Role of Echocardiography in Patients With Acute Coronary Syndrome


Applicable Modes of Echocardiography in the Coronary Care Unit

Transthoracic echocardiography (TTE) is ideally suited for cardiac imaging in the coronary care unit. It offers major advantages compared with other imaging modalities, including its portability, its relative low cost, and the wealth of anatomic, hemodynamic, and functional information that can be obtained rapidly at the bedside. With further technologic advances, it continues to play a major role in the diagnostic assessment and risk stratification of patients in the coronary care unit ( Table 21.1 ).

TABLE 21.1
Appropriate Use a of TTE for Cardiovascular Evaluation in Acute Settings.
Adapted from Douglas PS, Garcia MJ, Haines DE, et al. ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 appropriate use criteria for echocardiography. A report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, American Society of Echocardiography, American Heart Association, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, Society of Critical Care Medicine, Society of Cardiovascular Computed Tomography, Society for Cardiovascular Magnetic Resonance American College of Chest Physicians. J Am Soc Echocardiogr . 2011;24:229–267.
Finding Score
Hypotension or Hemodynamic Instability
Hypotension or hemodynamic instability of uncertain or suspected cardiac origin A-9
Assessment of volume status in a critically ill patient U-5
Myocardial Ischemia/Infarction
Acute chest pain with suspected MI and nondiagnostic ECG when a resting TTE can be performed during pain A-9
Evaluation of a patient without chest pain but with other features of an ischemic equivalent or laboratory markers indicative of ongoing myocardial ischemia A-8
Suspected complication of myocardial ischemia or MI, including but not limited to acute mitral regurgitation, ventricular septal defect, free wall rupture/tamponade, shock, RV involvement, heart failure, or thrombus A-9
Evaluation of Ventricular Function After Acute Coronary Syndrome
Initial evaluation of ventricular function after acute coronary syndrome A-9
Re-evaluation of ventricular function after acute coronary syndrome during recovery phase when result will guide therapy A-9
ECG , Electrocardiogram; MI , myocardial infarction.

a Appropriateness is scored 1 to 9: A, appropriate indication (7–9); U, uncertain indication (4–6).

For patients with an established myocardial infarction (MI), early echocardiographic evaluation using routine measures of left ventricular (LV) systolic function, regional wall motion, LV diastolic function, right ventricular (RV) function, and mitral regurgitation (MR) greatly assists with management. The use of left-sided contrast agents for LV opacification improves interobserver agreement and is superior to routine evaluation for the measurement of LV ejection fraction (LVEF) and regional wall motion. Real-time three-dimensional (3D) echocardiography allows fast, semiautomated, dynamic measurement of LV volume and LVEF, automated detection of regional wall motion abnormalities (WMAs), and perfusion imaging.

Quantification with myocardial strain techniques is a further significant step to reduce interobserver variability in the assessment of regional WMAs. It may facilitate the exclusion of significant coronary artery stenosis among patients with suspected non–ST-segment elevation acute coronary syndromes (ACSs) who have inconclusive electrocardiographic (ECG) findings and normal cardiac biomarkers.

Because perfusion abnormalities precede WMAs in the ischemic cascade, myocardial contrast echocardiography has a higher sensitivity for the detection of coronary artery disease (CAD). Myocardial contrast echocardiography also has a significant role in the evaluation of myocardial viability. Progressive improvements and miniaturization of handheld echocardiographic instruments have led to its increasing use as an adjunct to physical examination. Several studies have shown the utility of these modalities, but they are not comparable to full-service systems, and care should be exercised to ensure that clinicians using and reporting studies with these instruments are appropriately trained.

With careful sedation and close monitoring, transesophageal echocardiography (TEE) can be performed safely in patients early after acute MI. If there is a concern about the patient’s hemodynamic state or respiration, intubation and ventilation by an anesthetist before TEE imaging should be strongly considered. The cause of hemodynamic instability in patients with MI often can be established by bedside TTE. However, TTE may be limited by mechanical ventilation, recent cardiac surgery, and an inability to adequately position the patient, and in such cases, TEE may be invaluable. Other potential uses of TEE in the coronary care unit include exclusion of other diagnoses, particularly aortic dissection (especially in patients with impaired renal function that limits the use of contrast computed tomography [CT]) and evaluation of left atrial appendage thrombus before cardioversion. Two-dimensional (2D) and three-dimensional (3D) TEE are commonly used to guide intracardiac catheter-based interventions, such as closure of a post-MI ventricular septal defect.

Echocardiography in the Diagnosis and Localization of Acute Myocardial Infarction

Diagnostic Role of Echocardiography

The accuracy of echocardiographic diagnosis of an MI depends on its ability to detect WMAs in the involved segment. The severity of the WMA depends on the transmural extent of the infarction, and the circumferential limits depend on the arterial distribution and collateral blood supply. Most patients with ST-elevation myocardial infarction (STEMI) have some hypokinetic LV segments unless there is very early reperfusion, but it is not unusual for patients who have non-STEMI with a small troponin rise to have no appreciable WMA. The most widely used scoring system for grading the severity of a WMA is shown in Table 21.2 .

TABLE 21.2
Scoring System for Grading Wall Motion.
Modified from Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr . 2015;28(1):1–39.e14.
Score Wall Motion Endocardial Motion a Wall Thickening a
1 Normal Normal Normal (>30%)
2 Hypokinesis Reduced Reduced (<30%)
3 Akinesis Absent Absent
4 Dyskinesis Outward Thinning
5 Aneurysmal Diastolic deformity Absent or thinning

a In systole.

Other causes of segmental LV dysfunction must be recognized ( Table 21.3 ). An increasingly recognized mimic of acute MI is apical ballooning syndrome, also known as takotsubo cardiomyopathy. It is estimated that approximately 2% of all patients with suspected ACS are ultimately diagnosed with takotsubo cardiomyopathy. In the International Takotsubo Registry, 90% of registrants were women older than 50 years of age. Women are most commonly affected by an emotional trigger, men by a physical trigger, and no trigger is evident in an estimated 28% of cases.

TABLE 21.3
Regional Wall Motion Abnormalities Unrelated to Coronary Artery Disease.
Condition Comment
Left bundle branch block May be an ECG manifestation of acute MI or an incidental and unrelated finding
Wolff-Parkinson-White syndrome May mimic inferior or posterior MI
Pacemaker May result in abnormal septal or apical motion depending on the site of attachment of the RV pacemaker lead
Previous cardiac surgery Septum may be hypokinetic
RV volume overload Ventricular septal flattening in diastole
RV pressure overload Ventricular septal flattening in systole
Constrictive pericarditis Diastolic wobble of the septum
Apical ballooning syndrome (takotsubo cardiomyopathy) Classically, akinesis or ballooning of the middle and apical LV segments and hyperkinetic basal LV segments
Myocarditis May result in global or regional LV systolic impairment
Dilated cardiomyopathy Usually global LV systolic impairment, but there may be regional variation in contractility and wall thickness
Sarcoidosis May cause areas of hypokinesis and/or thinning
ECG , Electrocardiogram; MI , myocardial infarction.

Earlier criteria for the diagnosis of takotsubo cardiomyopathy excluded CAD, but it is now recognized that this syndrome may occur in patients with CAD. The prevalence of CAD ranges from 10% to 61%, with a 15% prevalence in the International Takotsubo Registry. Specific criteria were proposed by Frangieh et al. to help differentiate takotsubo cardiomyopathy from STEMI and non-STEMI.

TTE is invaluable in the diagnosis of takotsubo cardiomyopathy and reveals characteristic features of LV impairment in a noncoronary distribution and early improvement of LV function consistent with myocardial stunning rather than MI. Although the classic presentation is with midwall and apical LV ballooning and hypercontractile basal LV segments ( Fig. 21.1 ), variant forms such as mid-ventricular ballooning and basal ballooning have also been described.

Fig. 21.1, Takotsubo cardiomyopathy (apical ballooning syndrome).

In a cardiac magnetic resonance (CMR) imaging series of 256 patients with takotsubo cardiomyopathy, 82% were of the apical variety, 17% were mid-ventricular, 1% were basal, and 34% had RV involvement. Up to one third of patients experience early complications, including dynamic LV outflow tract obstruction, acute MR, heart failure, cardiogenic shock, and arrhythmias. Mortality rates vary from 2% to 5%, similar to those for STEMI, and death occurs mainly from cardiogenic shock and ventricular arrhythmias. Natural history studies suggest improvement in LV function in most cases within weeks or months with reported recurrence rates of 5% to 22% at 6 months to 10 years after the index event.

Myocarditis is an important mimic of ACS. Patients typically present with chest pain, a rise in troponin levels, and nonspecific ECG changes. Regional WMAs may exist but with a normal or near-normal coronary angiogram. Shirani et al showed a predominance of subepithelial inflammation in the LV free wall. The posterolateral LV segments are most commonly involved, but other LV segments may be involved, or the LV may be globally dilated and/or impaired. In a study by Mahrholdt et al., patients with biopsy-proven myocarditis due to parvovirus PVB19, the lateral wall of the LV was predominantly affected, whereas in patients affected with herpesvirus HHV6, the anterior septum was predominantly affected.

Clues to the diagnosis of myocarditis rather than an ACS include clinical features such as a viral prodrome, pleuritic chest pain, a more persistent rise in troponin levels (rather than the typical rise and fall of troponin levels in an ACS), and a pericardial effusion. Magnetic resonance imaging (MRI) with gadolinium is a very accurate modality to confirm myocarditis.

Localization of Infarction

In an attempt to establish segmentation standards applicable to all types of imaging, including echocardiography, nuclear perfusion imaging, cardiovascular MRI, and cardiac CT, a 17-segment model of LV segmentation has been proposed. This model includes the apical cap, which is the segment beyond the end of the LV cavity that usually is seen only with some contrast and myocardial perfusion studies. With routine echocardiographic studies, the 16-segment model can be used without the apical cap. The LV segments and the approximate and most common coronary arterial distributions in relation to these segments are depicted in Fig. 21.2 . The extent of the segmental wall motion is related to the exact coronary anatomy in an individual patient but may vary among patients. The presence of collaterals and previous bypass surgery alters the distribution of ischemia and infarction relative to the involved arterial supply.

Fig. 21.2, Typical coronary artery distribution of blood flow is shown in apical and parasternal short-axis views.

Direct visualization of the ostia of the left main coronary artery and right coronary artery (RCA) and the proximal left anterior descending coronary artery (LAD) in adults may be achieved with the use of TTE ( Fig. 21.3 ). This may be helpful to exclude anomalous coronary artery origin, especially in younger patients.

Fig. 21.3, Ostia and proximal courses of the major epicardial coronary arteries.

RV Infarction

Although RV infarction was first described in the 1930s, it was only after the hemodynamic consequences were recognized in the 1970s that RV infarction was considered a clinical entity.

RV infarction occurs in up to 50% of inferior MIs, but hemodynamic compromise develops in fewer than half of such cases. The RV is predominantly supplied by acute marginal branches of the RCA, and occlusion of the RCA proximal to the origin of these branches results in ischemic dysfunction of the RV. When the occlusion is distal to the right atrial (RA) branches, augmented RA contractility enhances RV function and cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling and function, resulting in more severe hemodynamic compromise.

Less commonly, RV infarction is associated with acute anteroseptal MI. Isolated RV MI is reported to occur in less than 3% of all acute MIs. The clinical importance of RV infarction is emphasized by higher rates of hemodynamic compromise, arrhythmias, and in-hospital mortality compared with MI involving only the LV.

Echocardiography plays a vital role in the evaluation of patients with suspected RV infarction ( Table 21.4 ). In many cases, the LV inferior WMA may be relatively small with preserved LVEF. Assessment of RV systolic function is complex, and commonly used echocardiographic measures, including RV fractional area change and visual assessment, are associated with significant interobserver variability.

TABLE 21.4
Echocardiographic Signs of RV Infarction.
Primary Signs
RV dilation
Segmental wall motion abnormality of the RV free wall
Reduced TAPSE
Tricuspid valve annulus peak systolic velocity < 12 cm/s
Reduced RV global longitudinal strain
Reduced RV fractional area change
Secondary Signs
Paradoxical septal motion
Tricuspid regurgitation
Tricuspid papillary muscle rupture
Pulmonary regurgitant jet pressure half-time < 150 ms
Dilated inferior vena cava
Right-to-left interatrial septal bowing
Right-to-left shunting across patent foramen ovale
TAPSE, Tricuspid annular plane systolic excursion.

Tricuspid annular plane systolic excursion of less than 10 mm is a useful objective measure of RV dysfunction and should be measured in patients with suspected RV infarction. In a study of 60 patients with a first acute inferior MI, a tricuspid valve annulus peak systolic velocity of less than 12 cm/s had a sensitivity of 81%, a specificity of 82%, and a negative predictive value of 92% for RV infarction.

Global longitudinal strain of the RV can provide greater sensitivity and specificity than RV fractional area change or tricuspid annular plane systolic excursion for major adverse cardiovascular events after RV infarction. Reduced RV compliance can be detected by an increased A-wave velocity on the hepatic vein flow signal and by a short pressure half-time of the pulmonary regurgitant jet (<150 ms).

Characteristic echocardiographic features of RV failure with high RA pressures include bowing of the interatrial septum into the left atrium (LA) and dilation of the inferior vena cava with lack of inspiratory collapse. These indicators of RV function correlate with clinical status and prognosis. Hypoxemia resulting from right-to-left shunting across a patent foramen ovale may occur with a large RV infarction associated with elevated RA pressures.

In most cases of RV infarction, RV function improves and returns to near normal within 3 to 12 months, although the improvement may not be complete. Because the acutely ischemic dysfunctional RV represents predominantly viable myocardium, which may spontaneously recover or respond favorably to successful reperfusion even late after the onset of occlusion, it has been suggested that the term RV infarction is largely a misnomer and that the term RV ischemic dysfunction should be used. However, it is important to recognize that RV infarction is associated with relatively high in-hospital mortality rates, and early reperfusion enhances recovery of RV function with an improved clinical course and improved survival. The use of RV speckle tracking–derived longitudinal strain has prognostic value for patients with heart failure and may have a role after MI with RV involvement.

Detecting Complications of Acute Myocardial Infarction

In the acutely hemodynamically unstable patient, it is critical to exclude mechanical complications of MI before concluding that cardiogenic shock is the result of pump failure ( Table 21.5 ). In most cases, TTE (supplemented when necessary by TEE) is sufficient to exclude the major mechanical complications of papillary muscle rupture (PMR), ventricular free wall rupture (VFWR), and ventricular septal rupture (VSR).

TABLE 21.5
Echocardiography for Complications of Myocardial Infarction.
Hemodynamic States
Hypovolemia
RV infarction
Globally reduced LV contractility
Mechanical Complications
Papillary muscle rupture and severe mitral regurgitation
Ventricular septal rupture
Free wall rupture and tamponade
Other
LV aneurysm
Mural thrombus
Pericardial effusion

A single-center study of 2508 patients admitted with STEMI reported an overall mechanical complication rate of 1.1% (26 patients), including VSR in 17, VFWR in 2, a combination of VSR and VFWR in 2, and PMR in 5 patients. Older age, female sex, no history of angina or revascularization, multivessel CAD, and longer time between symptom onset and coronary angiography were more common factors for patients who developed a mechanical complication.

The prognosis of acute MI has markedly improved with the implementation of strategies for early restoration of culprit coronary artery flow and a reduction in the incidence of mechanical complications. However, the mortality rate remains very high when acute MI is complicated by cardiac rupture .

Papillary Muscle Rupture

Acute severe mitral valve regurgitation in the setting of MI is usually a result of necrosis and rupture of papillary muscle tissue. It is a life-threatening complication that almost always requires urgent surgical intervention. MR due to LV remodeling and distortion of ventricular architecture may also occur (discussed later).

2D imaging may detect abnormalities in the mitral valve apparatus, including flail leaflets and PMR. Even if not clearly visualized, PMR should be suspected when there is an eccentric jet of MR with a relatively normal-sized LA. Although color-flow parameters are those most often used, accurate grading of MR severity should also encompass other Doppler-echocardiographic signs. For patients with pulmonary edema, the unexpected findings of a small infarction, a hyperdynamic LV, or increased early mitral inflow velocity should prompt a careful search for MR even when color-flow Doppler is unrevealing.

In a review of PMR, 15 of 17 cases occurred in patients with inferior infarction and rupture of the posteromedial papillary muscle. The more common involvement of the posteromedial papillary muscle occurs because its blood supply is from a single coronary artery (i.e., the posterior descending artery) rather than a dual coronary artery supply, as in the anterolateral papillary muscle, which is supplied by the LAD and the left circumflex coronary artery (LCx) ( Fig. 21.4 ).

Fig. 21.4, Papillary muscle rupture.

Chordae to both leaflets arise from each of the papillary muscles, and in cases of complete rupture of the entire trunk of a papillary muscle, both leaflets are affected. In less severe cases, the rupture is incomplete, and only a single head is torn. The 2D echocardiographic findings may include prolapse of one or both leaflets, a flail leaflet, or liberation of a portion of the papillary muscle. In some patients, the ruptured muscle remains tethered to the chordae, and chaotic motion is present. If only a single head of the papillary muscle is affected (i.e., incomplete rupture), medical stabilization often is possible. When rupture is complete, involving the main trunk of the papillary muscle, the complication is fatal without immediate recognition and prompt surgical repair.

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