Following the withdrawal of CPB and onset of acute left heart failure, TEE showed a high-brightness massive shadow at the left coronary ostium (Fig. 3) that was absent prior to surgery (Fig. 2). The massive shadow was considered part of the intimal piece that peeled off during decalcification and removal of calcified lesions in the valve annulus. We believe that as the cardiac output is increased, the floating intimal piece obstructs the coronary origin, leading to coronary ostial stenosis.
Coronary ostial stenosis is a fatal condition resulting from obstruction of the coronary ostia in the subacute phase following AVR (typically 1–6 months post-AVR). It can lead to, e.g., angina, left heart failure, and acute pulmonary edema. Thus, early diagnosis and treatment are crucial. Its frequency of onset is 1 to 5% and is diagnosed by coronary angiography and treated by coronary artery bypass surgery or percutaneous coronary angioplasty [1–7].
Although the causes of coronary ostial stenosis are not clear, various reports have suggested potential pathogenic mechanisms. For instance, Funada [1] reported three patients who developed coronary ostial stenosis 1 to 6 months after AVR with direct myocardial protection/perfusion. These patients exhibited a wide range of ostial fibrosis by intravascular echocardiography. In another study, Roberts and Morrow [8] reported postoperative pathological changes including fibrotic thickening of the endothelium of the coronary artery upon necropsy of patients after AVR. Based on these observations, direct cannulation of the coronary artery ostium and myocardial protection/perfusion appear to cause acute traumatic tissue damage and tissue remodeling during the trauma healing process, leading to delayed coronary ostial stenosis [1].
Coronary ostial stenosis is generally regarded as a late-onset disease, and only three cases [9–11] have been reported with perioperative onset. In two of the three cases, the prosthetic valve itself was the cause of stenosis. In one report by Umran [9], calcified lesions remaining in the right coronary ostium was thought to have caused a calcium embolism. In that study, right heart failure and right coronary ostial stenosis were diagnosed after AVR but before withdrawal of CPB. Thus, CABG was performed to the right coronary artery and an intra-aortic balloon pump (IABP) was inserted, followed by withdrawal of CPB.
The pathogenesis of coronary ostial stenosis in the present case is similar to that reported by Umran, although the timing of onset differs. In the present case, once CPB was withdrawn and circulation dynamics stabilized, left heart failure due to left coronary ostial stenosis occurred. Thus, CPB was established again and CABG was performed. As left heart function improved after CABG, it was possible to withdraw the patient from CPB without the need for an IABP.
Coronary ostial stenosis due to remnant intimal calcified lesions may occur at any time after CPB establishment and can be effectively diagnosed by TEE.
Regional wall motion abnormality of left ventricle and left heart failure due to coronary air embolism sometimes occur at heart surgery with CPB. It often occurs in early stage of withdrawal of CPB because of left heart chamber’s remnant air. Although the onset time is the same at this case, there are some different points. First, the risk of air embolism is considered to be low because remnant air in the heart chamber was vented carefully observing with TEE. Second, a brightness massive shadow at the left coronary ostium was brighter than the shadow of air and did not move like floating air. After CABG, TEE showed remnant of high-brightness massive shadow with no mobility. Finally, in general, air embolism occurs in the right coronary artery which is on the belly side; however, in this case, left coronary embolism happened. Considering the above things comprehensively, massive air embolism was considered negative.
