Abstract
Acute and subacute complications of myocardial infarction are often life-threatening and should be recognized by the astute sonographer. These include acute mitral valve disruption and consequent mitral regurgitation (flail mitral valve), ventricular septal defect, and free wall rupture (leading to either ventricular pseudoaneurysm, contained left ventricular rupture, or tamponade with hemopericardium). The echocardiographic manifestations of these emergencies are comprehensively covered in this chapter.
Keywords
acute mitral regurgitation, cardiogenic shock, hemopericardium, mechanical complications of myocardial infarct, papillary muscle rupture, ventricular rupture
Introduction
There is a short list of structural complications of which every cardiologist and sonographer must be aware that may arise in the subacute period after myocardial infarct (MI), that, within the first week ( Box 19.1 ). These are caused by necrosis of the heart muscle, and are frequently lethal if not caught early enough and repaired. The mechanical complications are: acute mitral regurgitation (MR), ventricular septal defect (VSD), pseudoaneurysm, free wall rupture, and tamponade. In any patient with sudden hypotension, chest pain, congestive heart failure or hypoxia post-MI, or electromechanical dissociation, there must be a high index of suspicion for these entities. The incidence of these complications has cumulatively decreased to less than 1% since primary percutaneous coronary intervention has become standard treatment for acute MI, but when they do occur, mortality is high. Echocardiography with color flow Doppler is a crucial tool for bedside diagnosis and differentiation of these complications.
Acute mitral regurgitation (papillary muscle rupture)
Ventricular septal defect
Pseudoaneurysm
Free wall rupture
Tamponade
Other potential factors contributing to cardiogenic shock post-AMI
LV failure
LV outflow tract obstruction
RV failure: RV infarct, pulmonary embolus
Acute Mitral Regurgitation
The appearance of a new large color jet of MR after MI, particularly if turbulent (as indicated by a multicolored signal) or directed eccentrically against the left atrial wall, should prompt the sonographer to search for structural abnormalities of the mitral apparatus ( Fig. 19.1 and 
). As mentioned previously in Chapter 18 , the diagonal branches of the left anterior descending (LAD) and the left circumflex artery (LCx) both supply the anterolateral papillary muscle, but the posterior descending artery (PDA; usually a branch of the right coronary artery [RCA]) alone supplies the posteromedial papillary muscle. For this reason, posteromedial papillary muscle rupture is far more common (6–12 times more), and RCA infarcts have the highest incidence of acute MR. For the most part, the anterolateral papillary muscle connects via chordae tendinae to the anterior leaflet and the posteromedial papillary muscle connects to the posterior leaflet. Rupture of the papillary muscle trunk, heads, or chordae will cause the associated leaflet tip to flail backward into the left atrium (LA), with consequent MR in a jet that is directed away from that leaflet onto the opposing wall ( Fig. 19.2 ). Hence, infarct of the posteromedial papillary muscle will cause posterior leaflet flail, which directs the jet anteroseptally. (Clinically, the sudden presence of a new murmur in the aortic area could be a telltale sign.) Infarct of the anterolateral papillary muscle, which would require extensive damage in both diagonal and LCx territories, would cause MR directed posteriorly (where the MR murmur might only be detected if the patient’s back was auscultated).
. 
Depending on the extent and duration of hypoxemia, the level of injury may involve the entire papillary muscle, or be more limited to one or more papillary muscle heads, tips, or chordae. In reality, there is variation in the chordal fan configuration, with occasional overlap and crossover between the papillary muscle heads and chordae tendinae (see Chapter 39 , Fig. 39.2 .) Hence there are instances in which inferior infarcts can lead to anterior leaflet flail, or conversely, anterior infarcts can cause posterior mitral leaflet flail. In these cases a smaller segment of leaflet, such as the tip only, is usually involved.
A patient’s echocardiographic windows may be poor in the setting of acute shock due to mitral valve disruption caused by multiple factors such as suboptimal patient positioning, volume overload, and tachycardia. Furthermore, poor cardiac contractility overall or a wide open mitral valve will also theoretically diminish the left ventricular (LV)-LA pressure differences and cause the MR color Doppler jet to appear less impressive. A very eccentric jet that hugs the left atrial wall and escapes the usual transducer planes of insonation may also cause underdetection of MR. Hence, even if transthoracic echo windows are poor and nondiagnostic , if the clinical scenario strongly suggests acute MR, one should pursue transesophageal echocardiography while the patient is being treated supportively and surgical consultation is underway (i.e., without delaying either). Fig. 19.3 shows an entire head of the anterior papillary muscle that has ruptured, which can be seen on the corresponding 
(transthoracic echocardiogram [TTE] 2D and color views, of suboptimal image quality as might be obtained in real life, but showing a very eccentric mitral regurgitant jet) and subsequent transesophageal echocardiogram (TEE) confirming flail mitral valve in 
.
. Ventricular Septal Defect
The LAD septal branches supply the anterior two-thirds of the interventricular septum, and the remaining inferior portion is supplied by the PDA. VSDs occurring after MI are typically detected by a color flow Doppler jet penetrating from the left to right ventricle. VSDs may be described as simple in type, which means a direct perforation through both sides of the septum at the same level, or complex, with multiple serpiginous tracts through the septum. VSDs caused by anterior MIs tend to be simple and arise more apically ( Fig. 19.4A and ), whereas VSDs in the setting of inferior MIs are often more complex and involve the basal portions of the septum (see Fig. 19.4B and 
). The latter tissue defects may also (rarely) extend to involve the adjacent inferior and right ventricular wall. Inferobasal defects are difficult for the surgeon to reach and repair by virtue of their location, complex configuration, and thin myocardial walls.
. (B) Inferoseptal VSD seen as echo dropout in the tissue of the basal inferoseptum on subcostal short-axis windows (left panel) , and left-to-right flow by color Doppler (right panel, arrow) . See also corresponding 
. LV , Left ventricular; RV , right ventricular. The actual width and extent of the VSD may not be readily apparent on echocardiography as an actual defect or discontinuity in the muscle layer, except in large cases. The area of the defect may simply appear akinetic, or thinned, as opposed to a discrete area of echo dropout in the muscular septum. Careful “sweeping” of the transducer plane with color Doppler by tilting the transducer systematically through short-axis and long-axis planes may be required to detect and localize smaller VSDs. Using continuous-wave (CW) Doppler collinearly with the color jet, one can obtain the peak velocity difference between the left and right ventricles. This difference is inversely proportional to the size of the defect: smaller (restrictive) VSDs will have high gradients, and the larger (nonrestrictive) VSDs will display lower gradients. If one documents the patient’s systolic blood pressure (SBP) at the time of study (which should equal LV systolic pressure in the absence of aortic stenosis), then the right ventricular systolic pressure (RVSP) may be calculated as:
RVSP = SBP − 4 × ( maximal interventricular pressure gradient in m/s ) 2
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