Papillary Muscle Echo

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Apical 2-C hamber Parasternal /Apical Long Axis

Short Axis

Fig. 5. Coronary artery territories and segments. Anatomical left ventricular segments used in reporting regional wall motion (American Heart Association classification) and their corresponding blood supply. Significant overlap and congenital variations in coronary blood supply can occur.

individual myocytes, and thereby causes a wall motion abnormality in the respective segment. At least a 70% reduction in cross-sectional diameter is required before the stenosis becomes hemodynamically significant. A proximal lesion will tend to affect more territory, i.e., basal to apical segments, whereas a more distal blockage will affect only more apical segments. An acute left main coronary artery occlusion can be lethal, as it supplies an extensive territory, and only the inferior septum and inferior wall would be spared. A lesion in the

Fig. 6. An 89-yr-old male with multiple malignancies and pre-existing coronary artery disease. This 89-yr-old male with three-vessel disease and multiple malignancies presented with chest pains and dyspnea. Diastolic images show infero-postero basal hypokinesis that were less apparent during systole. Collateral circulation develops in response to significant ischemia, and make a significant contribution to blood flow and improved ventricular function.

Inferior Wall Hypokinesis

Fig. 6. An 89-yr-old male with multiple malignancies and pre-existing coronary artery disease. This 89-yr-old male with three-vessel disease and multiple malignancies presented with chest pains and dyspnea. Diastolic images show infero-postero basal hypokinesis that were less apparent during systole. Collateral circulation develops in response to significant ischemia, and make a significant contribution to blood flow and improved ventricular function.

Table 1

Utility of Echocardiography in Detecting Complications of Myocardial Infarction

Early complications

Regional wall motion abnormalities

Infarct expansion

Right ventricular infarction

Pericardial effusion

Mitral regurgitation

Papillary muscle rupture

Ventricular septal defect

Ventricular free wall rupture ± pseudoaneurysm

Late complications

Ischemic cardiomyopathy ± mitral regurgitation Intracavitary thrombus, esp. ventricular Left ventricular aneurysm Pericardial effusion proximal RCA can additionally cause RV dysfunction and infarction, which can contribute to hypotension during an inferior MI. When the RV is infarcted, RV dilation, RV segmental wall motion abnormalities, and tricuspid regurgitation may be seen on echocardiography.

The presence of previously existing coronary artery disease can modify the wall motion abnormalities seen during an acute MI. Small collateral vessels from other unobstructed coronary arteries can develop and perfuse the peripheral territory of affected vessels, thus diminishing the dysfunctional territory (Fig. 6).

A wall motion score index has been developed as a scale for quantitating the extent and severity of LV systolic function. The system uses a 14 or 16 segment division of the LV (similar to the AHA system previously detailed), and assigns a number to each wall segment from 0-5 (0, hyperkinetic; 1, normal; 2, hypokinetic; 3, akinetic; 4, dyskinetic; 5, aneurysmal [see Chapter 5, Fig. 1B]). The wall motion score index score is equal to the sum of these numbers/number of segments visualized, such that a normokinetic ventricle should have a score of 1.0. This score has prognostic value, as a higher score is correlated with morbidity and mortality following MI.

The Role of Echo in Evaluating Chest Pain

Echocardiography is often called into use during episodes of chest pain to determine whether ischemia is the cause of the chest pain, as opposed to a noncardiac cause. Echocardiography—specifically transthoracic studies—can play a crucial role in acute MI. This is especially true for detecting early and late complications of MI (Table 1). Wall motion abnormalities are pathognomic of ischemia or early infarct, and have been shown to precede ECG changes and chest pain. However, it should be kept in mind that smaller (subendocardial) coronary arteries can cause more subtle or more localized wall motion abnormalities, and thus the sensitivity of echocardiogra-phy for subendocardial ischemia is reduced. However, in the absence of visualized wall motion abnormalities, other causes of chest pain should be considered. Although noncardiac chest pain is frequently the case, other etiologies such as aortic or coronary artery dissection, pericarditis, myocarditis, and endocarditis should be considered in the differential diagnosis.

indications for transthoracic echocardiography during and after mi

When is an echocardiogram of clinical utility in the setting of an acute MI? Simply stated, TTE is appropriate when (1) the diagnosis is unclear, (2) complications of MI are suspected, and (3) the results add information that may be used to risk-stratify a patient and guide future therapy.

In the uncomplicated acute MI, symptoms are the direct result of ongoing ischemia, which causes chest pain, as well as systolic and diastolic dysfunction. The segmental myocardial dysfunction can be extensive enough to cause a drop in cardiac output, leading to left-sided (and occasionally right-sided) heart failure. In this situation, the diagnosis is clear from a focused history, physical, and ECG, and the first priority should be to stabilize the patient with medical therapy, then proceed as soon as possible to primary revascularization strategies, i.e., thrombolysis and/or angioplasty. Obtaining an echocardiogram in the setting of an uncomplicated MI would only delay appropriate therapy.

However, if the patient had persistent or recurrent chest pain, ECG changes, hypotension, a new murmur, congestive heart failure, stroke, or a late tach-yarrhythmia, an echocardiogram would be crucial to rule out serious post-MI complications in the acute and chronic setting (discussed in the remainder of this chapter).

In this patient's case, a TTE was ordered after the angioplasty to evaluate LV ejection fraction (EF), because a left ventriculogram was not performed during his catheterization. Of note, an echocardiogram is not automatically indicated in all postinfarct patients for risk stratification; if there is already enough clinical information from the patient's history, physical, and available data (e.g., ventriculogram) to estimate postinfarct cardiac function and guide therapy, echocardiography may be redundant. For instance, 93-98% of patients with interpretable EKGs, no history of Q-wave MI or congestive heart failure, and an index MI that is not a Q-wave or anterior infarction will have LVEFs more than 40% (Krumholz et al. and Silver et al.). However, this clinical predictor of EF has only been applied to elderly (>65 yr old) patients, and certain conditions (presentation >6 h after the onset of chest pain, a history of coronary artery bypass surgery, and diabetes mellitus) invalidate the rule.

Subacute Complications

Echocardiography is useful for detecting negative sequelae in the first 1-3 wk after MI. Many of these complications are associated with more extensive Q-wave or transmural infarcts, and their cumulative incidence appears to be decreasing in the current era of reperfusion by angioplasty or thrombolysis. Nevertheless, when they occur, they are often heralded by abrupt clinical decline (hypotension and flash pulmonary edema, i.e., cardiogenic shock), and echocardiography can be the key to a swift diagnosis.

Acute Severe Mitral Regurgitation

Acute severe mitral regurgitation (MR) is caused by infarct and subsequent rupture of the chordae tendinae (Fig. 7), a papillary muscle (Fig. 8; please see companion DVD for corresponding video), or a muscle head.

Clinically a new harsh holosystolic murmur may be appreciated, although if the patient is extremely hypotensive and in cardiac shock, one may not be appreciated. Because the anterolateral papillary muscle receives dual blood supply from both the LAD (diagonals) and LCx, it is far less likely to rupture than the posteromedial papillary muscle, which is supplied mainly by the RCA (posterior descending artery) alone. Hence, papillary muscle rupture is seen more frequently with inferior infarcts, and more frequently involves the posterior leaflet (although there is crossover between chordae from individual papillary muscles and the corresponding leaflet). It is more common to see one head, or tip, of a papillary muscle disrupted, rather than the entire muscle trunk.

By two-dimensional (2D) echocardiography, one will see a flail (or partially flail) leaflet corresponding to the ruptured supporting muscle and chordae, which prolapses into the left atrium during systole. A triangular or pyramidal mobile echodensity, which represents the head of the papillary muscle, attached to the tip of the flail leaflet is pathognomic. Color Doppler will usually show severe MR, which can be extremely eccentrically directed away from the defective leaflet. Thus, anterior flail mitral leaflets will cause the visualized MR color jet to be directed posterior and laterally; posterior flail leaflets cause an eccentric anteroseptally directed jet of MR.

Severe MR can also occur in the absence of rupture of the mitral apparatus. The mechanism involves incomplete closure of the valve, and is thought to be a result of papillary muscle dysfunction (particularly with occlusion of the LCx artery),

Fig. 7. Flail anterior mitral valve leaflet in a 53-yr-old male with dilated cardiomyopathy. This 53-yr-old male with dilated cardiomyopathy, mitral regurgitation, and atrial fibrillation developed partial flail of anterior mitral valve leaflet (A, arrow in parasternal long-axis [PLAX] view; B, M-mode view). Note the severe mitral regurgitation with a posteriorly directed jet (C,D).

Posterior Mitral Jet

Fig. 7. Flail anterior mitral valve leaflet in a 53-yr-old male with dilated cardiomyopathy. This 53-yr-old male with dilated cardiomyopathy, mitral regurgitation, and atrial fibrillation developed partial flail of anterior mitral valve leaflet (A, arrow in parasternal long-axis [PLAX] view; B, M-mode view). Note the severe mitral regurgitation with a posteriorly directed jet (C,D).

termed "ischemic MR" and/or lateral displacement of the papillary muscles by LV dilatation (see "Chronic Implications" section).

Pitfalls in detecting severe MR: this eccentricity of MR jet, particularly the "wall-hugging" jets can be severe enough to cause the diagnosis to be missed entirely on echocardiography. (1) Eccentric wall jets may escape the scan plane, and when they are seen by color Doppler jet area, are usually underestimated in volume by at least 40%. Other pitfalls which can cause severe MR to be undetected on echo include: (2) "wide-open" MR with a completely incompetent valve and very high left atrial pressures, in which there is less pressure gradient and flow turbulence between the left atrium and ventricle; (3) a failing LV that is unable to generate much driving pressure for forward or backward cardiac output; (4) very transient MR in a tachycardic patient; and (5) inappropriately high- or low-gain settings. It cannot be emphasized enough that when a strong clinical suspicion for acute MR or other subacute complications for MI exists, the absence of such a finding on TTE even after diligent scanning does not rule out the complication. In such cases, the decision tree should rapidly progress to either a TEE for confirmatory diagnosis if the patient can be stabilized, or else directly to the operating room for exploratory surgery.

Ventricular Septal Defect

Ventricular septal defect (VSD) owing to rupture once complicated 0.5-3% of acute MIs, before the widespread use of thrombolytic therapy. The risk of developing VSD was highest in patients who were female, hypertensive, 60 yr or older, and without a previous history of angina or MI (Birnbaum). The latter risk factor is presumed to be a result of the absence of collateral flow preserving infracted segments. However, a more recent analysis of the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial has revealed that the incidence of VSD after reperfusion therapy has declined to 0.2-0.3% in patients receiving thrombolysis, far lower than previous (Crenshaw). Infarctions of large territories, involving the RV, or those caused by total occlusion of the culprit vessel were more likely to develop VSD.

In the unreperfused patient, ruptures were rare early in the course of MI. When they did occur within the first 24 h, they are thought to be owing to large intramural hemotomas that dissect directly through a

Fig. 8. Ruptured papillary muscle in a 74-yr-old male post-myocardial infarction. This 74-yr-old male presented with severe dyspnea and mitral regurgitation post-myocardial infarction. Echocardiographic images revealed avulsed papillary muscle and chordae attached to anterior mitral leaflet that prolapsed intermittently into the left atrium (apical four-chamber and apical three-chamber [A3C] views, A,C). Severe mitral regurgitation with a posteriorly directed jet was seen (B,D). At surgery for emergency mitral valve replacement, two-thirds of the posterolateral papillary muscle was totally detached. (Please see companion DVD for corresponding video.)

Ruptured Papillary •4 S Muscle

LA Anterior Mitral Leaflet

Papillary Muscle Rupture

Ruptured Papillary •4 S Muscle

LA Anterior Mitral Leaflet

Common Thrombolytics

large infarcted area. VSDs are more common 3-5 d after the acute MI, when the pathogenesis involves necrosis and thinning of the septum, with tissue disintegration hastened by the release of lytic enzymes from inflammatory cells. Interestingly, although the use of thrombolytics reduces the size of the infarct and risk of septal rupture, the onset of septal rupture in thrombolysed patients appears to be earlier (median time from onset of MI to rupture was 1 d in GUSTO-I trial and 16 h in the Should We Emergently Revas-cularize Occluded Coronaries in Cardiogenic Shock (SHOCK) trial, perhaps because of more intramyo-cardial hemorrhage.

Although 2D echo alone has limited sensitivity detecting VSDs, the addition of color Doppler increases the sensitivity and specificity of TTE for detecting VSD to almost 100%. On echocardiogram, the VSD may be seen as a discrete discontinuity or echo "dropout" in the muscular portion of the interventricular septum (Fig. 9 A).

Because of the asymmetry of most defects, it is important to inspect the septum from multiple windows when a VSD is suspected. The actual orifice size may range from millimeters or up to several centimeters in maximal dimension, and often expands during systole compared to diastole. Color flow Doppler will demonstrate turbulence and left-to-right flow through the VSD, because LV pressures are higher than RV pressures continuously throughout the cardiac cycle (Fig. 9B; please see companion DVD for corresponding video). Injecting agitated saline intravenously ("bubble study") can occasionally help define left-to-right flow by showing a negative contrast effect in the RV emanating from the VSD orifice. Morphologically, septal ruptures can be described as a simple perforation (i.e., direct defect through both sides of the septum at the same level), or more complex, with irregular serpiginous tracts entering and exiting the septum at different levels. Anterior VSDs are usually simple and located toward the apex (as in the ensuing case

The Mid Septum

Fig. 9. (A) Postmyocardial infarction ventricular septal defect in a 72-yr-old male. This 72-yr-old male with a 1-wk history of chest pains and inferior myocardial infarction showed a breach in the mid-to-basal infero-septal segments on two-dimensional echocardiography (left panel, arrow). Color Doppler revealed a left-to-right shunt consistent with a ventricular septal defect. This was confirmed on ventriculography. Angiography revealed 100% right coronary artery occlusion. (B) Continuous-wave (CW) Doppler examination of postmyocardial infarction ventricular septal defect. CW Doppler of the ventricular septal defect showed a high-velocity left-to-right (3.0 m/s) flow with limited low-velocity flow (1.4 m/s) in the opposite direction during diastole. (Please see companion DVD for corresponding video.)

Fig. 9. (A) Postmyocardial infarction ventricular septal defect in a 72-yr-old male. This 72-yr-old male with a 1-wk history of chest pains and inferior myocardial infarction showed a breach in the mid-to-basal infero-septal segments on two-dimensional echocardiography (left panel, arrow). Color Doppler revealed a left-to-right shunt consistent with a ventricular septal defect. This was confirmed on ventriculography. Angiography revealed 100% right coronary artery occlusion. (B) Continuous-wave (CW) Doppler examination of postmyocardial infarction ventricular septal defect. CW Doppler of the ventricular septal defect showed a high-velocity left-to-right (3.0 m/s) flow with limited low-velocity flow (1.4 m/s) in the opposite direction during diastole. (Please see companion DVD for corresponding video.)

vignette), whereas inferior infarctions often involve the adjacent basal septum and are more likely to be complex.

Echocardiography of a patient with VSD should define the location, type (simple or complex), and size of the defect if possible. Additional useful information includes an estimate of the degree of left-to-right shunting (by the combined 2D and Doppler technique of estimating Qp and Qs), the pressure gradient across the septum (from which

RV systolic pressure [RVSP] can be calculated using the formula RVSP = systolic BP - 4[VSD velocity]2, or RVSP = right atrial pressure + 4[TR velocity]2), and RV function. In severe VSDs, there may be associated rupture of papillary muscles or even free wall rupture (see "Free Wall Rupture" section).

Clinically, a significant VSD will be heralded by the patient experiencing chest pain, dyspnea, and potentially cardiogenic shock. The shunting of blood across the VSD may be appreciated on physical exam as a harsh loud holosystolic murmur at the left sternal border and a palpable thrill. As the LV fails, systemic vascular resistance increases (to maintain blood pressure), and right-sided pressures increase, the amount of left-to-right shunting will decrease and biventricular failure ensues. Mortality of VSD is high, approx 24% in the first day and reaching up to 82% at 2 mo in medically treated patients, and, thus, operative repair (or in some cases, potentially closure with a percutaneous septal occluding device) should be initiated as soon as possible.

Pseudoaneurysm

A pseudoaneurysm is thought to be secondary to a subacute ventricular perforation that is locally contained. Pathologically, all three layers of the heart are disrupted, such that blood from the LV courses through endocardium and myocardial wall into the pericardial space (Fig. 10A,B; please see companion DVD for corresponding video). Local containment of the extruded blood by adherent parietal pericardium and scar tissue forms a globular echo-free space adjacent to and continuous with the LV internal chamber. Because of the local containment adjacent to the ventricle, this space appears similar to a ventricular aneurysm (Fig. 10C,D).

The distinction between these two entities is vitally important: a pseudoaneurysm is a surgical emergency because of risk of impending rupture, whereas a true aneurysm is less likely to rupture and can often be observed. A key difference is that there is no myocardium in the wall of a pseudoanuerysm. Both entities may contain associated formed thrombus. In general, echo characteristics associated with a pseudoaneurysm include:

1. A narrow neck (an orifice:pseudoaneurysm body diameter <0.5).

2. An abrupt or ragged interruption in the LV wall, indicating a through-and-through discontinuity of all layers of the heart, as opposed to the gradual tapering and thinning of the myocardial layer seen in a true aneurysm. (This criteria is better for anterior than inferior aneurysms.)

3. Color or pulse-waved Doppler showing bidirectional blood flow and increased turbulence within the neck of the aneurysm.

4. If the patient is stable enough and the diagnosis is unclear from standard echocardiography, the injection of intravenous echo-opaque contrast agents such as Optison or Definity may help define a pseudoa-neurysm, by delineating the myocardial tear and extravasating into the pericardial space.

The most frequent presentation of pseudoaneurysm is chest pain and congestive heart failure, although patients may also present with syncope, vagal symptoms, or nonspecific symptoms (Frances et al.). Sudden cardiac death occurs in a small percentage. However, in a completely contained rupture, more than 10% of patients are entirely asymptomatic. Persistent ST-segment elevations occur in 20% of patients with pseudo-aneurysms, and it is possible that recurrent ischemia or reinfarction may contribute to its pathogenesis. Pseudoaneurysms appear about twofold more common after inferior MIs, as opposed to anterior MIs, but have been seen arising from lateral and apical walls as well. The mortality is high owing to late rupture, and operative treatment should be undertaken urgently.

Free Wall Rupture

Free wall rupture is one of the most feared complications of MI, owing to its sudden onset and lethality. Unlike pseudoaneurysm, in a free wall rupture blood flows freely into the pericardium and thorax, causing car-diogenic shock and tamponade. It is seen 2-8 d after MI, with risk factors similar to those for VSDs: patients with Q-wave MI or their first MI are at highest risk. Female gender, advanced age, and hypertension increase the risk, as does delayed recognition of the MI or continued physical activity. Acute chest pain, agitation, and cardiogenic shock occur abruptly and 90% of cases are fatal.

Echocardiograms of acute free wall ruptures are rare, owing to the rapid lethality of this complication.

case presentation (continued)

Two days later, the patient developed recurrent chest pain. An ECG showed sinus tachycardia and persistent ST elevations. Echocardiogram showed akinetic aneurysmal apex and paradoxical septal motion. Post-MI VSD at the apical septum with L-R shunt flow, measuring 1.5-1.7 cm. The gradient across the gradient was 49 mmHg. The LV was hyperdynamic at the base and midventricle and the RV was dilated and diffusely hypokinetic. An emergent intra-aortic balloon pump was placed and the patient underwent surgical repair with a pericardial patch. Repeat TTE showed patch material and no residual shunting.

Inferior Wall Hypokinesis

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Responses

  • Bingo
    How to evaluate a vsd with echocardiography using definity?
    1 year ago
  • sophie
    How to assess papillary muscles on echo?
    3 months ago

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