Introduction
Cardiac transplantation and retransplantation have become more widespread and are being used more frequently to treat end-stage heart failure. The first cardiac retransplantation was reported in 1977, and, since then, sequential orthotopic transplantation has become a treatment of graft failure (Michler, 1993). Over time, improvement in techniques along with immunosuppressive agents have led to improved outcome. Criteria for candidate selection have also improved. Most patients must be classified in the New York Heart Association Class IV category where revascularization is not an option. Two types of transplant exist: orthotopic and heterotopic. Pretransplantation, the most critical predictor of operative risk is pulmonary vascular resistance (Bolman, 1997).
Posttransplantation patients present with a variety of complications and are at risk for sudden death. In the immediate posttransplant period, infections and acute rejection are the most common causes of death. Later, cardiac transplant vasculopathy is a major factor to survival. The risk of death from coronary allograft disease increases steadily post transplantation and accounts for nearly 25% of deaths between 1 and 10 years (Benza, 2004). At 5 years, 30-60% of cardiac transplant patients will have evidence of vasculopathy (Valentine, 2004). Coronary artery disease is evident in about 30-40% of patients at 3 years (Stark, 1991) and 50% by 5 years (Neish, 1992). Mechanisms are both immunologic and nonimmunologic mediated.
Ventricular arrhythmias, congestive heart failure (CHF), and sudden death may occur in the immediate posttransplant period and may even be the first symptom manifested.
Fatigue, dyspnea, constitutional symptoms, and vague nonspecific complaints are common presentations in these patients at the emergency department and are usually a manifestation of serious underlying illness.
Infections
Fever is one of the common complaints in patients presenting to the emergency department, but an afebrile patient may be just as acutely ill. Common infections encountered in cardiac transplant patients include Candida, cytomegalovirus (CMV), Pneumocystis carinii pneumonia (PCP), and herpes virus. Appropriate antibiotic and antiviral treatment must be implemented immediately if infection is suspected. Broad-spectrum antibiotics should be administered in most instances, especially if the specific pathogen is unknown.
Ganciclovir or acyclovir is used for treatment of CMV and herpetic infections. Bactrim is used for treatment of PCP, and pentamidine is used for treatment of patients with a history of allergy to sulfa medications.
Appropriate therapy for other infections such as those from indwelling lines and catheters must also be completed.
CMV is one of the most common pathogens affecting transplant patients usually occurring after the first month. CMV may induce rejection. It should be considered in all patients presenting to the emergency department. Constitutional symptoms with vague complaints, thrombocytopenia, fever of unknown cause, hepatitis, pneumonitis, nephritis, and myocarditis are all signs that the patient may have CMV infection. Serologies and antigen testing must be completed, and early therapy with intravenous ganciclovir should be instituted.
Acute Rejection
Acute rejection is T-cell mediated and can present with a variety signs and symptoms that can be vague and nonspecific. Signs and symptoms may be subtle and should not be dismissed. Patients may not present with a fever and may not have hard signs of organ rejection. Contrary to the normal population, some of these patients may look well and lack physical findings of being acutely ill but may have life-threatening illness.
Acute rejection is more common in the early months and first year after transplantation. Peak incidence of rejection occurs in the first year after transplantation. The incidence of graft rejection decreases after the first year, but, conversely, the incidence of graft atherosclerosis increases (Hauptman, 1995). The definitive diagnosis of acute cellular rejection is established by endometrial biopsy (Eisen, 2002).
Medications and Immunosuppressive Agents
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Table
| Agent | Mechanism | Side Effects |
| Corticosteroids | Cytokine production suppression | Cushingoid syndrome,infections |
| Cyclosporin (Neoral, Sandimmune) | Calcineurin inhibitor | Nephrotoxic, hepatotoxic, hypertension, hyperkalemia, hyperlipidemia, hyperglycemia, hirsutism, infections |
| Azathioprine (Imuran) | Antagonizes purine metabolism, which may inhibit DNA, RNA, and protein synthesis | Risk of malignancy, hepatotoxicity, thrombocytopenia, anemia, leukopenia |
| Mycophenolate mofetil (CellCept) | Reversible inhibitor of inosine monophosphate dehydrogenase (IMPDH) | Hypertension, peripheral edema, GI hemorrhage, infection, malignancy, leukopenia, myelosuppression |
| Everolimus | Analog of rapamycin with antiproliferative and immunosuppressive activity | Leukopenia, thrombocytopenia, GI upset, hyperlipidemia, infection, nephrotoxicity |
| Sirolimus (Rapamycin, Rapamune) | Antimigratory/antiproliferative effects on vascular smooth muscle | Anemia, thrombocytopenia, hypertension, hyperlipidemia, thrombosis, hepatotoxicity |
| Tacrolimus (FK506, Prograf) | Calcineurin inhibitor | Hepatotoxicity, nephrotoxicity, thrombocytopenia, hyperlipidemia, hyperkalemia |
| Agent | Mechanism | Side Effects |
| Corticosteroids | Cytokine production suppression | Cushingoid syndrome,infections |
| Cyclosporin (Neoral, Sandimmune) | Calcineurin inhibitor | Nephrotoxic, hepatotoxic, hypertension, hyperkalemia, hyperlipidemia, hyperglycemia, hirsutism, infections |
| Azathioprine (Imuran) | Antagonizes purine metabolism, which may inhibit DNA, RNA, and protein synthesis | Risk of malignancy, hepatotoxicity, thrombocytopenia, anemia, leukopenia |
| Mycophenolate mofetil (CellCept) | Reversible inhibitor of inosine monophosphate dehydrogenase (IMPDH) | Hypertension, peripheral edema, GI hemorrhage, infection, malignancy, leukopenia, myelosuppression |
| Everolimus | Analog of rapamycin with antiproliferative and immunosuppressive activity | Leukopenia, thrombocytopenia, GI upset, hyperlipidemia, infection, nephrotoxicity |
| Sirolimus (Rapamycin, Rapamune) | Antimigratory/antiproliferative effects on vascular smooth muscle | Anemia, thrombocytopenia, hypertension, hyperlipidemia, thrombosis, hepatotoxicity |
| Tacrolimus (FK506, Prograf) | Calcineurin inhibitor | Hepatotoxicity, nephrotoxicity, thrombocytopenia, hyperlipidemia, hyperkalemia |
Avoiding nonsteroidal anti-inflammatory drugs (NSAIDs) in these patients is especially important because of the compounding and additive effect on renal function. Such effects are even more severe with tacrolimus and cyclosporine.
Caution must be used when adding any new medication to the patient's regimen, and liberal consult with the transplant team is the rule rather than the exception. Have a low threshold to consult the transplant team on all patients as early as possible.
Certain medications will increase drug levels such as clarithromycin, erythromycin, cimetidine, calcium channel blockers, and ethanol.
Medications that decrease drug levels include phenytoin, rifampin and barbiturates.
Workup
Laboratory and imaging studies
Comprehensive laboratory studies should be performed including renal function and drug levels determinations. Pneumonia is a frequent occurrence; therefore, chest radiography is necessary. At times, a chest CT scan may be necessary.
Electrocardiography
Nonspecific ST changes are common. Occasionally, two distinct P waves may be seen representing one from the patient and the other from the donor.
Cardiac transplant vasculopathy may not and often does not present with specific territorial abnormalities because of the diffuse concentric nature of the disease affecting multiple vessels. Reduced limb lead voltage is a common finding that may be suggestive of rejection, but this finding is neither sensitive nor specific.
A normal resting baseline tachycardia is often seen in cardiac transplant patients.
Myocardial Infarction Post Cardiac Transplant
Cardiac transplant patients are at risk for myocardial infarction. Acute myocardial infarction in these patients presents differently from nontransplant patients. Myocardial injury is manifested as functional consequences of myocardial ischemia such as congestive heart failure, arrhythmias, and sudden death. Infrequently, hypertension, renal failure, and malignancy occur.
Symptoms of myocardial infarction are usually vague and nonspecific. Atypical presentations can be misleading and lead to errors and missed diagnoses. Myocardial infarction is usually clinically silent because the denervated transplanted heart is lacking afferent pain fibers and does not seem to experience angina pectoris (Gao, 1989). In one study, only 3 of 22 patients with myocardial infarction had any type of pain syndrome (Gao, 1989). Chest pain as a symptom of ischemia is the exception and not the rule. Furthermore, their predilection to new-onset diabetes further predisposes them to silent ischemia. The most frequent symptom is fatigue, malaise, or weakness followed by dyspnea, palpitation, dizziness, arm pain, nausea and vomiting, as well as diaphoresis. Rales is suggestive of acute ischemia, and syncope is also not uncommon. A new S3 or S4 gallop may be a clue to cardiac ischemia though its occurrence does not seem to be related to the usual risk factors for coronary artery
disease (Gao, 1989). Because the disease can be so diffuse, percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass graft (CABG) are not considered good options. Revascularization by PTCA and CABG in selected cardiac transplant patients has been demonstrated with limited success (Parry, 1996).
Cardiac Transplant Vasculopathy
Accelerated coronary artery disease in cardiac allograft patients is the major factor limiting long-term survival. Cardiac allograft vasculopathy (CAV) will affect 30-60% of all cardiac transplant patients (Valentine, 2004) within 5 years of surgery. Rapidly progressive, diffuse concentric luminal narrowing occurs rather than focal asymmetric lesions in native coronary disease (Benza, 2004; Rhodes, 2004). T cell and smooth cell has been implicated in the process affecting mid and distal vessels in a diffuse concentric manner in contrast to focal nonconcentric lesions affecting proximal vessels in native coronary artery disease. When focal nonconcentric lesions occur, they are thought to be a manifestation from preexisting disease in the donor heart (Eisen, 2002).
One study described 2 distinct types of lesions by biopsy: pigmented lesions and nonpigmented lesions (Eisen, 2002). From this study, it was surmised that nonpigmented lesions were associated with sudden death and pigmented lesions were more correlated with non–sudden death events such as myocardial infarction, graft failure, and need for revascularization. The use of Rapamycin, a potent immunosuppressant drug with antiproliferative and antimigratory effects, has been shown to slow the disease process in transplant vasculopathy (Mancini, 2003).
Coronary angiography
Cardiac denervation results in silent ischemia; therefore, frequent surveillance must be completed. Although techniques such as intracoronary ultrasonography, dipyridamole myocardial perfusion scanning, dobutamine stress echo, positron emission tomography (PET), and CT have been used to measure intimal proliferation, coronary angiography remains the study of choice in monitoring and measuring the development of vasculopathy in cardiac transplant patients (St. Goar, 1992). Patients usually have baseline study performed at the time of transplantation with annual surveillance thereafter. At times, biopsy is also performed as part of the surveillance.
Percutaneous transluminal coronary angioplasty
Percutaneous transluminal coronary angioplasty (PTCA) has been used in selected patients with vasculopathy limited to one artery (Eisen, 2002).
PTCA is of limited value because of the diffuse concentric nature of the disease affecting multiple vessels with poor collateral circulation. It is reserved for the selected patient with discrete lesion. One study showed immediate success rates of 92% and restenoses rate of 20-55% at 6-15 months (Eisen, 2002). Another study documented a high rate of restenosis with an incidence of 30-100% for PTCA and 14-56% with stents (Benza, 2004; Schnetzler, 2000). Azathioprine and mycophenolate mofetil have been shown to reduce the risk of restenosis in repeat PTCA occurring in the first 6 months after therapy (Benza, 2004). Thus, although PTCA and coronary stents are widely used in native coronary artery disease, their use for transplant vasculopathy has not been established.
Coronary stenting
The value of coronary stenting post transplantation is still unclear. One study with 27 transplant patients with vasculopathy showed that they had no clinical adverse events at 8 months (Wong, 1998). However, the study also showed that significant restenosis occurred in greater than 50% when measured by intracoronary ultrasonography and in 25% when measured by angiography. The study did conclude that the rate of restenosis was lesser for patients who were stented when compared with angioplasty alone.
Thrombolytic therapy in cardiac transplant patients
The role of thrombolytic therapy in cardiac transplant vasculopathy remains unclear. An occasional case report has been cited with use of thrombolytic therapy in cardiac transplant patients (Virk, 1995). Because of the diffuse pathogenesis of the disease, how much, if any, thrombosis plays a role in the acute setting is unclear. Although discrete traditional plaques may coexist with diffuse concentric intimal hyperplasia, this is difficult to determine in the acute setting. No strict guidelines exist regarding the use of thrombolytic therapy in cardiac transplant suspected of ST elevation MI. Such treatment intervention must be performed on a case-by-case basis, and, in the rare instance when it is considered, it must be performed in conjunction and consultation with the transplant team or the patient's cardiologist.
Ultrasonography
Bedside echocardiography is useful in detection of an effusion and should be utilized liberally. New wall motion abnormality may be an indication of cardiac ischemia as well as progression of disease. When combined, the use of angiographic surveillance and echocardiography can provide useful information regarding disease progression.
Arrhythmias
Cardiac arrhythmias are common in orthotopic cardiac transplant patients, and this is especially true in the early postoperative period (Eisen, 2002; Rothman, 2002). Premature atrial and ventricular complexes have an incidence rate of 60% in the early transplant period but with little morbidity. Sudden cardiac death occurs with frequency in cardiac transplant patients; thus, antiarrhythmic treatment should be done with urgency (Patel, 1996).
Fifty percent of patients will manifest a relative bradycardia secondary to sinus node dysfunction in the first few weeks of allograft transplant (Eisen, 2002; Rothman, 2002). Of these, 16% of patients will require a permanent pacemaker because of decreased cardiac output. Surgical trauma, rejection, medications, and ischemia during hypothermic preservation have been listed as potential causes of sinus node dysfunction.
Approximately 18% of cardiac transplant patients will manifest atrial fibrillation and atrial flutter. Patients presenting with such arrhythmias have a high incidence (up to 75%) of graft rejection. Therefore, graft rejection must be considered in any patient presenting with this type of arrhythmia.
Ventricular premature beats (PVCs) occur with frequency early in the transplant period and decreases with time.
The most common conduction delay is incomplete right bundle-branch block.
Nonsustained ventricular tachycardia (NSVT) occurs with frequency but decreases with time. Sustained ventricular arrhythmias may be a sign of graft rejection and atherosclerosis, which may lead to sudden death (Eisen, 2002; Rothman, 2002).
Antiplatelet treatment
There appears to be no benefit for aspirin use in patients with transplant vasculopathy (Eisen, 2002; De Lorgeril, 1992).
Retransplantation
Although not suitable for all patients, retransplantation remains the only definitive treatment for transplant vasculopathy. Retransplantation 1 year survival rates have been reported from 48-60% (Ensley, 1992), a much poorer outcome when compared with rates for initial transplantations.
Hypertension
Hypertension is a common occurrence following cardiac transplantation. The increasing incidence of hypertension is suggested to be a manifestation of denervation and immunosuppression. Cyclosporine leads to nephrotoxicity and inhibits endothelium-dependent vasodilation and activation of the sympathetic nervous system, therefore contributing to post transplant hypertension (Taegtmeyer, 2004). Captopril normalizes blood pressure and fluid homeostasis in these patients suggesting that post transplant hypertension is related to the inability to suppress the renin-angiotensin-aldosterone system (Valentine, 2004). Treatment may require more than one antihypertensive agent. Diltiazem has been shown to have beneficial effect in managing hypertension secondary to calcineurin inhibitors (Valentine, 2004).
Hypotension
Signs of hemodynamic compromise should be corrected with judicious fluid boluses. Hypotension not responding to fluid boluses and stress dose steroids may require inotropic agents. Dobutamine is usually the agent of choice. Refractory hypotension with metabolic acidosis and decreased systemic vascular resistance may be a sign of vasoplegic syndrome, which places the patient at risk for sudden death (Byrne, 2004).
Diabetes
Post transplant diabetes is common. Two percent of pediatric patients and 15-20% of adult patients will develop diabetes after cardiac transplant, and its development has a strong correlation with the type of immunosuppression agents used (Valentine, 2004). Variation exists in the degree of diabetogenicity of immunosuppressive agents, with corticosteroids being associated with the greatest risk of developing new-onset diabetes post transplantation (Valentine, 2004).
Noninvasive tests in transplant recipients
Brain natriuretic peptide (BNP) levels correlate with ventricular wall stress and are predictive of alterations in hemodynamic status in native cardiac function. The use of BNP as a marker in cardiac transplantation to predict hemodynamic alterations has not been extensively studied. One study evaluated the prognostic relation of high BNP levels long after (mean, 5 y) heart transplantation in relation to cardiac allograft function and survival rate (Mehra, 2004). Although the study population was small (62 patients), they concluded that patients with high BNP levels were at greater risk for allograft dysfunction and cardiac allograft vasculopathy and was predictive of cardiovascular death.
Use of noninvasive tests such as exercise electrocardiography and exercise radionucleotide ventriculopathy as surveillance for vasculopathy in cardiac transplant patients have low sensitivity and poor predictive ability (Smart, 1991). 2-D echocardiography seem to be of some value. In one study looking at 91 consecutive transplant patients whom were undergoing annual coronary arteriography and subjected to several other noninvasive tests (mean age 53 y), the authors concluded that echocardiographic ejection fraction greater than 60% significantly predicted survival free of myocardial infarction, heart failure, and cardiac death (Barbir, 1997).
Others have stated that rather than a specific 60% cut off, a better predictor would be progressive decrease of left ventricular ejection fraction over successive echocardiographies (Delahye, 1997). Angiographic surveillance remains the best study, and, even then, the diagnosis of coronary artery disease is difficult. In one study, 28% of patients who had cardiac events showed no evidence of coronary artery disease by angiogram (Uretsky, 1992).
C-reactive protein
C-reactive protein (CRP) is an inflammatory marker, and elevation of plasma levels is an important predictor of coronary artery disease and atherosclerosis in native hearts. Studies have suggested that this is also true for cardiac transplant patients (Labarrere, 2002). CRP concentration can be used to identify cardiac transplant patients at increased risk for coronary artery disease and graft failure (Labarrere, 2002).
Risk stratification
Accelerated coronary artery disease in cardiac transplant patients does not seem to be related to the risk factors in native CAD, making risk stratification difficult (Gao, 1989). Hyperlipidemia is a common occurrence in heart transplant patients, and elevation of low-density lipoprotein (LDL), total serum cholesterol, and triglyceride levels seem to correlate with the severity of the vasculopathy (Eisen, 2002). A retrospective analysis cited vasoplegia syndrome post orthotopic heart transplantation as a possible risk profile for these patients (Byrne, 2004). Vasoplegia syndrome is rare but lethal and is characterized by severe refractory hypotension, metabolic acidosis, and decrease in systemic vascular resistance (SVR). Of 147 patients, 28 (19%) developed vasoplegia syndrome; such patients had higher hospital mortality rates compared with those who did not (25% vs 9% [p = 0.031]). They concluded that vasoplegia syndrome following orthotopic heart transplantation is associated with high earlymortality.
Emergency Department Care
Emergency department care of the cardiac transplant patient
Consult the transplant team early in the workup. Be aggressive with even the most benign and what may seem as a mild or vague complaint. Overwhelming sepsis may present as mild, nonspecific symptoms. Stress dose steroids should be given early; be liberal with imaging studies. Studies have suggested that pulmonary infections may be evident on chest CT scan before being seen on chest radiograph.
Lumbar puncture should be considered in all patients with a headache even if mild to exclude CNS infections.
Cultures are an integral part of the workup. Obtain drug levels.
Early antibiotics, antiviral, and antifungal treatment should be used.
Most patients will be admitted, and this should be done in consultation with the transplantation service.
Summary
Avoid pitfalls of disregarding nonspecific and vague complaints.
Stress dose steroids should be used early in the treatment course.
Consult with the transplant or cardiology service early.
Obtain cultures and appropriate laboratory studies, including drug levels and imaging studies.
Institute broad-spectrum antibacterial therapy and antiviral therapy.
Liberal admission of all patients.
Keywords
heart transplant, heart transplantation, heart failure, cardiac transplantation, cardiac retransplantation, end-stage heart failure, ventricular arrhythmias, congestive heart failure, CHF, sudden death, orthotopic transplantation, heterotopic transplantation
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References
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Further Reading
Keywords
heart transplant, heart transplantation, heart failure, cardiac transplantation, cardiac retransplantation, end-stage heart failure, ventricular arrhythmias, congestive heart failure, CHF, sudden death, orthotopic transplantation, heterotopic transplantation
