Cardiac Transplantation Board Review. Brian W. Zagol, M.D. Department of Cardiology University of Tennessee. Introduction. More than 4000 patients in the United States are registered with the United Organ Sharing Network (UNOS) for cardiac transplantation.
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Brian W. Zagol, M.D.
Department of Cardiology
University of Tennessee
1. D: Multiple studies have shown that peak O2 uptake determined by maximal CPX testing accurately predicts short-term (<18 month) prognosis in patients with moderate to severe CHF. A peak VO2 < 10 to 12 ml/kg/min is associated with a 1 year survival of only 60% and is a powerful indicator of the need for transplant listing in suitable candidates. Its predictive value is only valid when patient reaches his anaerobic threshold ie cardiac limit. Conversely patients whose VO2 exceeds 15 ml/kg/min are likely to experience one year survival rates similar or better than after cardiac transplantation. LVEF loses its independent predictive value when below 25% and in patients with advanced symptomatic CHF. Cardiac index <2.2 l/min/m2 is associated with a poor outcome, but is highly variable depending on patients volume status and afterload medications. Norepinephrine levels >900 picrograms/ml are predictive of poor two year outcome, but are seldom measured outside of clinical trials. LV dilation portends a worse prognosis, but its prognosis in the setting of chronic CHF is unclear.
2. D. This patient is failing on appropriate regimen for CHF. His recent VO2 max score of less than 14ml/min/kg and inability to achieve BP of 120mmHg are markers for poor prognosis. Given patient’s age and lack of comorbidities, transplantation should strongly be considered. A study from the DIG trial demonstrated an increase mortality from serum digoxin dosing above 0.5 to 0.8 ng/ml range. The potential benefits of higher Aldactone dosing have not be demonstrated. The RALES trial used as dose of 25mg qd titrated to 50mg qd. Changing to torsemide from furosemide may benefit the patient if bowel wall edema is leading to decreased absorption and thus the effectiveness of furosemide, but would not be expected to affect the patients prognosis. The use of B-blockers have been shown to improve mortality and exercise tolerance in patients with cardiomyopathy.
3. C. The transplanted heart remains denervated (with rare exceptions) and thus transplant patients are incapable of experiencing the subjective symptom of angina pectoris. The cardiac allograft is prone to develop a very diffuse form of coronary vasculopathy this is independent of the usual coronary risk factors, is increasingly prevalent with time after transplantation, and can be rapidly progressive. A long-term transplant recipient who is on a stable low-dose immunosuppressive regimen is unlikely to develop allograft rejection or opportunistic infection, although both are within the realm of possibility. Patient is relatively hypotensive and to write his symptoms off to anxiety or an upper respiratory infection would be a great disservice.
4. A 54 y/o male heart transplant recipient arrives for an unscheduled visit in transplant clinic following 2 weeks of progressive fatigue, anorexia, and worsening SOB. He underwent transplantation 5 years ago for lymphocytic myocarditis and had an early postoperative course complicated by 2 bouts of symptomatic CMV viremia, and 2 episodes of moderate (ISHLT grade 2 rejection at 3 months; and ISHLT grade 3A rejection at 6 months) cellular rejection. Both episodes rapidly resolved after intervenous treatment with methylprednisolone. Subsequent biopsies have been ISHLT grade 0 or 1A. Chronic maintenance therapy has consisted of cyclosporin (3mg/kg qd), azathioprine (1.5mg/kg qd), amlodipine (10mg qd), and simvastatin (20mg qd). He has been entirely well and walking about 1 hour qd until symptoms suddenly appeared. PE revealed mildly Cushingoid appearance / NAD, BP 160/95, P 115 with occasional PVC’s, temp 98.8. Skin showed several AK’s over sun-exposed skin surfaces. Lung exam showed fine crackles at b/l bases. Cardiac exam showed non-displaced PMI, S2 paradoxically split, loud S4, 2/6 HSM at LLSB. JVD 8cm; 1+ peripheral edema. CXR showed mild CMG and 2+ pulmonary vascular redistribution. ECG showed Sinus tach at 114, occasional PVC, biatrial enlargement, LBBB, diffuse repolarization abnormalities, WBC 5600, Plt 210, pO2 80, pCO2 32, pH 7.45. An echo, RHC, and endomyocardial bx is contemplated. The most likely diagnosis is:
A. Chronic cellular rejection.
B. Acute mitral regurgitation.
C. Reactivation of cytomegalovirus pneumonitis.
D. Recurrent lymphocytic myocarditis.
E. Transplant coronary vasculopathy.
4. E. Accelerated coronary vasculopathy is the most common cause of symptomatic LV dysfunction in heart transplant recipients who survive beyond the 1st 3 years. The patients clinical presentation is characteristic of post-transplant vasculopathy. The patient probably had a “silent” AMI approximately 2 weeks ago due to an epicardial coronary occlusion. The cardiac allograft typically remains denervated in the majority of transplant recipients so typical anginal pain is typically absent. Heart faliure and sudden cardiac death are the two most common clinical presentation. This frequent complication remains the “Achilles heel” of heart transplantation and is the major cause of mortality in long-term transplant recipients. Angiographic evidence of coronary vasculopathy is evident in at least 50% of patients at 5 years. CMV infection is a significant risk factor for this complication. HMG co-reductase inhibitors have been shown to lower the incidence of transplant vasculopathy. Cellular rejection occurs in over 70% of transplant recipients but is rarely observed beyond 12 months unless immunosuppression has been decreased. CMV can produce an interstitial pneumonitis but reactivation of disease after 7 years in the absence of enhanced immusuppression is unlikely. The lack of fever or leukopenia also argues against this diagnosis. Finally recurrent lymphocytic and giant cell myocarditis in the cardiac allograft has been described, but is exceedingly rare.
5. D. The patient clearly fits the definition of “advanced heart failure” and is a candidate for “specialized” therapies. If she were elderly or had major comorbidities, a hospice referral would be appropriate. In this case she is an excellent candidate for cardiac transplantation. There is probably little to be gained in the long-term by minor adjustments in her medications.