AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Infections
• Acute Rejection
• Medications and Immunosuppressive Agents
• Workup
• Myocardial Infarction Post Cardiac Transplant
• Cardiac Transplant Vasculopathy
• Emergency Department Care
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Infections
• Acute Rejection
• Medications and Immunosuppressive Agents
• Workup
• Myocardial Infarction Post Cardiac Transplant
• Cardiac Transplant Vasculopathy
• Emergency Department Care
• References

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

Section 3 of 10  

• Authors and Editors
• Introduction
• Infections
• Acute Rejection
• Medications and Immunosuppressive Agents
• Workup
• Myocardial Infarction Post Cardiac Transplant
• Cardiac Transplant Vasculopathy
• Emergency Department Care
• References

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

Section 4 of 10  

• Authors and Editors
• Introduction
• Infections
• Acute Rejection
• Medications and Immunosuppressive Agents
• Workup
• Myocardial Infarction Post Cardiac Transplant
• Cardiac Transplant Vasculopathy
• Emergency Department Care
• References

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

Section 5 of 10  

• Authors and Editors
• Introduction
• Infections
• Acute Rejection
• Medications and Immunosuppressive Agents
• Workup
• Myocardial Infarction Post Cardiac Transplant
• Cardiac Transplant Vasculopathy
• Emergency Department Care
• References

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

Section 6 of 10  

• Authors and Editors
• Introduction
• Infections
• Acute Rejection
• Medications and Immunosuppressive Agents
• Workup
• Myocardial Infarction Post Cardiac Transplant
• Cardiac Transplant Vasculopathy
• Emergency Department Care
• References

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

Section 7 of 10  

• Authors and Editors
• Introduction
• Infections
• Acute Rejection
• Medications and Immunosuppressive Agents
• Workup
• Myocardial Infarction Post Cardiac Transplant
• Cardiac Transplant Vasculopathy
• Emergency Department Care
• References

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

Section 8 of 10  

• Authors and Editors
• Introduction
• Infections
• Acute Rejection
• Medications and Immunosuppressive Agents
• Workup
• Myocardial Infarction Post Cardiac Transplant
• Cardiac Transplant Vasculopathy
• Emergency Department Care
• References

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

Section 9 of 10  

• Authors and Editors
• Introduction
• Infections
• Acute Rejection
• Medications and Immunosuppressive Agents
• Workup
• Myocardial Infarction Post Cardiac Transplant
• Cardiac Transplant Vasculopathy
• Emergency Department Care
• References

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.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Infections
• Acute Rejection
• Medications and Immunosuppressive Agents
• Workup
• Myocardial Infarction Post Cardiac Transplant
• Cardiac Transplant Vasculopathy
• Emergency Department Care
• References

• Barbir M, Lazem F, Banner N, et al. The prognostic significance of non-invasive cardiac tests in heart transplant recipients. Eur Heart J. Apr 1997;18(4):692-6. [Medline].
• Benza RL, Zoghbi GJ, Tallaj J, et al. Palliation of allograft vasculopathy with transluminal angioplasty: a decade of experience. J Am Coll Cardiol. Jun 2 2004;43(11):1973-81. [Medline].
• Bolman III RM. X-cardiac and cardiopulmonary homotransplants. 15th ed. Ch. 20 1997. WB Saunders Co.
• Byrne JG, Leacche M, Paul S, et al. Risk factors and outcomes for 'vasoplegia syndrome' following cardiac transplantation. Eur J Cardiothorac Surg. Mar 2004;25(3):327-32. [Medline].
• Delahaye F, Gare JP. Which test for detecting accelerated coronary artery disease in the heart transplant patient?. Eur Heart J. Apr 1997;18(4):537-8. [Medline].
• Eisen HJ. Pathogenesis of cardiac transplant vasculopathy. UpToDate. 2002;10.2:1-10.
• Eisen HJ. Diagnoses and treatment of cardiac transplant vasculopathy. UpToDate. 2002;10.2:1-10.
• Ensley RD, Hunt S, Taylor DO, et al. Predictors of survival after repeat heart transplantation. The Registry of the International Society for Heart and Lung Transplantation, and Contributing Investigators. J Heart Lung Transplant. May-Jun 1992;11(3 Pt 2):S142-58. [Medline].
• Gao SZ, Schroeder JS, Hunt SA, et al. Acute myocardial infarction in cardiac transplant recipients. Am J Cardiol. Nov 15 1989;64(18):1093-7. [Medline].
• Hauptman PJ, Ting HH, Stone PH. Transplant-associated coronary artery disease: from chronic disease to acute myocardial infarction. Ann Emerg Med. Apr 1995;25(4):545-7. [Medline].
• Labarrere CA, Lee JB, Nelson DR, et al. C-reactive protein, arterial endothelial activation, and development of transplant coronary artery disease: a prospective study. Lancet. Nov 9 2002;360(9344):1462-7. [Medline].
• Mancini D, Pinney S, Burkhoff D, et al. Use of rapamycin slows progression of cardiac transplantation vasculopathy. Circulation. Jul 8 2003;108(1):48-53. [Medline].
• Mehra MR, Uber PA, Potluri S, et al. Usefulness of an elevated B-type natriuretic peptide to predict allograft failure, cardiac allograft vasculopathy, and survival after heart transplantation. Am J Cardiol. Aug 15 2004;94(4):454-8. [Medline].
• Michler RE, McLaughlin MJ, Chen JM, et al. Clinical experience with cardiac retransplantation. J Thorac Cardiovasc Surg. Oct 1993;106(4):622-9; discussion 629-31. [Medline].
• Neish AS, Loh E, Schoen FJ. Myocardial changes in cardiac transplant-associated coronary arteriosclerosis: potential for timely diagnosis. J Am Coll Cardiol. Mar 1 1992;19(3):586-92. [Medline].
• Parry A, Roberts M, Parameshwar J, et al. The management of post-cardiac transplantation coronary artery disease. Eur J Cardiothorac Surg. 1996;10(7):528-32; discussion 53. [Medline].
• Patel VS, Lim M, Massin EK, et al. Sudden cardiac death in cardiac transplant recipients. Circulation. 1996;94(suppl II):273-76.
• Rhodes LR. Cardiac allograft vasculopathy. Crit Care Nurs Q. Jan-Mar 2004;27(1):10-6. [Medline].
• Rothman SA, Eisen HJ. Arrhythmias following cardiac transplantation. UpToDate. 2002;10.2:1-7.
• Schnetzler B, Drobinski G, Dorent R, et al. The role of percutaneous transluminal coronary angioplasty in heart transplant recipients. J Heart Lung Transplant. Jun 2000;19(6):557-65. [Medline].
• Smart FW, Ballantyne CM, Cocanougher B, et al. Insensitivity of noninvasive tests to detect coronary artery vasculopathy after heart transplant. Am J Cardiol. Feb 1 1991;67(4):243-7. [Medline].
• St Goar FG, Pinto FJ, Alderman EL, et al. Intracoronary ultrasound in cardiac transplant recipients. In vivo evidence of "angiographically silent" intimal thickening. Circulation. Mar 1992;85(3):979-87. [Medline].
• Stark RP, McGinn AL, Wilson RF. Chest pain in cardiac-transplant recipients. Evidence of sensory reinnervation after cardiac transplantation. N Engl J Med. Jun 20 1991;324(25):1791-4. [Medline].
• Taegtmeyer AB, Crook AM, Barton PJ, Banner NR. Reduced incidence of hypertension after heterotopic cardiac transplantation compared with orthotopic cardiac transplantation: evidence that excision of the native heart contributes to post-transplant hypertension. J Am Coll Cardiol. Sep 15 2004;44(6):1254-60. [Medline].
• Uretsky BF, Kormos RL, Zerbe TR, et al. Cardiac events after heart transplantation: incidence and predictive value of coronary arteriography. J Heart Lung Transplant. May-Jun 1992;11(3 Pt 2):S45-51. [Medline].
• Valentine H. Cardiac allograft vasculopathy after heart transplantation: risk factors and management. J Heart Lung Transplantation. 2004;23:187-93.
• Virk AS, Antosia RE, Partridge RA. Use of thrombolytic therapy in a heart transplant recipient with acute myocardial infarction. Ann Emerg Med. Apr 1995;25(4):548-50. [Medline].
• Wong PM, Piamsomboon C, Mathur A, et al. Efficacy of coronary stenting in the management of cardiac allograft vasculopathy. Am J Cardiol. Jul 15 1998;82(2):239-41. [Medline].
• de Lorgeril M, Dureau G, Boissonnat P, et al. Platelet function and composition in heart transplant recipients compared with nontransplanted coronary patients. Arterioscler Thromb. Feb 1992;12(2):222-30. [Medline].

Article Last Updated: Mar 13, 2007