Cardiac arrest caused by coronary occlusion during transcatheter aortic valve implantation: a unique cause

Abstract

Coronary artery occlusion (CAO) is a rare but life‐threatening complication of transcatheter aortic valve implantation (TAVI). The mechanism of CAO is the displacement of the native calcified valve leaflet over the coronary ostium. Here, we report on a woman who experienced sudden cardiac arrest and abrupt CAO during TAVI, which was caused by two different original obstructions, a rupture of aortic plaque or a partial tear of the aortic intima blocking the upper 2/3 of the left main trunk (LMT) ostium, and the transcatheter heart valve (THV) blocking the lower 1/3 of the LMT ostium. She was eventually successfully treated with the chimney stenting technique. Aortography other than coronary angiography was used to ascertain CAO. In patients presenting with abrupt cardiac arrest or cardiogenic shock with LMT occlusion, there must be prompt identification, and the causes of CAO may be various and rare. The identification of CAO relies not only on CAG but also on aortography, especially if the locations and origins of obstructions are special. Supportive therapy with an attempt at percutaneous revascularization is necessary. Pre‐procedural assessment is crucial prior to TAVI interventions. In cases with high risk of CAO, upfront coronary artery protection can be provided.

Introduction

Coronary artery occlusion (CAO) is a rare but serious complication of transcatheter aortic valve implantation (TAVI) that is associated with a high mortality rate. ¹ It typically occurs within minutes of prosthetic valve deployment. ¹ Chimney stenting is an infrequently used technique to treat or prevent CAO in the setting of TAVI, and the acute procedural results of its use have been encouraging. ² Here, we report on a case of sudden cardiac arrest and abrupt CAO during TAVI, which was caused by two different original obstructions, a rupture of aortic plaque or partial tear of the aortic intima blocking the upper 2/3 of the left main trunk (LMT) ostium, and the transcatheter heart valve (THV) blocking the lower 1/3 of the LMT ostium. Eventually, the patient was successfully treated with the chimney stenting technique.

Case report

A 76‐year‐old woman with hypertension presented with sudden persistent chest pain lasting 6 h and associated with New York Heart Association functional class II dyspnoea. A grade III/VI systolic ejection murmur was auscultated at the right 2nd intercostal space in the parasternal line. Laboratory testing was notable for myocardial injury with myoglobin of 178.81 ng/mL (<110 ng/mL), creatine kinase isoenzyme‐MB of 20.3 μg/L (< 5.0 μg/L), high‐sensitive troponin I of 1.838 ng/mL (0–0.100 ng/mL), and brain natriuretic peptide of 128.87 pg/mL (0–100.00 pg/mL). The 12‐lead electrocardiography (ECG) showed a sinus rhythm with non‐specific lateral ST‐segment change. Transthoracic echocardiography (TTE) showed severe aortic stenosis (AS) jet a peak gradient of 94 mmHg, a mean gradient of 55 mmHg, and an aortic valve area of 0.4 cm² with 56% of the estimated ejection fraction (EF). A pre‐procedure computed tomography (CT) scan (Figure 1 A ) revealed the average annulus diameter was 20.2 mm (Figure 1 B ). The diameter of the sinus of Valsalva was 24.2 × 19.7 × 25.7 mm (Figure 1 C ). The sinotubular junction (STJ) diameter was 19.4 × 22.3 mm (Figure 1 D ), the left coronary artery (LCA) ostium height was 11.8 mm (Figure 1 E ), and the right coronary artery (RCA) ostium height was 17.6 mm (Figure 1 F ). Coronary CT angiography (CCTA) showed 50% stenosis in the LMT. Based on the patient's preference to refuse surgery, the decision was made to proceed with synchronous percutaneous coronary intervention (PCI) of the ostial LMT, as well as a TAVI.

Figure 1.

The measurements of computed tomography scan. (A) Illustration of aortic valve, aortic root and coronary height. (B) Annulus diameters and perimeter. (C) Sinus of Valsalva depths. (D) Sinotubular junction diameter. (E) Left coronary height. (F) Right coronary height.

As per institutional protocol for high‐risk cases, the patient was under general anaesthesia and intubated for airway protection to undergo the procedure. Coronary angiography (CAG) showed a moderate stenotic lesion (50%) in the LMT (Figure 2 A ). A Promus Premier 4.0 × 8.0 mm drug‐eluting stent (DES) was positioned to the stenosis of the LMT (Figure 2 B ). Then, the native aortic valve annulus was predilated with an 18‐mm AT Gold balloon under rapid pacing (Figure 2 C and Video S1 ). However, the filling defects that obstructed nearly 70% of the LMT ostium after valve predilation were ignored. Her haemodynamic stability was maintained, and X‐ray showed normal cardiac motion after valve predilation. A 23‐mm VenusA valve (VENUS MEDTECH, Hangzhou, China; Figure 3 ) was successfully deployed under rapid pacing into the annulus (Figure 2 D and Video S2 ). However, the patient's blood pressure suddenly dropped, and her cardiac motion weakened significantly, followed by cardiac arrest. Chest compression was immediately initiated and continued along with veno‐arterial extracorporeal membrane oxygenation (VA‐ECMO). Pericardial tamponade, aortic dissection, and significant aortic regurgitation were excluded by transesophageal echocardiography (TEE). With a high suspicion of CAO, repeated CAG was performed excluding CAO, and the coronary flow was stable (Figure 2 E and Video S3 ). Then, aortography showed an unidentified tissue obstructing the LMT ostium (Figure 2 F and Video S4 ). A DES (4.0 × 10.0 mm) was instantly deployed, extending from the proximal portion of the LMT ostium and parallel to the THV, thus establishing TIMI 3 flow—namely, via the chimney technique—overlapping with the previous DES (Figure 2 G,H and Video S5 ). After stent optimization, her heart rate and blood pressure were gradually recovered but remained unstable despite the use of VA‐ECMO and high‐dose vasoactive agents. Post‐procedural anatomical assessment was conducted via TEE, which revealed appropriate deployment and mildly impaired left ventricular function with 48% of EF. The time from cardiac arrest to successful resuscitation was about half an hour.

Figure 2.

Coronary artery and aortography images. (A) CAG showed a moderate stenotic lesion in LMT. (B) Deployment of DES to the stenosis of LMT. (C) Unidentified tissue (arrow) obstructed nearly half LMT ostium after native aortic valve predilatation (Video S1 ). (D) Deployment of Venus‐A valve (Video S2 ). (E) Repeated CAG showed no CAO (Video S3 ). (F) Repeated aortography showed left coronary artery did not developed (Video S4 ). (G,H) Deployment of chimney DES and repeated aortography (Video S5 ). CAG, coronary angiography; CAO, coronary artery occlusion; DES, drug‐eluting stent; LMT, left main trunk.

Figure 3.

The sizing chart of VenusA‐Valve L23 transcatheter aortic valve (the use of copyrighted illustration with permission from VENUS MEDTECH, Data S1 ).

The patient was transferred to a cardiac intensive care unit post‐procedure for monitoring with VA‐ECMO and ventilator‐assisted breathing. However, she was still hypotensive and in cardiogenic shock. Excluding the ST‐segment elevation and confirming diffuse hypokinesis of the left ventricular wall motion with only 25% of the EF—which was considered to be related to the myocardial injury and left ventricular stunning caused by the abrupt CAO—an intra‐aortic balloon pumping (IABP) was inserted. On post‐operative day one, her haemodynamics were gradually stable, and left ventricular function was recovered with 55% of EF. She was successfully weaned off the VA‐ECMO in the afternoon. On the third day after the procedure, she was also successfully weaned off the invasive ventilation and IABP. She remained stable and was discharged 8 days after the procedure. At her 80‐day post‐operative follow‐up, she had no symptoms or complications. TTE revealed only the subtle thickening of the base of the interventricular septum. ECG revealed sinus rhythm without Q waves and atrioventricular block or bundle branch block.

Discussion

The case described a female patient who underwent acute CAO, resulting in cardiac arrest during a TAVI procedure. The obstructions were formed of two different parts, a rupture of aortic plaque or a partial tear of the aortic intima blocking the upper 2/3 of the LMT ostium after valve predilation and THV blocking the lower 1/3 after THV deployment. The former obstructions were uncommon and autologous, and materials of unknown origin formed a valve structure. To the best of our knowledge, this is the first such report. Due to the specific location of the obstructions, aortography rather than conventional CAG first revealed the defects. The patient was eventually successfully treated with a chimney stenting technique.

Indications for the TAVI procedure are expanding as a result of multiple randomized trials of TAVI versus surgical aortic valve replacement (SAVR). For symptomatic patients who are 65–80 years of age and have no anatomic contraindication to transfemoral TAVI, either an SAVR or transfemoral TAVI is recommended after shared decision‐making. ³ , ⁴ If combined with coronary artery disease (CAD), coronary artery bypass grafting (CABG) is recommended in patients with a primary indication for aortic valve surgery and LMT stenosis ≥50%. The heart team proposed simultaneous SAVR and CABG may have been much better for her. However, with the patient's refusal for surgery and adequate pre‐operative assessments before TAVI, the decision was made to proceed with a synchronous PCI of the ostial LMT and a TAVI.

CAO is a rare but potentially devastating complication of a TAVI. ¹ The incidence has been reported as less than 1%. ⁵ It is often caused by displacement of the diseased native or bioprosthetic aortic valve leaflet by the implanted THV towards the coronary ostia and/or STJ. ⁶ Beyond that, two cases have been reported of other rare causes of CAO. Stinis et al. reported on a distal LMT bifurcation that became obstructed by an embolized piece of native valve leaflet material 16 h after a TAVI procedure, which was demonstrated by intravenous ultrasound (IVUS) imaging. ⁷ Andreas et al. reported a case in which a calcified native coronary leaflet was pushed by the stent frame of an aortic bioprosthesis towards the left coronary ostium, causing its subtotal occlusion. ⁸ However, the obstruction of the coronary ostium in our case was more rare and unique. We reviewed the procedure video and found that the filling defects had existed, leading to nearly 70% obstruction of the LMT ostium after valve predilation. The left coronary ostium was completely obstructed after THV implantation, and thus, cardiac arrest occurred. Aortography other than CAG showed the specific occlusions in the LMT ostium, which made the situation confusing. Filling defects of nearly 70% appeared after valve predilation, located on the upper 2/3 of the LMT ostium (Figure 2 C ), whereas the lower 1/3 of the LMT ostium was visible, and the left coronaries were normally developed. It was thus possible to exclude the cause of the CAO as the native valve leaflet because the leaflet obstruction occurred from bottom to top. Therefore, we considered that the obstructions originated from the rupture of the aortic plaque or partial tear of the aortic intima. The obstructions formed a valve structure that obstructed 2/3 of the LMT ostium. When the THV was deployed, the THV perhaps obstructed the lower 1/3 of the LMT ostium. Finally, the two different parts totally obstructed the LMT ostium, leading to cardiac arrest. When performing repeated CAG, a Tig catheter may be placed at the junction of the upper obstructions and the THV. The valve obstructions could be opened by the Tig catheter, and CAG was performed from bottom to top. Thus, the LCA was visualized. However, aortography was performed from top to bottom, and the obstructions of the LMT ostium were visualized. This demonstrated that the identification of CAO relies not only on CAG but also on aortography. An illustration of the procedure is shown in Video S6 . Due to the emergency event, continuous resuscitation, repeated angiography, and the worsening status of the patient, we had no time to perform IVUS imaging to clarify the property of the obstructions.

The risk factors of CAO include low coronary heights, bulky calcified leaflets, small sinus of Valsalva, the presence of a valve‐in‐valve TAVI with either an externally mounted leaflet or stentless bioprosthesis, and the use of a TAVI prosthesis. ⁹ Pre‐procedural assessment composed of the exact risk evaluation, precise multimodal imaging, and proper planning is crucial prior to TAVI interventions. In cases with a high risk of CAO, upfront coronary artery protection can be provided by positioning a coronary guidewire, balloon, undeployed stent, or guide extension in the arteries at risk prior to THV deployment. ¹⁰ An international chimney registry study enrolled 60 cases, of which 92.9% had one or more classical risk factors for CAO. ² Upfront coronary protection was performed in 44 patients (73.3%). The absence of upfront coronary protection was the sole independent risk factor for the combined endpoint of death, cardiogenic shock, or myocardial infarction. In the present case, the patient was pre‐operatively assessed with inadequate sinus of Valsalva width, which had one risk factor of CAO. Because of the patient's preference for intervention, and with a plan to rejudge the sinus of Valsalva by aortography, we thought a TAVI was feasible and eventually proceeded with it after comprehensive evaluation. However, the surprising filling defects at the LMT ostium after valve predilatation were ignored. Otherwise, such upfront coronary artery protection should be performed before the TAVI. Additionally, it is necessary to find new risk models and tools to better predict CAO in clinical practice, not simply limited to imaging. In patients presenting with abrupt cardiac arrest or cardiogenic shock with LMT occlusion, there must be prompt identification and supportive therapy with an initial attempt at percutaneous revascularization.

There are two bailout techniques to treat CAO—the chimney stenting, which we used in the case report, and the bioprosthetic or native aortic scallop intentional laceration (BASILICA) technique. Chimney stenting was defined as the deployment of a coronary stent extending from the proximal portion of a coronary artery cranially, exterior and parallel to the THV. ² This is a simple, effective, and frequently used technique to achieve and maintain patency of the coronary arteries after abrupt CAO during the TAVI. ² Chimney technique can also be used prophylactically in cases of impending CAO. However, it should be noticed that 30‐day and 1‐year mortality was considerably higher in patients who had ‘unplanned’ LMT stenting for a coronary‐related complication during TAVI compared with TAVI patients who had ‘planned’ LMT stenting (15.8% vs. 3.0% and 21.1% vs. 8.0%, respectively). ¹¹ The potential mechanisms of chimney stent failure may be persistent turbulent flow across the THV and the coronary stent, local inflammatory processes, and galvanic corrosion between both metallic frames and chimney stent thrombosis. ¹² The optimal antiplatelet or anticoagulant strategy after TAVI is unclear and may mean that dual‐antiplatelet therapy is appropriate. The patient in our case took aspirin and ticagrelor orally, and CCTA showed no in‐stent restenosis at the 80‐day post‐operative follow‐up. BASILICA is an early‐stage transcatheter procedure to prevent CAO and works by splitting the native or bioprosthetic leaflets so that they splay after the TAVI and preserve coronary artery inflow. ¹² It appears to be effective in preventing CAO in at‐risk patients with both bioprosthetic and native aortic valve failure. However, it is not suitable for dislodgement of thrombotic or degenerative material in TAVI‐induced ostial CAO, ¹² as shown in the present case study.

Conflict of interest

None declared.

Funding

This work was supported by the National Natural Science Foundation of China [81700301] and Scientific Research Foundation of Education Department of Liaoning Province [LZ2020058].

Supporting information

Video S1. Supporting Information.

Video S2. Supporting Information.

Video S3. Supporting Information.

Video S4. Supporting Information.

Video S5. Supporting Information.

Video S6. Supporting Information.

Data S1. Supporting Information.

Gao, X. , Chen, F. , Jiang, X. , Chen, N. , Liu, J. , Luan, Y. , Yang, G. , Yin, D. , and Guo, R. (2023) Cardiac arrest caused by coronary occlusion during transcatheter aortic valve implantation: a unique cause. ESC Heart Failure, 10: 1467–1472. 10.1002/ehf2.14319.