Spontaneous cardiac rupture as the initial presentation of acute myeloid leukaemia complicated by malignant lactic acidosis: a case report

Left ventricular free wall rupture (LVFWR) without coronary artery occlusion in the setting of acute myeloid leukaemia (AML) is exceedingly rare. We report a rare case of spontaneous cardiac rupture in a patient ultimately diagnosed with acute myeloid leukaemia.

A 77-year-old woman presented with acute chest pain and haemodynamic collapse. Coronary angiography revealed no significant stenosis, whereas left ventriculography demonstrated contrast extravasation from the apical region, consistent with LVFWR. The patient underwent emergent surgery; however, no discrete rupture site was identified. Following temporary weaning from cardiopulmonary bypass and re-inspection, no obvious rupture site was observed. Since it appeared that the blow-out–type rupture had transitioned to an oozing type, suture less repair with TachoSil® was chosen, achieving initial haemodynamic stabilization. Postoperatively, the patient remained haemodynamically stable without persistent bleeding. However, on Postoperative Day 3, the patient was diagnosed with AML, followed by rapidly progressive malignant lactic acidosis and multiorgan failure, leading to death despite intensive care.

This case underscores three key clinical considerations:

(1) In instances of LVFWR without culprit coronary artery occlusion, the possibility of leukaemia-associated myocardial pathology should be actively evaluated.

(2) For oozing-type LVFWR lacking a clearly identifiable rupture site, sutureless repair may represent a feasible and effective surgical option.

(3) The onset or progression of lactic acidosis in the setting of marked leucocytosis constitutes a medical emergency, warranting prompt initiation of cytoreductive therapy and empiric thiamine supplementation.