Role of echocardiography in acute myocardial infarction

INTRODUCTION — The echocardiogram is a standard tool in the management of patients with acute myocardial infarction (MI). The role of echocardiography in establishing the diagnosis, location, and extent of MI, in diagnosing mechanical complications of infarction, and in providing prognostic information that is important for risk stratification will be reviewed.

The use of transthoracic echocardiography and other noninvasive imaging for the evaluation of chest pain in the emergency department is discussed separately. (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department" and "Noninvasive testing and imaging for diagnosis in patients at low to intermediate risk for acute coronary syndrome".)

INDICATIONS FOR ECHOCARDIOGRAPHY IN MI — Echocardiography is indicated to evaluate regional and segmental ventricular function, which influences therapy, to evaluate for mechanical complications and intraventricular thrombosis, and to provide prognostic information in acute myocardial infraction [1]. In addition, stress echocardiography is one of the recommended methods for identifying residual ischemia post MI. (See 'Diagnosis of MI' below and 'Location and extent of MI' below and 'Detecting complications after MI' below and 'Use for prognosis and to guide therapy' below and 'Residual ischemia' below.)

DIAGNOSIS OF MI

Use of echocardiography — Echocardiography is not routinely performed for diagnosis of MI but may be helpful when a patient presents with one or more symptoms or signs of MI and the diagnosis is uncertain. As discussed separately, the diagnosis of an acute MI is typically based upon the history, electrocardiogram (ECG), and serum troponins. (See "Diagnosis of acute myocardial infarction".)

Echocardiography is an accurate noninvasive test that enables detection of evidence of myocardial dysfunction caused by ischemia or necrosis [1]. Evaluation of wall motion while a patient is experiencing chest pain can be useful when the ECG is nondiagnostic [2]. Evaluation of wall motion may also be useful if there is ECG or laboratory evidence of MI even in the absence of chest pain [2]. Severe ischemia produces regional wall motion abnormalities (RWMAs) that can be visualized echocardiographically within seconds of coronary artery occlusion (12±5 and 19±8 seconds in two series of patients evaluated during transient coronary occlusions induced by angioplasty) [3,4]. These changes occur prior to the onset of ECG changes or the development of symptoms (figure 1) [5]. The RWMAs reflect a localized decrease in the amplitude and rate of myocardial excursion, as well as a blunted degree of myocardial thickening and local remodeling.

Since ischemic RWMAs develop prior to symptoms, chest pain in the absence of RWMAs is rarely caused by active myocardial ischemia. However, the converse is not true; the presence of RWMAs does not establish the diagnosis of ischemia. For example, left bundle branch block limits the diagnostic value of RWMAs detected by echocardiography [6]. There are a number of other causes of RWMAs, including a prior infarction, focal myocarditis, prior surgery, ventricular preexcitation via an accessory pathway, and cardiomyopathy.

Thus, echocardiography for an acute coronary syndrome (MI or unstable angina) has a high sensitivity but a relatively lower specificity. These predictions were confirmed in a study of 180 patients with chest pain in the emergency department; the following findings were noted [7]:

●RWMAs were present in 27 of 29 patients with an acute MI (sensitivity 93 percent as two non-ST elevation MIs were not apparent). By comparison, the initial ECG was diagnostic (ST elevation with or without Q waves) in only nine of these patients, and eight had an ECG that was not interpretable for an acute MI (due to left bundle branch block, pacing, or LV hypertrophy with strain). Thirteen patients subsequently developed pathologic Q waves.

●RWMAs were indicative of acute MI in only 31 percent of 87 patients.

●Among the 88 patients without RWMAs, only 2 (2.2 percent) subsequently "ruled in" for a non-ST elevation MI by cardiac enzymes.

It may be impossible to distinguish RWMAs due to acute ischemia from those due to a previous MI. One clue, the preservation of normal wall thickness and normal reflectivity, suggests an acute event, while a thin akinetic reflective segment suggests chronicity. Most authorities recommend utilization of left-sided contrast for better delineation of the endocardial border when standard views are difficult to interpret [8].

The presence of reversible RWMAs, as well as reversible ECG changes, is consistent with the diagnosis of myocardial ischemia. The time course of recovery after the cessation of chest pain is variable, ranging from less than two hours in patients with a short duration of chest pain (≤10 minutes) to more than 24 hours in patients with prolonged angina [9]. This delay in recovery, which occurs in the absence of recurrent chest pain, may reflect myocardial stunning [9,10]. (See "Clinical syndromes of stunned or hibernating myocardium".)

Differential diagnosis — When evaluating suspected MI, other causes of new RWMAs should be considered including myocarditis and stress (also known as takotsubo or apical ballooning) cardiomyopathy. Patients with stress cardiomyopathy typically present with chest pain, ECG changes, and cardiac enzyme elevations with normal coronary arteries. Significant wall motion abnormalities can be identified with echocardiography, most commonly affecting the apical and mid portions of the ventricle; other variants, including a type with midventricular hypokinesis, have been described. Wall motion usually returns to normal after a period varying from days to several months. (See "Diagnosis of acute myocardial infarction" and "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy".)

LOCATION AND EXTENT OF MI — Echocardiography can identify the location and extent of the infarct (movie 1 and movie 2 and movie 3 and movie 4). Regional wall motion abnormalities (RWMAs) correlate closely with other methods of assessing an MI such as pathology [11], left ventriculography, computed tomography, magnetic resonance imaging, or nuclear perfusion imaging [12].

Location — For the purposes of localizing segmental wall motion abnormalities in a standardized format, the American Society of Echocardiography (ASE) has recommended dividing the ventricle into 16 segments (figure 2) [8,12]. The American Heart Association (AHA), as part of an effort to unify wall motion analysis among different imaging modalities, concluded that a 17-segment model was preferred (figure 3) [13]. The different echocardiographic views permit visualization of regions of the myocardium perfused by the different coronary artery branches (figure 4 and table 1).

Anteroapical — Involvement of the septum, apex, and anteroseptal regions of the LV are typical of occlusion of sites in the left anterior descending coronary artery circulation; they are best seen in the parasternal long axis and apical two- or four-chamber views. The presence of diastolic deformity, sharply demarcated, indicates aneurysm formation.

Inferobasal — Inferior infarctions usually arise from occlusion of the right coronary artery and occasionally from occlusion of a posterior descending branch arising from the circumflex artery in a left dominant system. Most RWMAs arising from right coronary occlusion are found at the base of the inferior or diaphragmatic wall; in contrast to anterior infarctions, the apex is often spared.

These wall motion abnormalities are well seen in the short axis but even better by using the apical two chamber view with a slight degree of posterior tilt. When an inferior infarction is encountered, the right ventricle (RV) should be carefully evaluated for possible coexisting RV infarction. (See 'Right ventricle' below.)

Lateral or free wall — The LV free wall is a less common site for isolated MI; though the lateral wall may become akinetic in circumflex artery occlusion, the lateral wall is more frequently involved as a component of multisegmental involvement. Left main disease may cause anterior, lateral, and apical wall motion abnormalities, and left anterior descending artery disease may involve the entire apex, including the lateral apex. The base of the free wall is the least likely site of an ischemic echocardiographic abnormality.

Right ventricle — Obstruction of the proximal right coronary artery proximal to the RV marginal branches may infarct the inferior wall of the LV and the RV. Some studies suggest that as many as 40 percent of inferior infarctions are complicated by some degree of RV dysfunction. However, there is a major difference between mild subclinical depression of RV contractile function, which is associated with subtle echocardiographic abnormalities, and severe impairment of RV performance, which can lead to hypotension or shock, due to reduced LV preload. (See "Right ventricular myocardial infarction".)

The 2019 American College of Cardiology (ACC) Guideline on Multimodality Imaging gave an appropriate indication for the use of echocardiography for the evaluation of patients with possible RV infarction [14]. Similarly, evaluation of suspected RV infarction was classified as appropriate in the 2011 Appropriate Use Criteria for Echocardiography [2].

The echocardiographic manifestations of RV infarction are abnormal RV free wall motion and RV dilation [15]. The most reliable echocardiographic signs of hemodynamically important RV infarction are [16]:

●Enlargement of the RV with or without segmental wall motion abnormalities

●Decreased descent of the RV base

●Plethora of the inferior vena cava (defined as a less than 50 percent decrease in inferior vena cava diameter after deep inspiration)

Since a patent foramen ovale is present in 20 to 30 percent of normal individuals, the elevation of right-sided filling pressures accompanying severe RV dysfunction can result in acute right-to-left shunting. This complication should be suspected when patients with an inferior MI have an otherwise unexplained reduction in the arterial oxygen saturation.

Right-to-left shunting can be readily detected by performing an intravenous agitated saline contrast study, which shows the passage of microbubbles from right to left across the middle of the atrial septum. A contrast study is performed by attaching two 5 mL syringes to a three-way stop cock to an indwelling 18 gauge needle in the right antecubital fossa vein. A mixture of saline and a minute amount of air (approximately 0.1 mL) is passed rapidly between the two syringes until the saline has a gray appearance. The valve is then rotated so that the syringe with the solution can be forcefully injected with the arm elevated and the upper arm massaged. If a patent foramen ovale is the cause of hypoxemia, saline bubbles will appear in the LV within one or two beats of their first appearance on the right side.

Multiple segment — When the apex and base are the site of RWMAs, the segment of the septum that lies across from the moderator band of the RV is occasionally spared. This pattern reflects the moderator band artery (ramus limbi dextri), arising from a relatively proximal portion of the right coronary artery, which provides collateral circulation to a limited segment of myocardium [17].

Extent of infarct — The 2019 ACC Multimodality Imaging Guideline and 2011 ACC/AHA/ASE appropriateness criteria classified as appropriate the initial evaluation of LV function following acute coronary syndrome and for reevaluation of LV function following acute coronary syndrome during the recovery phase when results will guide therapy [2,14].

Two-dimensional echocardiographic studies have shown that the extent of the infarction is underestimated in up to 95 percent of cases if judged solely by the electrocardiogram [18,19]. This can be particularly evident in the setting of posterior infarction [19], RV infarction [20-22], or apical infarction [23,24].

A wall motion score index (WMSI) can be derived by assigning a number to each segment that corresponds to its wall motion (1 = normal or hyperkinetic, 2 = hypokinetic, 3 = akinetic, 4 = dyskinetic, and 5 = aneurysm) (figure 2) [8]. The WMSI is calculated by dividing the sum of these numbers by the number of segments visualized [25].

DETECTING COMPLICATIONS AFTER MI — Echocardiography can detect and evaluate a number of complications after MI (table 2). Since the emergence and growth of primary percutaneous coronary intervention, the incidence of complications from MI is now significantly lower than in previous decades [26].

Mechanical complications — Mechanical complications after MI include ischemic mitral regurgitation (from extensive wall motion abnormalities or LV dilation) and cardiorrhexis mitral regurgitation (due to papillary muscle rupture, ventricular septal defect [VSD], or ventricular rupture). (See "Acute myocardial infarction: Mechanical complications".)

In some cases, the clinical findings are highly suggestive of such a complication. As an example, hypotension and shock with a new murmur should immediately raise concern for VSD or papillary muscle rupture. These dire complications are especially to be suspected in a low output state when LV function appears normal or hyperdynamic. In an echocardiographic study of 50 such patients, 43 had a ventricular septal defect and seven had papillary muscle rupture or severe dysfunction [27].

The 2019 American College of Cardiology (ACC) Multimodality Imaging Guideline recognized echocardiography as appropriate for the assessment of mechanical complications after acute MI [14]. Similarly, this is included as an appropriate indication in the 2011 appropriateness guidelines [2].

VSD — Septal perforation is detected by direct visualization of an abrupt interruption of the septal musculature, usually surrounded by an area of akinesis or dyskinesis. One or several perforations are often located in close proximity to the cardiac apex; they tend to change in size throughout the cardiac cycle, expanding during systole. Because of the initial high pressure differential between the LV and RV, there is a high velocity shunt through the septal defect. (See "Acute myocardial infarction: Mechanical complications".)

Color flow mapping often confirms the diagnosis (movie 5 and movie 6 and movie 7) [27,28]. In the series of 43 patients with a VSD post-MI cited above, only 40 percent were detected by two-dimensional (2D) imaging; the addition of color flow Doppler identified all 43 VSDs [27]. Transesophageal echocardiography (TEE) may be useful in cases in which the transthoracic images are nondiagnostic [29].

Three-dimensional (3D) echocardiography may be useful in evaluating anatomical complications of MI. Case reports and case series have shown incremental benefit of 3D echocardiography over 2D imaging in planning interventions to treat VSD or papillary muscle rupture [30].

Papillary muscle rupture — Papillary muscle rupture with acute mitral regurgitation is usually caused by necrosis of the head of the posteromedial papillary muscle, presumably because of its tenuous blood supply derived from the posterior descending artery. The anterolateral papillary muscle is typically spared because it has a dual blood supply from the left anterior descending and circumflex arteries [31]. (See "Acute mitral regurgitation in adults".)

On echocardiography, papillary muscle rupture is characterized by a flail mitral leaflet and severed papillary muscle head, which move freely between the LV and left atrium (movie 8 and movie 9) [27,32]. Color flow Doppler contributes to judging the severity of associated mitral regurgitation [27].

TEE may be required for diagnosis of papillary muscle rupture when standard transthoracic studies are not informative. TEE is most likely to be needed when the ruptured head, because of preserved chordal support from the unaffected papillary muscle, does not prolapse into the left atrium [33].

Papillary muscle displacement — A new mitral regurgitation murmur after MI in the absence of papillary muscle rupture may suggest papillary muscle displacement (previously known as papillary muscle dysfunction) due to severe regional wall motion abnormality of the wall supporting the papillary muscle or malalignment due to ventricular dilation [34]  (movie 10). Doppler studies document the regurgitant flow (movie 11 and movie 12).

Both papillary muscle displacement and mitral annular dilation can cause a failure of leaflet coaptation with a visible space between the leaflets in systole (rare) or coaptation (less than 5 mm) with systolic tenting into the LV (movie 10) [35].

Mitral regurgitation is predictive of an increased cardiovascular mortality after MI, even if it is mild. This is not surprising given the frequent association between mitral regurgitation and LV enlargement.

Free wall rupture — LV rupture is a mechanical complication that can rapidly lead to cardiac tamponade and death. Echocardiography can confirm the findings of tamponade in the setting or a pericardial effusion (see "Cardiac tamponade"). A contained free wall rupture may form a pseudoaneurysm (see below).

Tricuspid regurgitation — Significant tricuspid regurgitation may result from RV infarction or from elevated pulmonary artery pressure resulting from elevated LV end-diastolic pressure (movie 13 and movie 14). (See "Right ventricular myocardial infarction".)

LV thrombus — LV intracavitary thrombi used to be one of the most common complications of apical MI, but with the advent of interventional treatment of acute MI, they are encountered less frequently. Thrombi are important clinically because of their potential for embolic complications, including stroke. Echocardiography can document both the presence of thrombus and of risk factors for embolization. The 2019 ACC Multimodality Imaging Guidelines classified as appropriate the use of echocardiography for the assessment of mural thrombus after acute MI (movie 15) [14]. Similarly, the 2011 ACC/AHA/American Society of Echocardiography (ASE) task force classified this use of echocardiography as appropriate [2]. Issues related to the diagnosis, prevention, and treatment of LV thrombus are discussed in detail separately. (See "Left ventricular thrombus after acute myocardial infarction".)

Silent complications — Among the compelling reasons for echocardiographic evaluation after acute MI is the detection and evaluation of sometimes silent complications:

●Pericardial effusion (movie 16) (see "Pericardial complications of myocardial infarction")

●Apical LV thrombus (see 'LV thrombus' above)

●LV aneurysm

●LV pseudoaneurysm (an LV wall rupture contained by the pericardium)

Ischemic aneurysms are defined as a localized diastolic deformity of the LV, recognized as extending beyond the expected LV contour when the chamber is maximally filled (movie 17 and movie 18 and movie 19). Pseudoaneurysm differs from true aneurysm and forms after myocardial rupture (or cardiorrhexis) with extravasation of blood into a partially adherent parietal pericardial sac [36]. This containment is weak but life-saving. The differentiation between the two types of aneurysm is important because a pseudoaneurysm is an indication for urgent surgery. On echocardiography, pseudoaneurysms have a narrow inlet or neck that is less than 40 percent of the maximal aneurysm diameter, while true aneurysms have wide inlets. (See "Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction".)

USE FOR PROGNOSIS AND TO GUIDE THERAPY — Echocardiography early post-MI provides prognostic information and may help guide therapy (eg, the LV ejection fraction [LVEF] influences the strength of recommendation for beta blocker and angiotensin converting enzyme inhibitor therapy). The role of echocardiography for risk stratification is discussed elsewhere. (See "Risk stratification after acute ST-elevation myocardial infarction" and "Risk stratification after non-ST elevation acute coronary syndrome".)

The 2013 American College of Cardiology/American Heart Association (ACC/AHA) ST-elevation MI guideline provides a strong recommendation for evaluation of LVEF as one of the strongest predictors of survival [37]. This measurement can be made with either left ventriculography or by echocardiography. The 2014 ACC/AHA non-ST-elevation MI guideline states that because the presence and degree of valvular disease may influence the revascularization strategy, echocardiography rather than ventriculography is often preferred to evaluate LV function [38].

Left ventricular systolic function — The LVEF is a major predictor of long-term prognosis after both ST elevation and non-ST elevation MIs (figure 5 and figure 6). Echocardiography is usually the preferred test to measure the LVEF, since it can detect other abnormalities that are associated with a worse prognosis including diastolic dysfunction, concurrent RV involvement, increased left atrial volume, mitral regurgitation, and a high wall motion score index [25,39-44].

In the absence of a specific indication (eg, heart failure or suspected mechanical complication), the LVEF is usually measured before or even after discharge. LVEF is best measured using biplane method of disks [8]. The end-diastolic volume and end-systolic volume are used to compute the LVEF. Early measurements may be misleading, since improvement in LVEF, beginning by the third day and largely complete by 14 days, may occur in patients who have been reperfused and reflects recovery from myocardial stunning [45,46]. In a review of 249 patients with serial echocardiographic studies, 58 percent showed complete or partial recovery of LV function; most of those who improved had more than a 5 percent increase in LVEF [46]. (See "Clinical syndromes of stunned or hibernating myocardium", section on 'Acute myocardial infarction'.)

A higher wall motion score index reflects a greater number of abnormally functioning segments and is thus associated with more severe impairment in overall LV systolic function and worse prognosis [25,44]. (See 'Extent of infarct' above.)

LV end-systolic volume index (mL/m² body surface area) provides valuable prognostic data in patients with stable coronary disease [47]. The quintessential reversible RMWA is that seen after stress testing, with most RMWAs resolving within minutes. If end-systolic volume increases, this suggests severe multivessel disease [48].

Strain echocardiography may also provide additional prognostic information independent of LVEF, including the prediction of ventricular arrhythmia after MI [49]. Strain imaging performed some months after MI has greater sensitivity compared with traditional methods of detecting RWMAs for detecting regions of MI detected by cardiac magnetic resonance imaging [50]. (See "Tissue Doppler echocardiography" and "Tissue Doppler echocardiography", section on 'Assessment of global and regional left ventricular systolic function'.)

Left ventricular diastolic function — A restrictive mitral filling pattern (RFP) is an independent predictor of mortality after acute MI [51]. Restrictive filling is characterized by a high E to A ratio and short deceleration time and is indicative of stage 3 or 4 diastolic dysfunction. (See "Echocardiographic evaluation of left ventricular diastolic function in adults".)

In a meta-analysis (3396 patients in 12 prospective studies), RFP was associated with higher all-cause mortality (hazard ratio 2.7; 95% CI 2.2-3.2) and remained an independent predictor in multivariate analysis with age, sex, and LVEF [51]. The prevalence of an RFP was highest (36 percent) in the quartile of patients with lowest LVEF (<39 percent) and lowest (9 percent) in the quartile of patients with the highest LVEF (>53 percent). RFP predicted mortality within each quartile of LVEF and in different Killip classes. Furthermore, a study of 571 patients with acute MI found that irreversible RFP was associated with increased mortality as compared with reversible RFP [52].

The ratio of transmitral flow velocity to early mitral annulus velocity (E/E') >15 has been found to predict future LV remodeling and dilation [53]. This ratio is also an independent predictor of all-cause mortality after MI [54]. (See "Echocardiographic evaluation of left ventricular diastolic function in adults".)

Mitral regurgitation — The presence of mitral regurgitation, even if mild, is an adverse prognostic finding (figure 7) [43,55], a reflection of its association with LV dysfunction. (See 'Papillary muscle rupture' above.)

Residual ischemia — Patients with acute MI who are not taken to the cardiac catheterization laboratory within the first 48 hours, and who are candidates for percutaneous intervention, should be considered for stress testing to evaluate for ischemia. Stress echocardiography is an established method of achieving this evaluation.

The 2011 ACC/AHA/American Society of Echocardiography (ASE) appropriateness criteria classified as appropriate the use of stress echocardiography within three months of MI to evaluate the presence/extent of inducible ischemia for individuals who are hemodynamically stable, without recurrent chest pain symptoms or signs of heart failure, or who have not had coronary angiography since the MI [2]. Stress echocardiography is not appropriate early after MI for those who have been completely revascularized and are asymptomatic [2].

Other factors — Other findings on echocardiography that have been demonstrated to influence prognosis include:

●Left atrial enlargement [42].

●RV dysfunction [41]. RV myocardial function as assessed by longitudinal strain is an independent predictor of all-cause mortality. In a study of 621 patients with acute MI, RV longitudinal strain ≥-22.1 percent (ie, a lesser absolute value) was associated with a threefold mean increase in death (HR 3.43; 95% CI 1.87-6.29) in a univariable analysis [56]. RV strain remained a significant predictor in a multivariable model (HR 1.08; 1.03-1.13 per 1 percent increase in RV strain).

●Pulmonary artery pressure. In a study of 536 patients with acute MI without significant valve disease or known pulmonary hypertension, increase in pulmonary artery systolic pressure independently predicted all-cause mortality (adjusted HR 1.22 per 10 mm Hg; 95% CI 1.14-1.38) [57].

●Longitudinal strain. Although LV longitudinal strain is associated with poor prognosis after MI [58,59], its routine clinical use remains controversial due to technical problems such as image acquisition, signal-to-noise ratio, poor spatial resolution, and angle dependence [60].

Contrast echocardiography — Myocardial contrast echocardiography can be used after MI for both image enhancement and prognosis. Persistent contrast perfusion defect is associated with worse LV remodeling four weeks later [61]. (See "Contrast echocardiography: Clinical applications".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: ST-elevation myocardial infarction (STEMI)".)

SUMMARY

●Echocardiography has significant utility in the diagnosis of myocardial infarction (MI), detection of complications, and for establishing prognosis after MI. (See 'Indications for echocardiography in MI' above.)

●Reasonable scenarios in which to obtain an echocardiogram for confirmed or suspected acute MI include:

•Chest pain, abnormal troponin, or electrocardiogram suggestive of MI in the emergency department when a definite diagnosis has not been established. (See 'Diagnosis of MI' above.)

•Evaluation of complications of MI. (See 'Detecting complications after MI' above.)

•Evaluation of the possibility of residual ischemia. (See 'Residual ischemia' above.)

•For prognosis and to guide therapy after MI. (See 'Use for prognosis and to guide therapy' above.)