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Imaging of Cardiac Transplantation Complications

¹ Department of Radiology (E3/311 CSC), University of Wisconsin Hospital and Clinics, 600 Highland Ave, Madison, WI 53792-3252.

	Abstract

Top Abstract INTRODUCTION POSTOPERATIVE ANATOMY AND NORMAL... COMPLICATIONS DIRECTLY RELATED... COMPLICATIONS OF ENDOMYOCARDIAL... COMPLICATIONS RELATED TO... SUMMARY References Invited Commentary  Introduction References

 
Common complications of cardiac transplantation include infection, rejection, accelerated coronary artery atherosclerosis, and lymphoproliferative disease. The authors reviewed radiographic and computed tomographic (CT) features of cardiac transplantation and its complications in a series of 232 patients (with 89 complications and 49 deaths). Normal postoperative findings in the first few weeks after surgery included enlarged cardiac silhouette, pneumomediastinum, pneumothorax, pneumopericardium, subcutaneous emphysema, and mediastinal widening. Infection was the most common complication, with pneumonia being the leading infectious condition (28 cases, with Aspergillus [n = 11] and cytomegalovirus [n = 10] being the most common pathogens) and the cause of death in seven cases. Although many cases of pulmonary infections occur in the first 3–4 months after surgery, in this series several cases developed up to 3 years afterward. Radiographic signs of acute rejection were nonspecific in the eight patients affected who died, and endomyocardial biopsy was used to confirm the suspected diagnosis. Accelerated atherosclerosis occurred in 13 patients between 10 months and 6.5 years after transplantation and led to death in eight. Lymphoproliferative disorders, which range from benign lymphoid hyperplasia to malignant lymphoma and which are the third leading cause of death beyond the immediate perioperative period in heart transplant recipients, developed in four patients who later died. Other complications related to endomyocardial biopsy and cardiothoracic surgery (ie, pneumothorax, hemothorax, pneumomediastinum, mediastinitis, aortic dissection, aortic pseudoaneurysm, and pulmonary embolism) occurred in 31 cases and were diagnosed with radiography and CT.

Index Terms: Heart, transplantation, 51.458, 51.459 • Surgery, complications, 51.458, 51.459

	INTRODUCTION

Top Abstract INTRODUCTION POSTOPERATIVE ANATOMY AND NORMAL... COMPLICATIONS DIRECTLY RELATED... COMPLICATIONS OF ENDOMYOCARDIAL... COMPLICATIONS RELATED TO... SUMMARY References Invited Commentary  Introduction References

 
Since the first successful cardiac transplantation performed in 1967, over 34,000 such operations have been recorded by the Registry of the International Society for Heart and Lung Transplantation (1). Cardiac transplantation is the currently accepted treatment for end-stage cardiomyopathy and coronary artery disease and has 1- and 5-year survival rates of 79% and 63%, respectively (1). Improvements in immunosuppression techniques and the widespread use of endomyocardial biopsy to diagnose rejection account for most of the improvement in early survival statistics (2). Infection and rejection remain significant causes of morbidity and death despite improvements in immunosuppression techniques (2), with the most common complications of cardiac transplantation being infection, rejection, accelerated coronary artery atherosclerosis, and posttransplantation lymphoproliferative disease (3–5).

In this article, we present the chest radiographic and computed tomographic (CT) appearances of common complications seen in cardiac transplant recipients. We review the postoperative anatomy of the transplanted heart and its normal radiologic appearance and discuss the complications directly related to cardiac transplantation, those related to endomyocardial biopsy, and those related to cardiothoracic surgery.

Our observations are based on a review of the clinical course and imaging studies of 232 patients who underwent orthotopic (n = 231) and heterotopic (n = 1) cardiac transplantation at our institution from November 1989 to November 1996. Among our group of transplant recipients, the mean patient age was 52 years (range, 13–71 years); 189 of the patients were men, and 43 were women. Causes of cardiomyopathy were ischemic (n = 117), idiopathic (n = 97), viral (n = 6), congenital (n = 4), valvular (n = 4), sarcoidosis (n = 1), arrhythmia (n = 1), restrictive (n = 1), and doxorubicin toxicity (n = 1). Forty-nine deaths occurred related to 89 complications. The deaths were related to severe acute rejection (n = 8), accelerated atherosclerosis (n = 8), sepsis (n = 3), multisystem organ failure (n = 3), bleeding (n = 3), malignancy (n = 3), disseminated Aspergillus infection (n = 2), failure to wean from cardiopulmonary bypass (n = 2), and nonspecific graft failure (n = 2). In 15 cases, cause of death was unknown.

	POSTOPERATIVE ANATOMY AND NORMAL POSTOPERATIVE APPEARANCE OF TRANSPLANTED HEARTS

Top Abstract INTRODUCTION POSTOPERATIVE ANATOMY AND NORMAL... COMPLICATIONS DIRECTLY RELATED... COMPLICATIONS OF ENDOMYOCARDIAL... COMPLICATIONS RELATED TO... SUMMARY References Invited Commentary  Introduction References

 
Orthotopic Cardiac Transplant
In orthotopic cardiac transplantation, the recipient's heart is removed through a median sternotomy, and a cuff of both native atria and severed ends of the ascending aorta and main pulmonary artery is retained (Fig 1). The donor heart is joined to the recipient's atria, aorta, and pulmonary artery. The donor superior vena cava stump is tied just above the right atrium, and the donor inferior vena cava is incorporated into the right atrial anastomosis.

View larger version (75K): [in this window] [in a new window] [Download PPT slide]   Figure 1a.  Orthotopic cardiac transplantation. (a) Diagram shows intraoperative appearance of native and donor hearts before surgical connection of the atria, pulmonary artery, and aorta. (b) Illustration shows the four anastomoses in the completed orthotopic cardiac transplantation. AO = aorta, LA = left atrium, LV = left ventricle, PA = pulmonary artery, RA = right atrium, RV = right ventricle, SVC = superior vena cava.

View larger version (115K): [in this window] [in a new window] [Download PPT slide]   Figure 1b.  Orthotopic cardiac transplantation. (a) Diagram shows intraoperative appearance of native and donor hearts before surgical connection of the atria, pulmonary artery, and aorta. (b) Illustration shows the four anastomoses in the completed orthotopic cardiac transplantation. AO = aorta, LA = left atrium, LV = left ventricle, PA = pulmonary artery, RA = right atrium, RV = right ventricle, SVC = superior vena cava.

View larger version (137K): [in this window] [in a new window] [Download PPT slide]   Figure 2.  Orthotopic cardiac transplantation in a 64-year-old woman with ischemic cardiomyopathy. AP recumbent chest radiograph obtained immediately after transplantation shows an enlarged cardiac silhouette, pulmonary edema, and bibasilar atelectasis. Bilateral thoracostomy tubes, endotracheal tube, esophageal temperature probe, left subclavian venous catheter, pulmonary artery catheter, and sternal wires are also seen.

View larger version (91K): [in this window] [in a new window] [Download PPT slide]   Figure 3a.  Mediastinal lipomatosis in a 61-year-old man who underwent orthotopic cardiac transplantation for ischemic cardiomyopathy 3 years before. (a) AP upright chest radiograph shows a wide mediastinum, an appearance consistent with mediastinal adenopathy or mediastinal lipomatosis. (b) Nonenhanced chest CT scan shows a superior redundant main pulmonary artery (arrowhead), a large space (large arrow) between the recipient superior vena cava and donor ascending aorta, and aortic anastomosis suture lines (small arrows) and helps confirm that mediastinal lipomatosis accounts for the wide mediastinum. (c) CT scan obtained inferior to b shows pulmonic anastomosis suture lines (arrows).

View larger version (115K): [in this window] [in a new window] [Download PPT slide]   Figure 3b.  Mediastinal lipomatosis in a 61-year-old man who underwent orthotopic cardiac transplantation for ischemic cardiomyopathy 3 years before. (a) AP upright chest radiograph shows a wide mediastinum, an appearance consistent with mediastinal adenopathy or mediastinal lipomatosis. (b) Nonenhanced chest CT scan shows a superior redundant main pulmonary artery (arrowhead), a large space (large arrow) between the recipient superior vena cava and donor ascending aorta, and aortic anastomosis suture lines (small arrows) and helps confirm that mediastinal lipomatosis accounts for the wide mediastinum. (c) CT scan obtained inferior to b shows pulmonic anastomosis suture lines (arrows).

View larger version (109K): [in this window] [in a new window] [Download PPT slide]   Figure 3c.  Mediastinal lipomatosis in a 61-year-old man who underwent orthotopic cardiac transplantation for ischemic cardiomyopathy 3 years before. (a) AP upright chest radiograph shows a wide mediastinum, an appearance consistent with mediastinal adenopathy or mediastinal lipomatosis. (b) Nonenhanced chest CT scan shows a superior redundant main pulmonary artery (arrowhead), a large space (large arrow) between the recipient superior vena cava and donor ascending aorta, and aortic anastomosis suture lines (small arrows) and helps confirm that mediastinal lipomatosis accounts for the wide mediastinum. (c) CT scan obtained inferior to b shows pulmonic anastomosis suture lines (arrows).

View larger version (96K): [in this window] [in a new window] [Download PPT slide]   Figure 4a.  Anastomotic connections in a 45-year-old man who underwent orthotopic cardiac transplantation for idiopathic cardiomyopathy. (a, b) Sequential contrast material–enhanced CT scans reveal change in caliber from the recipient to donor ascending aorta (arrow). (c) CT scan obtained inferior to b shows remnant donor superior vena cava (large arrow) posterior to the donor ascending aorta (arrowhead) and medial to the recipient superior vena cava (small arrow).

View larger version (104K): [in this window] [in a new window] [Download PPT slide]   Figure 4b.  Anastomotic connections in a 45-year-old man who underwent orthotopic cardiac transplantation for idiopathic cardiomyopathy. (a, b) Sequential contrast material–enhanced CT scans reveal change in caliber from the recipient to donor ascending aorta (arrow). (c) CT scan obtained inferior to b shows remnant donor superior vena cava (large arrow) posterior to the donor ascending aorta (arrowhead) and medial to the recipient superior vena cava (small arrow).

View larger version (120K): [in this window] [in a new window] [Download PPT slide]   Figure 4c.  Anastomotic connections in a 45-year-old man who underwent orthotopic cardiac transplantation for idiopathic cardiomyopathy. (a, b) Sequential contrast material–enhanced CT scans reveal change in caliber from the recipient to donor ascending aorta (arrow). (c) CT scan obtained inferior to b shows remnant donor superior vena cava (large arrow) posterior to the donor ascending aorta (arrowhead) and medial to the recipient superior vena cava (small arrow).

View larger version (105K): [in this window] [in a new window] [Download PPT slide]   Figure 5.  Heterotopic cardiac transplantation. Illustration shows the anastomoses and the relationship of the donor heart to the recipient heart. AO = aorta, LV = left ventricle, PA = pulmonary artery, RA = right atrium, RV = right ventricle, SVC = superior vena cava.

View larger version (118K): [in this window] [in a new window] [Download PPT slide]   Figure 6.  Heterotopic cardiac transplantation in a 55-year-old man with ischemic cardiomyopathy for whom orthotopic cardiac transplantation was precluded because of severe pulmonary hypertension. PA upright chest radiograph obtained 6 years after transplantation shows an enlarged cardiac silhouette, with the donor heart in the right hemothorax, lateral to the patient's native heart. Radiosynthetic patch encircles the aortic anastomosis (arrows).

	COMPLICATIONS DIRECTLY RELATED TO CARDIAC TRANSPLANTATION

Top Abstract INTRODUCTION POSTOPERATIVE ANATOMY AND NORMAL... COMPLICATIONS DIRECTLY RELATED... COMPLICATIONS OF ENDOMYOCARDIAL... COMPLICATIONS RELATED TO... SUMMARY References Invited Commentary  Introduction References

Most pulmonary infections occur within the first 3–4 months following heart transplantation, with most fatal infections developing during this period (15). About 20%–25% of infection-related deaths are caused by multiple pathogens (15). Empyema and mediastinitis, in addition to pneumonia, are often associated with an unfavorable outcome (17).

Reported frequency of and death from Aspergillus pneumonia in cardiac transplant recipients ranges from 11% to 16% (9,10) and 54% to 86% (2,18), respectively. In our group, 11 cases of Aspergillus pneumonia occurred between 11 days and 17 months after transplantation (mean, 6 months) (Fig 7), and this infection was related to the cause of death in six patients (Fig 8). Four patients died of pneumonia, and two developed disseminated Aspergillus infection and eventually died: In one patient, infection spread to the skin, kidney, and adrenal gland, and in the other patient, infection spread to the brain.

View larger version (144K): [in this window] [in a new window] [Download PPT slide]   Figure 7a. Figures 7, 8. (7) Pulmonary A fumigatus infection in a 40-year-old man who developed dyspnea 10 months after cardiac transplantation for idiopathic cardiomyopathy. (a) PA upright chest radiograph shows numerous ill-defined nodular opacities in the right lung. (b) CT scan reveals multiple, fuzzy nodules in the right lung, consistent with pulmonary Aspergillus infection. Diagnosis was confirmed with bronchoalveolar lavage, and the patient recovered after a course of amphotericin. (8) Aspergillus pneumonia in a 60-year-old man who developed productive cough and dyspnea 8 months after cardiac transplantation for idiopathic cardiomyopathy. (a) PA upright chest radiograph shows a cavitary mass (arrows) in the right lower lobe and diffuse interstitial lung disease. (b) Thin-section CT scan shows the cavitary mass with a ground-glass "halo" (arrows) representing hemorrhage, a finding consistent with invasive Aspergillus infection. Basilar honeycombing is consistent with idiopathic pulmonary fibrosis.

View larger version (108K): [in this window] [in a new window] [Download PPT slide]   Figure 7b. Figures 7, 8. (7) Pulmonary A fumigatus infection in a 40-year-old man who developed dyspnea 10 months after cardiac transplantation for idiopathic cardiomyopathy. (a) PA upright chest radiograph shows numerous ill-defined nodular opacities in the right lung. (b) CT scan reveals multiple, fuzzy nodules in the right lung, consistent with pulmonary Aspergillus infection. Diagnosis was confirmed with bronchoalveolar lavage, and the patient recovered after a course of amphotericin. (8) Aspergillus pneumonia in a 60-year-old man who developed productive cough and dyspnea 8 months after cardiac transplantation for idiopathic cardiomyopathy. (a) PA upright chest radiograph shows a cavitary mass (arrows) in the right lower lobe and diffuse interstitial lung disease. (b) Thin-section CT scan shows the cavitary mass with a ground-glass "halo" (arrows) representing hemorrhage, a finding consistent with invasive Aspergillus infection. Basilar honeycombing is consistent with idiopathic pulmonary fibrosis.

View larger version (135K): [in this window] [in a new window] [Download PPT slide]   Figure 8a. Figures 7, 8. (7) Pulmonary A fumigatus infection in a 40-year-old man who developed dyspnea 10 months after cardiac transplantation for idiopathic cardiomyopathy. (a) PA upright chest radiograph shows numerous ill-defined nodular opacities in the right lung. (b) CT scan reveals multiple, fuzzy nodules in the right lung, consistent with pulmonary Aspergillus infection. Diagnosis was confirmed with bronchoalveolar lavage, and the patient recovered after a course of amphotericin. (8) Aspergillus pneumonia in a 60-year-old man who developed productive cough and dyspnea 8 months after cardiac transplantation for idiopathic cardiomyopathy. (a) PA upright chest radiograph shows a cavitary mass (arrows) in the right lower lobe and diffuse interstitial lung disease. (b) Thin-section CT scan shows the cavitary mass with a ground-glass "halo" (arrows) representing hemorrhage, a finding consistent with invasive Aspergillus infection. Basilar honeycombing is consistent with idiopathic pulmonary fibrosis.

View larger version (115K): [in this window] [in a new window] [Download PPT slide]   Figure 8b. Figures 7, 8. (7) Pulmonary A fumigatus infection in a 40-year-old man who developed dyspnea 10 months after cardiac transplantation for idiopathic cardiomyopathy. (a) PA upright chest radiograph shows numerous ill-defined nodular opacities in the right lung. (b) CT scan reveals multiple, fuzzy nodules in the right lung, consistent with pulmonary Aspergillus infection. Diagnosis was confirmed with bronchoalveolar lavage, and the patient recovered after a course of amphotericin. (8) Aspergillus pneumonia in a 60-year-old man who developed productive cough and dyspnea 8 months after cardiac transplantation for idiopathic cardiomyopathy. (a) PA upright chest radiograph shows a cavitary mass (arrows) in the right lower lobe and diffuse interstitial lung disease. (b) Thin-section CT scan shows the cavitary mass with a ground-glass "halo" (arrows) representing hemorrhage, a finding consistent with invasive Aspergillus infection. Basilar honeycombing is consistent with idiopathic pulmonary fibrosis.

View larger version (102K): [in this window] [in a new window] [Download PPT slide]   Figure 9.  Fungal pneumonia in a 46-year-old woman who developed pleuritic right-sided chest pain 3 months after cardiac transplantation for ischemic cardiomyopathy. Thin-section CT scan shows multiple 1–3-mm subpleural nodules (small arrows) and a nodule in the medial right lower lobe (large arrow), compatible with systemic spread of a rare fungal (Exophiala) infection of her toe that responded to multidrug antifungal therapy.

View larger version (112K): [in this window] [in a new window] [Download PPT slide]   Figure 10.  CMV pneumonia in a 57-year-old woman who developed fever and shortness of breath 10 weeks after cardiac transplantation for restrictive cardiomyopathy. Contrast-enhanced CT scan reveals a consolidated right lower lobe with air bronchograms and a small right pleural effusion. Transbronchial biopsy specimens from the right lung showed large CMV intracytoplasmic inclusion bodies.

View larger version (106K): [in this window] [in a new window] [Download PPT slide]   Figure 11.  Haemophilus influenzae pneumonia in a 60-year-old man who presented with productive cough, fever, and chills 8 weeks after cardiac transplantation. Nonenhanced CT scan shows bilateral pleural effusions and left lower lobe consolidation. Sputum cultures were positive for H influenzae, and the patient responded to intravenous treatment with antibiotics.

View larger version (114K): [in this window] [in a new window] [Download PPT slide]   Figure 12.  Pulmonary abscess in a 44-year-old man who developed increasing shortness of breath and fatigue after cardiac transplantation for familial cardiomyopathy. Nonenhanced CT scan shows a 3.5-cm mass in the right upper lobe with a central area of low attenuation consistent with necrosis and surrounding air-space disease. The patient developed gram-negative sepsis leading to multisystem organ failure and died 8 days later.

Acute Allograft Rejection
Acute rejection is defined histologically as lymphocytic infiltration of the myocardium with myocyte necrosis and usually occurs between 2 weeks and 3 months after transplantation (3). According to the Cardiac Transplant Research Database, rejection risk is highest in the first postoperative months and decreases dramatically within 6 months of transplantation (20). Death from acute rejection occurs in approximately 3% of patients at 18 months after transplantation (20).

Patients experiencing acute rejection present clinically with dyspnea, lethargy, weakness, hypotension, or heart failure. Cardiomegaly may be demonstrated on chest radiographs; however, this sign is neither specific nor sensitive for rejection (Fig 13).

View larger version (105K): [in this window] [in a new window] [Download PPT slide]   Figure 13a.  Acute allograft rejection in a 62-year-old man who developed hypotension and congestive heart failure 10 weeks after cardiac transplantation for dilated cardiomyopathy. (a) AP upright chest radiograph shows an enlarged cardiac silhouette, pulmonary edema, and bilateral pleural effusions. The postoperative image also reveals sternal wires, endotracheal tube, nasogastric tube, right subclavian venous catheter, and pulmonary artery catheter in the distal right lower lobe interlobar pulmonary artery. (b) High-power photomicrograph (original magnification, x400; hematoxylin-eosin stain) shows diffuse lymphocytic infiltration of the myocardium with patchy myocyte necrosis.

View larger version (159K): [in this window] [in a new window] [Download PPT slide]   Figure 13b.  Acute allograft rejection in a 62-year-old man who developed hypotension and congestive heart failure 10 weeks after cardiac transplantation for dilated cardiomyopathy. (a) AP upright chest radiograph shows an enlarged cardiac silhouette, pulmonary edema, and bilateral pleural effusions. The postoperative image also reveals sternal wires, endotracheal tube, nasogastric tube, right subclavian venous catheter, and pulmonary artery catheter in the distal right lower lobe interlobar pulmonary artery. (b) High-power photomicrograph (original magnification, x400; hematoxylin-eosin stain) shows diffuse lymphocytic infiltration of the myocardium with patchy myocyte necrosis.

In our group, eight patients developed severe acute rejection and were treated with high doses of steroids and with monoclonal antibody OKT3, but all eight died. OKT3 is an anti–T-lymphocyte antibody used in the treatment of acute cardiac allograft rejection. These rejection episodes developed from 1 day to 9 months (mean, 2.6 months) following transplantation.

Accelerated Graft Atherosclerosis
Accelerated graft atherosclerosis is defined histologically as concentric intimal proliferation composed of modified smooth muscle cells, macrophages, and lymphocytes (23). Progressive intimal thickening diffusely obliterates coronary artery lumens, causing ischemic allograft failure. Angiographic evidence of accelerated coronary artery atherosclerosis is seen in up to 50% of transplant recipients by 5 years after transplantation (24). Approximately 40% of deaths and cases of retransplantation are related to accelerated graft atherosclerosis (24). In our group, accelerated atherosclerosis occurred in 13 of 232 patients, between 10 months and 6.5 years after transplantation (mean, 2.25 years).

Coronary angiography and intracoronary ultrasonography are methods currently used to detect accelerated coronary artery atherosclerosis (25). Recent studies indicate that coronary artery calcification is a marker of active atherosclerotic plaque development (26). Early work with noninvasive ultrafast CT showed good correlation between coronary artery calcification seen on CT scans and angiograms, and the quantity of calcifications on CT scans was a good predictor of subsequent cardiac events (27).

Malignancy
The prevalence of malignancy after transplantation is estimated to be 4% or 100 times greater than that for the general population (28). The most frequently observed tumors are squamous cell carcinoma of the skin, adenocarcinomas of the lung and gastrointestinal tract, Kaposi sarcoma, acute leukemia, and lymphoma (29). The increased prevalence of malignancy is thought to be related to the use of cytotoxic agents for immunosuppression.

Posttransplantation lymphoproliferative disorder occurs in 2%–6% of cardiac transplant recipients (30). Most lymphoproliferative disorders are of B-cell origin and are associated with Epstein-Barr virus infection (31). The third leading cause of death beyond the immediate perioperative period in heart transplant recipients is lymphoproliferative disorders, which range from benign lymphoid hyperplasia to malignant lymphoma (5). Pulmonary manifestations of posttransplantation lymphoproliferative disorder include a solitary mass, multiple noncavitating nodules, and mediastinal or hilar adenopathy (32,33).

In our group, two patients developed posttransplantation lymphoproliferative disorder at 8 and 9 months after the surgery (Fig 14). Reduction of immunosuppression was the treatment for both patients; however, both died 2 and 10 months later of an unknown cause and an arrhythmia, respectively. Two patients developed lymphoma at 11 and 12 months (Fig 15). Both died shortly after diagnosis, related to gram-negative sepsis and rectus sheath hemorrhage, respectively. One patient developed biopsy-proved Kaposi sarcoma of the lower extremity, which was diagnosed shortly before the patient died of sepsis. One patient developed squamous cell carcinoma at her tracheostomy site 4 years after transplantation; the cancer was treated with surgical resection. One patient died as a result of metastatic adenocarcinoma of the lung 3 months after cardiac transplantation (Fig 16). A recent report showed a high prevalence of bronchogenic carcinoma in cardiac transplant recipients (34). An earlier report described sporadic cases of carcinoma of the lung, breast, and colon in these patients (35).

View larger version (124K): [in this window] [in a new window] [Download PPT slide]   Figure 14a.  Lymphoproliferative disorder in a 65-year-old man who presented without symptoms after cardiac transplantation for ischemic cardiomyopathy. (a) PA upright chest radiograph reveals a lingular mass and small left pleural nodular opacity (arrow). (b) Nonenhanced CT scan reveals a left pleural-based nodule. (The patient's allergy to contrast material prevented its use.) (c) CT scan obtained inferior to b reveals a mass abutting the left atrium (arrow). (d) T1-weighted magnetic resonance image shows frank invasion of the mass into the left atrium. Findings from open lung endomyocardial biopsy were consistent with lymphoproliferative disorder. The patient died 7 months later of an arrhythmia.

View larger version (120K): [in this window] [in a new window] [Download PPT slide]   Figure 14b.  Lymphoproliferative disorder in a 65-year-old man who presented without symptoms after cardiac transplantation for ischemic cardiomyopathy. (a) PA upright chest radiograph reveals a lingular mass and small left pleural nodular opacity (arrow). (b) Nonenhanced CT scan reveals a left pleural-based nodule. (The patient's allergy to contrast material prevented its use.) (c) CT scan obtained inferior to b reveals a mass abutting the left atrium (arrow). (d) T1-weighted magnetic resonance image shows frank invasion of the mass into the left atrium. Findings from open lung endomyocardial biopsy were consistent with lymphoproliferative disorder. The patient died 7 months later of an arrhythmia.

View larger version (115K): [in this window] [in a new window] [Download PPT slide]   Figure 14c.  Lymphoproliferative disorder in a 65-year-old man who presented without symptoms after cardiac transplantation for ischemic cardiomyopathy. (a) PA upright chest radiograph reveals a lingular mass and small left pleural nodular opacity (arrow). (b) Nonenhanced CT scan reveals a left pleural-based nodule. (The patient's allergy to contrast material prevented its use.) (c) CT scan obtained inferior to b reveals a mass abutting the left atrium (arrow). (d) T1-weighted magnetic resonance image shows frank invasion of the mass into the left atrium. Findings from open lung endomyocardial biopsy were consistent with lymphoproliferative disorder. The patient died 7 months later of an arrhythmia.

View larger version (143K): [in this window] [in a new window] [Download PPT slide]   Figure 14d.  Lymphoproliferative disorder in a 65-year-old man who presented without symptoms after cardiac transplantation for ischemic cardiomyopathy. (a) PA upright chest radiograph reveals a lingular mass and small left pleural nodular opacity (arrow). (b) Nonenhanced CT scan reveals a left pleural-based nodule. (The patient's allergy to contrast material prevented its use.) (c) CT scan obtained inferior to b reveals a mass abutting the left atrium (arrow). (d) T1-weighted magnetic resonance image shows frank invasion of the mass into the left atrium. Findings from open lung endomyocardial biopsy were consistent with lymphoproliferative disorder. The patient died 7 months later of an arrhythmia.

View larger version (104K): [in this window] [in a new window] [Download PPT slide]   Figure 15a.  Lymphoma in a 64-year-old man who developed shortness of breath 13 months after cardiac transplantation. (a) PA chest radiograph shows a right paratracheal mass (arrow) and right pleural effusion. (b) Contrast-enhanced CT scan shows the large anterior mediastinal mass lateral to and abutting the aortic arch, causing extrinsic compression on the superior vena cava and left brachiocephalic vein. Analysis of right thoracentesis fluid revealed findings consistent with monoclonal large cell lymphoma. The patient developed sepsis and died 3 weeks later of a major retroperitoneal hemorrhage while receiving heparin for pulmonary embolus.

View larger version (105K): [in this window] [in a new window] [Download PPT slide]   Figure 15b.  Lymphoma in a 64-year-old man who developed shortness of breath 13 months after cardiac transplantation. (a) PA chest radiograph shows a right paratracheal mass (arrow) and right pleural effusion. (b) Contrast-enhanced CT scan shows the large anterior mediastinal mass lateral to and abutting the aortic arch, causing extrinsic compression on the superior vena cava and left brachiocephalic vein. Analysis of right thoracentesis fluid revealed findings consistent with monoclonal large cell lymphoma. The patient developed sepsis and died 3 weeks later of a major retroperitoneal hemorrhage while receiving heparin for pulmonary embolus.

View larger version (110K): [in this window] [in a new window] [Download PPT slide]   Figure 16a.  Bronchogenic carcinoma in a 65-year-old man who developed shortness of breath 3 months after cardiac transplantation for ischemic cardiomyopathy. (a) PA upright chest radiograph shows recurrent right pleural effusion, a left upper lobe mass (arrow), and peripheral interstitial disease. (b) CT scan shows air bronchograms within the left upper lobe mass, as well as low-attenuation areas throughout the lung parenchyma consistent with emphysema and superimposed interstitial disease consistent with amiodarone toxicity. Findings from transbronchial biopsy were consistent with bronchogenic carcinoma. The patient died of cardiopulmonary arrest related to metastatic bronchogenic carcinoma 1 week later.

View larger version (131K): [in this window] [in a new window] [Download PPT slide]   Figure 16b.  Bronchogenic carcinoma in a 65-year-old man who developed shortness of breath 3 months after cardiac transplantation for ischemic cardiomyopathy. (a) PA upright chest radiograph shows recurrent right pleural effusion, a left upper lobe mass (arrow), and peripheral interstitial disease. (b) CT scan shows air bronchograms within the left upper lobe mass, as well as low-attenuation areas throughout the lung parenchyma consistent with emphysema and superimposed interstitial disease consistent with amiodarone toxicity. Findings from transbronchial biopsy were consistent with bronchogenic carcinoma. The patient died of cardiopulmonary arrest related to metastatic bronchogenic carcinoma 1 week later.

	COMPLICATIONS OF ENDOMYOCARDIAL BIOPSY

Top Abstract INTRODUCTION POSTOPERATIVE ANATOMY AND NORMAL... COMPLICATIONS DIRECTLY RELATED... COMPLICATIONS OF ENDOMYOCARDIAL... COMPLICATIONS RELATED TO... SUMMARY References Invited Commentary  Introduction References

In our group, two patients developed pneumothorax (one in the left lung, one in the right) following endomyocardial biopsy that resolved with chest tube placement (Fig 17). Of the two patients who developed hemothorax (one in the left lung, one in the right), one suffered cardiovascular collapse and died; the second required no intervention (Fig 18).

View larger version (118K): [in this window] [in a new window] [Download PPT slide]   Figure 17.  Pneumothorax following endomyocardial biopsy in a 57-year-old man who developed shortness of breath after the biopsy 6 months after cardiac transplantation. AP upright chest radiograph reveals a large right pneumothorax. The patient recovered following chest tube placement and returned home 6 days later.

View larger version (106K): [in this window] [in a new window] [Download PPT slide]   Figure 18.  Hemothorax following endomyocardial biopsy in a 59-year-old man who developed mild shortness of breath after the biopsy. Nonenhanced CT scan shows a high-attenuation left pleural effusion consistent with hemothorax (arrow). The patient recovered without intervention.

	COMPLICATIONS RELATED TO CARDIOTHORACIC SURGERY

Top Abstract INTRODUCTION POSTOPERATIVE ANATOMY AND NORMAL... COMPLICATIONS DIRECTLY RELATED... COMPLICATIONS OF ENDOMYOCARDIAL... COMPLICATIONS RELATED TO... SUMMARY References Invited Commentary  Introduction References

At radiography, acute mediastinitis appears as mediastinal widening, pneumomediastinum, obliteration of fat planes, localized fluid collections, and abscess formation. Patients with mediastinitis are often very ill, presenting with fever, chills, tachycardia, chest pain, and elevated white blood cell counts. Sternal infection is frequently associated with deeper mediastinal infection, and sternal dehiscence is frequently associated with osteomyelitis of the sternum (11).

In our group, noninfectious and infectious events involving the chest wall accounted for 10 of 89 complications. Two patients developed sternal dehiscence, one 10 days and the other 17 months after transplantation (Fig 19). The latter patient received a direct blow to the chest from a truck door. Both patients survived the acute episode, with the first patient requiring sternal débridement and muscle flap reconstruction for bacterial wound infection and pleuromediastinosternal cutaneous fistula (Fig 20).

View larger version (79K): [in this window] [in a new window] [Download PPT slide]   Figure 19a.  Sternal dehiscence in a 52-year-old man who sustained blunt chest trauma 17 months after cardiac transplantation. (a) CT scan shows distraction of sternal fragments. (b) CT scan obtained inferior to a shows anterior fluid collection consistent with resolving hematoma.

View larger version (109K): [in this window] [in a new window] [Download PPT slide]   Figure 19b.  Sternal dehiscence in a 52-year-old man who sustained blunt chest trauma 17 months after cardiac transplantation. (a) CT scan shows distraction of sternal fragments. (b) CT scan obtained inferior to a shows anterior fluid collection consistent with resolving hematoma.

View larger version (117K): [in this window] [in a new window] [Download PPT slide]   Figure 20a.  Pleuromediastinal cutaneous fistula in a 51-year-old man who developed coagulase-negative staphylococcal sternal wound infection 10 days after cardiac transplantation. (a) CT scan shows subcutaneous emphysema in the left chest wall. (b) Nonenhanced CT scan obtained inferior to a shows air in the sternal dehiscence and in infiltrated anterior mediastinal fat, findings consistent with infection. (c) CT scan obtained inferior to b shows more extensive pneumomediastinum and a right pneumothorax.

View larger version (105K): [in this window] [in a new window] [Download PPT slide]   Figure 20b.  Pleuromediastinal cutaneous fistula in a 51-year-old man who developed coagulase-negative staphylococcal sternal wound infection 10 days after cardiac transplantation. (a) CT scan shows subcutaneous emphysema in the left chest wall. (b) Nonenhanced CT scan obtained inferior to a shows air in the sternal dehiscence and in infiltrated anterior mediastinal fat, findings consistent with infection. (c) CT scan obtained inferior to b shows more extensive pneumomediastinum and a right pneumothorax.

View larger version (123K): [in this window] [in a new window] [Download PPT slide]   Figure 20c.  Pleuromediastinal cutaneous fistula in a 51-year-old man who developed coagulase-negative staphylococcal sternal wound infection 10 days after cardiac transplantation. (a) CT scan shows subcutaneous emphysema in the left chest wall. (b) Nonenhanced CT scan obtained inferior to a shows air in the sternal dehiscence and in infiltrated anterior mediastinal fat, findings consistent with infection. (c) CT scan obtained inferior to b shows more extensive pneumomediastinum and a right pneumothorax.

View larger version (119K): [in this window] [in a new window] [Download PPT slide]   Figure 21a. Figures 21, 22. (21) Mediastinal abscess in a 62-year-old man who developed a substernal fluid collection 6 weeks after cardiac transplantation. (a) Lateral chest radiograph reveals retrosternal air bubbles (arrows) and a moderate left pleural effusion. (b) Contrast-enhanced CT scan shows the anterior mediastinal loculated fluid collection with air pockets. Specimen obtained from CT-guided drainage revealed gram-positive cocci, and the patient responded to antibiotic therapy and drainage. (22) Mediastinal abscess in a 55-year-old man who developed a candidal incisional infection requiring rectus abdominis muscle flap reconstruction, recurrent débridements, and antifungal therapy. (a) Nonenhanced CT scan reveals a small retrosternal fluid collection with air bubbles (arrow) and left pleural effusion. (b) Nonenhanced CT scan obtained 6 months later shows anterior rectus abdominis muscle flap (arrow), sternal dehiscence, and residual retrosternal fluid.

View larger version (101K): [in this window] [in a new window] [Download PPT slide]   Figure 21b. Figures 21, 22. (21) Mediastinal abscess in a 62-year-old man who developed a substernal fluid collection 6 weeks after cardiac transplantation. (a) Lateral chest radiograph reveals retrosternal air bubbles (arrows) and a moderate left pleural effusion. (b) Contrast-enhanced CT scan shows the anterior mediastinal loculated fluid collection with air pockets. Specimen obtained from CT-guided drainage revealed gram-positive cocci, and the patient responded to antibiotic therapy and drainage. (22) Mediastinal abscess in a 55-year-old man who developed a candidal incisional infection requiring rectus abdominis muscle flap reconstruction, recurrent débridements, and antifungal therapy. (a) Nonenhanced CT scan reveals a small retrosternal fluid collection with air bubbles (arrow) and left pleural effusion. (b) Nonenhanced CT scan obtained 6 months later shows anterior rectus abdominis muscle flap (arrow), sternal dehiscence, and residual retrosternal fluid.

View larger version (93K): [in this window] [in a new window] [Download PPT slide]   Figure 22a. Figures 21, 22. (21) Mediastinal abscess in a 62-year-old man who developed a substernal fluid collection 6 weeks after cardiac transplantation. (a) Lateral chest radiograph reveals retrosternal air bubbles (arrows) and a moderate left pleural effusion. (b) Contrast-enhanced CT scan shows the anterior mediastinal loculated fluid collection with air pockets. Specimen obtained from CT-guided drainage revealed gram-positive cocci, and the patient responded to antibiotic therapy and drainage. (22) Mediastinal abscess in a 55-year-old man who developed a candidal incisional infection requiring rectus abdominis muscle flap reconstruction, recurrent débridements, and antifungal therapy. (a) Nonenhanced CT scan reveals a small retrosternal fluid collection with air bubbles (arrow) and left pleural effusion. (b) Nonenhanced CT scan obtained 6 months later shows anterior rectus abdominis muscle flap (arrow), sternal dehiscence, and residual retrosternal fluid.

View larger version (89K): [in this window] [in a new window] [Download PPT slide]   Figure 22b. Figures 21, 22. (21) Mediastinal abscess in a 62-year-old man who developed a substernal fluid collection 6 weeks after cardiac transplantation. (a) Lateral chest radiograph reveals retrosternal air bubbles (arrows) and a moderate left pleural effusion. (b) Contrast-enhanced CT scan shows the anterior mediastinal loculated fluid collection with air pockets. Specimen obtained from CT-guided drainage revealed gram-positive cocci, and the patient responded to antibiotic therapy and drainage. (22) Mediastinal abscess in a 55-year-old man who developed a candidal incisional infection requiring rectus abdominis muscle flap reconstruction, recurrent débridements, and antifungal therapy. (a) Nonenhanced CT scan reveals a small retrosternal fluid collection with air bubbles (arrow) and left pleural effusion. (b) Nonenhanced CT scan obtained 6 months later shows anterior rectus abdominis muscle flap (arrow), sternal dehiscence, and residual retrosternal fluid.

View larger version (115K): [in this window] [in a new window] [Download PPT slide]   Figure 23a.  Pneumomediastinum in a 63-year-old man who developed extensive subcutaneous emphysema 4 days after cardiac transplantation. (a) AP upright chest radiograph shows right anterior pneumomediastinum (arrows) and left subcutaneous emphysema. (b) CT scan shows anterior mediastinal and bilateral subcutaneous air collections. The patient underwent mediastinal chest tube placement and recovered.

View larger version (133K): [in this window] [in a new window] [Download PPT slide]   Figure 23b.  Pneumomediastinum in a 63-year-old man who developed extensive subcutaneous emphysema 4 days after cardiac transplantation. (a) AP upright chest radiograph shows right anterior pneumomediastinum (arrows) and left subcutaneous emphysema. (b) CT scan shows anterior mediastinal and bilateral subcutaneous air collections. The patient underwent mediastinal chest tube placement and recovered.

View larger version (89K): [in this window] [in a new window] [Download PPT slide]   Figure 24.  Sternal wire protrusion in a 34-year-old man that developed 17 months after cardiac transplantation. Contrast-enhanced CT scan reveals the tip of a sternal wire (arrow) protruding through the anterior skin surface (arrowheads) and right pleural effusion. The wire was surgically removed and the patient recovered.

View larger version (130K): [in this window] [in a new window] [Download PPT slide]   Figure 25.  Mediastinal bleeding in a 61-year-old man who developed sudden decrease in hematocrit level 1 day after cardiac transplantation. AP supine chest radiograph shows a massive right hemothorax and wide mediastinum. The patient recovered after repair of right atrial and aortic anastomosis suture line bleeding sites.

Aortic Dissection and Pseudoaneurysm
The prevalence of aortic dissection after cardiac transplantation has been reported as less than 1% (10). Aortic pseudoaneurysm occurs even less often. Any aortic wall incision increases a patient's risk for aortic dissection or pseudoaneurysm. Mediastinal infection may weaken suture lines, predisposing the patient to aortic dissection or pseudoaneurysm (40,41). These conditions may occur weeks to years after surgery.

Aortic dissection or pseudoaneurysm manifests radiographically as a widened mediastinum or anterior mediastinal mass. At CT, pseudoaneurysm manifests as a focal, contrast material–filled outpouching from the ascending aorta. The pseudoaneurysm occurs along the cannulation site for cardiopulmonary bypass, and thrombus may be present.

Unlike sterile aortic pseudoaneurysms, mycotic pseudoaneurysms usually manifest with fever and leukocytosis, and, unless treated, they enlarge rapidly and are fatal. CT findings of iatrogenic aortic dissection include two contrast material–filled channels separated by an intimal flap. An aortic pseudoaneurysm and dissection rarely coexist. In such cases, the false channel of a dissection may develop a contained rupture, forming a pseudoaneurysm.

In our group, one patient developed an aortic dissection 11 months after transplantation (Fig 26) and was treated with conservative medical therapy.

View larger version (104K): [in this window] [in a new window] [Download PPT slide]   Figure 26a.  Aortic dissection in a 60-year-old man who developed severe low back pain and hypertension 17 months after cardiac transplantation for ischemic cardiomyopathy. (a) Baseline PA upright chest radiograph obtained 9 months after surgery shows minimal left lower lobe atelectasis. (b) PA upright chest radiograph reveals the newly enlarged aortic arch. (c) Contrast-enhanced CT scan shows an aortic dissection involving the aortic arch and descending thoracic aorta. The intimal flap (arrows) separates the medial true channel from the lateral false channel. The patient was managed medically as he was not considered a surgical candidate and died 16 months later of disseminated Aspergillus infection.

View larger version (113K): [in this window] [in a new window] [Download PPT slide]   Figure 26b.  Aortic dissection in a 60-year-old man who developed severe low back pain and hypertension 17 months after cardiac transplantation for ischemic cardiomyopathy. (a) Baseline PA upright chest radiograph obtained 9 months after surgery shows minimal left lower lobe atelectasis. (b) PA upright chest radiograph reveals the newly enlarged aortic arch. (c) Contrast-enhanced CT scan shows an aortic dissection involving the aortic arch and descending thoracic aorta. The intimal flap (arrows) separates the medial true channel from the lateral false channel. The patient was managed medically as he was not considered a surgical candidate and died 16 months later of disseminated Aspergillus infection.

View larger version (106K): [in this window] [in a new window] [Download PPT slide]   Figure 26c.  Aortic dissection in a 60-year-old man who developed severe low back pain and hypertension 17 months after cardiac transplantation for ischemic cardiomyopathy. (a) Baseline PA upright chest radiograph obtained 9 months after surgery shows minimal left lower lobe atelectasis. (b) PA upright chest radiograph reveals the newly enlarged aortic arch. (c) Contrast-enhanced CT scan shows an aortic dissection involving the aortic arch and descending thoracic aorta. The intimal flap (arrows) separates the medial true channel from the lateral false channel. The patient was managed medically as he was not considered a surgical candidate and died 16 months later of disseminated Aspergillus infection.

View larger version (98K): [in this window] [in a new window] [Download PPT slide]   Figure 27a.  Pulmonary embolus in a 64-year-old man who developed shortness of breath 13 months after cardiac transplantation. (a) AP upright chest radiograph shows a relatively lucent left upper lobe, representing the Westermark sign of decreased perfusion due to pulmonary embolus. Fullness in the right paratracheal region represents lymphoma adjacent to the aorta. (b) Anterior lung perfusion scan shows relative decreased perfusion to the left upper lobe with normal ventilation in the left upper lobe, findings consistent with a high probability of pulmonary embolus. The patient was treated with heparin but died related to a major retroperitoneal hemorrhage 9 days later.

View larger version (92K): [in this window] [in a new window] [Download PPT slide]   Figure 27b.  Pulmonary embolus in a 64-year-old man who developed shortness of breath 13 months after cardiac transplantation. (a) AP upright chest radiograph shows a relatively lucent left upper lobe, representing the Westermark sign of decreased perfusion due to pulmonary embolus. Fullness in the right paratracheal region represents lymphoma adjacent to the aorta. (b) Anterior lung perfusion scan shows relative decreased perfusion to the left upper lobe with normal ventilation in the left upper lobe, findings consistent with a high probability of pulmonary embolus. The patient was treated with heparin but died related to a major retroperitoneal hemorrhage 9 days later.

	SUMMARY

Top Abstract INTRODUCTION POSTOPERATIVE ANATOMY AND NORMAL... COMPLICATIONS DIRECTLY RELATED... COMPLICATIONS OF ENDOMYOCARDIAL... COMPLICATIONS RELATED TO... SUMMARY References Invited Commentary  Introduction References

Currently, endomyocardial biopsy and coronary angiography are the standard methods for diagnosing acute rejection and accelerated atherosclerosis, although Ga-67 cardiac scintigraphy and ultrafast CT are being studied as potential alternative, less invasive, tests. Chest radiography and CT maintain a prominent role in diagnosis of infection and malignancy. Specific diagnoses that can be made or suggested include Aspergillus pneumonia, lymphoproliferative disorder, bronchogenic carcinoma, pneumothorax, hemothorax, pneumomediastinum, mediastinitis, aortic dissection, aortic pseudoaneurysm, and pulmonary embolism.

	Acknowledgments

 
The authors thank Joan S. Kozel, senior medical illustrator, University of Wisconsin Medical School, Madison, for preparation of the medical illustrations.

	Footnotes

 
Address reprint requests to: B.L.K.

See the commentary by Leung following this article.

Presented as a scientific exhibit at the 1997 RSNA scientific assembly.

Presented as a scientific exhibit at the 1997 RSNA scientific assembly.

Abbreviations: AP = anteroposterior CMV = cytomegalovirus PA = posteroanterior

CME FEATURE This article meets the criteria for 1.0 credit hour in category 1 of the AMA Physician's Recognition Award. To obtain credit, see the questionnaire on pp 472–480.

LEARNING OBJECTIVES After reading this article and taking the test, the reader will: • Understand the normal postoperative radiographic and CT appearance of cardiac transplantation. • Understand the radio-graphic and CT findings of cardiac transplantation complications. • Understand the radio-graphic and CT findings of complications related to cardiothoracic surgery.

Received for publication February 2, 1998. Revision received April 29, 1998. July 10, 1998. Accepted for publication July 13, 1998.

	References

Top Abstract INTRODUCTION POSTOPERATIVE ANATOMY AND NORMAL... COMPLICATIONS DIRECTLY RELATED... COMPLICATIONS OF ENDOMYOCARDIAL... COMPLICATIONS RELATED TO... SUMMARY References Invited Commentary  Introduction References

 

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5. McGiffin DC, Kirklin JK, Naftel DC, Bourge RC. Competing outcomes after heart transplantation: a comparison of eras and outcomes. J Heart Lung Transplant 1997; 16:190-198.[Medline]
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7. Shirazi KK, Amendola MA, Tisnado J, et al. Radiographic findings in the chest of patients following cardiac transplantation. Cardiovasc Intervent 1983; 6:1-6.
8. Hastillo A, Thompson J, Szentpetery S, Lower R, Hess M. Cyclosporine-induced pericardial effusions in patients who have undergone heart transplantation. Am J Cardiol 1987; 59:1220-1222.[Medline]
9. Florence SH, Hutton LC, McKenzie FN, Kostuk WJ. Cardiac transplantation: postoperative chest radiographs. Can Assoc Radiol J 1988; 39:115-117.[Medline]
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13. Adey CK, Schwartz M, Nath PH, et al. Heterotopic heart transplantation: a radiographic review. RadioGraphics 1987; 7:151-160.[Abstract]
14. Hofflin JM, Potasman I, Baldwin JC, Oyer PE, Stinson EB, Remington JS. Infectious complications in heart transplant recipients receiving cyclosporine and corticosteroids. Ann Intern Med 1987; 106:209-216.
15. Austin JH, Schulman LL, Mastrobattista JD. Pulmonary infection after cardiac transplantation: clinical and radiologic correlations. Radiology 1989; 172:259-265.[Abstract/Free Full Text]
16. Gorensek MJ, Stewart RW, Keyus TF, Mehta AC, McHenry MC, Goormastic M. A multivariate analysis of risk factors for pneumonia following cardiac transplantation. Transplantation 1988; 46:860-865.[Medline]
17. Trento A, Dummer GS, Hardesty RL, Bahnson HT, Griffith BP. Mediastinitis following heart transplantation: incidence, treatment, and results. J Heart Transplant 1984; 3:336-340.
18. Jamieson SW, Oyer PE, Reitz BA, et al. Cardiac transplantation at Stanford. J Heart Transplant 1981; 1:86-92.
19. Detry O, Defraigne JO, Meurisse M, et al. Acute diverticulitis in heart transplant recipients. Transpl Int 1996; 9:376-379.[Medline]
20. Kobashigawa JA, Kirklin JK, Naftel DC, et al. The Transplant Cardiologists Research Database Group: pretransplantation risk factors for acute rejection after heart transplantation—a multi-institutional study. J Heart Lung Transplant 1993; 12:355-366.[Medline]
21. Billingham ME. Endomyocardial biopsy diagnosis of acute rejection in cardiac allografts. Prog Cardiovasc Dis 1990; 33:11-18.[Medline]
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25. St Goar FG, Pinto FJ, Alderman EL, et al. Intracoronary ultrasound in cardiac transplant recipients: in vivo evidence of "angiographically silent" intimal thickening. Circulation 1992; 85:979-987.[Abstract/Free Full Text]
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31. Young L, Alfieri C, Hennessy K, et al. Expression of Epstein-Barr virus transformation–associated genes in tissues of patients with EBV lymphoproliferative disease. N Engl J Med 1989; 321:1080-1085.[Abstract]
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	Invited Commentary

Top Abstract INTRODUCTION POSTOPERATIVE ANATOMY AND NORMAL... COMPLICATIONS DIRECTLY RELATED... COMPLICATIONS OF ENDOMYOCARDIAL... COMPLICATIONS RELATED TO... SUMMARY References Invited Commentary  Introduction References

 

Department of Radiology, Stanford University Medical Center, Stanford, California

	Introduction

Top Abstract INTRODUCTION POSTOPERATIVE ANATOMY AND NORMAL... COMPLICATIONS DIRECTLY RELATED... COMPLICATIONS OF ENDOMYOCARDIAL... COMPLICATIONS RELATED TO... SUMMARY References Invited Commentary  Introduction References

 
Use of cardiac transplantation as a viable option for treatment of end-stage heart disease was first realized in December 1967 with successful performance of the first human-to-human heart transplant operation by Barnard (1). In the ensuing 30 years, over 40,000 cardiac transplantations have been performed in 297 institutions worldwide (2). Because cardiac transplantation serves as a treatment modality rather than a curative procedure, its potential benefits of improved survival and quality of life for transplant recipients depend on prevention, early detection, and successful treatment of posttransplantation complications (3).

The preceding article by Knisely and colleagues describes their 7-year institutional experience of cardiac transplantation complications that were observed in a total of 232 transplant recipients. The article is a comprehensive review in which the authors have logically organized imaging findings into three main categories: normal postoperative appearance, complications directly related to cardiac transplantation, and complications related to cardiothoracic surgery.

According to the 1997 report of the registry of the International Society for Heart and Lung Transplantation (2), the actuarial 1-year survival rate for cardiac transplant recipients is 79%. Heart transplant recipient half-life (ie, elapsed time after transplantation at which 50% of recipients remain alive) is 8.6 years, and for patients who survive the first year, recipient half-life increases to 11.0 years, with a constant mortality rate of 4% per year from years 1–13 (2). Causes of death in cardiac transplant recipients are well documented and are usually classified according to the time period (early, 0–30 days; intermediate, 31 days to 1 year; and late, >1 year) in which they occur after transplantation (2).

In the early period, infection and graft failure, either nonspecific in nature or related to acute rejection, account for the majority of deaths (4,5). In the intermediate period, acute rejection and infection account for approximately equal numbers of deaths (2,4). In the late period, accelerated graft atherosclerosis, malignancy, and acute rejection become the most common causes of death (2,6).

Infection screening is one of the most common indications for postoperative imaging in the cardiac transplant population. The majority of life-threatening infections develop in the first 3 months after transplantation, when use of immunosuppressants is maximal (7). Sternal wound infection occurs in approximately 7% of cardiac transplant recipients but is associated with up to 25% of deaths (8). Although CT has been shown to be highly sensitive in detection of mediastinal fluid and air collections in the perioperative period (9,10), the specificity of these CT findings for mediastinitis is time dependent. As shown by Jolles et al (10), the presence of mediastinal fluid and air collections becomes specific for mediastinitis only after the 14th postoperative day; retrosternal collections visualized before that time require aspiration to differentiate normal postoperative findings from superimposed infection.

The lung is the most common site of infection in cardiac transplant recipients (8). In the early period, bacteria are the most common pulmonary pathogens, with nosocomial pneumonias typically caused by Staphylococcus aureus, Pseudomonas aeruginosa, and other gram-negative organisms (7). Opportunistic pathogens such as cytomegalovirus and Aspergillus species predominate 2–6 months after transplantation (8,11). After 6 months, the degree of immunosuppression required to maintain allograft function determines the susceptibility of individual cardiac transplant recipients to infection (11). In the approximately three-quarters of survivors who require only minimal immunosuppression, infection risk is relatively low, with pneumonias typically caused by "community-acquired" bacteria or viruses (8,11). Cardiac transplant recipients who continue to require high doses of immunosuppressants for treatment of rejection continue to be at high risk for developing opportunistic infections. Although in the past Pneumocystis carinii and Nocardia asteroides were frequent causes of pneumonia in the immunocompromised cardiac transplant population (12), these infections have essentially been eliminated by the current practice of prophylaxis with trimethoprim and sulfamethoxazole (11).

Radiologic detection of single or multiple pulmonary nodules or masses in a cardiac transplant recipient usually denotes the presence of infectious or malignant disease. In the series of Haramati et al (13) in which the cause for newly developed, single or multiple nodules or masses was determined in 25 of 257 cardiac transplant recipients, 75% of cases were related to infection, with the two most common pathogens being Aspergillus and Nocardia organisms. Posttransplantation lymphoproliferative disorder was diagnosed in two of the 25 cases (8%) and, in each case, was associated with multiple nodules (about 20 and 50 nodules, respectively) and hilar and mediastinal lymphadenopathy (13). Although less common than lymphoproliferative disorder, bronchogenic carcinoma is another malignant diagnostic possibility that should be considered. Based on large institutional series (14,15), the overall prevalence of lung cancer after cardiac transplantation is estimated to be 1%–2%, with a median time to diagnosis of 34 months after surgery (16).

Cardiac transplant recipients who develop bronchogenic carcinoma typically have extensive histories of smoking and undergo cardiac transplantation because of ischemic cardiomyopathy (14,16). Despite ongoing medical surveillance (which includes frequent chest radiographic studies), affected recipients usually present at advanced stages of cancer and, accordingly, have a dismal prognosis (14–16). Because retrospective review of radiographs obtained before diagnosis often reveals the developing tumor (14), several investigators (16,17) have suggested that lung cancer screening be performed with more sensitive techniques such as CT to improve survival in this high-risk population.

In summary, the major complications that currently limit survival in the cardiac transplant population are infection, acute rejection, accelerated graft atherosclerosis, and malignancy. Radiologic studies have an integral role in the management of cardiac transplant recipients and are particularly useful in the evaluation of postoperative complications, infections, and neoplasms.

	References

Top Abstract INTRODUCTION POSTOPERATIVE ANATOMY AND NORMAL... COMPLICATIONS DIRECTLY RELATED... COMPLICATIONS OF ENDOMYOCARDIAL... COMPLICATIONS RELATED TO... SUMMARY References Invited Commentary  Introduction References

 

1. Rodeheffer RJ, McGregor CGA. The development of cardiac transplantation. Mayo Clin Proc 1992; 67:480-484.[Medline]
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12. Austin JHM, Schulman LL, Mastrobattista JD. Pulmonary infection after cardiac transplantation: clinical and radiologic correlations. Radiology 1989; 172:259-265.
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