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The Diagnosis and Management of Cardiac Allograft Vasculopathy

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The Diagnosis and Management of Cardiac Allograft Vasculopathy Denton A. Cooley's 50th Anniversary New Developments in in Medicine the Diagnosis and Management of Cardiac Allograft Vasculopathy Mandeep R. Mehra, MD The major cause of late death in cardiac transplant recipients is cardiac allograft vascu- Hector 0. Ventura, MD lopathy, also referred to as cardiac transplant atherosclerosis, which occurs in as many Frank W. Smart, MD as 45% of transplant who survive than 1 It differs from Dwight D. Stapleton, MD recipients longer year. typical Tyrone J. Collins, MD atherosclerosis in that intimal hyperplasia is concentric and diffuse, the internal elastic Stephen R. Ramee, MD lamina remains intact, calcification is rare, and the disease tends to develop rapidly. Joseph P. Murgo, MD Intravascular ultrasound and coronary angioscopy are more sensitive diagnostic mea- Christopher J. White, MD sures of cardiac allograft vasculopathy than is coronary angiography. Although re- transplantation at present seems to be the only definitive therapy for cardiac allograft vasculopathy, it has shown only fair results. Recent studies have suggested that cal- cium entry blockers and angiotensin-converting enzyme inhibitors may play a beneficial role in delaying the progression of cardiac allograft vasculopathy. (Tex Heart Inst J 1995; 22:138-44) A dvances in immunosuppression and improved recipient selection have resulted in an increased survival of cardiac allograft recipients, with 1-year survival rates approaching 85%.1-3 Despite this improvement in patient survival, the most common cause of late death is cardiac allograft vascu- lopathy, a unique and unusually accelerated form of coronary artery disease. Early experiments with canine cardiac transplantation in the late 1960s by Kosek and colleagueS4s 1st reported this phenomenon, and its occurrence in human cardiac This series in recognition allografts was subsequently verified by Thomson6 and by Bieber's group. Car- of Dr Cooley's 50th diac allograft vasculopathy is angiographically evident in as many as 45% of heart anniversary in mediclne is continued from the transplant recipients who survive 3 or more years;8 and these patients have a 5- December 1994 and fold greater relative risk of developing other cardiac events, such as myocardial March 1995 issues. infarction, terminal heart failure, and sudden death.8 This report reviews the current concepts in the diagnosis and management of Key words: Angioscopy; cardiac allograft vasculopathy, with specific consideration of the pathologic char- coronary vessels/ultra- acteristics, diagnosis, and treatment of the disease. sonography; graft occlusion, vascular; transplantation, homologous Pathologic Characteristics From: The Ochsner Medical Several histopathologic studies by Billinghamr"" have established the diffuse na- Institutions, Section of ture of cardiac allograft vasculopathy, which affects the major epicardial vessels Internal Medicine, Depart- along their entire length from the base of the heart to the apex and the epicardial ment of Cardiology, New Orleans, Louisiana 70121 and intramyocardial branches. In fact, this disease is not limited to the coronary vasculature, for it has been demonstrated to involve the venous structures" and the great vessels within the cardiac The classic lesion consists Section editors: allograft.'2 allograft Grady L. Hallman, MD of progressive concentric myointimal proliferation that appears as intimal thick- Robert D. Leachman, MD ening and ultimately results in luminal occlusion.'0 John L. Ochsner, MD There are several differences between this condition and the more commonly seen native atherosclerosis (Table I). The latter demonstrates eccentric, focal, and Address for reprints: proximal lesions of major epicardial coronary arteries.9 These lesions contain Hector D. Ventura, MD, calcium, disrupt the internal elastic and over many Con- Ochsner Medical Institutions, lamina, develop years. 1514 Jefferson Highway, versely, cardiac allograft vasculopathy is associated with concentric, diffuse, and New Orleans, LA 70121 distal lesions of the coronary vessels and branches. The internal elastic lamina is 1,38 Cardiac Allograft Vasculopathy Volume 22, Nitinber 2, 1995 TABLE 1. Histopathologic Findings in Cardiac Allograft duration of 2.5 years. Patients underwent an annu- Vasculopathy and Coronary Artery Disease al follow-up examination, including 2-dimensional echocardiography, supine rest and bicycle exercise- Cardiac Allograft gated wall-motion study, 48-hour Holter recording, Factors under Vasculopathy: Coronary Artery Comparison Findings Disease: Findings oral dipyridamole thallium-201 SPECT (single pho- ton emission computed tomographic) imaging, and Localization Diffuse, distal Focal, proximal coronary angiography. In regard to the presence of arrhythmia, ambulatory electrocardiographic moni- Intimal proliferation Concentric Eccentric toring detected significant differences between the Internal elastic lamina Intact Disrupted groups with and without cardiac allograft vascu- lopathy. The sensitivity and specificity of dipyri- Vasculitis Infrequent Never damole thallium-201 SPECT imaging were 21% and Calcium deposit Absent Present 80%, respectively, comparable with a sensitivity and specificity for supine bicycle exercise radionuclide Rate of development Months Years angiography of 21% and 77%, respectively. The in- ability of noninvasive studies to detect differences in myocardial uptake or redistribution may ensue intact, calcification is rare, a low grade of vasculitis from the diffuse nature of the disease. is occasionally present, and the disease tends to de- velop rapidly.9"10 Invasive Diagnosis Histopathologic studies, however, have demon- Coronary Angiography. Both the patient's inabil- strated that more typical focal and complicated ath- ity to experience angina pectoris and the poor pre- erosclerotic plaques may also be present in older dictive value of noninvasive tests have led to the cardiac allografts, indicating that cardiac allograft establishment of annual surveillance angiography as vasculopathy has a spectrum of pathologic features. the primary method used to detect and follow the Thus, it has been demonstrated that early intimal development of cardiac allograft vasculopathy. proliferation progresses after transplantation, as sub- A grading system has been developed by Gao and sequent increases in lipid deposits and calcification associates"' for the standard definition of coronary occur in the coronary vessels.'3 Over time, these lesions on the basis of angiographic appearance. more typical atherosclerotic processes are likely su- Lesions can be classified as Type A, B, or C. Type A perimposed upon the cardiac allograft. lesions are discrete and tubular stenoses of the prox- imal epicardial vessels; Type B lesions are character- Diagnosis ized by diffuse concentric narrowing of the middle or distal coronary vessels and can be subclassified Clinical Symptoms into Type Bi lesions (indicating an abrupt narrow- To rely on the presentation of clinical symptoms for ing) or B2 lesions (indicating smooth concentric ta- the diagnosis of cardiac allograft vasculopathy can pering); Type C lesions are characterized by distal be perilous, since the lack of afferent autonomic in- narrowing and irregularities and by loss of small nervation results in the inability of most allograft branches.'5 In patients with cardiac allograft vascu- recipients to experience angina pectoris. Although lopathy, angiographic Type Bi, B2, and C lesions are partial restoration of the allograft's nerve supply more commonly found, whereas Type A lesions are occurs in up to one third of heart transplant recipi- seen only rarely. Conversely, in patients with typical ents who survive at least 1 year, cardiac allograft coronary atherosclerosis, Type A lesions predomi- vasculopathy rarely presents with angina. Therefore, nate and Type Bi, B2, and C lesions are almost never silent myocardial infarction, heart failure with the seen.'5 Although coronary angiography may have a loss of allograft function, and sudden death are its high specificity in diagnosing cardiac allograft vas- most common forms of presentation.8 culopathy, it has been shown to underestimate the presence of disease and, therefore, has not proved Noninvasive Diagnosis to be a sensitive method. The insensitivity of coro- Noninvasive studies routinely used to diagnose con- nary angiography in diagnosing cardiac allograft ventional coronary artery disease have not been vasculopathy has been demonstrated both by histo- found to be useful in diagnosing cardiac allograft pathologic studiesl6l8 and by comparison with intra- vasculopathy. vascular ultrasound diagnosis.'9 In 1 histopathologic A study by Smart and coworkers'4 assessed the study of 10 failed human allografts, Johnson and use of several noninvasive tests for detecting allo- associates'7 showed the presence of significant inti- graft vasculopathy in 73 cardiac transplant recipients mal hyperplasia in 75% of angiographically normal who were followed prospectively for an average coronary segments. Quantitative coronary angiog- Texas Heart Institutejournal Cardiac Allograft Vasculopathy 139 raphy, performed either manually or by automated video densitometry, may improve the estimation of coronary narrowing. It may, therefore, be a more sensitive method of diagnosing cardiac allograft vas- culopathy.20 Other Coronary Artery Imaging Techniques. Cor- onary angioscopy and intravascular ultrasonog- raphy, 2 novel intracoronary imaging methods, have been used recently in heart
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