Myocardial Infarction

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In patients with suspected or evolving acute myocardial infarction (AMI), emergency echocardiography is appropriate when the diagnosis is unclear or complications of AMI are suspected. It may also provide valuable information (e.g. functional infarct size, concomitant right ventricular infarction, etc.) that can be used to guide and monitor therapy [1].

Since the clinical course of acute myocardial infarction is highly variable, routine (and sometimes serial) echocardiographic studies may be needed in all patients to assess actual risks and to correct therapeutic strategy, but obtaining an echocardiogram in a patient with uncomplicated AMI must not delay reperfusion therapy.

The role of echocardiography in patients with myocardial infarction comprises:


Differential diagnosis of chest pain

In patients with atypical clinical presentation and/or a nondiagnostic electrocardiogram, echocardiography is frequently used to determine whether myocardial ischemia is the cause of the chest pain. This is possible due to the fact that left ventricular (LV) wall motion abnormalities (i.e. LV asynergy) are the earliest detectable changes in the ischemic cascade – they were shown to precede both ECG changes and chest pain. Nevertheless, apart from acute infarction, LV asynergy can be detected during transient anginal attack, in chronic ischemia (hibernated myocardium) or in patients with previous infarctions (myocardial scar). In patients without wall motion abnormalities, echocardiography may be used to diagnose other life-threatening conditions with similar clinical presentation, such as massive pulmonary embolism or aortic dissection. It is noteworthy that emergency echocardiography in patients with ongoing chest pain is highly demanding procedure and should be preformed only by echocardiographers with adequate training for image acquisition and interpretation [2] [3].

Wall motion abnormalities

In an AMI, an (in)complete occlusion of coronary artery by intraluminal thrombus reduces downstream blood flow resulting in impaired contractility of affected segments, i.e. wall motion abnormalities. For the visual assessment of regional function, the left ventricle is divided into 17 segments [Figure 1], and segmental function is related to common perfusion territories of the three coronary arteries [4] This approach allows identification of infarct-related artery, but the inherent variability of coronary supply should also be considered [Figure 2].

An acute left main coronary artery occlusion is usually lethal, sparing only inferior wall and inferior septum and resulting in severe LV dysfunction and cardiogenic shock. If the left anterior descending coronary artery (LAD) is involved, hypo/akinesia of the anterior wall, anterior septum, and left ventricular apex is typically present [Videos 1-4].

Lateral wall dyssynergy points to the left circumflex artery (LCx) as an infarct-related artery [Video 5], while dyssynergy of the inferior wall and inferior septum suggests right coronary artery (RCA) lesion [Video 6]. Of note, a culprit lesion in the proximal right coronary artery causing inferior wall AMI may also cause right ventricular infarction associated with hypotension and cardiogenic shock despite only mild-to-moderate LV systolic dysfunction.

The extent of regional LV dysfunction can also be reported in a semi-quantitative manner, with the function of each segment graded and/or scored, as follows:

- Score 1: normokinetic (preserved wall thickness in diastole and normal contractility)

- Score 2: hypokinetic (reduced wall thickening and/or reduced longitudinal shortening)

- Score 3: akinetic (no deformation) and

- Score 4: dyskinetic (outward motion of the segment during systole).

Thin, akinetic /dyskinetic, and bright segments are strongly suggestive of myocardial scar due to old infarction [Video 7].

The average of the scores of all LV segments is referred to as wall motion score index (WMSI) and provides comparable prognostic information as LV ejection fraction.

The magnitude of LV asynergy caused by actual AMI is related to the location of the culprit lesion in the infarct-related artery, the presence of collateral circulation, and the extent of coronary artery disease. In the absence of collateral circulation, a proximal lesion usually affects basal, mid-ventricular and apical segments, while the distal lesions will impede perfusion and contractility of apical segments only [Videos 1-2 vs. Videos 3-4]. Overall, sensitivity of the LV asynergy for the detection of an AMI is high (over 90%), but specificity and positive predictive value are less convincing [5][6] Apart from subjectivity of the visual assessment of LV asynergy, interpretation difficulties may also arise from both poor imaging technique and poor echogenicity [Video 6]. While the latter problem can be partially overcomed by the use of contrast agents, the first two can be addressed only by adequate training and experience of echocardiographers. It has been shown that detectable LV asynergy will occur with >50% reduction of resting coronary flow, if >20% of myocardial thickness is jeopardized by actual ischemia, or if at least 1–6% of the left ventricular mass is involved [7] [8][9] Thus, echocardiography may miss very small or non-transmural myocardial infarctions.

Assessment of left ventricular function

Echocardiography is a useful tool to assess the functional infarction size and monitor contractile recovery which has been related to viability of the infarcted but timely reperfused segments. Both initial values and the pattern of temporal changes of various parameters of LV systolic and diastolic function have prognostic implications.

Functional infarction size

It has been shown that the ECG changes may not correlate well with the extent of dysfunctional myocardium in both the acute and chronic phase of a myocardial infarction. Furthermore, functional infarct size is often considerably larger than the anatomical size of actual necrosis, since it includes the zone of actual infarction, but also stunned and hibernated segments, and dysfunction from previous infarctions [10].

Systolic LV function

Although low postinfarction ejection fraction (LVEF) is a strong predictor of poor outcome [11], measuring LVEF in the acute phase of the event may underestimate true infarction size due to transient hypercontractility of myocardial segments not affected by actual infarction [12]. Apart from the immediate decline in LV function due to necrosed segments, adverse LV remodeling (i.e. infarct expansion), characterized by the enlargement of the initial hypo/akinetic zone and LV dilation, additionally contributes to the development of heart failure [13]. Increased initial left ventricular volumes indicate extensive myocardial damage and require serial echocardiographic evaluation for early detection of adverse LV remodeling, which has important clinical (therapeutic and prognostic) implications [14].

Permanent LV systolic dysfunction and heart failure symptoms are among the strongest predictors of risk for sudden cardiac death, and currently, LVEF of < 30-35% is a cut-off for device (ICD and/or CRT) implantation [15]. Of note, functional recovery after reperfusion/revascularization and initiation of optimal medical treatment may improve LVEF above the cut-off, and premature ICD implantation has shown no benefit [16]. According to myocardial perfusion studies, in approximately 40% of well-reperfused segments, contractile recovery will occur within 2 weeks from the infarction. Significant recovery can still be observed within 6 weeks in segments with homogeneous contrast enhancement, indicating resolved myocardial stunning. Finally, in up to 25% of segments with heterogeneous contrast enhancement, contractile recovery may be expected, while the absence of tissue perfusion is highly suggestive of the permanent contractile impairment [17]. In patients with recent myocardial infarction, therefore, repeat LVEF assessment (at approximately 40 days after the event) is necessary to confirm candidacy for ICD [18]. A high WMSI is generally associated with significantly reduced LVEF, and renders similar prognostic information.

Diastolic function

Assessment of LV diastolic function has been detailed in the Assessment of diastolic function. It is noteworthy that in the settings of an AMI, almost all Doppler-derived indices are influenced by numerous physiologic factors (e.g. heart rate) and may not reliably reflect LV filling [19][20]. However, it has been shown that various quantitative measures of LV filling have prognostic value, but their independence from LV systolic function is less convincing [21].

Detection of complications

Acute mitral regurgitation

Acute mitral regurgitation may occur due to infarction and rupture of the mitral apparatus (the chordae tendinae, the papillary muscles or a muscle head) or as a consequence of impaired mitral leaflet coaptation (arising from papillary muscle ischemia, LV dilation, remodeling, and associated dysynergy of the LV wall underlying the papillary muscle). The anterolateral papillary muscle receives dual blood supply (from both the LAD and LCx) and is far less likely to rupture than the posteromedial papillary muscle, which is supplied only by RCA. This explains why, unlike ventricular septal rupture which complicates large infarctions, papillary muscle rupture is usually associated with smaller (inferior wall) infarctions. In patients with complete papillary muscle transection, the findings on two-dimensional echocardiography include a flail leaflet, with a triangular echogenic mass that prolapses into the left atrium in systole, and moves back into the LV in diastole. The attached mass corresponds to ruptured papillary muscle or its portion (a muscle head), connected by chordal apparatus to the flail leaflets [Videos 8-10]. Even though mitral regurgitation is always severe in patients with the rupture of the mitral apparatus, color Doppler will sometimes underestimate its severity due to tachycardia, high left atrial pressure and eccentric regurgitant jets. In patients with poor echogenicity and high clinical suspicion of acute mitral regurgitation, transesophageal echocardiography may be needed to rule out this complication [Videos 11-12].

Ventricular septal rupture

The incidence of ventricular septal rupture (VSR) declined from 0.5-3% in pre-reperfusion era to 0.2-0.3% with reperfusion treatment [22]. Clinically, this rare complication is presented as a new holosystolic murmur accompanied by chest pain, dyspnea, and potentially hemodynamic compromise. A combined 2D and Doppler echocardiography and multiple standard and modified echocardiographic views are generally required for detection and evaluation of VSR [Videos 13-15]. Echocardiographic assessment in a patient with VSR should define location and size of the defect, but should also include the estimation of interventricular pressure gradient and right ventricular systolic pressure (RVSP).

The defects may be seen as a direct discontinuity of the septal wall (defects entering and exiting the septum at the same level) or as serpiginous tunnels with entry points at different levels on the left and right side of the septum. The site of the rupture is often localized at the border of the infarction zone, but sometimes there are multiple small orifices. Anterior defects are frequently located in the vicinity of the apex [Video 13] and have a better prognosis than inferior defects involving the basal septum [Video 14] [23]. Color Doppler may reveal systolic turbulent left-to-right flow across the ventricular septum, indicating the presence of a pathological communication even when the discontinuity of the septum could not be detected by 2D echocardiography. The maximal width of the turbulent jet by Color flow Doppler correlate well with intraoperative and autopsy findings and can be used to assess the defect size when direct 2D measurement is not possible.

Right ventricular function is crucial in maintaining hemodynamic stability and RVSP should be estimated in all patients, using the following formulas:

RVSP= Right atrial pressure + 4[TR velocity]2

RVSP= Systolic blood pressure – 4[VSR velocity]2

Mortality of VSR is high in conservatively treated patients.

Free wall rupture

Due to abrupt onset of cardiac tamponade, electromechanical dissociation and sudden death, echocardiograms of patients with acute free wall ruptures are rare. On the other hand, up to 40% of patients may present with a subacute from of free wall rupture which typically evolve over hours or even days [24]. Echocardiographic findings in a patient with a subacute free wall rupture may include large pericardial effusion (hemopericardium), segmental akinesia due to myocardial infarction, and echocardiographic signs of tamponade. In some cases, the site of the free wall rupture can be visualized, and color Doppler may reveal flow across the defect to the pericardial space [Videos 16-19].

Urgent surgical repair is the only life-saving treatment for this complication.

True versus pseudo-aneurysm

True aneurysm formation is closely related to infarct expansion which is defined as acute dilation and thinning of the area of infarction that cannot be explained by additional myocardial necrosis. On echocardiography, true aneurysms appear as highly echogenic areas of thinned, scarred myocardium. True aneurysms most commonly involve LV apex [Video 20] but can be seen anywhere in the LV [Video 21]. Due to the stagnant blood flow, LV thrombi may frequently be seen within the aneurysms [Videos 20, 22, 23].

In contrast to true aneurysms, pseudo-aneurysms are formed when free wall rupture is contained by pericardial adhesions or thrombosis at the rupture site. Echocardiographic distinction between these 2 entities is summarized in Table 1 and has important clinical implications: patients with true aneurysms can generally be followed whereas pseudo-aneurysms are considered surgical emergency. Pathologically, both entities may contain a thrombus, but there is no myocardial layer in the wall of the pseudo-aneurysm.

True aneurysm Pseudoaneurysm
Orifice (Neck) Wide Narrow
LV wall Uninterrupted with gradual thinning Abrupt interruption
Doppler No flow Bidirectional blood flow
Contrast No extravasation Extravasation into the pericardial space

Left ventricular thrombus

Left ventricular thrombi are most often found in patients with large infarctions and severely depressed LV systolic function, but can also be found in those with small apical infarctions and preserved LVEF [Video 22]. The overall incidence of this complication is approximately 5%. Thrombus is always located in the akinetic/dyskinetic zone and typically appears as a homogeneous echogenic mass [Video 23]. Its embolic potential is determined by the presence of mobile portions or protruding filaments.

In order to improve detection rate, both standardized and modified views should be used and all efforts should be made to visualize true LV apex. In some cases, the use of contrast agents is necessary, while transesophageal echocardiography is less sensitive due to difficulty visualizing LV apex.

Viability assessment

The identification of dysfunctional, but viable myocardium is of utmost importance in patients with a history of MI since those with viable myocardium can benefit from revascularization procedures. Despite not being a gold standard technique, echocardiography has a major role in distinguishing scarred from viable (stunned or hibernating) myocardium. Even simple echocardiographic parameters taken at rest, such as systolic wall thickness (> 7 mm) or LV filling pattern (absence of restrictive filling), can provide some prognostic information on recovery following revascularization [25][26]. Low-dose dobutamine stress echocardiography (DSE) is considered a modality with acceptable accuracy for identifying viable myocardium, but it prognostic value has been recently questioned [27]. Previously, a number of studies reported high predictive value of low-dose DSE even in patients not suitable for revascularization. Furthermore, DSE was able to predict the quantitative improvement in global LV systolic function, which was related to the number of myocardial segments with contractile. This relationship, however, may not be valid if the infarct-related artery is severely stenotic. In this case, viable myocardium can be identified by a biphasic response (improvement of contractility at low dose and worsening at high dose) or by a new dyssynergy in segments within the infarct-related area. Thus, the presence of a flow-limiting stenosis will induce ischemia at high dose, diminishing wall thickening despite the presence of viable myocardium. In line with this, it must be recognized that persistence of akinesia during the dobutamine test does not necessarily imply absence of residual viability.


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