An 80-year-old man was referred to our hospital for syncope caused by severe AS. Twelve years previously, he had undergone CABG that comprised bypass grafting of the left internal thoracic artery (LITA) to the left anterior descending coronary artery (LAD) and of the saphenous vein from the ascending aorta to circumflex branch. He had also undergone pericardiectomy for constrictive pericarditis 10 years prior to the surgery. Unfortunately, the details of the surgical procedure and findings were unknown because the surgery for pericarditis was performed at another hospital. Preoperative computed tomography indicated that the pericardium around the aorta and right-sided left atrial area were almost intact. However, severe adhesion appeared to be present from the anterior to diaphragmatic aspects of the heart. Echocardiography showed severe progressive AS with moderate aortic regurgitation. Other examination data were as follows: aortic valve area of 0.6 cm2, mean trans-aortic valvular pressure gradient of 86 mmHg, bicuspid aortic valve, and left ventricular ejection fraction of 70%. Although the patency of the LITA–LAD graft was confirmed, computed tomography and coronary arteriography showed that the saphenous vein graft was occluded. We discussed the treatment strategy (TAVR or AVR) in a “heart team.” The heart team considered TAVR not to be suitable for his deformed bicuspid aortic valve. We decided to use a right parasternal minimally invasive approach, which is optimal for performing AVR to avoid median sternotomy-related injury, especially to the patent LITA–LAD graft.
A 7-cm right parasternal incision extending from the inferior edge of the second costal cartilage to the superior edge of the fourth costal cartilage was made (Fig. 1a). Both the third and fourth costal cartilages were totally excised following exposure of the second and third intercostal spaces by division of the pectoralis major muscle. The right ITA was ligated immediately inferior to the second costal cartilage and immediately superior to the fifth costal cartilage. The intercostal muscles and pleura were incised. The pericardium around the aorta was intact as estimated by computed tomography, and the adhesion around the aorta was less severe than predicted preoperatively. Pericardial stay sutures were placed, providing excellent exposure of the ascending aorta. Next, the ascending aorta was exposed and controlled (Fig. 1b). Cardiopulmonary bypass (CPB) using the femoral artery and vein was initiated. A left ventricular vent cannula was placed in the right superior pulmonary vein, and then the patient was cooled to 28 °C. Because of severe adhesion around the right atrium, a retrograde catheter could not be inserted. We only injected antegrade cardioplegia solution after the ascending aorta was cross-clamped. Once cardioplegic arrest was obtained, ventricular fibrillation developed. Therefore, we administered 40 meq/L potassium via the CPB to maintain a blood potassium concentration of 8 meq/L. Antegrade cold blood cardioplegia was induced intermittently every 20 min. A 19-mm Mosaic pericardial bioprosthesis (Medtronic, Minneapolis, MN, USA) was implanted (Fig. 1c). After the patient had been placed in the Trendelenburg position, the aorta was unclamped and de-airing was accomplished through suction on the cardioplegia aortic root needle with flooding of CO2 gas in the operative field. The aortic cross-clamping time was 83 min. A ventricular pacemaker wire was placed in the right ventricle while the CPB was running, and the heart was decompressed. The patient was smoothly separated from CPB. The operation time and CPB time were 348 and 158 min, respectively. Immediately after surgery, the absence of ischemic damage to the myocardium was confirmed based on the serum creatine kinase MB concentration and electrocardiography findings. Echocardiography also showed normal movement of the left ventricle. The postoperative course was uneventful, and the patient was discharged on postoperative day 7.
