What is the management of ventricular septal rupture (VSR) in a patient with myocardial infarction (MI)?

Types and Management of Ventricular Septal Rupture in Myocardial Infarction

Overview and Prognosis

Ventricular septal rupture (VSR) is a catastrophic mechanical complication of myocardial infarction requiring urgent surgical intervention, as mortality without surgery reaches 54% within the first week and 92% within the first year. 1

VSR occurs in approximately 1-2% of all myocardial infarctions and typically presents early after the acute event. 1

Types of VSR by Location

Anterior VSR

• Occurs in 32% of cases 2
• Associated with left anterior descending artery territory infarction 1
• Generally carries better prognosis with 46% operative mortality 2

Posterior VSR

• Occurs in 68% of cases 2
• Associated with right coronary or circumflex artery territory infarction 1
• Posterior location is an independent predictor of poor postoperative outcome 1
• Higher operative mortality of 74% compared to anterior defects 2

Clinical Presentation and Diagnosis

Clinical Features

• Severe clinical deterioration is often the first sign 1, 3
• A loud systolic murmur is typically present, though it may be soft or absent in some cases 1
• Cardiogenic shock develops in approximately 71% of patients 2
• Acute heart failure with pulmonary edema 3

Diagnostic Workup

• Echocardiography is the primary diagnostic tool, revealing the location and size of the defect 1, 3
• Color Doppler depicts the left-to-right shunt and quantifies it with pulsed Doppler 1
• Continuous-wave Doppler measures peak flow velocity to estimate right ventricular systolic pressure 1
• Right heart catheterization demonstrates oxygen step-up in the right ventricle, confirming the diagnosis 1
• Pre-operative coronary angiography must be performed to identify coronary anatomy and plan bypass grafting 1, 3

Management Algorithm

Immediate Stabilization (All Patients)

Step 1: Hemodynamic Support

• Oxygen therapy 3
• Intra-aortic balloon pump (IABP) is the most effective method of providing circulatory support while preparing for surgery 1, 3
• Consider extracorporeal membrane oxygenation (ECMO) or ventricular assist devices in hemodynamically compromised patients to bridge to surgery 4
• Hemodynamic assessment with balloon flotation catheter 3

Step 2: Pharmacological Management (if no cardiogenic shock)

• Intravenous nitroglycerin or other vasodilators may produce some improvement 1, 3
• Inotropic agents (dopamine and/or dobutamine) for severe heart failure 1, 3
• Diuretics: furosemide 20-40 mg intravenously, repeated at 1-4 hourly intervals as needed 1, 3
• Ventilatory support if inadequate oxygen tension 1, 3

Definitive Treatment: Surgical Timing Decision

For Patients with Cardiogenic Shock:

• Urgent surgery offers the only chance of survival in large post-infarction VSR with cardiogenic shock 1, 3
• Surgery should be performed at the time of surgical repair, with concomitant coronary artery bypass grafting as necessary 1, 3
• In patients under 75 years with cardiogenic shock developing within 36 hours of STEMI who have severe multivessel or left main disease, emergency CABG with VSR repair should be performed within 18 hours of shock onset 1

For Hemodynamically Stable Patients:

• Early surgery is usually indicated even without hemodynamic instability, because the defect may increase over time 1
• However, studies suggest delaying surgery when possible allows for myocardial recovery and maturation of VSR with scarring at the defect edges, improving surgical outcomes 5, 4, 2
• The optimal timing balances the risk of ongoing hemodynamic deterioration against the fragility of infarcted myocardium in the early phase 4, 2
• Median interval from MI to VSR repair is approximately 7 days 2
• Shorter time between AMI and surgery is an independent predictor of mortality (HR=0.90, P=0.015) 2

Surgical Technique

• Pre-operative coronary angiography is mandatory 1, 3
• Bypass grafts are inserted as necessary during the procedure 1, 3
• Surgical closure remains the definitive treatment 3, 5

Alternative: Percutaneous Closure

• Percutaneous device closure has been reported but requires more experience before it can be recommended as standard therapy 1
• May represent a valuable therapeutic alternative in patients with prohibitive surgical risk 6
• Current experience is mainly restricted to chronic and subacute settings 7
• Immediate shunt reduction can prevent further hemodynamic deterioration 6
• Certain drawbacks have hampered widespread application 6

Predictors of Poor Postoperative Outcome

Independent Risk Factors:

• Cardiogenic shock 1, 3
• Posterior location of VSR 1, 3
• Right ventricular dysfunction 1, 3
• Older age (HR=1.11, P=0.0001) 2
• Shorter time between AMI and surgery (HR=0.90, P=0.015) 2
• Long delay between septal rupture and surgery 1

Outcomes

• Hospital mortality after surgery ranges from 25% to 60% 1, 3
• Overall 30-day operative mortality is approximately 65% 2
• 95% of survivors achieve NYHA class I or II functional status 1, 3

Critical Pitfalls and Caveats

Diagnostic Pitfalls

• The murmur may be soft or absent, particularly in patients with severe pulmonary hypertension or cardiogenic shock 1
• Do not rely solely on auscultation; echocardiography is essential 1

Management Pitfalls

• Operating too early on fragile, infarcted myocardium increases the risk of recurrent septal defects and mortality 4
• Delaying surgery too long risks severe heart failure and organ dysfunction 4
• In hemodynamically compromised patients who cannot be stabilized, immediate surgery after diagnosis is recommended to prevent further deterioration 4
• Concomitant CABG does not influence early or late survival but should still be performed based on coronary anatomy 2

Late Complications

• Remain vigilant for late VSR development in patients with chronic septal MI, presenting with new systolic murmur, acute heart failure, or cardiogenic shock 8
• Risk of ventricular remodeling and progression if surgery is delayed 5

Pathophysiology

VSR results from myocardial necrosis, inflammatory response, and enzymatic degradation of the extracellular matrix, particularly mediated by matrix metalloproteinases (MMPs), leading to structural weakening and subsequent rupture. 5 Hemodynamically, VSR creates left-to-right shunting, increased pulmonary blood flow, and potentially catastrophic hemodynamic instability. 5