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Acute Left Main Coronary Occlusion Following Transcatheter Aortic Valve Implantation

DOI: 10.4236/wjcd.2024.1411061, PP. 695-700

Keywords: TAVI (Transcatheter Aortic Valve Implantation), LMCA (Left Main Coronary Artery), CAD (Coronary Artery Disease), TEE (Transoesophageal Echocardiography), Intravascular Ultrasound, Severe Calcific Aortic Stenosis, CABG (Coronary Artery Bypass Grafting)

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Abstract:

Background: Aortic stenosis (AS) is caused by either age-related degeneration of aortic valve or congenital malformation of aortic cusps. Severe aortic valve stenosis is a clinically emerging diagnosis in the current world. The three cardinal signs of severe AS are dyspnea, syncope, and angina. Transcatheter aortic valve implantation is one of the safe and effective methods for treating severe aortic valve stenosis, and an alternative to surgery in high-risk patients. Aortic valve calcification and changes after TAVI were specifically assessed by computed tomography. Excessive aortic valve calcification is related to procedural complications. A possible consequence is obstruction of coronary ostia. Heavy calcification of the aortic valve and surrounding structure is an important risk factor for coronary obstruction, heart block, and embolization during aortic valve implantation (TAVI). Here we present a case of an elderly old man, where critical ostial left main coronary artery (LMCA) disease was caused by shifting of a calcium speck rather than obstruction with native leaflet. He was successfully rescued by an emergent CABG. Methods and Results: This is a case of a 69-year-old man with severe calcific aortic stenosis and single-vessel CAD who underwent TAVI with a relatively unremarkable course. Notably, his pre-operative TAVI angiography showed no LMCA stenosis. But 10 days later he presented to the ER with acute myocardial infarction with peak high-intensity troponins, diffuse ST changes, and cardiogenic shock. Urgent coronary angiography and intravascular ultrasound showed critical LMCA stenosis caused by a speck of calcium externally abating the vessel. He underwent emergency coronary artery bypass grafting; intraoperative TEE confirmed the etiology. He had an uneventful postoperative course and was successfully weaned off vasoactive medications. Conclusion: This case illustrates that obstruction of coronary ostia could be a possible complication of TAVI. Calcium distribution should factor in TAVI versus surgical candidacy. Calcium shifting should be watched closely during valve deployment, post-TAVI coronary angiogram should be considered if shifting was significant or suspected to compromise coronary arteries.

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