Successful Treatment of Post-Myocardial Infarction Ventricular Septal Rupture

A 61-year-old man with no previous history visited the emergency room due to a sudden onset of chest pains since 2 days. Initial electrocardiography (ECG) showed a 15 mm ST segment elevation in precordial leads with pathologic Q waves (Figure 1A). Initial supine anteroposterior chest radiography showed cardiomegaly (cardiothoracic ratio 0.56) with pulmonary congestion (Figure 1B). Since the patient presented with hypotension (blood pressure: 78/62 mmHg) and persistent chest pain, emergency percutaneous coronary intervention was planned under the support of norepinephrine (0.1 μg/kg/min). The initial coronary angiography revealed total occlusion of the middle left anterior descending (LAD) artery (Supplementary Video 1). After successful implantation of a sirolimus-eluting stent (3×24 mm), angiography showed no-reflow phenomenon (Supplementary Video 2). Intra-coronary nicorandil infusion and intravascular abciximab were administered, and TIMI flow of grade 1 was confirmed by follow-up angiography (Supplementary Video 3). Post-procedural ECG showed partially resolved ST segments, but abnormal Q waves persisted (Figure 1C). Laboratory findings revealed the following: creatine kinase-myocardial band, 110 ng/mL; Troponin I 59.4 ng/mL; lactic acid, 4.4 mmol/L; and total bilirubin, 1.63 mg/dL. Transthoracic echocardiography (TTE) showed severely decreased left ventricular (LV) ejection fraction with akinesia of the anterior and septal walls and aneurysm formation of the apical wall. Color Doppler imaging revealed shunt flow at the apical portion of the interventricular septum due to ventricular septal rupture (VSR) (1.6 cm) (Figure 1E). Since the patient's pain was tolerable, and his vital signs and laboratory findings were stabilized without increment of positive inotropes (norepinephrine 0.1 μg/kg/min), our multidisciplinary cardiac team including a cardiac intensivist, cardiac surgeon, and cardiac imaging specialist, decided to delay surgery and closely monitor the patient at the cardiac intensive care unit. On the ninth day following admission, the patient reported worsening dyspnea. Chest radiography showed abrupt exacerbation of bilateral pulmonary edema and systolic blood pressure dropped under 90 mmHg, requiring additional norepinephrine infusion to 0.15 μg/kg/min (Figure 1D). Immediate extracorporeal membrane oxygenation (ECMO) was performed with mechanical ventilator support (Flow rate 3.8 liter per minute [LPM], 3565 revolution per minute [RPM], FiO2 0.65). Chest radiography confirmed the resolution of pulmonary edema. The patient's vital signs and laboratory findings were stabilized. However, on the sixth day of ECMO, lactic acid and bilirubin level increased to 6.5 mmol/L and 5.63 mg/dL, respectively, indicating progression of inadequate tissue perfusion and venous congestion despite the ECMO support. Conservative management such as diuretics and ursodeoxycholic acid use was not effective. Therefore, the heart team finally decided to perform VSR correction surgery on post-admission day 14. The follow up echocardiography revealed severely decreased LV systolic function and still noted left to right shunt. Mean arterial pressure was 78 mmHg, and heart rate was 80 beat per minute under the full ECMO support (Flow rate 3.7 LPM, 3525 RPM, FiO2 0.75) with dobutamine (5 μg/kg/min) infusion. The surgery was performed with a median sternotomy. Anterior ventriculotomy was performed parallel to the LAD coronary artery, and a 1.5 cm VSR was exposed (Figure 2A). Interrupted pledgeted sutures (5–0 polypropylene) were placed along the surrounding healthy tissue, and repair was performed using a 5.5 cm bovine pericardial patch (Figure 2B). The ventriculotomy site was repaired using 3–0 polypropylene mattress sutures reinforced with a felt strip (Figure 2C) and a bovine pericardial patch (Figure 2D). Surgery was completed after intra-operative transesophageal echocardiography confirmed no abnormal flow between the ventricles. ECMO support was maintained after the surgery because of the severely decreased LV systolic function. Five days post-operatively, TTE revealed a hematoma around the heart compressing the right ventricle. Hematoma evacuation surgery was performed, and the patient was successfully weaned from ECMO, which took 11 days after its initiation. The patient was discharged on post-operative day 30 after cardiac rehabilitation.

Figure 1. Electrocardiography showing ST-elevation in precordial leads. Initial electrocardiography (A). Initial chest radiography (B). Post-percutaneous coronary artery intervention electrocardiography (C). Bilateral pulmonary edema on post-admission day 9 (D). Echocardiography showing ventricular septal rupture at the apex (yellow triangles) (E). Final chest radiography before discharge (F).

RV = right ventricle; LV = left ventricle.

Figure 2. Surgical finding showing ventricular septal rupture. The VSR was exposed after anterior ventriculotomy parallel to the LAD coronary artery (A). Interrupted pledgeted sutures were placed along the surrounding healthy tissue, and patch repair was performed using a bovine pericardial patch (B). The ventriculotomy site was repaired using felt strip polypropylene mattress sutures (C). The ventriculotomy site was covered with a bovine pericardial patch (D).

LAD = left anterior descending artery; VSR = ventricular septal rupture.

Post-myocardial infarction (MI) VSR is a well-known complication following acute MI, and surgical repair is mandatory to restore hemodynamic stability. Older age, female gender, prior stroke, ST segment elevation, elevated cardiac markers, higher heart rate, lower blood pressure, higher Killip class, and delayed or lack of reperfusion are associated with developing post-MI VSR.¹⁾ Without surgical repair or percutaneous closure, the mortality rate can reach 94%. When treating a patient with post-MI VSR, clinicians must decide whether to proceed with emergency surgical repair or delay surgery under conservative management to stabilize the friable myocardium. The time interval between the occurrence of VSR and surgery is important to form firmer scars at the friable margin of the defect which is a critical component to determine successful outcome.^2),3) A previous study investigating the timing of post-MI VSR surgery reported that patients who underwent surgery within 7 days of presentation had a 54.1% mortality rate.⁴⁾ When the surgery was delayed until after 7 days, the mortality rate was only 18.4%. Another study showed that the mortality rate for patients who had surgery 3 weeks after MI was only 10%.³⁾ There was a report even showing no deaths in patients who underwent surgery 4–6 weeks after MI and suggesting that surgery could be delayed in hemodynamically stable patients after 3–4 weeks with the support of mechanical circulatory support (MCS).^2),5) In patients with hemodynamic instability, early MCS can be a bridge to delayed surgical repair, transplantation, or palliative treatment.³⁾ In this case, the patient was relatively young, and no serious comorbidity which can deteriorate condition during waiting period was present. We therefore planned surgical repair instead of proceeding urgent alternative strategy such as device closure. Since the patient's vital sign was stable, we decided to postpone surgery and optimize medical management with the readily prepared MCS for our patient.

Management of post-MI VSR requires a stepwise strategy at each stage of disease (Figure 3). At the time of acute MI presentation, routine auscultation and TTE prior to revascularization can lead to early detection of VSR. Additional mechanical complications affect the therapeutic strategy. In some cases, delayed coronary artery bypass grafting with VSR repair may be required. After the detection of post-MI VSR, evaluation of hemodynamic and metabolic stability via vital signs, laboratory findings, ECG, and chest radiography is crucial to determine the timing of MCS and surgery. The timing of surgical repair is dependent on the patient's condition. If the patient shows signs of instability, such as lactic acidosis or pulmonary edema, MCS needs to be applied immediately. If the patient is stable, surgical repair can be delayed for at least 7 days after post-MI VSR, and optimally until after 3 weeks as the risk of mortality after surgery is decreased. Immediate post-operative management should involve close observation for surgical complications such as surgical site bleeding or hematoma. Cardiac rehabilitation is crucial for early recovery, and long-term management of heart failure is also mandatory to maintain long-term survival.

Figure 3. Schematic figure showing considerations over the courses of post-MI VSR and the risk of mortality.

MI = myocardial infarction; TTE = transthoracic echocardiography; VSR = ventricular septal rupture; IABP = intra-aortic balloon pump; MCS = mechanical circulatory support; ECMO = extracorporeal membrane oxygenation; HF = heart failure.

The key to success during the management of post-MI VSR is optimal decision making based on the multidisciplinary cardiac team discussions and the delicate management of highly vulnerable patients.

SUPPLEMENTARY MATERIALS

Supplementary Video 1

The initial coronary angiography (right anterior oblique cranial view) showing total occlusion of the middle left anterior descending artery.

Supplementary Video 2

No reflow phenomenon after the implantation of a sirolimus-eluting stent (3×24 mm).

Supplementary Video 3

Final angiography showing TIMI flow grade 1 after the infusion of intra-coronary nicorandil and intravascular abciximab.