Acute Decompensated Heart Failure after Transcatheter Aortic Valve
Implantation: A Case Report
Hong Nyun Kim1,2,3, Dong Heon
Yang1,3
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
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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.