Acute Decompensated Heart Failure after Transcatheter Aortic Valve Implantation: A Case Report

Hong Nyun Kim^1,2,3, Dong Heon Yang^1,3

¹Division of Cardiology, Department of Internal Medicine, Kyungpook National University Hospital, Daegu, Korea

²Division of Cardiology, Department of Internal Medicine, Kyungpook National University Chilgok Hospital, Daegu, Korea

³Department of Internal Medicine, School of Medicine, Kyungpook National University, Daegu, Korea

Abstract

Transcatheter aortic valve implantation (TVAI) is a widely used treatment modality for severe aortic stenosis. The complication rates of the procedure have gradually decreased over time, owing to the improvements in procedural skills and development of TVAI devices. However, several rare but serious complications can still occur after TAVI. We recently encountered acute decompensated heart failure as a rare and fatal complication of TAVI, and would like to share our experience.

Keywords: Acute decompensated heart failure, stress-induced cardiomyopathy, left ventricular stunning, transcatheter aortic valve implantation

INTRODUCTION

Since the first transcatheter aortic valve implantation (TAVI) was performed two decades ago, the TAVI procedure had gone through numerous advances. Currently, it is firmly established as the treatment of choice for severe aortic stenosis (AS) with a high risk of surgical aortic valve replacement (SAVR).¹ Although TAVI is less invasive than SAVR, it can also cause several periprocedural complications, including cerebrovascular accidents, ventricular perforation, valvular complications, arrhythmias, coronary artery occlusion, myocardial infarction, cardiogenic shock, and death.² We recently encountered a case of acute decompensated heart failure (ADHF) after TAVI and herein report the details of the case.

CASE DESCRIPTION

A 76-year-old female was transferred to our institution’s emergency room due to exertional chest pain and dyspnea for a week. Two days before being transferred to our hospital, the patient visited a local hospital because of the aforementioned symptoms and subsequently underwent coronary angiography (CAG) and transthoracic echocardiography (TTE). CAG found no significant luminal stenosis in the coronary arteries; however, TTE showed severe AS. The patient had no prior medical history and was not taking any medications. Initial vital signs taken at the emergency room were as follows: blood pressure, 123/72 mmHg; heart rate, 78 bpm; respiratory rate, 18 breaths/min; and peripheral O2 saturation, 100% on room air. Cardiomegaly was observed on chest radiography, but no pulmonary edema or pleural effusion was noted (Figure 1A). An initial electrocardiogram (ECG) indicated sinus rhythm with a heart rate of 73 beats/min and a left ventricular (LV) hypertrophy pattern (Figure 1B). Laboratory examination did not indicate any abnormal findings, except for a slight increase in N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels to 5618.0 pg/mL (reference range < 665.0 pg/mL) and high-sensitivity cardiac troponin I (hs-cTnI) to 0.552 ng/mL (reference range < 0.034 ng/mL). TTE revealed very severe AS and mild decrease of left ventricular ejection fraction (LVEF) with global hypokinesia; LVEF of 40% by Simpson’s method, aortic valve area (AVA) of 0.51 cm² on planimetry, indexed AVA of 0.10 cm²/m², mean pressure gradient of 95.50 mmHg, and peak aortic jet velocity of 6.23 m/s (Figure 2). The patient’s perioperative mortality rate was evaluated and she was subsequently classified into the intermediate-risk group with a Society of Thoracic Surgeons Risk Score of 6.806%. We discussed the treatment options (SAVR vs. TAVI) with the patient, in the presence of a multidisciplinary team of interventional cardiologists, cardiac surgeons, and anesthesiologists until the decision to perform TAVI was reached. Prior to TAVI, a computerized tomography scan was performed to evaluate the type and size of the prosthetic valve required and peripheral vascular approach needed.

The TAVI procedure was performed 2 days after hospitalization under general anesthesia. We performed the procedure via the right femoral artery and implanted an Edwards SAPIEN 3 prosthetic aortic valve (23mm; Edwards Lifesciences, Irvine, CA, USA) (Figure 3). No specific events or complications occurred during the procedure. However, in this particular case, four rapid ventricular pacings (RVP) at a pacing rate of 160 bpm were conducted, which would normally be conducted once, to achieve appropriate implantation depth and position. After the procedure, minimal paravalvular leakage (PVL) and trace aortic regurgitation (AR) were observed on transesophageal echocardiography, and the implanted aortic valve functioned well (Figure 4). Coronary blood flow was intact on aortography (Figure 4). Finally, the patient’s vital signs were stable with blood pressure 128/66 mmHg and heart rate of 76 bpm, and the procedure concluded without acute complications. After the procedure, the patient was admitted to the intensive care unit for observation. The patient was alert and did not complain of discomfort. However, one hour after the procedure, the patient’s blood decreased to 42/25 mmHg. Intravenous hydration was promptly started with normal saline and inotropic support with norepinephrine was administered to restore vital signs. Subsequently, the patient’s vital signs stabilized at a blood pressure of 130/67 mmHg and heart rate of 83 bpm. We checked the peripheral procedure site, but there were no specific complications, such as bleeding and hematoma, and no difference was found in the ECG compared with the previous examination. A complete blood count (hemoglobin, 13.4 g/dL; hematocrit, 39.9%) showed normal values; however, metabolic acidosis was detected (pH 7.253; PCO2, 41.0 mmHg; HCO3, 16.6 mmol; base excess, -9.1 mEq) in the arterial blood gas study. Cardiac enzyme, hs-cTnI was 1.402 ng/ml, modest increased compare to the initial value. On TTE, the implanted aortic valve was functioning well, and the amount of AR and PVL noted were similar to the last images taken. There were no significant abnormal findings in the other valves, and there was no pericardial effusion. In spite of these results, the patient’s systolic heart function continued to deteriorate, with an LVEF of 25% and global hypokinesia. After that, the patient’s blood pressure continued to decrease, and despite inotropes administration of epinephrine and vasopressin, the lactic acid levels rose to 17 mmol/L. Seven hours post-TAVI, we applied mechanical ventilation, continuous renal replacement therapy, and veno-arterial extracorporeal membrane oxygenation (VA-ECMO) in an effort to improve patient hemodynamics. We continued supportive care with mechanical support, but the patient’s heart function further deteriorated and fail to recover. The patient eventually died, 3 days after the TAVI procedure.

DISCUSSION

TAVI has revolutionized the treatment of severe AS since its inception in 2002. TAVI was initially indicated for inoperable patients or those deemed too high-risk for SAVR, but the scope of its application gradually expanded due to technological advances and various successful study results.¹ Despite its advanced technique and widespread use, TAVI can incur several life–threatening complications such as coronary obstruction, ventricular rupture, vascular injury, stroke and death.² ADHF may also occur after TAVI from numerous causes including LV dysfunction (due to coronary obstruction, “stunning” via rapid pacing, or stress induced cardiomyopathy), arrhythmia, annular rupture, pericardial effusion, mitral valve insufficiency, peripheral vascular injury, and a “suicide ventricle” (hyperdynamic intraventricular obstruction after unloading by TAVI).^2-5

In the present case, the possibility of coronary obstruction due to an implanted aortic valve was considered low as the patency of the coronary artery was confirmed through an aortogram post-TAVI. During the progression of cardiogenic shock, neither ST segment changes nor ventricular arrhythmias, such as ventricular fibrillation or ventricular tachycardia, were observed on ECG monitoring. TTE was performed repeatedly, but other than a severe decrease in LVEF with global hypokinesia, abnormal findings, such as implanted aortic valve insufficiency, mitral valve insufficiency, pericardial effusion, ventricular septal defect, and left ventricular outflow tract (LVOT) obstruction, which could cause cardiogenic shock, were not found. Complications, such as bleeding and hematoma, were also not observed in the peripheral vessels that were used the TAVI procedure, and the red blood cell count and hematocrit levels were within the normal ranges. After the procedure, continuous ECG monitoring was performed, and conduction abnormalities, such as bradycardia or atrioventricular block, were not detected.

Therefore, two possible causes of ADHF were considered in this patient. First, it is conceivable that the patient experienced post-procedural stress-induced cardiomyopathy accompanied by heart failure with midrange ejection fraction (HFmrEF). Stress-induced cardiomyopathy is a clinical syndrome characterized by acute and transient (< 21 days) LV systolic and diastolic dysfunction often related to an emotional or physical stressful event.⁶ Clinically, it is recognized that stress-induced cardiomyopathy exhibits a benign course with an in-hospital mortality rate of 1-2%, but some meta-analyses report an in-hospital mortality rate of 3.5-4.5%.⁷Furthermore, a study of patients with high severity of illness reported up to 16% mortality during hospitalization, suggesting a poor prognosis when the severity of underlying disease is high or when stress-induced cardiomyopathy perpetuates a vicious cycle in the course of the disease.⁸ Although stress-induced cardiomyopathy related to the TAVI procedure is very rare, some cases have been reported in the literature.^4,5 In this particular case, we performed four RVPs for pre-balloon dilation, prosthetic valve implantation, and post-balloon dilation. Each RVP induces a drop in blood pressure that can lead to stress-induced cardiomyopathy. Moreover, pre- and post-balloon dilation can also induce stress-induced cardiomyopathy. Second, transient ventricular stunning due to RVP and balloon aortic valvuloplasty (BAV) could have caused ADHF in the patient. Ventricular stunning is an established clinical entity that has already been described in TAVI.^3,9-11 Both RVP and BAV induce short periods of myocardial ischemia that can precipitate cardiogenic collapse due to profound ventricular stunning in susceptible patients. Patients with coronary artery disease, with greatly reduced oxygen levels during RVP, or patients with marked LV hypertrophy, which may increase oxygen demand, are at risk of myocardial ischemia during RVP.³ In general, patients undergoing TAVI are older adults with coronary artery stenosis, and patients with severe AS often present with LV hypertrophy; therefore, the possibility of ventricular sunning due to RVP is higher in this group than that in the general population. In this case, the patient had LV hypertrophy and underwent four RVPs and three balloon inflations during the TAVI procedure, which could have triggered ventricular stunning.

Therefore, when planning and performing TAVI, we must prepare for the serious but rare complications such as stress-induced cardiomyopathy and LV stunning. Elderly female, low body weight, hypertrophied ventricles, discontinuation of beta-blockers, and coronary artery disease are factors known to increase the risk of stress-induced cardiomyopathy and LV stunning.¹² Thus, strategies that could reduce the risk of stress-induced cardiomyopathy and LV stunning in these high-risk patients, which include reducing the number and rate of RVPs, avoiding pre-balloon dilation, using a smaller balloon size for pre-balloon dilation, and implanting a self-expandable prosthetic aortic valve should be considered.

CONFLICT OF INTEREST

All authors have no potential conflicts of interest to disclose.

AUTHOR CONTRIBUTIONS

Kin HN: conceptualized the study. Kim HN: investigated the study. Kim HN: wrote original draft preparation. Kim HN, Yang DH: wrote review and editing. All authors approved the final manuscript.

ETHICS STATEMENT

The study protocol was reviewed and approved by the Institutional Review Board of the School of Medicine, Kyungpook National University (IRB No. 2022-09-021), Daegu, Korea

CONSENT

Written informed consent was obtained from the patient to publish this report in accordance with the journal’s patient consent policy

ORCID

Hong Nyun Kim https://orcid.org/0000-0002-9903-1848

Dong Heon Yang https://orcid.org/0000-0002-1646-6126

REFERENCE

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2. Grube E, Sinning JM. The ”Big Five” complications after transcatheter aortic valve replacement: do we still have to be afraid of them? JACC Cardiovasc Interv . 2019 Feb 25;12(4):370-372.

3. Fabbro M, Goldhammer J, Augoustides JG, et al. Case 1-2016 problem-solving in transcatheter aortic valve replacement: cardiovascular collapse, myocardial stunning, and mitral regurgitation. J Cardiothorac Vasc Anesth . 2016 Jan;30(1):229-36.

4. Harhash A, Koulogiannis KP, Marcoff L, et al. Takotsubo cardiomyopathy after transcatheter aortic valve replacement. JACC Cardiovasc Interv . 2016 Jun 27;9(12):1302-1304.

5. Steinecker M, Benvenuti C, Digne F, et al. Case report: Takotsubo cardiomyopathy after transcatheter aortic valve-in-valve replacement.Eur Heart J Case Rep . 2020 Dec 20;5(1):ytaa457.

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9. Shivaraju A, Thilo C, Sawlani N, et al. Aortic valve predilatation with a small balloon, without rapid pacing, prior to transfemoral transcatheter aortic valve replacement. Biomed Res Int . 2018 Apr 30;2018:1080597.

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12. Yong ZY, Wiegerinck EM, Boerlage-van Dijk K, et al. Predictors and prognostic value of myocardial injury during transcatheter aortic valve implantation. Circ Cardiovasc Interv . 2012 Jun;5(3):415-23.

Figure Legends

Fig. 1. On the day of admission, Chest X-ray (A) reveled cardiomegaly, but pulmonary edema and pleural effusion were not observed. Initial electrocardiogram (B) showed sinus rhythm and left ventricular hypertrophy with QRS widening.

Fig. 2. Initial transthoracic echocardiography (TTE) findings. (A, B) TTE showed left ventricular hypertrophy and degenerative aortic valve with severe calcification. (C) The aortic valve area (AVA) was 0.51 cm² on the planimetry. (D) The mean systolic pressure gradient of aortic valve was 95.50 mmHg, and peak aortic jet velocity was 6.23 m/s on the continuous wave Doppler.

Fig. 3. Transcatheter aortic valve implantation (TAVI) procedure. (A) Pre-balloon dilation was performed under rapid ventricular pacing (RVP). (B) An Edwards SAPIEN 3, 23mm, prosthetic aortic valve was successfully implanted. (C) Post-balloon dilation was performed under RVP to reduced paravalvular leakage.

Fig.4. Post TAVI procedural findings (A) Transesophageal echocardiography showed minimal paravalvular leakage (arrow). (B, C) Coronary artery blood flow was intact on aortography after the TAVI procedure.