The patient is a 52-year-old male who was admitted to the hospital. He presented with chest distress for 2 years and another half-hour episode with psychiatric change. Results of physical examination after admission showed the following: blurred mind, passive position, thick breathing in both lungs, dry and wet rales, Heart rate 96 beats per minute, and blood pressure of 63/43 mmHg; N-terminal pro brain natriuretic peptide (NT-proBNP): 2,425 (pg/ml); Highly sensitive troponin T (TnT-HS): 10,000 (ng/L); Creatine kinase (CK): 14,147 (U/L); And creatine kinase isoenzyme (CK-MB): 587 (U/L). ECG showed that:sinus tachycardia and acute anterior and lateral myocardial infarction (Fig. 1). Cardiac colour ultrasound indicated that the left ventricular wall activity was generally weakened. The following were observed: left atrial and LV enlargement, incomplete mitral valve closure (mild-moderate) and ejection fraction EF: 0.18. So the patient was diagnosed acute myocardial infarction and cardiogenic shock. The patient was given a 0.2 ug/kg.min dose of adrenaline and norepinephrine at 0.2 ug/kg.min to Pump injection.The blood pressure was 63/43 mmHg. The lactate was 6 mmol/L. The patient’s limbs were wet and cold, and he was unconscious. The patient was intubated and mechanically ventilation, Then he was immediately given ECMO assistance.
In venous-arterial ECMO oxygenation (V-A ECMO) mode, the right femoral artery-venous catheterisation was performed, and the following were used: systemic heparin sodium (1 mg/kg), 17Fr femoral arterial catheter (Medtronic) with a depth of 15 cm and 21Fr femoral venous catheter (Medtronic) with a depth of 45 cm. An 8Fr end-end reperfusion catheter was inserted to prevent ischemia of the lower limbs. After the ECMO establishment was completed, we ran the ECMO perfusion system (Medtronic) with a flow rate of 3.5 L/min and MAP of 80 mm Hg. The ECMO was fully established, and the patient underwent interventional therapy.
The patient had acute myocardial infarction 2 years ago, the coronary angiography showed that: about 40–50% left trunk stenosis, anterior descending branch opening-proximal stenosis, recent acute occlusion and distal flow grade TIMI 0; and about 40–60% distal branch stenosis, about 50–70% OM opening-proximal stenosis and distal flow grade TIMI(Fig. 2) .Descending stenting and IABP implantation were performed, and the patient was successfully discharged 30 days later. In this operation,the coronary angiography showed that: the left main trunk, three vessel lesions and the cyclotron branch were acute occlusion, stent implantation and IABP implantation. The operation process was smooth (see Fig. 3). After surgery, he was transferred to the intensive care unit for fluid expansion, and the infusion of red blood cells was performed to improve anaemia. The infusion of blood products and other blood products was performed to improve coagulation function, piperacillin tazobactam sodium anti-infection and haemostasis.
After 7 days of ECMO-assisted support and active treatment, the patient showed no significant recovery of cardiac function. After re-examination of NT-proBNP: 33553 (pg/ml), chest X-ray indicated that the texture of both lungs was slightly thickened and blurred, the heart shadow was enlarged. Cardiac insufficiency was considered. Cardiac colour ultrasound suggested the following: weak left ventricular wall activity, left atrial and left ventricular enlargement, mild mitral valve closure, poor left ventricular systolic function and ejection fraction EF of 0.19. Mechanical assistance needed to continue for patient survival. Left ventricular MCE was performed, and the contrast filling defect in the anterior left ventricular wall, anterior interstitial wall and apex myocardium was found in segments 7, 8, 13, 14 and 15 (Section 17) (Fig. 4). End-stage heart failure was diagnosed with indications for heart transplantation, and orthotopic allotransplantation was decided after multidisciplinary consultation in the whole hospital. On day 8 of admission, the patient underwent heart transplantation. The procedure was smooth, and the patient returned to the intensive care unit. ECMO, IABP auxiliary support, balaliximab anti-rejection, vancomycin and meropenem anti-infection procedures were continued. Erythrocyte infusion was performed to alleviate anaemia and improve coagulation function, haemostasis and sedation. Extensive myocardial ischemic necrosis and thrombosis were seen (see Fig. 5). Myocardial pathology was determined, and results showed the following: large coagulative necrosis in microscopic myocardial tissue; nuclear fragmentation and disappearance; red-dyed cytoplasm or irregular coarse granular appearance; formation of a contractile zone; interstitial oedema; scattered surrounding neutrophils infiltration; and congested bleeding zone in the infarct area. The left ventricle was predominant, and a small focal infarct area appeared in the right ventricle (see Fig. 6). On the first postoperative day. The patient had stable respiratory and stable circulation, and the IABP assistance was removed. Review of cardiac colour ultrasound indicated the following: the left ventricular systolic function was normal; ejection fraction EF was 0.62; cardiac function was good; and stable hemodynamic status. ECMO assistance was removed, and the respiratory circulation was stable after withdrawal. On the eighth postoperative day, the patient’s respiratory function was normal. The oxygenation index was normal after shutdown. The tracheal tube was removed, and the breathing was smooth after extubation. On the eleventh day, the patient had stable vital signs and was transferred to the general ward. The patient was successfully discharged after 86 days of hospitalisation.