Coronary Artery Disease: Ischemia, Infarction, and Complications

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11 Coronary Artery Disease

Ischemia, Infarction, and Complications

Wall Motion Abnormalities and Their Relation to Blood Flow

Due to the high myocardial extraction of oxygen (the greatest O₂ extraction by any organ in the body), myocardial function is dependent on adequate perfusion. The correlation of coronary blood flow and myocardial motion and thickening is the flow–function relationship. Reduced coronary flow results in reduced wall motion (translation) and thickening. Hence, the echocardiographic hallmark of ischemia/infarction is segmental wall motion disturbance. Systolic wall thickening is viewed as a superior (more specific) depiction of myocardial function than is translation for the following reasons:

Translation of a segment of myocardium may be passive and may be due to

• Translation of adjacent myocardial segments

• Systolic pressure

• Systolic right ventricle (RV): left ventricle (LV) pressure differential

Conduction disturbances render translation more difficult to assess than thickening. Given the prevalence of coronary artery disease (CAD), wall motion abnormalities (WMAs) are seen most commonly in the context of CAD, but are not specific for it.

Although echocardiographic estimates using wall motion correlate well with autopsy estimates of infarction,^1,² in general, echocardiography tends to overestimate the amount of ischemic/infarcting muscle.³ Pathologic:echocardiographic correlations

Are best for first Q-wave infarctions

Are less good for

• Non–Q-wave infarctions

• Second and third infarctions

Echocardiography for Wall Assessment in Acute Myocardial Infarction

Wall motion score index at the time of acute myocardial infarction (MI) is prognostic of the in-hospital course. A wall motion score index >2 has a higher incidence of the following:

• Congestive heart failure

• Ventricular tachycardia/ventricular fibrillation

• Ventricular septal defect/rupture

• Free wall rupture

• In-hospital mortality

In terms of 1-year mortality, a WMS <2 has high predictive value for a good prognosis and low complication rate. A WMS >7 on admission predicts Killip Class 3 or 4 with a sensitivity of 88%, specificity of 57%, positive predictive value of 35%, and negative predictive value of 95%, and may, therefore, be helpful in identifying early low-risk patients.⁴ The degree of systolic function of the nonischemic/infarcting myocardial segments is largely a function of the adequacy of perfusion to these other territories. The normal response of noninfarcting myocardium is hyperkinesia. The absence of hyperkinesia correlates with more extensive CAD (e.g., prior infarction, acute ischemia, stunning, or hibernation), and high risk for early mortality.^4,⁵ Echocardiography is superior to electrocardiography in determining infarct extension.⁶ Echocardiographic assessment of left ventricular systolic function (presence/absence of WMAs) in patients presenting to the emergency department with cardiac-related symptoms is able to stratify patients (Table 11-1).

TABLE 11-1 Cardiac Events According to the Presence or Absence of Left Ventricular Systolic Dysfunction^*

Echocardiographic Views to Assess Left Ventricular Wall Motion and its Relation to Coronary Arteries

The LV segmental nomenclature suggested by the American Society of Echocardiography lends itself to inference of underlying coronary artery anatomy and lesions.

Parasternal Long-Axis View

The basal 1 to 2 cm of the interventricular septum are generally perfused by the first septal perforator (i.e., proximal left anterior descending artery); hence, the presence of a basal anterior septal WMA suggests either proximal left anterior descending coronary artery (LAD) or left-main disease. However, there are variants to septal perforator anatomy.

Caveat: The parasternal long-axis view does not image the apex, and no conclusions should be drawn about apical wall motion or lesions until apical views have been obtained. A normal parasternal long-axis view may fail to reveal an apical aneurysm, clot, or apical septal rupture.

Parasternal Short-Axis View

The parasternal short-axis views provide a very useful plane to assess the LV, although several problems are regularly encountered:

The lateral wall remains obscured by lung artifact.

The apical segment(s) are not imageable.

Oblique cross-sectional views are obtained, not truly short-axis views.

Apical 2-Chamber View

The A2CV is comparable with the right anterior oblique contrast ventriculogram (reflecting perfusion from both the left anterior descending and posterior descending arteries, but principally from the LAD).

Coronary Care Unit Echocardiographic Studies

Reporting Issues

Beyond describing the LV grade and ejection fraction, it is important to describe the stroke volume and the cardiac output. Recall that for any given degree of depression of LV systolic function, the impact on stroke volume is greatest when the LV is not dilated, which is the typical state during an acute MI. Hemodynamic parameters are the strongest determinant of mortality in acute MI, and ESV and ejection fraction are probably the most powerful prognosticator post-infarction and should be offered routinely. Cardiogenic shock with normal or near-normal LV systolic function strongly suggests the following:

Mechanical complication

• Papillary muscle rupture

• Septal rupture

When transthoracic echocardiography (TTE) is not adequate to evaluate the clinical concerns, then transesophageal echocardiography (TEE) should be offered.

Echocardiography for the Assessment of Complications of Acute Myocardial Infarction

Pump Failure

Left Ventricular Systolic Dysfunction and Failure

LV pump failure is the dominant cause (>65%) of in-hospital mortality from acute MI. It may occur with a first, and massive, infarction, or with a second or third infarction. Severe WMAs in extensive territories are expected in cardiogenic shock due to pump failure. The LV may or may not be dilated. Massive acute first MI is unlikely to have prominent dilation. It is the combination of abrupt fall in ejection fraction and lack of dilation that is responsible for the low stroke volume, and resultant low output, despite tachycardia.

Right Ventricular Infarction

RV infarction is a common cause of hypotension and the principal cause of shock in inferior infarction. The RV is under-assessed on most echocardiograms; therefore, a diligent effort to assess it regionally and globally is required. The size of RV infarction relates, in general, to how proximally the right coronary artery is occluded. A posterior RV infarction is common in the context of most inferior infarctions. An anterior RV infarction is common in the context of anterior LV infarction, as an apical RV infarction is common in the setting of an LV apical infarction. The right ventricular outflow tract (seen on the posterior long-axis view) usually is spared in RV infarction. The hemodynamically significant, important RV infarction involves the lateral RV (seen on the apical four-chamber view and the posterior short-axis view) and the posterior RV (seen on the posterior short-axis view and the subcostal view). Rarely, complications other than hemodynamic compromise—such as RV thrombi, RV papillary muscle rupture, and RV rupture—will arise from RV infarction. The most severe RV infarctions also involve the right atrium, which is difficult to assess by echocardiography.

Mechanical Complications of Infarction

Free Wall Rupture

Free wall rupture accounts for approximately 10% of postinfarction sudden deaths. Rupture typically occurs through the lateral (but it may be through any) wall of the left ventricle. The right ventricle is one-seventh as likely to rupture as the LV. Rupture occurs only following a transmural infarction. The time is typically 3 to 5 days following MI, but may be earlier, especially if the patient received fibrinolytics. A subset of patients with free wall rupture will not experience immediate sudden death: this group is said to have “subacute rupture”⁷ with echocardiographic signs of tamponade, pericardial effusion >5 mm, and echodensities in the pericardial space that represent coagulated blood. Suspected clot in the pericardial space, which appears as an echo-dense mass in the pericardial space, may be a sign of free wall rupture⁸ and renders the likelihood of evacuation through a pericardiocentesis needle unlikely. Urgent surgical repair will salvage some cases. Bedside echocardiography is the most suitable test to identify free wall rupture. Ultimately, there is no perfect echocardiographic sign to distinguish severe early postinfarction tamponade from rupture. Identification of clot in the pericardial space is useful, however.

Left Ventricular (or Other) False Aneurysm

Ventricular false or “pseudo” aneurysms contain no myocardial layer; a free wall rupture is contained by adherence of overlying pericardium or by a thin layer of epicardium beneath pericardium. A false aneurysm develops because a tear into a portion of recently transmurally infarcted myocardium extended up to the epicardium or even through it, and complete rupture of the LV into the pericardial cavity was avoided because pericardial adhesions (the result of prior pericarditis) contained the rupture. Thus, a false aneurysm is to be considered an intermediate form of rupture, and reparative surgery is urgently indicated. The contained rupture typically extends away from the neck to appear as an echo-free space with the shape of a mushroom cap. The neck usually is less than half the width of the body of the false aneurysm. This is in contradistinction to the wide neck of a (true) aneurysm, which usually is as wide as the body of the aneurysm itself (the dimension of the neck/the dimension of the body is 0.9 to 1.0).⁹ It is the width of the neck, more than any other detail, that renders the outpouching of the LV a false aneurysm rather than a true aneurysm. In systole, the false aneurysm typically bulges out as it receives part of the LV stroke volume. The flow in and out (or “to-and-fro”) is evident by color and spectral Doppler.¹⁰ Two-dimensional echocardiography is the procedure of choice to establish the presence of a pseudoaneurysm. Cineangiography and MRI also are excellent means to image false aneurysms. Confusion occurs about aneurysms of the base of the LV between the body of the posteromedial papillary muscle and the mitral annulus. Often the traction of the papillary muscle keeps the neck narrow, replicating the sign of a false aneurysm. Thus the “neck” sign is best applied away from the trouble spot on the posterolateral wall, where both aneurysms and false aneurysms occur, but where they cannot be easily distinguished by neck morphology alone.

The diagnosis can be made by TTE in most cases. TEE offers confirmation in some cases that the neck is narrow, and the wall disrupted. TEE is probably better able to image posterior wall false aneurysms and may increase the detection rate of small posterior false aneurysms.

Septal Rupture

Ventricular septal ruptures are less common than free wall ruptures (about 1–3% of MI). They are almost invariably associated with a septal dilation (aneurysm) with thinning. Septal ruptures may occur in anterior/apical locations, or basal–posterior locations.

Associated RV MI is common, which indicates a poor prognosis.¹¹ Two-dimensional echocardiography identifies the defect in more than half of cases, but color Doppler will find nearly 100% of defects.¹²^–¹⁴ Agitated saline contrast studies are not needed. Urgent surgical repair is indicated. Patients with large concurrent RV infarctions do very poorly with or without surgery.

TTE is able to make the diagnosis in almost all cases, and detects and localizes the septal rupture by color flow mapping. TEE will give more detail of the anatomic disruption, which may be necessary for the surgeon. Intraoperative TEE is required to determine adequacy of the repair (ablation of the shunt) and to assist with elucidating the all too common hemodynamic problems coming off pump.

Papillary Muscle Rupture

Papillary muscle rupture causes severe disruption of the mitral apparatus and leads to severe mitral insufficiency and marked reduction in forward cardiac output. Clinically, papillary muscle rupture is a severe event, progressive, and usually fatal if not successfully operated upon (80% mortality within 1 week). In the setting of inferior infarction, the posteromedial papillary muscle usually is the affected one. In the setting of anterolateral infarction, the anterolateral papillary muscle usually is the affected one. Overall, the posteromedial papillary muscle, which usually is supplied by the posterior descending artery alone, is 5 to 10 times more likely to rupture than the anterolateral one, which usually is supplied by both the posterior descending artery and the left circumflex coronary artery.¹⁵ In a short-axis view, the anterolateral papillary muscle is seen at 3 o’clock, and the posteromedial papillary muscle is seen at 7 o’clock. Of note, even tricuspid papillary muscles can rupture in the case of RV MI. Rupture may be complete or partial. Partial rupture results in severe MR, not cardiogenic shock. In a posterior long-axis view, the posteromedial papillary muscle or muscles are seen. On an A4CV, the anterolateral papillary muscle is seen. On TEE transgastric short-axis views, as with transthoracic short-axis views, both papillary muscle sets are seen. On a TEE long-axis view, both papillary muscles can be seen, although often with slight angulations to optimize the imaging of each. Imaging of papillary muscles requires specific views to assess their integrity. Zoom views are helpful. The echocardiographic signs of papillary muscle rupture depend on whether the rupture is complete or partial.

Complete papillary muscle rupture

• Flailing mass attached to the mitral leaflets, moving back and forth between the left atrium and the LV

• If the papillary muscle head becomes “wrapped-up” in its chordae, the appearance of the mass is less obviously that of a ruptured papillary muscle trunk.

• Severe MR. The absence of a large jet does not exclude the diagnosis of severe MR. The size of the jet depends on the transmitral gradient, which may be low if there is systemic hypotension and the left atrial pressure is high.

Partial papillary muscle rupture

• “Wobbling” of the body of the papillary muscle

• Stretching of the body of the papillary muscle

• Usually, there is severe MR due to prolapse of the mitral valve. Conspicuously, the mitral valve leaflet thickness is normal, suggesting that myxomatous disease is not responsible for the prolapse and that another cause should be sought.

A WMA may not be apparent.

There typically are two posteromedial papillary muscle bodies or heads; seeing one of them does not establish that the entire apparatus is intact. The left atrium, even if not enlarged, may show systolic bulging secondary to the large volume load of severe MR. The maximal velocity is reached in early systole, with a rapid systolic decline, indicating rapid equilibration of the left ventricular and left atrial pressures.

Although TTE, carefully performed (i.e., with zoom views of each of the papillary muscles) is able to establish the diagnosis in most cases, TEE can be confirmatory when uncertainty persists or diagnostic when images are poor by TTE or when the echocardiographer is unsure of the diagnosis.

Left Ventricular Aneurysm

An LV aneurysm is a localized dilation of the LV, with the wall intact but usually thinned. To clinicians, aneurysms are recognized by the following:

Their diastolic dilation

Two-dimensional echocardiography is the procedure of choice to establish the presence and size of ventricular aneurysms (sensitivity 93%, specificity 94%).¹⁶ Aneurysms may occur anywhere, but most commonly occur over the anterior or apical regions. Typically, a recently formed aneurysm is dyskinetic. Chronically, as they scar and often calcify, they become less dyskinetic. Early formation of aneurysm (<5 days) is associated with high mortality (80% at 1 year).^17,¹⁸ True aneurysms of the LV only rarely rupture. They commonly are associated with intracavitary clot, as the flow within them is stagnant, and permissive of thrombus formation.¹⁹^–²² The size of the aneurysm may be described in several ways, including the ratio of the circumferential length of the aneurysm to that of the overall LV, and area of the aneurysm to the overall LV area. Patients with circumference ratios >0.4 or area ratios >0.3 have significantly more congestive heart failure and mortality.^18,²² The location of the aneurysm and the systolic function of the remainder of the LV are considered when surgical aneurysmectomy is entertained. Surgical aneurysmectomy is not a primary indication for surgery, but may be entertained when coronary bypass or valve surgery is the primary indication. If the aneurysm involves the papillary muscles, then surgical results are less good, as the mitral apparatus will be affected by the surgery. Similarly, if the condition of the nonaneurysmal LV (what will be left after the surgery) is poor, then the outcome will be poor.^19,²⁰

Inferior/posterior aneurysms often lead to MR, and hence to mitral valve replacement with aneurysmectomy. Ventricular aneurysms frequently contain thrombus.

The role OF TEE in assessing aneurysms is very small, unless TTE views are very poor. Because most aneurysms are apical, TEE is less well suited to depict most aneurysms, because of the longer distance to the apex using an inherently higher frequency transducer, and the invariably foreshortened view of the apex from the lower esophageal four-chamber view.

Other Complications

Intracavitary Thrombus

Intracavitary thrombus may occur in almost any location of the heart where regional aneurysm or dyskinesis (or possibly akinesis) has occurred. Thrombus typically is seen at the apex, which is prone to the most stagnant flow following infarction. The second most common site is over the anterior wall. Thrombi may be laminated and flat, round and pedunculated, single or multiple, obvious or difficult to distinguish from trabeculations. Thrombi are a sign of low flow within that region of the heart, and potentially of overall low cardiac output. When they form very early postinfarction, they are associated with high mortality.

The echocardiographic signs of thrombi are as follows:

Thrombus to blood pool interface

Specular echoes within the thrombus

Endocardial to thrombus interface underneath

False-positives include prominent trabeculations, false tendons, and near-field artifacts. False tendons are linear and have blood pool on both sides. Near-field artifacts typically cross tissue borders. False-negatives occur because of insufficient time taken to scan an enlarged apex (where a small thrombus resides), an overlying near-field artifact, or poor image quality. Intravenous echo contrast may help to recognize some thrombi not seen on poor quality TTE, as may TEE. The thrombi most likely to embolize are those that are mobile and located at the margin of an infarct that is subject to violent rocking motion.

Dynamic Left Ventricular Outflow Tract Obstruction

Dynamic left ventricular outflow tract obstruction can occur post–apical infarction or stunning. The predisposing factor is a small-cavity dynamic LV. With apical infarction or stunning, the basal (noninfarct) portion becomes hyperdynamic and develops a dynamic obstruction at the base of the left ventricular outflow tract. The condition has a favorable prognosis, unlike most postinfarction causes of hypotension or shock, but is load and inotrope sensitive.

“Functional” Mitral Regurgiation

By objective testing, at least 20% of MI cases develop “functional” MR, which may be transient or persistent. Any peri-infarction MR portends higher risk. The term “functional” MR denotes that the mitral components are intact (using zoom views, it is necessary to exclude papillary muscle rupture). The basis of “functional” mitral insufficiency post-MI is distortion of the LV and tethering/malalignment of the chordae and leaflets. Apical or lateral displacement of the papillary muscles exerts traction on the mitral leaflets that results in loss of coaptation. The greater the regional or overall remodeling of the LV, the greater the likelihood of development of MR. Hence, functional MR postinfarction is an indirect descriptor of LV function, geometry, or remodeling.

BOX 11-1 Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Coronary Artery Disease

Transthoracic Echocardiography

ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography ²³

Hypotension or Hemodynamic Instability with TTE

Hypotension or hemodynamic instability of uncertain or suspected cardiac etiology

Appropriateness criteria: A; median score: 9

Assessment of volume status in a critically ill patient

Appropriateness criteria: U; median score: 5

Evaluation of Ventricular Function after ACS with TTE

Initial evaluation of ventricular function following ACS

Appropriateness criteria: A; median score: 9

Re-evaluation of ventricular function following ACS during recovery phase when results will guide therapy

Appropriateness criteria: A; median score: 9

Respiratory Failure with TTE

Respiratory failure or hypoxemia of uncertain etiology

Appropriateness criteria: A; median score: 8

Respiratory failure or hypoxemia when a noncardiac etiology of respiratory failure has been established

Appropriateness criteria: U; median score: 5

ACC/AHA/ASE 2003 Guideline Update for the Clinical Application of Echocardiography ²⁴

Recommendations for Echocardiography in Risk Assessment, Prognosis, and Assessment of Therapy in Acute MI Syndromes

• Assessment of infarct size and/or extent of jeopardized myocardium

• In-hospital assessment of ventricular function when the results are used to guide therapy

• In-hospital or early postdischarge assessment of the presence/extent of inducible ischemia whenever baseline abnormalities are expected to compromise electrocardiographic interpretation ^†

• Assessment of myocardial viability when required to define potential efficacy of revascularization ^‡

• In-hospital or early postdischarge assessment of the presence/extent of inducible ischemia in the absence of baseline abnormalities expected to compromise ECG interpretation ^†

• Assessment of myocardial viability when required to define potential efficacy of revascularization ^‡

• Re-evaluation of ventricular function during recovery when results are used to guide therapy

• Assessment of ventricular function after revascularization

• Assessment of long-term late prognosis (≥2 years after acute MI)

• Routine re-evaluation in the absence of any change in clinical status

Cardiac Computed Tomography

ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT ²⁵

Evaluation of Ventricular Morphology and Systolic Function

Initial evaluation of LV function

Following acute MI or in HF patients

Appropriateness criteria: I; median score: 2

Evaluation of LV function

Following acute MI or in HF patientsInadequate images from other noninvasive methodsAppropriateness criteria: A; median score: 7

Elevated Troponin of Uncertain Clinical Significance

Elevated troponin without additional evidence of ACS or symptoms suggestive of CAD

Appropriateness criteria: U; median score: 6

Nuclear

ACCF/ASNC/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging ²⁷

Ischemic Cardiomyopathy/Assessment of Viability

Known severe LV dysfunction

Patient eligible for revascularization

Appropriateness criteria: A; median score: 9

Evaluation of LV Function

Assessment of LV function with radionuclide angiography (ERNA or FP RNA)

In absence of recent reliable diagnostic information regarding ventricular function obtained with another imaging modality

Appropriateness criteria: A; median score: 8

Routine ^† use of rest/stress ECG-gating with SPECT or PET MPI

Appropriateness criteria: A; median score: 9

Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain.

ACS, acute coronary syndrome; CAD, coronary artery disease; ECG, electrocardiogram; HF, heart failure; LV, left ventricle; MI, myocardial infarction/ischemia; MPI, myocardial perfusion imaging; PET, positron emission tomography; RV, right ventricle; SPECT, single-photon emission computed tomography; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

^* TEE is indicated when TTE studies are not diagnostic.

^‡ Dobutamine stress echocardiogram.

^† Exercise or pharmacologic stress echocardiogram.

Figure 11-1 Right ventricular (RV) myocardial infarction with RV failure and shock. Persistent, refractory hypoxemia was due not to pulmonary edema, but to right-to-left shunting across a patent foramen ovale. Right-to-left shunting was first detected on transthoracic echocardiography by saline contrast. Both images are transesophageal. Left: Dilation of the right atrium and bowing of the interatrial septum to the left side, as well as obvious patency. Right: Right-to-left flow by color Doppler flow mapping.

Figure 11-2 Post–myocardial infarction septal rupture (anterior/apical). The actual defect is seen on the left; the right image demonstrates the left-to-right flow.

Figure 11-3 Post–myocardial infarction septal rupture (inferobasal). The actual defect is seen on the left image; however, most septal ruptures in this location are poorly defined on two-dimensional imaging, as they are anatomically complex. The right image demonstrates the left-to-right flow.

Figure 11-4 Free wall rupture (transesophageal echocardiographic images of different patients). Left: A small (compressed) left ventricular cavity and blood clot (fine specular echoes) in the pericardial space. Right: A clear depiction of the appearance of the blood clot (crescent-shaped) in the pericardial space. The heart cavities are to the left and distorted by compression.

Figure 11-5 Free wall rupture (transthoracic images from different patients). Left: The posterior short-axis view demonstrates a small (compressed) left ventricular (LV) cavity and blood clot (fine specular echoes) in the pericardial space posterior to the LV. Right: The subcostal view clearly depicts the appearance of the thick blood clot (same echo-texture as liver) in the pericardial space. The heart cavities are displaced deeply.

Figure 11-6 Post–myocardial false aneurysm of the lateral wall. Left: The A4CV shows the “thumb-like” narrow neck of the false aneurysm, and the “mushroom cap” shape of the contained rupture. Right: The corresponding ventriculogram.

Figure 11-7 Post–myocardial infarction false aneurysm of the posterior wall. Left: The off-axis posterior long-axis view shows the small false aneurysm and its narrow neck. There is no adjacent contained rupture. Right: The corresponding ventriculogram.

Figure 11-8 Post–myocardial infarction false aneurysm of the lateral wall (transesophageal short-axis images). Left: The A4CV shows the contained rupture beside the posterolateral wall. The neck is not apparent. Right: Color Doppler flow mapping reveals the neck.

Figure 11-9 Dynamic left ventricular outflow tract (LVOT) obstruction post–myocardial infarction (MI). Upper left: The A4CV shows that the LV cavity is small at the base and dilated at the apex (anterior MI). There is systolic anterior motion of the mitral valve. Upper right: A3CV. Color Doppler flow mapping reveals flow acceleration in the LVOT (large proximal isovelocity surface area). Lower left: A3CV view. Color Doppler also reveals associated mitral regurgitation to the LVOT obstruction. Lower right: Continuous wave Doppler across the LVOT shows a 77-mm Hg gradient. The gradient was abolished with saline and beta-blockers.

Figure 11-10 Transesophageal echocardiographic images of a complete rupture of the posteromedial papillary muscle.

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