Successful treatment of cardiac dysfunction due to left main trunk obstruction and severe acute aortic regurgitation secondary to acute type A aortic dissection using Impella: a case report

Abstract

Background

Acute type A aortic dissection (A-AAD) with severe acute aortic regurgitation (AR) and coronary involvement is a potentially fatal condition that causes left ventricular volume overload and catastrophic acute myocardial infarction. We present the successful management of a patient using Impella 5.5 following cardiopulmonary arrest caused by A-AAD with severe acute AR and left main trunk (LMT) obstruction.

Case presentation

A 50-year-old man presented with acute anterior chest pain. The patient subsequently experienced a cardiac arrest, and veno-arterial extracorporeal membrane oxygenation (VA-ECMO) was administered accordingly. Contrast-enhanced computed tomography indicated type A aortic dissection extending from the sinotubular junction to the left common iliac artery. Transthoracic echocardiography revealed inversion of the aortic flap into the left ventricular outflow tract, resulting in acute severe AR and LMT obstruction. Based on these findings, the patient was diagnosed with A-AAD accompanied by severe acute AR and LMT obstruction. Emergent total arch replacement with a frozen elephant trunk (FET) was performed. However, the patient could not be weaned from cardiopulmonary bypass owing to cardiogenic shock, necessitating the introduction of VA-ECMO. Pulmonary capillary wedge pressure remained high at 22 mmHg. Subsequently, Impella 5.5 was introduced via a branch of the vascular graft to address the extensive myocardial damage due to preoperative LMT obstruction, acute AR-induced left ventricular volume overload, and increased afterload from VA-ECMO. The patient’s cardiac function gradually improved. VA-ECMO and Impella 5.5 were weaned on postoperative day 8 and 20, respectively. However, three months postoperatively, a MitraClip was used to progress secondary mitral regurgitation associated with left ventricular remodeling after myocardial infarction. The patient gradually recovered from the neurological deficit and was transferred for physical rehabilitation five months postoperatively.

Conclusions

The patient exhibited severe cardiac dysfunction due to extensive myocardial infarction and acute AR from A-AAD. Retrograde perfusion via VA-ECMO was required for systemic organ perfusion but was expected to hinder cardiac recovery. This report demonstrates that Impella effectively aids the restoration of cardiac function in such desperate conditions.

Background

Acute type A aortic dissection (A-AAD) with severe acute aortic regurgitation (AR) and coronary involvement is a potentially fatal condition that causes left ventricular (LV) volume overload and catastrophic acute myocardial infarction. To manage this condition, the reestablishment of adequate coronary blood flow, postoperative treatment of post-ischemic myocardial recovery, and a low cardiac output must be considered. Primary coronary revascularization and early aortic repair are reported to be necessary to prevent extensive myocardial damage and rescue critically ill patients [1]. However, in our case, percutaneous coronary revascularization was not feasible for the aortic flap. In this report, we present a case of cardiopulmonary arrest due to A-AAD with severe acute AR and left main trunk (LMT) obstruction successfully managed using Impella 5.5.

Case presentation

A 50-year-old man with a history of hypertension and hyperlipidemia developed acute anterior chest pain and was admitted to our hospital. The patient’s hypertension and hyperlipidemia were untreated, but he was taking an oral hypoglycemic medication for diabetes. There was no family history of cardiovascular disease. On arrival at the emergency department, the patient was in a disturbed state, with a Glasgow Coma Scale of E3V3M5. The patient’s height, weight, and body mass index were 172 cm, 80 kg, and 27 kg/m², respectively. His heart rate and SpO₂ were 74 bpm and 85% with 10 L/min oxygen supply, respectively, whereas the blood pressure was unmeasurable. Laboratory data showed levels of creatine kinase (CK), CK-muscle brain (CK-MB), lactate, troponin T, and hemoglobin A1c (HbA1c) of 348 IU/L, 49 IU/L, 6.0 mmol/L, 0.023 ng/mL, and 7.2%, respectively. The blood gas analysis revealed the following values: pH 7.101, pCO2 36.3 mmHg, pO2 47.6 mmHg, HCO3 10.8 mmol/L, and base exces (BE) -18.2 mmol/L. The electrocardiogram (ECG) showed elevated ST-segment in lead aVR. Transthoracic echocardiography (TTE) revealed inversion of the aortic flap into the LV outflow tract, resulting in acute severe AR and LMT obstruction (Fig. 1a), as well as mild mitral regurgitation (MR).

Fig. 1

(a) Transthoracic echocardiography shows an inversion of the aortic flap into the left ventricular outflow tract. (b) Contrast-enhanced computed tomography reveals type A aortic dissection extending from the sinotubular junction and narrowed true lumen

During the TTE, the patient experienced a cardiac arrest. After approximately 10 min of cardiopulmonary resuscitation (CPR), spontaneous circulation was restored. However, ventricular fibrillation occurred, necessitating the introduction of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) via the right common femoral artery and vein. The interval between CPR and initiation of ECMO, defined as CPR duration, was 18 min. Subsequently, a contrast-enhanced computed tomography (CT) revealed A-AAD extending from the sinotubular junction to the left common iliac artery (Fig. 1b). Intraoperative transesophageal echocardiography (TEE) revealed inversion of the aortic flap into the LV outflow tract (Fig. 2a).

Fig. 2

Operative findings. (a) Transesophageal echocardiography shows an inversion of the aortic flap into the left ventricular outflow tract. (b, c) The dynamic obstruction of the left main trunk (LMT) was repaired by repositioning the aortic flap. (d) Proximal reinforcement was performed with a Teflon felt inside and outside using continuous mattress sutures

Emergent total arch replacement (J graft 4 branched 24 mm, Japan Lifeline, Tokyo, Japan) with a frozen elephant trunk (FET) (Frozenix 25 × 90 mm, Japan Lifeline, Tokyo, Japan) was performed. A 5 − 0 polypropylene single purse-string suture was placed on the exposed anterior axillary artery. Bilateral axillary cannulation was performed directly using a 14 F cannula (PCKC-A-14, Senko Medical Instrument Mfg, Co., Ltd., Tokyo, Japan) using the Seldinger technique. A quadfurcated circuit from the main pump was used for arterial perfusion as follows: two branches for the bilateral axillary artery, one for the femoral artery, and one for the fourth branch of the J graft for rewarming. The second pump was used to perfuse the left common carotid artery (LCCA) for antegrade selective cerebral perfusion. The arterial pressure was monitored from three arterial lines, including bilateral radial and left femoral arteries. Cardiopulmonary bypass (CPB) was initiated at half flow via cannulation of the bilateral axillary arteries and the superior vena cava. The inflow and outflow cannulas of ECMO inserted in the right common femoral artery and vein were connected to the CPB, which was set to full flow. An LV vent was inserted through the right upper pulmonary vein. After the rectal temperature reached 28 °C, a retrograde cardioplegic catheter was inserted directly into the coronary sinus. Under circulatory arrest and after proximal clamping of the brachiocephalic trunk and the left subclavian artery (LSA), perfusion of the right carotid artery, bilateral vertebral, and axillary arteries was initiated through direct insertion of cannulas. Antegrade selective cerebral perfusion was initiated after the insertion of a perfusion catheter in the LCCA. Subsequently, the aorta was open and transected distal to LCCA. Cardioplegia was simultaneously administered in a retrograde manner. The entry was observed in the ascending aorta. Distal anastomosis was performed at zone 2. The orifice of the transected LSA located distal to the distal anastomosis site was closed with felt strips. The FET was inserted into the true lumen with the proximal tip of the stent portion placed 1 cm deeper from the distal anastomosis site under direct vision. The device was secured in that position, and the FET was deployed by pulling back the outer sheath. Consequently, the distal end of Frozenix was positioned at the Th5 level. The excess proximal portion of the non-stented polyester tube was cut at the distal anastomosis site to ensure that the proximal non-stented portion remained inside the aorta due to its porosity. The circumference of the stump was reinforced with a felt strip placed outside the adventitia and the graft of the FET placed inside the intima using horizontal mattress continuous sutures. The reinforced aorta was sutured end-to-end to a J graft, which was cut at 2 cm distal from the origin of the branch for the LSA, and the fourth branch was directed toward the superior vena cava for guidance to the right anterior thoracic region to introduce Impella. Systemic distal reperfusion and rewarming were initiated in an antegrade manner from the fourth branch of the J graft with de-airing from the proximal end of the graft. There was no dissection or tear involving the LMT and aortic root. The obstruction was determined to be dynamic and caused by the inverted aortic flap. The aortic flap was repositioned (Fig. 2b and c), followed by proximal reinforcement with a Teflon felt inside and outside using continuous mattress sutures (Fig. 2d). After that, proximal anastomosis was performed with the J graft using running sutures. Subsequently, the LSA, LCCA, and brachiocephalic arteries were anastomosed to the branches of the J graft in an end-to-end fashion with felt strip reinforcement. TEE showed mild AR and coronary flow at the left and right coronary ostia.

Following the procedure, the patient could not be weaned from the CPB because of cardiogenic shock secondary to the extensive myocardial damage caused by preoperative LMT obstruction, acute AR-induced LV volume overload, and increased afterload from preoperative VA-ECMO. Subsequently, CPB was switched to VA-ECMO. Total CPB, aortic cross-clamp, total circulatory arrest, and selective cerebral perfusion times were 427 min, 130 min, 60 min, and 238 min, respectively. The patient, requiring VA-ECMO for weaning off CPB and exhibiting a high pulmonary capillary wedge pressure (PCWP) of 22 mmHg, was diagnosed with left heart failure and elevated LV end-diastolic pressure (LVEDP), necessitating the introduction of Impella. Impella 5.5 (Abiomed, Danvers, MA, USA) was introduced via the fourth branch of the J graft guided to the right anterior thoracic region. The circulatory support rate was 3.6 L/min on VA-ECMO and P4 (1.2 L/min) on Impella 5.5. After decannulation of the bilateral axillary arteries, the mean arterial pressures of the bilateral radial and left femoral arteries were 60–70 mmHg, and hemodynamics were stable. The mean pressure in the left femoral artery suddenly increased from 60 to 110 mmHg just before chest closure, whereas the mean pressure in both radial arteries remained the same at approximately 60 mmHg. TEE revealed an enlarged false lumen of the descending thoracic aorta, and the Frozenix was narrowed at the distal anastomotic site (Fig. 3a). A guidewire was inserted from the left femoral artery into the Frozenix while confirming the true lumen with intravascular ultrasound (IVUS). IVUS findings revealed the collapse of the true lumen of the descending aorta and the proximal end of the Frozenix, impeding the IVUS catheter from passing through (Fig. 3b). A 5Fr pigtail catheter with a marker was able to advance to the ascending aorta, and the wire was replaced with a stiff wire (0.035-inch, EGoist Ultimate, double J curve, Medicos Hirata Inc., Japan) to secure the route. After the wire was replaced, the Frozenix dilated slightly, and the difference in blood pressure between both radial arteries and the left femoral artery disappeared. The stent graft (cTAG 26 × 100 mm; W.L. Gore & Associates, Newark, DE, USA) was placed to cover the entire length of the Frozenix (Fig. 3c). Aortography following the deployment of cTAG showed a predominance of retrograde perfusion from VA-ECMO over the antegrade perfusion from the LV (Fig. 3d). These findings suggest that the predominant retrograde perfusion from VA-ECMO enlarged the false lumen via reentry, narrowed the true lumen, and completely collapsed the Frozenix at the distal anastomosis, the blind end of the false lumen, thus preventing blood flow through the true lumen beyond the distal anastomosis to the central side; it was thought to have caused increased pressure in the left femoral artery. Inhaled nitric oxide (iNO) therapy was also initiated to manage right-sided heart failure. Postoperatively, an ECG revealed that the elevated ST-segment in lead aVR was resolved. On postoperative day (POD) 1, the CK level was 10,781 IU/L, whereas CK-MB and myocardial troponin T reached peak values of 536 IU/L and 50.500 ng/ml, respectively, and subsequently declined. These findings were indicative of extensive myocardial infarction and successful reperfusion. On POD 6, TTE revealed mild MR. The patient’s cardiac function gradually improved. VA-ECMO, Impella 5.5, and iNO were weaned on POD 8, 20, and 31, respectively. However, the patient required maintenance dialysis postoperatively. One month after the surgery, intradialytic hypotension complicated hemodialysis, likely attributable to the progression of secondary MR associated with LV remodeling after myocardial infarction. This assessment was based on TTE findings, which revealed leaflet tethering due to LV dilatation without mitral leaflet prolapse. The patient remained on hemodialysis. However, three months postoperatively, a MitraClip was necessary to reduce MR, after which TTE revealed trivial mitral valve regurgitation, and the LV ejection fraction improved to 36%. Postoperative CT angiography revealed residual dissection extending from the descending thoracic aorta to the left internal iliac artery, demonstrating a patent false lumen without narrowing of the true lumen and adequate organ perfusion. Postoperative complications included newly required maintenance dialysis and visual field impairment due to cerebral infarction. The patient gradually recovered from the neurological deficit and was transferred for physical rehabilitation five months postoperatively.

Fig. 3

(a) Transesophageal echocardiography reveals that the true lumen and Frozenix were narrowed from the distal anastomotic site (white arrow). (b) Intravascular ultrasound shows that the true lumen and Frozenix were narrowed from the distal anastomotic site (white arrow). (c) A guidewire was inserted into the true lumen of the descending aorta, and the stent graft (cTAG 26 × 100 mm; W.L. Gore & Associates, Newark, DE, USA) was placed to cover the entire length of the Frozenix. (d) Blood flow to the lower extremity was improved

Discussion

A-AAD complicated by coronary artery malperfusion is reported to occur in 7% of individuals [2]. The operative mortality rate for A-AAD is approximately 8.2–12%; however, the rate for those complicated by coronary malperfusion is significantly higher, ranging from 20 to 33% [2]. Patients cannot be weaned from CPB and may either die intraoperatively or postoperatively due to low cardiac output [3]. Although primary coronary revascularization and early aortic repair are necessary to prevent extensive myocardial damage and rescue critically ill patients, primary coronary revascularization to the LMT in patients with an inversion of the aortic flap into the LV outflow tract is technically challenging. The patient in this report required preoperative support with VA-ECMO via a femoral approach to maintain systemic circulation following cardiac collapse caused by coronary malperfusion secondary to A-AAD. Since the coronary malperfusion was caused by an inversion of the flap into the LV outflow tract due to dissection of the ascending aorta, VA-ECMO, although necessary to maintain systemic circulation, was detrimental to the heart owing to its contribution to AR, and its ability to assist coronary perfusion was questioned. Postoperative cardiogenic shock persisted, necessitating VA-ECMO for cardiopulmonary support to wean from CPB. VA-ECMO can provide end-organ perfusion with retrograde aortic flow. However, it may result in a rightward shift of the pressure-volume loop (PVL), an increase in afterload, subsequent rises in end-diastolic and end-systolic volumes, and an elevation in PCWP. Impella offers effective hemodynamic support for left heart failure. An increase in the pump flow rate progressively unloads the LV, as evidenced by a leftward shift in the PVL, leading to a reduction in the peak LV pressure. In addition, the pressure-volume area (PVA) and myocardial oxygen consumption (MVO2) significantly decrease. Concurrently, arterial pressure rises, resulting in an increasing disparity between peak LV pressure and arterial pressure [4]. Impella is beneficial during coronary reperfusion for reducing myocardial damage, decreasing infarct size, and preventing progression to advanced-stage heart failure [5]. Impella insertion is generally contraindicated in cases of acute aortic dissection (AAD) owing to the potential risk of exacerbating the dissection or causing aortic rupture. Therefore, we introduced Impella after aortic repair using a vascular prosthesis. Shojima et al. [5] reported the successful management of primary percutaneous coronary intervention and Impella support prior to aortic repair in a case of AAD with LMT malperfusion. They stated that the lower pulsatile pressure and ability of Impella to pump blood directly from the LV into the true aortic lumen may have helped prevent aortic rupture. In our case, Impella implantation after aortic repair could rescue a patient with extensive myocardial damage after cardiac arrest, LMT obstruction, LV volume overload induced by acute AR, and increased afterload from VA-ECMO.

Conclusions

The patient in this case presented with severe cardiac dysfunction resulting from extensive myocardial infarction and acute AR secondary to A-AAD. Retrograde perfusion via VA-ECMO was necessitated to maintain systemic organ perfusion; however, this intervention was anticipated to negatively impact the recovery of cardiac function in a severely dysfunctioning heart. This report demonstrates that Impella efficiently facilitates the restoration of cardiac function under these desperate circumstances.