J Apical 3Chamber

Fig. 10. (A) Pseudo-aneurysm (postmyocardial infarction [post-MI]). This 64-yr-old woman suffered an inferior MI and required implantable cardioverter defibrillator placement. Her apical two-chamber images show a narrow-necked cavity (left panel) that communicated with the left ventricular cavity. No intracavitary thrombus was seen. Surgical removal confirmed it was a pseudo-aneurysm. (B) Pseudo-aneurysm: anatomy. A post-MI pseudoaneurysm of the left ventricular wall is essentially a contained ruptured of the ventricular wall that is not lined by myocardium. (C) 77-yr-old female with history of previous MI and of ventricular aneurysm. Her parasternal long-axis (PLAX) and apical long axis images show aneurysmal remodeling of the basal infero-posterior wall. No intracavitary thrombus was seen. (D) Anatomy: true aneurysm. In a true ventricular aneurysm, the entire wall of the aneurysm is still lined by endocardium/myocardium. (Please see companion DVD for corresponding video.)

dysfunctional territories, or LVEF less than 40% are at the highest risk. Anticoagulation is usually indicated to prevent systemic embolization.

Transthoracic echocardiography has a sensitivity of nearly 95% and specificity of 90% for LV thrombi. (TEE is less sensitive, and therefore an inappropriate test for detecting LV thrombi; this is because of difficulty visualizing the apex, which is more distant from the TEE probe, particularly in patients with large dilated ventricles.) Thrombi are usually detected between 4 and 14 d after the infarct, and typically appear as discrete, echogenic, homogenous speckled masses lying adjacent to an akinetic or dyskinetic segment of endocardium. The individual characteristics of thrombi vary widely; many appear fixed and adherent to the endocardial wall ("mural thrombi") with smooth laminar surfaces, but they may also be rounded or pyramidal, have independently mobile portions and protruding filaments, or be pedunculated. Those that are mobile or protruding are at particularly high risk of embolization, and adjacent hyperkinetic myocardial segments also increase embolic potential. Older or well-organized thrombi are often observed to include more echo-bright elements.

With anticoagulation, LV thrombi have been observed to resolve in 47% of patients by 1 yr and 76% by 2 yr of follow-up, although they are less likely to resolve in those patient with apical dyskinesis.

Pericardial Complications: Infarct-Related Acute Pericarditis, Tamponade

Less severe complications of MI frequently involve the pericardium. Early or acute pericarditis, as defined by a pericardial friction rub with or without chest discomfort and/or ECG changes typical of pericarditis, is estimated to occur in 5-20% of patients with MI, with the lower incidence in patients who have smaller infarcts or those who are thrombolysed. The rub is generally transient and lasts 3 d or less. A pericardal effusion occurs in up to one-third of cases—similar to the other complications of MI, larger infarctions or concurrent RV infarctions appear to be risk factors. The effusions are usually asymptomatic, small in size, and only rarely cause tamponade. However, the effusions may take weeks to months to resolve, and patients with significant effusions appear to have higher morbidity and mortality.

Post-MI pericarditis, or Dressler's syndrome, may occur as a late complication of MI (and cardiac surgery) weeks to months after the acute event. It is characterized by pleuritic chest pain, a pericardial rub, fever, and elevated leukocyte count.Echocardiography of the pericardium may show a thickened pericardium and/or pericardial effusion, often with associated "shaggy" echodensities, which represent fibrin, and inflammatory material within the pericardium adherent to the visceral or parietal pericardium. Adjacent "sympathetic" pleural effusions may be present as well. The incidence of post-MI pericarditis was estimated in up to 3-4% of infarcts before the thrombol-ysis era, but appears to have declined enormously in reperfused patients.

Chronic Implications

Heart Failure: Decline in Systolic and Diastolic Function

Echocardiography is a useful tool for risk assessment and determining prognosis in the weeks to months after an MI. The EF is the most frequently used index of clinical heart failure, and both EF and infarct size have been shown to be a strong predictors of survival post-MI (see Chapter 5). Emerging indications for automatic implantable cardioversion defibrillator placement post-MI include an EF of 30% or less, with or without ventricular tachyarrhythmias.

Diastolic dysfunction (see Chapter 6) is also abnormal both early and late in the course of MI, and quantitative measures of LV relaxation or restriction can have prognostic and therapeutic implications as well.

Dilation and Remodeling: Heart Failure

Although an infarct causes immediate local myocar-dial dysfunction in the necrosed segments, further adjacent and even distal territories may be negatively affected and become functionally abnormal in the few months following an acute infarct. This process has been termed cardiac remodeling, or infarct expansion (see Chapter 5, Fig. 6). On cardiac ultrasound, this is manifested by enlargement of the hypokinetic or akinetic zones, which are still viable, as well as overall dilatation of the LV chamber. The ventricle often takes on a more spherical shape, with an aneurysmal apex. Pathologically, LV hypertrophy is usually present as measured by overall LV mass, but because the overall internal chamber size has increased, the measured wall thicknesses on echocardio-graphy may remain within normal limits. Angiotensin-converting enzyme inhibitors have been shown to limit the process of remodeling after MI.

Aneurysm (and Thrombus)

Injured myocardial segments may become scarred, and if extensive enough can "balloon out" to form aneurysmal segments (Fig. 11; please see companion DVD for corresponding video). These appear as thinned, highly echogenic areas of scarred myocardium, which are in continuity with the adjacent viable myocardium, have wide necks, and appear to bulge from the LV cavity in systole. See "Pseudoaneurysm" and "Free Wall Rupture" sections for the distinction between aneurysms and pseudoaneurysms; these can be difficult to discriminate, and in some cases may require surgical/pathological determination. Although they can

Left Ventricular Noncompaction

Fig. 11. A 74-yr-old male with a 2-mo history of myocardial infarction (MI) and congestive heart failure. This 74-yr-old man with a history of MI 2 mo earlier presented with wide-complex tachycardia requiring implantable cardioverter defibrillator placement. Echocardiography revealed large left ventricular aneurysm measuring approx 9 X 9 cm in two dimensions. Ejection fraction was estimated at 10% (A,C). Moderate mitral regurgitation was seen by color Doppler. (B) No left ventricular thrombus was observed. Higher frequency echocardiogram revealed the presence of spontaneous echocontrast in the aneurysmal segment (D). (Please see companion DVD for corresponding video.)

Fig. 11. A 74-yr-old male with a 2-mo history of myocardial infarction (MI) and congestive heart failure. This 74-yr-old man with a history of MI 2 mo earlier presented with wide-complex tachycardia requiring implantable cardioverter defibrillator placement. Echocardiography revealed large left ventricular aneurysm measuring approx 9 X 9 cm in two dimensions. Ejection fraction was estimated at 10% (A,C). Moderate mitral regurgitation was seen by color Doppler. (B) No left ventricular thrombus was observed. Higher frequency echocardiogram revealed the presence of spontaneous echocontrast in the aneurysmal segment (D). (Please see companion DVD for corresponding video.)

Mural Thrombus Echo

Fig. 12. A 40-yr-old male with left ventricular thrombus. Apical four-chamber image shows moderately directed left ventricle with global hypokinesis and estimated ejection fraction of 25%. An echodensity was observed in the apical region (A, arrow), which, on higher frequency and color Doppler imaging, showed appearances consistent with a thrombus. (Please see companion DVD for corresponding video.)

Fig. 12. A 40-yr-old male with left ventricular thrombus. Apical four-chamber image shows moderately directed left ventricle with global hypokinesis and estimated ejection fraction of 25%. An echodensity was observed in the apical region (A, arrow), which, on higher frequency and color Doppler imaging, showed appearances consistent with a thrombus. (Please see companion DVD for corresponding video.)

arise from anywhere in the LV, the majority involve the apex. Many (from 34 to 77%) of these aneurysms are associated with indwelling mural thrombi, with comprises a stroke risk (see Fig. 12; please see companion

DVD for corresponding video; see also "Free Wall Rupture" section). Finally, because the scar comprising the aneurysm cannot conduct electrical impulses, it can form the substrate for ventricular tachycardias.

Mitral Regurgitation (Without Flail Leaflet) Mild or greater degrees of MR often accompany remodeling post-MI, and increasing severity is associated with increased cardiovascular mortality. In the absence of a flail leaflet owing to rupture of a papillary muscle or chordae, the MR appears to be caused by incomplete valve closure, which in turn is because of displacement of the papillary muscles, with the laterally displaced chordae tethering the leaflets open. On echocardiogram, the anterior leaflet appears elongated and both leaflet tips are angulated toward the lateral apex. The mitral leaflet tips appear not to coapt fully at end-diastole, and a clear jet of color flow Doppler originating at or just proximal to the central orifice can be seen. Whether interventions such as mitral annuloplasties or LV aneurysectomies, which decrease the amount of MR, actually decrease cardiac morbidity or mortality remains to be seen.

In summary, echocardiography serves as a diagnostic and prognostic tool to guide therapeutic intervention in both the acute myocardial infarct as well as the aftermath. It should be used judiciously to answer specific questions in a given clinical scenario, and an appropriately high suspicion for the development of acute or chronic complications should be borne in mind.

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