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Key Concepts

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  • Epidemiology

    • Six to ten percent of patients develop cardiogenic shock after myocardial infarction.

    • Mitral regurgitation (MR) occurs in 8 to 50 percent of patients after myocardial infarction.

    • Post-infarct ventricular septal defects (VSD) occurs in <0.5 percent of myocardial infarction (MI) patients.

    • Only 24 percent of medically treated patients with post-infarct VSD survive 30 days.

    • In autopsy series, 30 percent of myocardial infarction (MI) is accompanied by ventricular free wall rupture (VFWR).

    • The incidence of left ventricular aneurysms depends on exact definition; 10 to 35 percent of patients will develop region of systolic akinesia or dyskinesia after transmural myocardial infarction (MI).

  • Pathophysiology

    • In cardiogenic shock associated with MI, worsening ventricular function leads to decreased coronary perfusion, worsening ischemia, and an enlarging infarct zone.

    • Three primary pathologic mechanisms exist for post-infarct MR:

      • Papillary muscle rupture

      • Acute ischemic MR

      • Chronic ischemic MR.

    • Post-infarct VSD follows large transmural infarction with weakening of the septal wall.

    • Post-infarct VSD results in left-to-right shunt of variable magnitude with diversion of blood flow from systemic to pulmonary circulation and low-cardiac-output state, ultimately into cardiogenic shock.

    • VFWR occurs after large, transmural MI in myocardium without collaterals.

    • Traditionally ventricular aneurysm is defined as region of myocardium exhibiting abnormal diastolic contour with systolic dyskinesia and paradoxic bulging.

    • Ventricular remodeling after large transmural infarct leads to infract expansion and aneurysm formation.

  • Clinical features

    • Symptoms of systemic and coronary hypoperfusion, including cold, clammy extremities, cyanosis, oliguria, and altered sensorium.

    • Cardiogenic shock associated with MI leads to pulmonary edema, chest pain, and shortness of breath.

    • New holosystolic murmur best heard at the apex is noted in MR associated with MI.

    • Post-infarct VSD typically occurs 5 to 6 days after MI

    • Eighty percent of VFWR occur within 7 days after infarct.

    • Subacute VFWR results in a worsening pericardial effusion and hypotension without pulseless electrical activity and cardiac arrest.

    • Pseudoaneurysm formation from VFWR occurs approximately 3 months after MI with variable symptomatology.

    • Commonly presents with congestive heart failure

    • LV aneurysm commonly presents with congestive heart failure, angina, and/or dyspnea.

    • Mural thrombus present in 50 percent of ventricular aneurysm patients at surgery.

  • Diagnostics

    • Invasive hemodynamic monitoring important in optimizing both coronary and systemic perfusion.

    • Electrocardiography (ECG) confirms cardiac ischemia; chest X-ray rules out pneumothorax.

    • Emergent echocardiography (ECHO) to rule out other mechanical causes of shock, including papillary muscle or ventricular rupture.

    • Echocardiography (ECHO) allows evaluation of left ventricular (LV) function and mitral apparatus; can accurately diagnose pulmonary muscle (PM) rupture as well as exclude other mechanical causes of cardiovascular collapse.

    • Location of infarct of echocardiography (ECHO) correlates with location of post-infarct VSD.

    • ECHO is important to differentiate post-infarct VSD from acute, severe mitral regurgitation (sensitivity and specificity ~100 percent).

    • Angiography allows delineation of coronary anatomy, estimation of ventricular aneurysm size, and guided placement of intra-aortic balloon pump (IABP).

    • Rapid pericardiocentesis is both diagnostic and therapeutic for VFWR.

    • Echocardiography (ECHO) identifies effusion with pericardial clots for VFWR; Doppler evaluation may identify rupture site.

    • MRI may be useful in evaluating pseudoaneurysms.

  • Treatment

    • Medical

      • No pharmacologic agent has ...

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