Overcoming the Boundaries of Heart Warm Ischemia in Donation After Circulatory Death: The Padua Case

Abstract

A 45 year old male obese patient with a previous history of repaired congenital heart disease developed worsening heart failure making heart transplantation listing mandatory. Unfortunately, due to his anthropometric measures, the search for a suitable brain-dead donor was unsuccessful. For this reason, he accepted to be enrolled in the controlled donation after circulatory death (cDCD) program. According to the Italian Law regulating death declaration after cardiac arrest (no-touch period of 20 minutes-one of the longest in the world), we faced a 34 minute cardiac asystole, after which the heart was recovered through a thoraco-abdominal normothermic regional perfusion excluding the epiaortic vessels. The heart was then preserved by means of cold static storage. Heart transplantation was performed successfully without any signs of primary graft failure. Postoperative endomyocardial biopsies were negative for acute cellular and antibody-mediated rejection. Furthermore, echocardiographic and cardiac magnetic resonance evaluation of the heart did not show any functional abnormalities. The patient was discharged on post-operative day (POD) #39 in good clinical conditions.

Figure 1.

Laboratory assessment during heart donation after circulatory death. A: Trends of troponin and CK-MB levels soon after in situ reperfusion of the donor heart. B: Metabolic profile after in situ reperfusion of the donor heart. CK-MB, creatine kinase-myoglobin binding.

Figure 2.

Posttransplant cardiac magnetic resonance. Basal (A, F, L), mid (B, G, M), and distal (C, H, N) short axis slice T2 mapping (A–C), T1 mapping (F–H), ECV (L–N). Bull’s-eye representation of the native T2 values (E), T1 values (I), and ECV (O) in the 16 myocardial segments (according to the American Heart Association). ECV, extracellular volume values.

Figure 3.

Posttransplant endomyocardial biopsies. Microscopic view of postoperative endomyocardial biopsies. A, B: First EMB (one of the three fragments) showing mild interstitial inflammatory lymphomonocytic infiltration not associated to necrosis and mild ischemic damage, with focal cardiomyocytes damage. C4d and CD68 were negative for AMR. A: Hematoxylin–Eosin stain, original magnification ×5. B: High power view showing the nature of inflammatory cells infiltration, ×10. C, D: Second EMB (one of the three fragments) showing absence of acute cellular rejection, mild ischemic damage with early reparative changes in the subendocardium. C: Hematoxylin–Eosin stain, original magnification ×5. D: High power view of C, original magnification ×10. E–G: Third EMB (one of the three fragments) showing again mild focal ischemic damage with packed granulocytes in the vessels and in the perivascular space. E: Hematoxylin–Eosin stain, original magnification ×5. F: High power view of E, original magnification ×10. G: Inset highlighting the granulocytes. AMR, acute myocardiac rejection; EMB, endomyocardial biopsies.