Post Myocardial Infarction Ventricular Septal Rupture

Post infarction ventricular septal rupture (VSR) is a full thickness necrotic perforation of the interventricular septum producing a left to right shunt.

Incidence is about 0.2% of STEMI in the reperfusion era (previously 1 to 2%). Peaks at 3 to 5 days, with a range of 24 hours to 2 weeks.

Risk factors: first anterior infarction, older age, female sex, hypertension, absence of collaterals, late or failed reperfusion, thrombolysis.

Anterior infarcts cause apical ruptures, inferior infarcts cause basal posterior ruptures (more complex, worse prognosis).

Mortality is 40 to 80% even with surgery, about 90% without treatment.

Complications: cardiogenic shock, biventricular failure, multiorgan failure.

• Sudden clinical deterioration with chest pain, dyspnoea, hypotension and pulmonary oedema.
• New loud holosystolic murmur at the left sternal border with a palpable thrill.
• Signs of right heart failure, raised jugular venous pressure and cardiogenic shock.
• Differentiate from acute mitral regurgitation (soft murmur at apex, no thrill, pulmonary oedema).

• Urgent transthoracic echocardiography with colour Doppler shows the defect, shunt direction and ventricular function. TOE for complex defects.
• Right heart catheterisation: oxygen saturation step up from right atrium to right ventricle (over 5%). Qp:Qs ratio quantifies shunt (over 2 is significant).
• Coronary angiography to plan revascularisation.
• Lactate, creatinine, liver tests to assess organ perfusion.

Stabilisation

• Intra aortic balloon pump reduces afterload and shunt.
• Vasodilators if blood pressure permits: sodium nitroprusside 0.25 to 0.5 micrograms/kg/min.
• Inotropes (dobutamine 2.5 to 10 micrograms/kg/min) and diuretics for failure. Mechanical support (Impella, VA ECMO) as a bridge in selected cases.
• Avoid excessive afterload augmentation by vasopressors.

Definitive closure

• Early surgical repair (infarct exclusion patch repair, David technique) is recommended for all suitable patients regardless of haemodynamics, because of rapid deterioration. Delay of 2 to 3 weeks improves tissue strength but carries risk for those with shock.
• Concomitant coronary bypass when indicated.
• Percutaneous device closure with a septal occluder is an option for delayed, haemodynamically stable patients, or as a bridge. Residual shunts and device embolisation are common.
• Operative mortality 20 to 50% (highest with shock and posterior defects). Residual or recurrent shunt in up to 25%.

After repair

Standard post infarct therapy (aspirin, P2Y12 inhibitor, beta blocker, ACE inhibitor, statin), heart failure therapy and follow up echocardiography.