Regional wall motion abnormalities (RWMA) occur before the ECG changes or the onset of symptoms in the ischemic cascades. Left ventricular (LV) diastolic dysfunction occurs before systolic dysfunction; ECG abnormalities and chest pain are relatively late events (Fig. 1).5) RWMA detected by echocardiography correspond with the coronary artery territories, although there is some variation depending on the individual coronary artery anatomy6) and dominance of the right coronary artery (RCA) and left circumflex arteries (LCX).

The severity of the wall motion abnormality depends on the transmural extent of the infarction, and the circumferential limits depend on the coronary arterial distribution. The ischemic myocardium continues to demonstrate some degree of passive forward motion because of the pulling action of adjacent nonischemic myocardium, but the contractility (systolic thickening) of the ischemic myocardial segments decreases or is absent. In a normal person, the LV free wall thickness increases by more than 40% during systole. Hypokinesis is defined as systolic wall thickening of less than 30%, and akinesis is defined as systolic wall thickening of less than 10%. Dyskinesis means that a myocardial segment moves outward during systole, usually in association with systolic wall thinning.7)

To detect RWMA, the LV is divided into several segments. American Society of Echocardiography scoring system is used most widely for grading the severity of a wall motion abnormality (Table 3).8) A 17-segment model has been proposed recently, which adds the apical cap.9) This 17-segment model (Fig. 2) is preferred for myocardial perfusion studies, which can be compared with other perfusion modalities {cardiac single photon emission computed tomography (SPECT), cardiac magnetic resonance image (MRI), cardiac computed tomography (CT) etc.}. Each segment is assigned a score on the basis of visual assessment of contractility: normal: 1, hypokinesis: 2, akinesis: 3, dyskinesis: 4, and aneurysmal: 5. The wall motion score index (WMSI) is calculated to provide a semi-quantitative measure of the extent of RWMA. For example, a normal contracting LV has a WMSI of 1 (16/16), whereas a dysfunctional LV will have an increasing WMSI proportional to the severity of RWMA. This score correlates with the myocardial infarction size compared with the perfusion defect size on cardiac SPECT imaging. Patients with a WMSI greater than 1.7 have a perfusion defect larger than 20%.10)

The coronary arterial territories of the LV wall are depicted in Fig. 3.9) The anterior, anterolateral, anteroseptal, and apical segments are in the distribution of the left anterior descending artery (LAD). The lateral wall and lateral apex correspond to the LCX distribution. The inferolateral wall is supplied by the posterior descending artery. In 80% of the population, the posterior descending artery arises from the RCA. In the other 20%, the posterior descending artery arises from the LCX (so called, left-dominant). The right ventricle (RV) is supplied by acute marginal branches arising from the RCA. The coronary artery anatomy may differ between individual patients, so the extent of segmental wall motion abnormalities may also differ between patients. In addition, the presence of collateral vasculatures and bypass graft must be considered.

Echocardiography can be useful for direct visualization of coronary arteries.11)12) Detection of the ostia of the left and right coronary arteries and proximal part of the LAD and their flow is helpful for excluding an anomalous origin of a coronary artery, coronary aneurysm, and coronary fistula, associated with chest pain or sudden death. Use of a high-frequency transducer and a special setting of low Nyquist limits allow visualization of the coronary artery tree and evaluation of the coronary flow.12) For instance, coronary flow reserve (CFR), expressed as the ratio of the peak diastolic flow velocity during maximal vasodilatation to that of the basal diastolic flow velocity, can predict coronary artery stenosis and can be used to elucidate other causes of chest pain, including myocardial hypertrophy, microvascular disease, and aortic stenosis.13-15) TTE allows the evaluation of the diastolic coronary flow velocity in the distal LAD. An extremely slow diastolic velocity of less than 13 cm/s may suggest the pathologic flow, which can mean impairment of myocardial perfusion.12)16) The slow diastolic velocity can explain the "slow dye progression" phenomenon of coronary angiography in patients with angina-like chest pain. Retrograde flow at the anterior apex of the heart reflects the presence of collateral flow, which means the total occlusion of the LAD.12)17)

In most cases, a patient's cardiovascular symptoms are worsened by activity or stress. An adequate supply of oxygen to the myocardium is essential for preventing the development of ischemia and infarction. For example, coronary artery stenosis limits an appropriate increase in perfusion in response to an increased demand for blood flow, as occurs during exertion or emotional stress. Stress echocardiography compares the wall motion, myocardial perfusion, pressure gradient, pulmonary pressure, valvular regurgitation, or filling pressure before and after a stress to identify a pathologic condition, that is not apparent at rest. During a stress echocardiography, two-dimensional echocardiographic images at rest and during stress are digitized and displayed in a side-by-side format so that induced RWMAs can be detected easily.

The most common indication for stress echocardiography is the evaluation of myocardial ischemia, but this modality is also available in the evaluation of valvular heart disease, pulmonary hypertension, LV filling pressure (e.g. diastolic heart failure), and exertional dyspnea.

Echocardiography related to exercise or pharmacologic stress to assess the presence of ischemia is safe and effective in patients with acute chest pain, except myocardial infarction (MI) or unstable angina.

Stress echocardiography is performed during exercise or administration of pharmacologic agents. Exercise stress includes a treadmill exercise protocol (e.g. Bruce protocol) or a supine bicycle protocol. For a treadmill study, the patient is imaged at baseline and just after peak exercise. Because exercise-induced RWMA due to ischemia usually lasts for a few minutes after termination of exercise, it is important to acquire the immediate postexercise image to compare with the baseline preexercise image. The supine bicycle protocol can be used to obtain images throughout exercise, which allows for image comparison at low, medium, and high workloads.18) Exercise echocardiography should be terminated if any of the following conditions occurs: (1) severe symptoms (chest pain, dyspnea), (2) severe ischemia (ST-segment depression ≥5 mm or ST-segment elevation), (3) complex ectopy or ventricular tachycardia, (4) hypertensive blood pressure response (>220 mmHg systolic, >110 mmHg diastolic), (5) hypotension (>20 mmHg decrease compared with previous stage), or (6) reaching the target heart rate.19) In one study, with using the wall motion criteria, the sensitivity and specificity of exercise stress echocardiography were 85% and 88%, respectively, compared with 85% and 81% for an exercise thallium scan.20)

When a patient cannot exercise properly, a pharmacologic stress test can be performed to induce ischemia with dobutamine, adenosine or dipyridamole. Dobutamine is used most commonly in stress echocardiography (Fig. 4). Baseline images are obtained, followed by the infusion of dobutamine at incremental levels (usually 5, 10, 20, 30 and 40 ㎍/kg/min) of 3 minutes duration. Patients who do not reach target heart rate even after being given 40 ㎍/kg/min of dobutamine can perform handgrip maneuvers or be given intravenous atropine in doses of 0.1 to 0.25 mg up to total of 1 mg, unless they have contraindications. The test is terminated when the patient's heart rate reaches 85% of maximum predicted heart rate or the evidence of myocardial ischemia, hypotension, significant arrhythmia or drug-related side effects is developd.21) In one study, dobutamine stress echocardiography was found to have a sensitivity of 89.5%, a specificity of 88.9%, and a negative predictive value of 98.5%.22)

Tissue Doppler imaging (TDI), strain rate imaging, or color kinesis are anticipated to improve the accuracy of stress echocardiography.

The LV opacification with imaging microbubbles improves the definition of the LV endocardial border (Fig. 5). This provides better quantification of LV volume and assessment of wall motion analysis. The administration of an echocardiographic contrast enhancing endocardial border has increased the sensitivity of stress echocardiography in the diagnosis of CAD. In one study, the percentage of wall segments visualized increased from 94.4% to 99.8% with the use of LV opacification during peak exercise.23)

Myocardial contrast echocardiography (MCE) allows the assessment of myocardial perfusion with microbubbles, delivered to small myocardial vessels for ventricular enhancement. Hypoperfused areas of myocardium lack the enhancement by a contrast agent. MCE is a reproducible and reliable technique for evaluating of the risk area after coronary occlusion, regional coronary flow reserve, myocardial viability, and the outcome of reperfusion.24)

Innovative ultrasound methods using harmonic imaging have been developed to exploit the interaction between microbubbles and ultrasound and to allow assessment of perfusion.

Harmonic imaging has recently been shown to provide improved endocardial definition relative to tissue harmonic imaging for specific regions of the endocardium, in particular the base and anterior wall.25) In conventional echocardiography, images are derived from ultrasound waves returned at the same frequency as the transmitted waves. However, harmonic frequencies are also produced by the transmitted wave; in harmonic imaging, the machine uses the returning second harmonic to construct images. This improves image quality because there is less distortion of the returned ultrasound waves (they are generated in the heart and only have to pass through tissue once), and few harmonics are produced close to the chest wall where many artifacts arise.26) This technique has recently been shown to be superior to routine evaluation to detect of CAD.27)28) If the amount of microbubbles in the myocardium is sufficient, they can be destroyed with a high mechanical index (>1.5) of ultrasound. In the normal myocardium, the microbubbles are replenished within five to seven cardiac cycles. However, in the myocardium with low or no perfusion, the microbubbles are not replenished normally, and the areas of myocardium affected appear dark or patchy.29)30)

In the hemodynamically unstable patients after acute MI, it is very important to identify immediately the underlying cause and to exclude cardiac rupture to ensure proper treatment. Two-dimensional echocardiography and color Doppler study are useful for identifying the cause in these patients, especially for checking mechanical complications (e.g. ventricular septal rupture, papillary muscle rupture, free wall rupture). Therefore, echocardiography is the mainstay of diagnosis of mechanical complications of MI,31) and patients with unexplained hemodynamic deterioration should be evaluated immediately (Table 4). Thrombolytic therapy and primary percutaneous coronary intervention have been reported to reduce the incidence of mechanical complications.

Ventricular septal rupture occurs in 1-3% of patients after MI, and it occurs during the early phase of acute infarction (almost within the first week). The typical clinical presentation is a new systolic murmur, with abrupt hemodynamic deterioration. The risk factors for development of ventricular septal rupture include old age (>65 years), hypertension, anterior wall infarction, first infarction, or lack of collateral circulations.32) Two-dimensional echocardiography may show a discrete defect, but there may also be multiple serpiginous channels in the necrotic myocardium (Fig. 6). The diagnosis can usually be made by TTE, and experience is essential because the most useful views depend on the location of defect. Subcostal views are particularly useful in the critically ill, supine patient with inferior infarction. Small defects may not be visible, but color Doppler is very sensitive. When TTE is suboptimal for examination, transesophageal echocardiography (TEE) is very useful for detecting the site of the defect, and the presence of multiple defects.

The therapeutic strategy for ventricular septal rupture is early surgery. Without a repair, the outcome is very poor. Early surgical intervention improves the outcome compared with conservative therapy.33) Intra-aortic counterpulsation can be used to stabilize the patient with cardiogenic shock before surgery.

The necrosis and rupture of a papillary muscle causes acute mitral regurgitation (MR) in patients with acute MI. The clinical presentation of papillary muscle rupture is variable. About 50% of patients with acute MR do not have a systolic murmur because of rapid equalization of the LV and left atrial (LA) pressure. In addition, the murmur can be attenuated by a crackled lung sound caused by pulmonary edema. Rupture usually involves the posteromedial papillary muscle, perfused from the posterior descending artery alone, whereas the anterolateral papillary muscle has a dual blood supply from both the diagonal and circumflex arteries.

Two-dimensional echocardiography can detect abnormalities of the mitral valve apparatus, including prolapse of one or both leaflets, a flail leaflet, and liberation of a portion of the papillary muscle (Fig. 7). A papillary muscle rupture should be suspected when there is eccentric jet of MR with a relatively normal-sized LA. TEE is a particularly suitable imaging modality34) and should be performed immediately if this diagnosis is suspected because it provides high-resolution images of the papillary muscles and accurate assessment of the severity of MR.

Papillary muscle rupture and acute severe MR is a life-threatening condition that requires urgent surgical intervention. Once a papillary muscle rupture has been diagnosed, immediate mitral valve replacement and coronary revascularization is necessary for patient's survival.

Rupture of the free wall of the LV is a fatal mechanical complication of acute MI that occurs in about 1% of patients with MI. Free wall rupture is prone to the patients with a transmural MI involving the inferolateral wall in association with the LCX. The administration of thrombolytic agents may promote cardiac rupture, presumably because of a hemorrhagic tendency. Free wall rupture usually presents clinically as hemodynamic collapse and sudden death.

Direct visualization of the free wall rupture is often difficult because it may be only a "slit" in the myocardium and the location of pericardial fluid may not correlate with the area of rupture (Fig. 8). It is rare for a color Doppler study to show blood flow into the pericardium. When the diagnosis is uncertain, the use of left heart contrast may delineate the tear. An intrapericardial thrombus is often present and is very characteristic. It appears as an echo-dense mass that may be mobile and undulating within the pericardial space or immobile and impinging on cardiac chambers.35) Negative echocardiographic findings should not exclude myocardial rupture, if the clinical suspicion is high.

The mortality is so high unless appropriate treatment is given, that clinical suspicion, early detection and prompt surgical intervention are indispensable for good clinical outcome.

A pseudoaneurysm is characterized by a small neck communication that connects the LV and aneurismal cavity. The majority of pseudoaneurysms are located in inferoposterior or inferolateral regions, in association with the RCA or LCX.

It is important to distinguish a pseudoaneurysm, which has a high possibility of spontaneous rupture, from a true aneurysm, which seldom ruptures spontaneously. In a true aneurysm, there is continuity of the myocardium in the region of dilatation, in contrast to the loss of this continuity in a pseudoaneurysm with an abrupt area of rupture. An echocardiographic feature of pseudoaneurysm is the narrow neck. The ratio of the diameter of entry and the maximal diameter of the pseudoaneurysm is usually <0.5, although this feature is not always reliable and has only a 60% sensitivity.36) Spectral and color Doppler studies demonstrate characteristic "to-and-pro" flow through the rupture site. Contrast echocardiography can be helpful in locating the point of communication. Fig. 9 demonstrates the difference between a true aneurysm and a pseudoaneurysm.

The RV is involved in acute MI frequently. RV infarction occurs in up to 50% of inferior wall MI, but hemodynamically significant RV infarction occurs infrequently.37) Many RCA occlusions do not result in significant RV infarction because of the lower RV oxygen demand, higher oxygen extraction ratio, greater systolic/diastolic flow ratio, and collateral supply. However, once a patient develops cardiogenic shock due to RV infarction, the mortality is so high that initial recognition and treatment are very important. The clinical settings of a suspected RV infarction are unexplained hypotension or low cardiac output after acute MI, marked hypotension after administration of nitrates, and unexplained hypoxemia after acute MI. Patients who have an RV infarction present with increased jugular venous pressure but clear lung fields. Echocardiography plays an important role in the diagnosis and assessment of RV infarction. The RV is dilated and hypokinetic to akinetic (Fig. 10). Tricuspid regurgitation may appear and become significant because of dilatation of the tricuspid annulus. TDI may provide additional evidences of RV infarction. In one study, a tricuspid valve annulus peak velocity less than 12 cm/s had a sensitivity of 81%, specificity of 82%, and negative predictive value of 92% for RV infarction.38)

When a segmental wall motion abnormality is present in the LV cavity, it is prone to form a thrombus, most commonly in the LV apex resulting from occlusion of the LAD. The peak timing of thrombus formation after MI is 3 days, but thrombus may occur as early as within few hours in large areas of apical akinesis and may occur a few weeks after acute MI.

Because of concern about a potential embolic event, patients with a large apical infarction or ventricular aneurysm should be given anticoagulation properly.

Two-dimensional echocardiography is the most practical and reliable imaging modality for detecting a LV thrombus. The echocardiographic finding of a thrombus is a mass that is distinct from the endocardium and protruding to a variable extent into the LV cavity (Fig. 11). Characteristically, a thrombus has a nonhomogeneous echo density. The base of attachment to the wall may be broad in a sessile thrombus, or narrow in a pedunculated thrombus, which has a greater chance of embolization. Contrast echocardiography is also helpful in detecting a LV thrombus.

Hemodynamically insignificant pericardial effusion is common after MI, especially after a large transmural infarction. Pericardial friction rubs and/or pericardial pain are frequently encountered in patients with a transmural MI. It is important to identify the chest pain of pericarditis accurately, because failure to be aware of it may lead to the incorrect diagnosis of recurrent ischemic pain and/or infarct extension, with resulting inappropriate use of anticoagulants, nitrates, beta-blockers, or coronary angiography.

Echocardiography is a sensitive technique for diagnosing pericardial effusion, although the absence of fluid does not exclude pericarditis. Echocardiography can identify a site for percutaneous drainage if required and can be used to monitor the procedure. The effusion does not increase morbidity and mortality in MI but serves as another indicator of a large area infarction. Larger effusion or echocardiographic dense effusions representing hemorrhage should always make the clinicians consider a free wall rupture.39)

In patients with severe hemodynamic compromise, TTE may be limited by mechanical ventilation, recent cardiac surgery, or an inability to position the patient adequately. In this situation, TEE has proven to be efficacious, especially in ruling out complications related to cardiac rupture and for assessing global and regional ventricular function.40) With careful sedation and close monitoring, TEE can be performed safely even in patients with early acute MI.41) However, it does have chances of potential complications, TEE should be performed by an experienced physician. It is relatively contraindicated in patients with esophageal diseases-for example, varices, stricture, esophagitis, scleroderma-and may be hazardous in patients with severe coagulopathy or poor respiratory function.

The filling of the pericardial space with fluid or blood results in a pericardial effusion, detected as an echo-free space. A small amount of effusion may be detected usually as a posterior echo-free space in the parasternal long axis view in the ventricular systolic phase. When the amount of pericardial effusion is massive, the heart may have a "swinging" motion in the pericardial cavity. However, the swinging motion is not always present in cardiac tamponade. Cardiac tamponade can occur with a small amount of pericardial effusion if the effusion accumulates rapidly.43)

Two-dimensional echocardiographic features of a tamponade include early diastolic collapse of the RV, late diastolic right atrial inversion, abnormal ventricular septal motion, respiratory variation in ventricle chamber size, and plethora of the inferior vena cava with blunted respiratory changes.

The Doppler echocardiographic findings of pericardial effusion and tamponade are more sensitive than the two-dimensional echocardiographic features.44) Cardiac tamponade makes the four cardiac chamber pressures equal. During inspiration, the venous return and RV filling increase and that result in a leftward septal shift. Therefore, the Doppler ultrasound shows that tricuspid and pulmonic valve flow velocities increase markedly during inspiration, while pulmonic vein, mitral, and aortic flow velocities diminish.

The most effective therapy of tamponade is elimination of the pericardial fluid. If manifestations of tamponade appear, pericardial drainage must be performed immediately because relief of the intrapericardial pressure may be lifesaving. Intravenous saline may be administered as the patient is being readied. Pericardiocentesis is very useful for lifesaving in tamponade, but a blind percutaneous attempt has a high rate of complications, including pneumothorax, puncture of the cardiac wall, and even death. Two-dimensional echocardiography provides guidance of the needle by locating the optimal site of the puncture, by determining the depth of the pericardial effusion, usually from the subcostal view. The position of the puncture needle can be confirmed by imaging with administration of agitated saline.45) Two-dimensional echocardiography can be used to monitor the result of pericardiocentesis.