Mechanical Complications of Myocardial Infarction

True Aneurysm vs. Pseudoaneurysm

Both entities are late mechanical complications of transmural myocardial infarction, but they differ fundamentally in wall composition, neck geometry, and rupture risk, and distinguishing them is one of the highest-stakes calls in echocardiography.

• True LV aneurysm — the wall consists of thinned, scarred myocardium; all native layers remain present, just fibrotic, akinetic, or dyskinetic, and the sac is continuous with the adjacent normal wall through a wide, broad-based neck. On echo, the ratio of the neck (orifice) width to the maximal sac diameter is greater than 0.5. True aneurysms most commonly involve the anteroapical wall in the LAD territory and carry a relatively low risk of rupture, but they predispose to mural thrombus formation, ventricular arrhythmia, and heart failure. Management is typically medical, with anticoagulation if thrombus is present.
• Pseudoaneurysm (false aneurysm) — results from a contained free-wall rupture: the myocardium has actually ruptured, and the "wall" of the resulting sac is formed only by adherent pericardium and thrombus, with no myocardial layer at all. This produces a characteristically narrow neck, with an orifice-to-sac diameter ratio of 0.5 or less, and often a beak-like configuration in which the narrow channel can be traced extending behind an intact segment of ventricular wall. Color Doppler frequently shows to-and-fro flow through the narrow neck. Because the sac wall has no myocardial integrity, pseudoaneurysms carry a high risk of rupture and represent a surgical emergency; anticoagulation should generally be avoided, and urgent surgical resection is indicated rather than observation.

LV Thrombus

Regions of akinesis or dyskinesis — especially apical aneurysms — create blood stasis that predisposes to mural thrombus formation. On echo, thrombus appears as a discrete echodensity distinct from the underlying endocardium, typically layered along an akinetic or dyskinetic segment and best seen at the LV apex using dedicated, non-foreshortened apical views. Ultrasound-enhancing contrast agents substantially improve detection when the true apex is poorly seen on fundamental imaging, since apical thrombus is the single most commonly missed diagnosis on suboptimal studies. A mobile or protruding thrombus, as opposed to a flat, laminated, mural thrombus, carries a substantially higher embolic risk and must always be described explicitly in the report rather than simply noted as present.

Ventricular Septal Rupture

A mechanical complication from necrosis of the interventricular septum, ventricular septal rupture classically presents three to five days after infarction, with a reported range of one to fourteen days, producing a new, harsh, holosystolic murmur and rapid hemodynamic deterioration. Location correlates closely with the infarct territory:

1. Anteroapical septal rupture — follows LAD (anterior) infarction; typically a simple, apical defect.
2. Basal posteroseptal rupture — follows RCA (inferior) infarction; often a more complex, serpiginous defect that is technically harder to close.

Color Doppler demonstrates a left-to-right shunt, with turbulent flow crossing the septum from the LV into the RV, corresponding to a step-up in RV oxygen saturation on right-heart catheterization. The resulting acute RV volume overload frequently precipitates cardiogenic shock, and emergent surgical or transcatheter closure is generally required rather than medical management alone.

Papillary Muscle Rupture

Papillary muscle rupture, whether partial or complete, causes sudden, severe, acute mitral regurgitation from a flail leaflet, usually presenting two to seven days after infarction with abrupt pulmonary edema and cardiogenic shock, since the large regurgitant volume is poorly tolerated by a left atrium that has not had time to dilate or become compliant. The posteromedial papillary muscle ruptures far more often than the anterolateral papillary muscle because of a key difference in blood supply: the posteromedial muscle receives a single source, the posterior descending artery, typically from the RCA, while the anterolateral muscle has dual supply from diagonal branches of the LAD and obtuse marginal branches of the LCx, making it considerably more resistant to ischemic necrosis. As a result, even a small, non-transmural inferior infarction can cause posteromedial papillary muscle rupture. Echocardiography shows a flail or grossly hypermobile leaflet segment with a ruptured papillary head or chordal remnant still attached, along with a severe, often eccentric, mitral regurgitant jet directed away from the affected leaflet.

Timing Summary of Mechanical Complications

Recognizing these complications promptly on echo, and correctly distinguishing look-alikes such as a true aneurysm from a pseudoaneurysm, directly changes management from watchful observation to emergency surgical referral, making this one of the most clinically consequential skills in the post-MI echocardiographic examination.