The effectiveness of extracorporeal membrane oxygenation in a patient with post myocardial infarct ventricular septal defect

A 62-year-old woman with a history of hypertension was admitted with complaints of chest pain and shortness of breath of 3 days duration. Her heart rate was 89 bpm, blood pressure 105/70 mmHg, and temperature 36.5 °C. Chest X-ray revealed cardiomegaly and pulmonary edema. On admission, blood tests revealed Hb 10.9 g/dl, troponin I 5.26, CK-MB 4 ng/ml. Arterial blood gas revealed pH 7.32, pCO 2 21.6, pO 2 80.2 mmHg, bicarbonate 11 mmol/l and SaO 2 92.8 % on room air. Electrocardiography (ECG) showed ST-segment elevation and Q waves in leads V1-4 and coronary catheterization revealed total proximal occlusion of the anterior interventricular branch of the left coronary artery. Angioplasty and stent implantation were performed, and chest pain, shortness of breath, and general malaise disappeared after the procedure. However, the day after angioplasty and stenting, the patient suddenly experienced fatigue, dyspnea, and tachycardia. At this time, her blood pressure was 70/50 mmHg and heart rate 120 bpm. On physical examination, auscultation revealed a 3/6 pan-systolic murmur in the left parasternal area.

Transthoracic echocardiography (TTE) with Doppler showed an akinetic area in the apex, an ejection fraction of 43 %, and confirmed 15 mm and 8 mm VSDs in the apicoanterior and mid anterior ventricular septum (Fig. 1). Tricuspid regurgitation was mild with moderate pulmonary arterial hypertension with systolic pulmonary artery pressure of 50 mmHg. The total pulmonary to total systemic blood flow ratio (Qp/Qs) of VSD was 5.7.

Symptoms of congestive heart failure progressed due to low cardiac output, and the patient was transferred to the intensive care unit to treat the heart failure and to prevent progression of cardiogenic shock. After her intubation, we administered maximum dose of inotropics and vasopressors. Despite optimal medical treatment, pulmonary hypertension and pulmonary congestion gradually increased, and urine output decreased. We decided to insert an extracorporeal membrane oxygenation (ECMO) device for stabilization purposes before surgical repair, and ECMO support was emergently initiated via a left femoral artery and right femoral vein. Arterial and venous cannulations were performed percutaneously, and distal limb perfusion was achieved with an introducer sheath (7 Fr). Stabilization of the patient was immediate and her clinical status improved. Accordingly, surgical VSDs repair was postponed. After 4 days from the implantation, signs of left leg ischemia developed; hence, we decided to perform surgical repair. On the same day, closure of the VSDs was performed using two patches of bovine pericardium by bilateral ventriculotomy. Using interrupted mattress suture, one patch was placed on the left ventricular (LV) side and the other on the RV side of the VSD. Lastly, both ventriculotomies were closed using Teflon strips to buttress the suture lines. Cardiopulmonary Bypass (CPB) and aortic cross clamp (ACC) times were 219 and 194 min, respectively. Immediately following the surgery, the patient was stable and had a good urine output. Her postoperative course was uneventful. On the third postoperative day, the patient was extubated and transferred to the general ward on the fourth postoperative day.

The TTE prior to discharge showed a residual 6 mm VSD in the mid anterior ventricular septum, and at this time, the total pulmonary to total systemic blood flow ratio (Qp/Qs) of the residual VSD was 1.1. However, the patient’s hemodynamics were stable. The patient was discharged on the fourteenth postoperative day without symptoms of heart failure.

After thirty months postoperatively, the patient remained in good condition clinically. The patient’s blood pressure was well controlled and renal function was normal. Follow-up TTE revealed no significant changes.