What causes ventricular septal rupture (VSR)?

Causes of Ventricular Septal Rupture (VSR)

Ventricular septal rupture is primarily caused by acute myocardial infarction (AMI), occurring in approximately 1-2% of all infarctions, with extremely high mortality rates of 54% within the first week and 92% within the first year without surgical intervention. 1, 2

Pathophysiology of VSR

• VSR typically appears early after myocardial infarction, most commonly within the first 24 hours in patients treated with fibrinolytic therapy 1
• The rupture occurs due to necrosis of the interventricular septum following coronary artery occlusion, most commonly affecting the left anterior descending artery (84.4% of cases) 3
• The necrotic tissue is exposed to shear forces and macrophage-mediated removal processes, which can cause the rupture site to expand abruptly 1
• VSR can occur in both anterior (more common) and inferior/posterior locations, with posterior ruptures having worse outcomes 1, 2

Risk Factors for VSR

• First-time myocardial infarction 1
• Female sex (significantly higher risk with odds ratio 14.043) 3
• Advanced age (mean age of occurrence is 68-72 years) 4, 5
• Hypertension (present in 72% of VSR cases) 4
• Lower platelet count on admission 3
• Single-vessel disease, particularly involving the left anterior descending artery 3
• Lack of collateral circulation to the infarct area 1
• Delayed presentation after symptom onset 1

Clinical Presentation

• Severe clinical deterioration is often the first sign of VSR 2
• A loud systolic murmur is typically present over the third to fourth intercostal space, often with a palpable thrill 6, 2
• The murmur may be soft or absent in some cases 1
• Patients frequently present with signs of cardiogenic shock or heart failure 1, 2
• Killip class 3 or 4 is present in approximately 60% of patients at diagnosis 4

Diagnostic Evaluation

• Echocardiography is the primary diagnostic tool, revealing the location and size of the defect 1
• Color Doppler can demonstrate the left-to-right shunt 1, 2
• Continuous-wave Doppler can estimate right ventricular pressure 1, 2
• Right heart catheterization may detect an oxygen step-up in the right ventricle, confirming the diagnosis 1, 2
• Coronary angiography is recommended to assess coronary anatomy before surgical repair 1, 2

Prognostic Factors

• Non-anterior wall AMI and non-apical VSR are associated with poorer survival 4
• Lower left ventricular ejection fraction correlates with higher mortality (36.6% vs. 51% in survivors) 5
• Higher EuroSCORE II values predict worse outcomes 5, 7
• Early surgery (within 8 days of MI) is associated with higher mortality (HR 2.7) 7
• Need for renal replacement therapy post-surgery indicates poor prognosis 5

Management Considerations

• Urgent surgical repair is the definitive treatment and offers the only chance of survival in large VSRs with cardiogenic shock 1, 2
• Initial stabilization should include vasodilators (IV nitroglycerin) and intra-aortic balloon counterpulsation 2
• Surgical mortality ranges from 25% to 60%, with 95% of survivors achieving good functional status (NYHA class I or II) 1, 2
• Percutaneous closure has been reported but requires more experience before being widely recommended 1, 2, 8
• The strategy of total coronary revascularization during surgical repair provides long-term survival benefit 5

Temporal Trends

• The incidence of VSR has decreased over time with modern reperfusion therapies 4, 7
• In-hospital mortality has decreased significantly since 1990, though it remains high 7
• Patients with Killip class <3 and EuroSCORE <20 may benefit from delayed surgery (>8 days after MI) 7