Acute Decompensated Congestive Heart Failure in a Heart Transplant Patient: Too Sugar, Too Bad

Abstract

Introduction Diabetic cardiomyopathy (CMP) is an under-recognized type of CHF with a prevalence of 1.1%. Heart transplantation (HT) patients are at risk of developing de novo or worsening diabetes mellitus (DM) secondary to their immunosuppressive therapy. Thus, they are at risk of having diabetic CMP. We present a case of a patient with HT who presented with acute decompensated CHF (ADCHF) secondary to uncontrolled DM. Case A 43-year-old male with a medical history of ischemic cardiomyopathy (EF of 5-10%) status post HT [EF of 50-55% with normal right ventricular (RV) function via TTE 6 months ago], DM type II, CKD stage III who presented with progressive shortness of breath and leg swelling. His immunosuppressive therapy included tacrolimus, mycophenolate mofetil, and prednisone. Labs showed BNP of 30000 pg/mL, Cr 2.1 mg/dL, blood glucose > 600 mg/dL, and Hb A1C 14. TTE showed a significant reduction in EF to 5-10% with moderate to severe RV dysfunction. The patient was started on milrinone infusion, insulin infusion, and IV diuresis. Left heart cath (LHC) showed mild luminal irregularities without significant coronary stenoses. Right heart cath (RHC) on milrinone showed RA 23, RV 50/11, PA 54/32, PCWP 29 mmHg, CO 4.2 L/min, CI 2.1 L/min/m2. Endomyocardial biopsy (EMB) revealed no acute cellular or humoral rejection. The patient was diagnosed with ADCHF secondary to diabetic CMP secondary to uncontrolled DM. He improved clinically during his hospital stay. His insulin regimen was adjusted and he was discharged to follow up with HF and Endocrinology. Discussion In our patient, the initial diagnostic work-up (LHC, RHC, and EMB) aimed to investigate cardiac allograft vasculopathy and acute allograft rejection, the two most common causes of ADCHF in HT patients. However, after excluding these conditions, patient's poorly controlled DM with HbA1C of 14 led to diagnosing him diabetic CMP. During the follow-up period, patient's DM became under better control with Hb A1C of 6-7 which resulted in an improvement in his EF to 30-40% (after 4 months) and to 50-55% (after 7 months). Figure 1 demonstrates the fluctuation of patient's ejection fraction before and after his HT along with his highest Hb A1C levels. As shown, periods of poorly controlled DM were associated with lower EF. Conclusion Diabetic CMP is an under-recognized type of CHF. It is a diagnosis of exclusion that requires a low threshold of suspicion. As demonstrated in our case, attaining better DM control in patients with diabetic CMP results in an improvement in their cardiac function.