Title : Management of post heart transplant complications
Abstract:
Heart transplant rejection remains a significant challenge, threatening the long-term success of heart transplantation. Acute Cellular Rejection (ACR) is most common type and occurs within first year of transplant. Common cause of ACR is decreased blood level of immunosuppressants making the recipient’s T-cells active against the allograft. ACR can also occur without any identifiable cause and many risk factors like genetic mismatch, cytomegalovirus infection, donor coronary artery disease etc. have been described. We describe a patient who developed ACR 5months post-heart transplant and he recovered after a long course of treatment.
A 45 year male diagnosed with endstage heart failure due to valvular cardiomyopathy. He underwent heart transplantation within a year of enlistment and recovered slowly with a longer hospital stay due to bleeding, transfusions, lung injury, uncontrolled diabetes, infection. Donor and recipient both were cytomegalovirus negative. The patient was discharged home with triple maintenance immunosuppressive therapy 6weeks after transplantation. On 5th month post-transplant, he presented with dyspepsia, bloating sensation and breathing difficulty. Clinical examination did not reveal any feature of heart failure, blood pressure was 108/84mmHg, SpO2 100%. ECG showed normal sinus rhythm @98/min heart rate, Echocardiography revealed dilated heart, global hypokinesia, mild MR and moderate TR with RVSP=25+RAP, no PE. His blood tacrolimus level was low @2.87ng/ml, NT pro BNP was 35000pg/ml, Troponin I-128pg/ml. Endomyocardial biopsy revealed grade 2 ACR (2R ISHLT 2004).
The patient was admitted to intensive care unit, invasive monitoring started, his hemodynamics was supported with dobutamine and adrenaline infusion. Methyl prednisolone pulse therapy @20mg/kg/day was initiated, tacrolimus dose was increased and mycofenolate continued. Frusemide infusion was started as urine output decreased, blood sugar was controlled with insulin infusion. The patient developed bilateral severe pleural effusion, became dyspneic and required oxygen supplementation with positive airway pressure. The patient did not improve with pulse steroid and escalation of tacrolimus levels even after 2weeks, so we Administered Antithymocyte Globulin (ATG). 1week after completing the course of ATG the heart started recovering. Inotropes were tapered, tacrolimus dose adjusted with target level 10ng/ml and prednisolone was tapered @ 5mg/week till 5mg daily dose. The heart recovered and the patient was discharged home after 3 months with diuretics. We could avoid mechanical circulatory support, but this ACR was very resistant to treatment.
