowledge of the role of these pathways in CAV development and the possibility of manipulating these pathways as a means to treat heart allograft vascular disease and atherosclerosis. Key Words: transplantation Ⅲ rejection Ⅲ T cell-mediated immunity Ⅲ arteriosclerosis Ⅲ atherosclerosis Ⅲ smooth-muscle cell C ardiac transplantation provides long-term survival for patients with end-stage heart disease. The percentage of patients surviving to 1 year after heart transplantation continues to increase; however, the percentage of patients surviving beyond 1 year has not changed significantly over the past 20 years. 1 Long-term functional deterioration of allografts is caused by chronic rejection. The pathologic features of chronic rejection include reduced vessel size and parenchymal fibrosis. Development of cardiac allograft vasculopathy (CAV) has been a major cause of morbidity and mortality following heart transplantation. 1 The mechanism of CAV is not known despite extensive basic and clinical studies; however, inflammation and immunity are known to be associated with the pathogenesis of CAV. CAV lesions contain immune competent cells; among these cells, activated T lymphocytes are the most conspicuous. Therefore, T cell-mediated immunity and subsequent inflammation appear to be an important feature of initiation and progression of CAV. There are similarity and difference among CAV, atherosclerosis, and restenosis after balloon angioplasty as shown in Table 1. The pathophysiology of CAV should be recognized in a spectrum of wide range of arterial lesions. Risk Factors for and Treatment of Graft VasculopathyOne of the major risk factors for CAV is the episodic frequency and severity of acute rejection. Donor-recipient differences in major histocompatibility complexes and ineffective immunosuppression increase the risk. 2,3 Nonimmunologic factors are also known to confer risk. In cases of kidney transplantation, cadaveric donor kidneys are more likely to have stenotic arterial lesions than living-related donor kidneys, suggesting the importance of ischemia/reperfusion injury in the pathophysiology of allograft vasculopathy. 4 Both clinical and experimental studies have indicated that cytomegal...

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“…Recent studies indicate a potential role of systemic inflammation and infectious agents in the development of graft coronary disease [7]. Graft coronary disease is associated with both worse functional status [8] and worse survival [9,10]. Most patients who have undergone cardiac transplantation lack an adequate anginal mechanism, necessitating a regular screening strategy.…”

Section: Opinion Statementmentioning

confidence: 99%

“…In patients with established graft coronary disease, substituting sirolimus for azathioprine or MMF (in combination with corticosteroids and a calcineurin inhibitor) resulted in a significant decrease in disease progression [20]. Coronary angioplasty [9,10], stenting [37], and intracoronary brachytherapy [38] have all been employed with acceptable results in the treatment of graft coronary disease. In addition, standard, off-pump [39], and minimally invasive coronary bypass grafting [40] have been successfully performed in highly selected patients following cardiac transplantation.…”

Section: Atorvastatinmentioning

confidence: 99%

Management of the patient after heart transplant

Mathier

McNamara

2004

Curr Treat Options Cardio Med

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Cardiac transplantation is a highly effective therapy for selected patients with end-stage cardiac disease. The management of the patient after heart transplant involves three main strategies: optimization of immunosuppressive therapy, prevention of complications resulting from the transplant or the immunosuppressive agents, and treatment of those complications when they arise. For most patients, optimal current immunosuppression in the first year after transplantation consists of combination therapy with a calcineurin inhibitor (eg, cyclosporine or tacrolimus), corticosteroids, and an antimetabolite agent (eg, azathioprine or mycophenolate mofetil). Ideally, the corticosteroid is weaned and discontinued 1 to 2 years following transplantation and the patient is managed chronically with a two-drug immunosuppressive regimen. The major complications that occur following cardiac transplantation include infection, hypertension, diabetes, dyslipidemia, osteoporosis, graft coronary disease, renal insufficiency, and malignancy. Preventive efforts focused on infection, osteoporosis, renal insufficiency, and malignancy include minimization of immunosuppression. Once established, treatment of any of the above conditions generally relies on standard pharmacologic therapies; however, an understanding of potential drug interactions is critical. In addition, although standard nonpharmacologic therapies may be used to treat several of these conditions, one must be cognizant of special issues related to the post-transplant state.

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Percutaneous coronary intervention versus medical therapy for coronary allograft vasculopathy

Cited by 46 publications

References 16 publications

Drug‐eluting stenting of unprotected left main coronary artery stenosis in patients with orthotopic heart transplantation: Initial clinical experience

Drug‐eluting stenting of unprotected left main coronary artery stenosis in patients with orthotopic heart transplantation: Initial clinical experience

T Cell Costimulation in the Development of Cardiac Allograft Vasculopathy

Management of the patient after heart transplant

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