Case Report
A 26-year-old female patient was referred to our tertiary center because
her dyspnea did not decrease 2 months after percutaneous balloon mitral
valvuloplasty (PBMV) for rheumatic mitral stenosis. She had no family
history of CHD. At the admission, her functional capacity was NYHA-III.
Arterial blood pressure was 125/80 mmHg, peripheral oxygen saturation
was 97%, and heart rate was 75/beats per minute. There was a 2/6-degree
systolic murmur on auscultation besides a wide split-second heart sound
(S2). ECG showed sinus rhythm and did not show any specific changes. Two
months ago, just after the PBMV procedure, mitral valve area (MVA) was
reported as 1.8 cm2. The patient was admitted to the
emergency department several times with palpitation attacks after
discharge and had some transthoracic echocardiography (TTE) reports
performed by different cardiologists during this period. Her MVA
measurements ranged between 1.2 cm2 and 1.9
cm2 on TTE.
On our TTE examination, ejection fraction (EF) was normal, mitral valve
area (MVA) was 1.72 cm2, and we observed a secundum
type atrial septal defect (ASD) accompanied by dilatation in the right
heart chambers (Figure-1) with moderate tricuspid regurgitation (TR).
Pulmonary arterial systolic pressure (PASP) was also measured as 48
mmHg. Transesophageal echocardiography (TOE) showed that MVA was 1.65
cm2 by pressure half time on 2-D evaluation and a
diastolic D-sign on the interventricular septum (IVS) (Figure-2). With
the 3-dimensional Multiplanar reconstruction (MPR) measurement of MVA
was 1.63 cm2 (Figure-3). The mitral valve gradient was
9/5 mmHg, and as such, it was evaluated as mild mitral stenosis.
Moderate TR was observed, PASP was 50 mmHg, and tricuspid annular
diameter was 37.5 mm. The interatrial septum was aneurysmatic and a
1.22x0.67 cm of atrial septal defect was observed with the 3-D
examination (Figure-4), and left to right shunt was seen through this
defect. Also, the patent foramen ovale (PFO) tunnel was observed.
Although the drainage of the left upper, left lower, and right lower
pulmonary veins into the left atrium were observed, a cardiac MRI
evaluation was planned because the right upper pulmonary vein drainage
could not be adequately evaluated. Interestingly, the patient applied
PBMV two months ago, and she was assessed with TOE before; no ASD
finding was found in that period. In this case, we concluded that the
current ASD is an iatrogenic defect secondary to the PBMV.
On cardiac MRI, dilatation in the right chambers, diastolic D-sign on
IVS, secundum type ASD (Qp/Qs ratio: 2.82) were also observed,
consistent with TOE. We found that the right upper and middle lobe
pulmonary veins drained into the superior vena cava on cardiac computed
tomography (CT), and it was interpreted as a partial pulmonary venous
return anomaly (Figure-5). Then, we performed a cardiac catheterization,
and our main findings are followings; 1) Qp/Qs: 6.28, 2) pulmonary
vascular resistance was 1.04 wood unit, 3) systemic vascular resistance
was 10,42 wood unit, 4) pulmonary capillary wedge pressure was 7 mm Hg,
5) mean pulmonary artery pressure was 15 mm Hg. Hence, the results of
catheterization consisted of left-to-right shunt. At this stage, the
evaluation made with the patient gained importance, and the heart team
decision was determined because the patient was young and considering
pregnancy.
Surgical treatment for pulmonary venous return anomaly and ASD was
decided in the heart team council for the patient. A follow-up with
medical treatment was planned for the mitral valve depends on low
pulmonary capillary wedge pressure. The PAPVR was repaired by robotic
intracardiac routing using the da-Vinci system, and the ASD was closed
successfully.
In the TTE evaluation performed 2 months after the surgery, the right
heart chambers were in normal size (Figure-6), MVA was 1.63
cm2, mitral valve gradient was 9/6 mmHg, mild
tricuspid regurgitation, and PASP was 24 mmHg. The patient was
symptom-free, and her functional capacity was NYHA-I.