Left Ventricular Systolic Dysfunction and Failure

LV pump failure is the dominant cause (>65%) of in-hospital mortality from acute MI. It may occur with a first, and massive, infarction, or with a second or third infarction. Severe WMAs in extensive territories are expected in cardiogenic shock due to pump failure. The LV may or may not be dilated. Massive acute first MI is unlikely to have prominent dilation. It is the combination of abrupt fall in ejection fraction and lack of dilation that is responsible for the low stroke volume, and resultant low output, despite tachycardia.

Right Ventricular Infarction

RV infarction is a common cause of hypotension and the principal cause of shock in inferior infarction. The RV is under-assessed on most echocardiograms; therefore, a diligent effort to assess it regionally and globally is required. The size of RV infarction relates, in general, to how proximally the right coronary artery is occluded. A posterior RV infarction is common in the context of most inferior infarctions. An anterior RV infarction is common in the context of anterior LV infarction, as an apical RV infarction is common in the setting of an LV apical infarction. The right ventricular outflow tract (seen on the posterior long-axis view) usually is spared in RV infarction. The hemodynamically significant, important RV infarction involves the lateral RV (seen on the apical four-chamber view and the posterior short-axis view) and the posterior RV (seen on the posterior short-axis view and the subcostal view). Rarely, complications other than hemodynamic compromise—such as RV thrombi, RV papillary muscle rupture, and RV rupture—will arise from RV infarction. The most severe RV infarctions also involve the right atrium, which is difficult to assess by echocardiography.

Free Wall Rupture

Free wall rupture accounts for approximately 10% of postinfarction sudden deaths. Rupture typically occurs through the lateral (but it may be through any) wall of the left ventricle. The right ventricle is one-seventh as likely to rupture as the LV. Rupture occurs only following a transmural infarction. The time is typically 3 to 5 days following MI, but may be earlier, especially if the patient received fibrinolytics. A subset of patients with free wall rupture will not experience immediate sudden death: this group is said to have “subacute rupture”⁷ with echocardiographic signs of tamponade, pericardial effusion >5 mm, and echodensities in the pericardial space that represent coagulated blood. Suspected clot in the pericardial space, which appears as an echo-dense mass in the pericardial space, may be a sign of free wall rupture⁸ and renders the likelihood of evacuation through a pericardiocentesis needle unlikely. Urgent surgical repair will salvage some cases. Bedside echocardiography is the most suitable test to identify free wall rupture. Ultimately, there is no perfect echocardiographic sign to distinguish severe early postinfarction tamponade from rupture. Identification of clot in the pericardial space is useful, however.

Left Ventricular (or Other) False Aneurysm

Ventricular false or “pseudo” aneurysms contain no myocardial layer; a free wall rupture is contained by adherence of overlying pericardium or by a thin layer of epicardium beneath pericardium. A false aneurysm develops because a tear into a portion of recently transmurally infarcted myocardium extended up to the epicardium or even through it, and complete rupture of the LV into the pericardial cavity was avoided because pericardial adhesions (the result of prior pericarditis) contained the rupture. Thus, a false aneurysm is to be considered an intermediate form of rupture, and reparative surgery is urgently indicated. The contained rupture typically extends away from the neck to appear as an echo-free space with the shape of a mushroom cap. The neck usually is less than half the width of the body of the false aneurysm. This is in contradistinction to the wide neck of a (true) aneurysm, which usually is as wide as the body of the aneurysm itself (the dimension of the neck/the dimension of the body is 0.9 to 1.0).⁹ It is the width of the neck, more than any other detail, that renders the outpouching of the LV a false aneurysm rather than a true aneurysm. In systole, the false aneurysm typically bulges out as it receives part of the LV stroke volume. The flow in and out (or “to-and-fro”) is evident by color and spectral Doppler.¹⁰ Two-dimensional echocardiography is the procedure of choice to establish the presence of a pseudoaneurysm. Cineangiography and MRI also are excellent means to image false aneurysms. Confusion occurs about aneurysms of the base of the LV between the body of the posteromedial papillary muscle and the mitral annulus. Often the traction of the papillary muscle keeps the neck narrow, replicating the sign of a false aneurysm. Thus the “neck” sign is best applied away from the trouble spot on the posterolateral wall, where both aneurysms and false aneurysms occur, but where they cannot be easily distinguished by neck morphology alone.

The diagnosis can be made by TTE in most cases. TEE offers confirmation in some cases that the neck is narrow, and the wall disrupted. TEE is probably better able to image posterior wall false aneurysms and may increase the detection rate of small posterior false aneurysms.

Septal Rupture

Ventricular septal ruptures are less common than free wall ruptures (about 1–3% of MI). They are almost invariably associated with a septal dilation (aneurysm) with thinning. Septal ruptures may occur in anterior/apical locations, or basal–posterior locations.