INDICATIONS FOR THE PROCEDURE
This is a 63-year-old patient with not known history of coronary artery disease who complained of chest pain. She came to the Emergency Room on 01/04/2019. She was ruled in for an ST elevation acute myocardial infarction . The patient went to the catheterization lab and a coronary angiogram was done, which showed a preserved left ventricular function, totally occluded right coronary artery. A PCI with stent placement of the right coronary artery was performed successfully with an opening with placement of the stents in the distal right coronary artery and flow in the PDA. However, the patient became unstable, at that point, with signs of acute pulmonary edema, which was difficult to explain based on the coronary angiogram finding. A transthoracic echo was performed which showed a possibility of a right ventricular wall dissection with impending rupture and the possibility of a ventricular septal defect as a complication of the acute myocardial infarction. The patient’s blood pressure was in the 90s, heart rate 130-140. She became dyspneic with significant shortness of breath on oxygen. Cardiac surgery was consulted, I reviewed the echo as well as coronary angiogram with and a decision was made to bring the patient emergently to the operating room. The patient was intubated in the CCU in preparation for her surgery.

PROCEDURE IN DETAIL
The patient was brought to the operating room and laid in a supine position on the table. She was prepped and draped in the usual sterile fashion after antibiotics were given. The chest was opened through a standard median sternotomy and then very cautiously opened the pericardium. There was some bloody fluid, but not obvious blood and no signs of acute bleeding. The patient was heparinized intravenously. I examined the heart and I noticed that the inferior wall of the right ventricle had a large area affected by an acute myocardial infarction. This involved of the area adjacent to the diaphragm.( inferior wall ). The anterior wall seems to be normal, unaffected by the myocardial infarction. Basically the area affected was between an acute marginal branch and the PDA. I could hear a significant thrill just by palpating that area. I also noticed that the wall was extremely thin, so it was a communication with at least one of the ventricles, the right ventricle but possible the LV also, creating a VSD.

The aorta was cannulated with a 21-French aortic cannula, the superior vena cava with a 30-French venous cannula and the IVC with a 32-French venous cannula.

Cardiopulmonary bypass was commenced without any hemodynamic problems. The aorta was cross-clamped and 800 mL of cold blood cardioplegia were given through the aortic root. This arrested the heart in diastole without any distention. Again, I examined the heart very carefully. I could not see anything abnormal except this inferior wall of the right ventricle, again between the acute marginal and the PDA; This area was beefy red and very thin on a couple of the places in a way that I could visualize the blood through the epicardium. Appeared like an impending rupture of the RV. Based on those specific findings, I decided to open the right ventricle through the pseudoaneurysm. The incision was from cranial to caudal (toward the apex). I was able to open the pseudoaneurysm chamber of the right ventricle, which seems to communicated with the right ventricle. may also had a communication with the left ventricle but it was difficult to find it because of the anatomy created by the RV wall dissection. This might have been the reason why it seems that there was a ventricular septal defect on the transthoracic echo. The pseudoaneurysm area was fairly well defined, so I decided to open it, excise the portion which was obviously not viable ( resection of the pseudoaneurysm sac ). Then, I very carefully opened the right ventricle and inspected visually and by palpation, the septum all the way from the tricuspid valve, including under the leaflets and to the apex. I could not see any ventricular septal defect and actually the septum did not seem to be involved in the acute myocardial infarction. As I mentioned before, the communication might have been betwen the LV and the pseudoaneurysm sac. After the debridement and excision of the pseudoaneurysm I did a careful inspection of the inside of the right ventricle, and not finding anything abnormal except the area affected by acute myocardial infarction, I decided to close the right ventricular wall in a way that the area of dissection and possible communication with LV was securely closed . This was done in 2 layers, the first layer was a horizontal mattress using 3-0 Prolene with pledgets on both sides. The second layer was an over and over layer again with a Teflon felt on top of the suture line. In this way, the suture line was protected with three rows of a Teflon felt; one to the left and one to the right, and one on top of the suture line.

The patient was positioned in Trendelenburg with the vent on and the crossclamp was removed. Two temporary pacer wires were attached to the right atrium and right ventricle and the patient was paced AI with a rate of 80 per minute. Then the lungs were ventilated. The patient was rewarmed and then the patient was weaned off cardiopulmonary bypass without the need of any inotropic support. The heparin was reversed with protamine and the venous and aortic cannula were removed.

Potential bleeding sites including closure of the right ventricular and cannulation sites were checked. There was no significant bleeding. Considering the fact the patient was given 180 mg of Brilinta in the cath lab with the PCI procedure, I administered 2 units of platelets to avoid postop bleeding.

Two chest tubes were placed using 19-French Blake drains. The sternum was closed with stainless steel wires. The linea alba and presternal fascia with #1 Vicryl suture, the skin with 3-0 Monocryl. Sterile dressing was applied. The patient tolerated the procedure well and left the Operating Room in stable condition.