Case
A 95-year-old woman with a history of hypertension was referred to our
hospital with signs of progressive dyspnea. Upon arrival, she was
tachypneic (respiratory rate: 27 breaths/min), hypotensive (blood
pressure: 95/67 mmHg), and tachycardic (heart rate: 110 beats/min). She
had high-grade fever (body temperature: 38.5℃) and her oxygen saturation
was 83% on room air. Physical examination revealed coarse crackling and
wheezing in both lungs, a Levine IV/VI systolic murmur at the upper
right sternal border, and bilateral lower extremity pitting edema.
Laboratory test results were normal except for B-type natriuretic
peptide levels of 5908.8 pg/mL, creatinine levels of 1.97 mg/dL,
C-reactive protein levels of 4.2 mg/dL, white blood cell count of 12,000
/μL, hemoglobin levels of 115 g/L, albumin levels of 23 g/L, and pyuria
with nitrituria. A chest radiograph showed pulmonary congestion with a
butterfly shadow and an increased cardiothoracic ratio
(Figure 1A ). Transthoracic echocardiography revealed
severe AS with severely decreased left ventricular ejection fraction
(LVEF: 30.3%) and stroke volume (SV index to body surface area: 22
ml/m2) (Video S1 ). The aortic valve
area calculated with the continuity equation was 0.38
cm2 with a mean transaortic pressure gradient of 45.2
mmHg. Pulmonary hypertension was suggested by a systolic tricuspid
regurgitation pressure gradient of 47.4 mmHg. Multidetector computed
tomography demonstrated a severely calcified aortic valve with aortic
annulus area of 360.3 mm2 with the maximum diameter of
25.4 mm and the minimum diameter of 17.8 mm (Figure 2 ).
The patient suffered from severe heart failure owing to
low-flow-high-gradient AS with reduced LVEF and urinary tract infection.
Noninvasive ventilatory support and intravenous furosemide
administration were ineffective and urgent intervention for AS was
required before the results of blood cultures were available. Our heart
team dismissed the option of a surgical aortic valve replacement because
of advanced age and high-surgical risk (Society of Thoracic Surgeons
Predicted Risk of Mortality of 9.217%). In addition, the patient was
considered not to be an immediate candidate for TAVR because of the
risks of subsequent endocarditis in the case of prosthesis implantation.
Accordingly, we decided to perform a retrograde BAV as a bridge to TAVR.
Retrograde BAV was performed at day 3. To avoid rapid ventricular pacing
considering the severely decreased LVEF, the newly invented Inoue
balloon for retrograde BAV use was utilized (Figures 3A to
3C, Video S2 ). Systemic blood pressure decreased only during balloon
inflation and recovered several seconds after balloon deflation
(Figure 3D ). After six times inflations of the 20-mm
Inoue balloon in the absence of rapid ventricular pacing, an adequate
acute gain was achieved without any complications (Figures
3E and 3F ). Transthoracic echocardiography performed after the
procedure showed improvement in LVEF to 41.1% and the aortic valve area
of 0.60 cm2 with a mean transaortic pressure gradient
of 36.9 mmHg. The patient’s urine output immediately increased after
BAV, and her heart failure was completely compensated at day 8
(Figure 1B ). After the signs of infection improved,
transfemoral-TAVR with the 23-mm SAPIEN 3 (Edwards Lifesciences, Irvine,
California) was performed at day 23 (Video S3 ), and the
patient was ambulatorily discharged after 4 days.