Left Main Coronary Artery Dissection During Aortic Valve Replacement

A 73-year-old man was scheduled to undergo aortic valve replacement (AVR) for severe aortic stenosis. Transthoracic echocardiography showed normal left ventricular function with no regional wall motion abnormalities (RWMA). Preoperative coronary artery angiography showed no significant stenosis. Written informed consent was obtained from the patient for publication of this report.Figure 1.: Intraoperative transesophageal echocardiography at the midesophageal aortic valve short-axis view after aortic valve replacement with a bio-prosthesis. A mass with linear density in the left main coronary artery can be seen (solid arrow). A, Two-dimensional imaging. B, Schematic diagram. AV indicates aortic valve; LA, left atrium; LMCA, left main coronary artery.Figure 2.: Pulsed wave Doppler measurement of left main coronary flow velocity, which was obtained from the modified midesophageal aortic valve short-axis view. Peak velocity, which was oriented in the positive direction in diastole, was 1.4 m/s. Note: ECG demonstrates atrial pacing rhythm with first-degree atrioventricular block. “A” indicates an atrial pacing pulse. “B” indicates a QRS complex. ECG indicates electrocardiogram.Figure 3.: Postoperative optical coherence tomography imaging. An intimal tear divides the true and false lumens (arrow). FL indicates false lumen; TL, true lumen.Transesophageal echocardiography (TEE) before initiating cardiopulmonary bypass (CPB) showed no additional findings compared with preoperative transthoracic echocardiography. During CPB, myocardial protection was achieved by antegrade (via the ascending aorta) and retrograde (via the coronary sinus) administration of cardioplegia. The aortic root was markedly calcified. After removal of calcification, the aortic valve was replaced with a bio-prosthesis. After aortic cross-clamp release, normal function of the prosthetic valve was confirmed. However, during weaning off CPB, a localized linear density was observed in the proximal left main coronary artery in the short-axis view of the midesophageal (ME) aortic valve (Figure 1; Supplemental Digital Content, Video 1, https://links.lww.com/AA/B725). This linear density suggested a coronary artery dissection flap. No aortic root dissection was detected. In the short-axis view of the modified ME aortic valve, coronary blood flow velocity was measured by pulsed wave (PW) Doppler and showed a marked increase in diastole (1.4 m/s), which suggested coronary artery stenosis (Figure 2). Neither RWMA by TEE nor ischemia-related changes by electrocardiogram in perfusion territories of the left main coronary artery were observed. Therefore, we elected to continue weaning from CPB and perform coronary artery angiography postoperatively. Weaning from CPB was performed without difficulty, and surgery was completed with stable hemodynamics. Postoperative coronary artery angiography showed 75% stenosis in the left main coronary artery. Optical coherence tomography, a catheter-based invasive imaging system for clearly visualizing lumen morphology, showed a localized dissection (Figure 3). A drug-eluting stent was placed at the dissection site of the left main coronary artery. The patient was discharged, and the clinical course did not show any hemodynamic changes. DISCUSSION Coronary artery dissection is spontaneous or iatrogenic (Table).1–3 Iatrogenic coronary artery dissection results from catheters during percutaneous coronary intervention or cardioplegia administration, or handling during surgical procedures, such as implantation of the coronary ostia during aortic root surgery.2,3 Spontaneous coronary artery dissection typically follows aortic dissection, or it is caused by atherosclerosis, hypertension, coronary vasospasm, or pregnancy and may occur in connective tissue diseases.4 Aortic dissection can extend to a coronary artery, and it involves the right coronary artery, typically.5 In our case, there was neither an ascending aorta nor right coronary artery dissection. Additionally, the coronary artery ostia were not directly cannulated as intraoperative myocardial protection was achieved using antegrade and retrograde administration of cardioplegia. We speculate that the cause of dissection was an intimal tear at the ostium of the left main coronary artery when calcification of the aortic root was removed.Table.: Etiology of Coronary Artery DissectionThis case presented a considerable challenge in decision making regarding the treatment strategy. Although TEE is useful for diagnosing coronary artery ostial dissection, detailed assessment of the coronary artery lumen, progression of dissection, or the number of affected branches is difficult.6 Following AVR, an intracoronary mass should be differentiated from ultrasound artifacts as well as an intimal flap, suture material, and calcified debris. A dissection flap has a similar echogenicity to the wall of a coronary artery and does not cross physical boundaries. On the other hand, masses, such as retained sutures or calcified debris, appear highly echogeneic.7 Measurement of coronary blood flow velocity with TEE is challenging because it is difficult to position the PW Doppler sample volume inside the moving coronary artery. The diagnostic accuracy of PW Doppler is improved by using a lower frequency transducer and scanning at a decreased depth, in order to increase the pulse repetition frequency, parallel alignment with blood flow, and proper setting of the velocity scale. To obtain more accurate findings, epicardial ultrasound imaging might help in the definitive diagnosis. Stenosis of the left main coronary artery should be suspected if coronary blood flow velocity is increased above the normal range of 0.3–0.4 m/s.8 If new RWMA consistent with left main coronary artery perfusion zones appear intraoperatively, surgical revascularization should be undertaken without hesitation. Clinician’s Key Teaching Points By Kent H. Rehfeldt, MD, and Nikolaos J. Skubas, MD Coronary artery dissection is an iatrogenic complication or occurs spontaneously. Percutaneous interventions, direct administration of cardioplegia into the coronary ostia, or surgical manipulation of the aortic root are the most frequent iatrogenic causes. Coronary artery dissection can occur spontaneously from retrograde progression of aortic dissection or in the setting of hypertension, pregnancy, or coronary vasospasm. Echocardiographic features consistent with coronary artery dissection include the visualization of a linear density within the coronary lumen. Additionally, the dissection flap can elevate blood flow velocities above the normal range of 0.3–0.4 m/s. The finding of new RWMA in the corresponding myocardial territory is suggestive of an acute reduction in coronary blood flow. In this case, a linear density, suspicious for a dissection flap, was observed by TEE (short-axis view of the ME aortic valve) in the left main coronary artery lumen following aortic root decalcification and AVR. Additionally, the diastolic flow velocity in the left main coronary artery was increased to 0.7 m/s. However, given the absence of associated RWMA, the lack of ascending aorta dissection, and the hemodynamic stability of the patient, the operation was completed and the patient was transferred to the catheterization laboratory where the diagnosis of left main coronary dissection was confirmed and treated by stent placement. Coronary artery dissection should be distinguished from other causes of echogenic material within the vessel lumen. A dissection flap has an echo density similar to that of the coronary artery wall and does not cross anatomic boundaries. Sutures or calcified debris display an increased echo density compared with a dissection flap, whereas artifacts may extend beyond the coronary lumen. ACKNOWLEDGMENTS We appreciate Dr Yoshihiro Takeda for the assessment. DISCLOSURES Name: Kenta Nakao, MD. Contribution: This author was in charge of the patient and helped prepare the manuscript. Name: Toshiyuki Sawai, MD, PhD. Contribution: This author helped manage the manuscript, figures, video, and table. Name: Junko Nakahira, MD, PhD. Contribution: This author helped prepare the figures and the video. Name: Ayako Hamakawa, MD. Contribution: This author helped prepare the references. Name: Hisanari Ishii, MD, PhD. Contribution: This author was in charge of the patient and helped prepare the manuscript. Name: Toshiaki Minami, MD, PhD. Contribution: This author helped perform a native check. This manuscript was handled by: Nikolaos J. Skubas, MD, DSc, FACC, FASE.