A 72-year-old man presented to emergency room with 8-h fatigue and 4-h mild exertional dyspnea, palpitation, and blurred vision. He was a nonsmoker and denied previous history of cardiovascular disease. Physical examination showed sinus tachycardia (117 bpm) and normal blood pressure (120/70 mmHg). The position and range of apical impulse were normal. There were no heart murmurs, no crackles or wheezes on chest auscultation. In ECG, the ST-segment was elevated by 2–3 mm in leads II, III, and aVF, with Q-waves (Fig. 1A). Cardiac troponin T was 3.33 ng/mL (normal range 0–0.04). A diagnosis of acute inferior myocardial infarction was established.
Dual anti-platelet therapy (loading doses: aspirin 300 mg and clopidogrel 300 mg) was initiated to prepare for primary PCI. Coronary angiography (CAG) showed multi-vessel lesions, including a total occlusion of the distal portion of a dominant right coronary artery (RCA), 90% stenosis of the proximal portion of the left anterior descending artery (LAD), and diffuse stenosis (50–60%) of the left circumflex artery (LCX) (Fig. 2A–C). The culprit lesion was in the distal portion of the RCA. The patient received a loading dose of glycoprotein IIb/IIIa inhibitor (tirofiban) after the angiography. Percutaneous balloon angioplasty was then conducted; one BuMATM 2.5 × 20 mm sirolimus-eluting stent was placed to restore blood flow in RCA (TIMI grade 3) (Fig. 2D). ST-segment elevation and depths of the Q-waves were attenuated after the primary PCI (Fig. 1B). Secondary PCI was planned for LAD lesions 5 days later.
Immediately prior to transfer to the cardiac intensive care unit (CCU), the patient developed severe dyspnea. Heart rate (HR) was 120 bpm, and blood pressure (BP) decreased to 90/60 mmHg. Auscultation revealed a loud harsh holosystolic murmur along the left sternal border and crackles throughout both lungs. NYHA functional class of heart failure was IV. A mechanical complication was suspected, but not investigated immediately. We immediately placed an IABP (1:1 augmentation ratio) from femoral access, and the patient received 3-mg morphine, 20-mg furosemide, and 0.1-mg recombinant human brain natriuretic peptide (rhBNP). Once the IABP was inserted, symptoms became alleviated. The BP stabilized at 110/70 mmHg and the augmentation pressure was 120 mmHg. Then the patient was transferred to CCU safely.
Transthoracic echocardiography (TTE) was performed the next day and revealed a left-to-right shunt in the posterior portion of the interventricular septum with a size of 11.4 mm (Fig. 3). The left ventricle end-diastolic diameter (LVED) was 50 mm, and the diameter of the right ventricle was 20 mm. We also detected regional wall-motion akinesia of the left ventricle in the inferior and posterior sections. Left ventricular ejection fraction (LVEF) was 59%. The estimated pulmonary arterial pressure and right ventricular systolic pressure were 48 mmHg. A calculated Qp/Qs was 2.905. There was no regurgitation of the mitral valve or pericardial effusion. An updated diagnosis of ventricular septal rupture was made. We decided to continue IABP to support cardiac function. Medications included aspirin (100 mg orally once a day), clopidogrel (75 mg orally once a day), atorvastatin (20 mg orally once a day), furosemide, spironolactone, and nitrates, as well as an intravenous infusion of rhBNP. The patient received a subcutaneous injection of 40-mg enoxaparin every 12 h to prevent deep vein thrombosis. Omeprazole (40 mg per day) was used to prevent gastrointestinal mucosal injury.
An attempt to wean IABP was made on day 12 on the ground of stable hemodynamics and disappearance of all symptoms. Five minutes after reducing the augmentation ratio from 1:1 to 1:2, the patient felt dyspnea, and the BP decreased from 116/68 mmHg to 71/50 mmHg. The augmentation ratio was increased back to 1:1. Dyspnea gradually dissipated, and the BP normalized. We realized the shunt was in a large amount according to the Qp/Qs. IABP can decrease the shunt, so we decided to implement a prolonged use of IABP, which continued at 1:1 ratio for another 16 days. During the use of IABP, we enhanced the medical and nursing concern including checking the circulatory status of the lower limb of the puncture with Doppler ultrasound every day, limiting its movement to avoid dislocation of the balloon catheter and bleeding, and continuous administration of anticoagulation by subcutaneous injection of enoxaparin to prevent deep vein thrombosis. The aspirin, clopidogrel, atorvastatin, spironolactone, and rhBNP were administered during the month when IABP was used. An antibiotic (cefamandole 2000 mg intravenously every 12 h) was given for prophylaxis for bacteremia during invasive IABP insertion from day 21 to 27. Psychological therapy was adopted to enable the patient to cooperate on prolonged use of IABP.
Surgical repair was offered to the patient on day 27 since the friable tissue in the ischemic myocardium should be sufficiently mature at this time to allow repair. However, the surgeons considered that it was too risky to perform the surgical repair due to the limitation of technique at that time. Firstly, the VSR located at the posterior muscular part of the ventricular septum was lower and deeper than a perimembranous ventricular septal defect approached through a right atriotomy and the tricuspid valve, so the surgical repair was more difficult and beyond the techniques of the surgeons, when they only had experience in the treatment of perimembranous ventricular septal defects at that time. Secondly, the EuroSCORE [17] of this case they calculated was 16, and the predicted mortality was 59.07%, which was too high for them to operate safely. Meanwhile, we also consulted the anesthesiologist to evaluate the patients for general anesthetization, and the anesthesiologists deemed there would probably be high risk in the process of a general anesthesia for the open surgery and especially under extracorporeal circulation support. Surgery was also declined by the patient and his family due to the high risk of open surgery and under general anesthesia and extracorporeal circulation support. Instead, the patient opted to receive percutaneous closure of the VSR. So we decided to choose percutaneous VSR closure for this specific high-risk senior patient.
On day 28 (4 weeks after VSR), the patient didn’t feel dyspnea or any other discomfort with stable vital signs (HR 90 bpm, BP 98/67 mmHg, augmentation pressure 112 mmHg). We believed the waiting period for the infarcted myocardium to recover was enough according to the documented experiences [18, 19]. Left ventriculography confirmed an 11-mm left-to-right shunt (Fig. 4A). Transcatheter closure was conducted via the femoral artery and subclavian vein. Upon establishment of the transseptal wire loop as a rail, the patient developed ventricular fibrillation, and he lost consciousness followed by. A 200-J electrical shock was delivered immediately and restored sinus rhythm. Then the patient regained consciousness. After the wire loop through the rupture was established, the HR suddenly decreased to 30 bpm. A temporary pacemaker was placed, and we proceeded to implant a 24-mm double-umbrella AGA AMPLATZERTM occluder to close the VSR (Fig. 4B). The vital signs were stable (HR 78 bpm, BP 110/72 mmHg). Echocardiography after the procedure revealed no residual shunt, and no interference of valve functions by the occluder. The estimated Qp/Qs was 1.086. The temporary pacemaker was removed after the closure operation.
Two days later, the augmentation ratio was decreased to 1:2 and then to 1:3. IABP was weaned off on day 31. Secondary PCI was conducted on day 35 for LAD lesions (Fig. 5). The patient was discharged on day 41.
At the last follow-up 6 years later, CAG and TTE revealed no in-stent restenosis, no left-to-right shunt, no mitral regurgitation, and 51% LVEF. He kept taking aspirin, atorvastatin, and metoprolol regularly as the medication therapy.
All procedures performed in this study involving human participants were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient.
