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Echocardiography in acute and remote myocardial infarction
Echocardiography in Acute and Remote Myocardial Infarction
ALFRED F. PARISI, PAUL F. MOYNIHAN EDWARD
MD,
D. FOLLAND,
WILLIAM
E. STRAUSS,
G.V.R.K.
SHARMA,
ARTHUR
A.
Two dimensional echocardiography is just beginning to be used to char-
FACC MD,
FACC
MD
MD
SASAHARA,
MD,
FACC
Boston, Massachusetts
acterize cardiac damage in patients with acute myocardial infarction. The two dimensional approach allows for a more comprehensive evaluation of cardiac anatomy and is able to detect with high sensitivity changes in regional wall motion that previously were sometimes missed or only found with difficulty using M mode echocardiography. Two dimensional echocardiography appears to offer a basis for quantifying the extent of myocardial damage in acute myocardial infarction and thus may permit objective assessment of therapeutic modalities and prognosts. In addition, the technique facilitates recognition of specific complications in acute myocardial infarction. In particular, the technique offers the ability to distinguish true from false ventricular aneurysm, postinfarction ventricular septal defect from papillary muscle dysfunction and rupture, and right ventricular infarction from cardiac tamponade.
By its nature clinical coronary artery disease is a process that impairs coronary blood flow in one or more segments of the coronary arterial tree. When coronary flow is reduced to a point inadequate to meet the demands of metabolism in a given area of the heart, tissue ischemia leads to regional myocardial dysfunction. Experimental and clinical characterization of the regional myocardial dysfunction, which occurs in coronary artery disease, has been the subject of continued investigation over the past half century. This review will outline some of the experimental background pertaining to regional myocardial dysfunction in coronary artery disease and will describe in detail observations made during the past decade using both M mode and two dimensional echocardiography in patients with acute and remote myocardial infarction. Observations
From the Cardiology Section and Department of Medicine, West Roxbury Veterans Administration Medical Center, Peter Sent Brigham Hospital and Harvard Medical School, Boston, Massachusetts. This study was supported by the Medical Research Service of the U.S. Veterans Administration, Washington, D.C. Manuscript received April 14, 1980, accepted April 18, 1980. Address for reprints: Alfred F. Parisi, MD, Veterans Administration Medical Center, 1400 VFW Parkway, West Roxbury, Massachusetts 02132.
in Experimental Animals
Over the past five decades a number of acute animal experiments using differing techniques have shown abnormalities of regional contraction to occur in the distribution of an acutely ligated coronary artery shortly after its occlusion. Most frequently cited are the original studies of Tennant and Wiggersl in which epicardial myographic recordings showed within seconds after coronary occlusion new systolic aneurysmal bulging of the acutely ischemic distal area. M mode echocardiography in experimental coronary occlusion: During the past 10 years, ultrasonic methods have been used to study the effects of acute and sustained ischemia further. Appreciation of regional contraction abnormalities within, rather than on the surface of the heart has been possible by implanting ultrasonic sonomicrometers in pairs in control subendocardial regions preserved from and in test areas subiected to exnerimental ischemia.2 Conventional single crystal M mode echocardiograms have also been used to study endocardial motion during induced acute ischemia either by placing the transducer on the wall of the closed chest dog or more commonly on the surface of
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TABLE I Regional Wall Motion Abnormalities Detected in Experimental Animals With Ultrasonic Techniques
opposite wall, will show compensatory hyperactivity; that is, the septum will show increased velocity and amplitude of motion when the posterior wall is ischemic and the posterior wall will show similar changes when the septum is ischemic. The abnormalities of left ventricular wall motion commonly detected with echocardiography in acute animal experiments are recapitulated in Table I. Two dimensional echocardiography in acute myocardial infarction: This method is beginning to be used to observe the effects of acute myocardial infarction in closed chest dogs. The two dimensional technique enables the investigator to examine the extent of abnormal wall motion associated with acute coronary occlusion; in one recent study the amount of wall motion abnormality correlated with infarct size determined with technetium pyrophosphate scintigraphy.5 Wall motion abnormalities have also been positively correlated with peak rise in serum creatine kinase values.6 Attention is also being paid to analysis of changes in A mode echocardiographic signals backscattered from the acutely ischemic myocardium. Acute ischemia and injury increase the amplitude and change the frequency distribution of backscattered signals; computer-aided signal analysis can distinguish such evidence of injury from normal myocardium.7*8 Using two dimensional echocardiography, Kisslo et al9 reported a qualitatively echo-dense “speckle” pattern appearing in acutely infarcted canine myocardial walls. These hard echoes appear in the first few days of infarction and perhaps represent an evolution of the increased amplitude A mode signals seen shortly after acute coronary ligation.
lschemic or Injured Area Abnormal bulging during isovolumic systole Decreased amplitude of motion during systolic ejection Decreased velocity of motion during systolic ejection Impaired systolic wall thickening Normally Perfused
Area
Compensatory hyperactivity in healthy remote areas Transitional wall motion abnormalities in adjacent areas
the heart of the open chest dog. By passing the ultrasonic beam through the interventricular septum and left ventricular posterior wall, the behavior of opposite sides of the heart can be observed when one or the other wall is made ischemic.3*4 Abnormalities of contraction as seen in the transmyocardial view rendered by M mode echocardiography are also apparent within seconds after experimental coronary occlusion. During isovolumic systole there is aneurysmal bulging of the ischemic segment away from the center of the left ventricular cavity; during the ejection phase of systole the amplitude and velocity of motion of the ischemic wall are reduced compared with control values; the wall fails to thicken and may even be observed to become thinner. Regions adjacent to the ischemic area can show transitional forms of motion abnormalities between normal and ischemic regions. Often remote regions, particularly the
mode echocardic+ grams from normal patient (A), patient with acute inferoposterior myocardial infarctiin (B) and patient with remote anteroseptal myocardial infarction (C). The amplitude of left ventricular posterior wall motion and its systolic thickening are diminished in the patient with acute infarction (B). Also, there is hyperactivity of the interventricular septum which can be conceptualized as compensating for the poor posterior wall motion. In the patient with remote anterior infarction (C) the same features affecting the interventricular septum are evident. In addition, the septum is relatively echo-dense compared with the posterior wall end Is thin in d&stole (approximately 6 mm).
FIGURE 1. M
A.
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TABLE II Wall Motion Amplitude in Normal Subjects and Patients With Acute Myocardial Infarction*
Observations
1111 Mode Echocardiography One of the earlier observations made with M mode echocardiography in a patient with acute myocardial ischemia is directly analogous to the results of the animal experiments cited. ‘These occurred in a patient with Prinzmetal’s angina who had angiographically documented coronary arterial spasm but no fixed obstructions in the distribution of the left anterior descending coronary artery.lO This patient had a striking loss of the amplitude of systolic septal motion during ischemic episodes characterized1 by chest pain and associated with S-T segment elevation and T wave peaking in mid precordial electrocardiographic leads. The amplitude of septal motion returned to normal as the clinical episodes abated and electrocardiographic manifestations of the ischemic process resolved. This observation underscores the appropriateness of the animal models discussed because co:mparable regional myocardial dysfunction is seen with clinical episodes of ischemic pain and the changes appear immediately with evidence of onset of the ischemic process. Abnormal left ventricular wall motion: Several systematic studies performed in patients admitted to coronary care units with the diagnosis of acute myocardial infarction have further confirmed the observation that impaired amplitude of wall motion is a finding highly associated with regional myocardial damage. A typical example is shown in Figure 1. In a series of 64 patients with acute transmural myocardial infarction, Corya et al.ll reported abnormal left ventricular wall motion in the echocardiogram corresponding to the electrocardiographic s.ite of infarction in 84 percent of the group. Thirty percent of these patients had exaggerated motion in noninfarcted areas, an observation consistent with the compensatory hyperactivity noted in the animal experim’ents cited. Table II summarizes the echocardiographic measurements of the amplitude of motion compared with the normal range in those patients in the series of Corya et al.ll with well localized anterior and inferior myocardial infarction. Detection of wall motion abnormalities with M mode echocardiography is critically dependent on traversing the abnormally contracting myocardial segment with the echographic beam. Because some myocardial infarcts are not necessarily in the path of the standard M mode study, further techniques have been developed with this study and successfully used particularly to detect abnormal anterior wall motion in patients with anterior infarction. These techniques usually involve further lateral exploration of the left precordium at multiple sites in a search for a “window” through which the anterior left ventricular wall can be directly imaged. When this approachl:! is used, absent or paradoxical anterior left ventricular wall motion is a frequent finding in patients with anterior infarction, whereas anterior wall motion abnormalities are rarely seen in patients with inferior infarction. Dynamic changes in wall thickness: Because ab-
Normal Septal amplitude Range (cm) Mean % decreased % increased Posterior wall amplitude Range (cm) Mean % decreased % increased l
Site of Infarction Anterior Inferior
0.3-0.8
O-O.6
O-2.0
0.63 -
0.08 80% 0%
0.81
0.8-2.1 1.40 0% 16%
O-l.7 0.66 57% 7%
0.8-1.6 1.29 -
393;
Adapted from Cotya et al. 11
normalities of wall motion, particularly of the interventricular septum, are nonspecific findings and occur in patients with other conditions, notably right ventricular volume overload and chronic cardiomyopathy, closer scrutiny has been devoted to other local properties of the myocardium in the affected region in patients with acute infarction. In this regard, dynamic changes in wall thickness in transition from diastole to systole have received a great deal of attention as a manifestation of impaired regional function in contraction caused by myocardial ischemia. In a series of 40 patients with acute myocardial infarction (composed of equal numbers with anterior and inferior infarcts),13 18 of the 20 with an anterior infarct had abnormally decreased septal systolic thickening, 19 had abnormally decreased septal motion and 18 had both decreased septal thickening and abnormal wall motion. Interestingly, 11 of these patients had systolic septal thinning. Of the 20 patients with inferior infarction, 65 percent had abnormally decreased posterior wall thickening, 18 abnormally decreased posterior wall motion and 13 both the thickening and motion abnormalities. Systolic thinning of the posterior wall was infrequently recorded, being seen in only one patient. Abnormalities of wall motion and systolic thickening can be seen, although less frequently, in patients with chronic coronary artery disease, particularly if there has been an antecedent myocardial infarction. However, systolic thinning is highly suggestive of acute injury since it is an unusual finding outside of the setting of acute myocardial infarction. Changes in myocardial scarring: Further observations have resulted in the emergence of criteria that identify myocardial scar tissue as a residual of previous myocardial infarction. In a series of 182 patients Rasmussen et a1.14 showed that scar tissue was very likely to be present if (1) the myocardium was less than 7 mm thick in diastole and more echo-producing than the adjacent or opposing wall, or (2) an area of myocardium was 30 percent less thick than an adjacent area in the same scan (Fig. 10 These observations were confirmed in all instances by surgical observations and in 34 cases by histologic examination of either autopsy or surgical
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FIGURE 2. Epicardial and endocardial diastolic outlines of short axis views of the left ventricle at the level of the papillary muscles in a patient with an acute transmural anterior infarction and evidence of infarct expansion over the course of serial studies. The development of regional dilatation and thinning in the infarcted areas is apparent from the tracing of day 7. (Reprinted by permission, from Eaton et al.“)
PL
resection specimens. Ninety percent of these patients had a clinical history of antecedent myocardial infarction and most had consistent electrocardiographic findings as well. Two Dimensional Echocardiography Acute myocardial infarction: Two dimensional echocardiography offers the ability to evaluate regional abnormalities of myocardial motion with much greater facility than M mode examination since the field of the examination is not restricted to the narrow M mode beam and the spatial orientation of the tomographic sections can be appreciated. As early as 1977 Kisslo et a1.15 reported that two dimensional echocardiograms lent themselves as readily to qualitative examination of regional wall motion abnormalities as did left ventricular cineangiograms. More recently several observers have looked specifically at two dimensional echocardiography for its ability to detect wall motion abnormalities that are associated with acute myocardial infarction. Most observers have depended on one or more short axis views that allow evaluation of departures from the normally concentric contraction of the left ventricle around its perimeter. Heger et a1.r6 devised a nine segment subdivision of the left ventricle that included anterior, medial, posterior and lateral quadrants at the mitral and papillary muscle levels and an apical segment recorded by placing the transducer directly over the apex and obtaining a long axis scan. Complete studies, allowing evaluation of these nine segments, was accomplished in 37 of 44 attempts. Nineteen of 20 patients with inferior infarction had asynergy in posterior segments, 14 patients with anterior infarction had asynergy in anterior segments and 3 patients with both anterior and inferior infarction had appropriately localized wall motion abnormalities. In four patients pathologic lo-
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end diastole end systole
FIGURE 3. Schematic drawing illustrating short axis views of the left ventricle obtained with two dimensional echocardiography. The insert shows diastolic and systolic outlines of the left ventricle at either level as a pair of outlines that approximate concentric circles. The axis system used for analysis is superimposed. Regional function of the left ventricle can be characterized with use of either segmental areas or chords (see text). A = anterior; AL = anterolateral; AS = anteroseptal; L = lateral; P = posterior; PL = posterolateral; PS = posteroseptal; S = septal.
calization of infarction corresponded to the asynergic areas detected on two dimensional echocardiography, thus confirming that this technique is a reliable method of detecting and localizing regional contraction abnormalities that occur in acute myocardial infarction. Eaton et a1.17 performed serial two dimensional echocardiographic examinations in 28 patients during the first 2 weeks after myocardial infarction. Diastolic short axis two dimensional echocardiograms at the level of the papillary muscle tips were evaluated serially in this study in patients whose first echocardiogram had been obtained within 60 hours of the acute event. Endocardial and epicardial outlines were traced; segment lengths and wall thickness were calculated using a computer-aided semiautomated contouring system. Eight of the patients showed evidence of infarct expansion with disproportionate transmural thinning of the infarcted zone and associated left ventricular dilatation, whereas the remaining 20 patients had no evidence of these findings. Patients with anterior and anteroseptal infarction seemed particularly prone to infarct expansion (Fig. 2). At 8 weeks after infarction 4 of the 8 patients who showed infarct expansion had died, whereas all 20 patients without infarct expansion were
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living. On the basis of this study these investigators contended that infarct expansion, rather than further extension of the’ischemic process with further necrosis of myocardial tissue, might play a more important role than had previously been appreciated in patients surviving acute myocardial infarction. This study demonstrates that two dimensional echocardiography can be used as an indicator of topographic changes that occur in the evolution of an acute myocardial infarction and may have considerable clinical importance, not only in assessing survival but potentially in assessing interventions that may influence survival of such patients. Remote myocardia.1 infarction: Using a computer-aided approach in our laboratory, wel*Jg have also been interested with the ability of two-dimensional echocardiography to define and quantify regional wall motion abnormalities. We obtained cross-sectional short axis views of the left ventricle in a series of normal volunteers, patients with coronary artery disease without remote myocardlial infarction as well as patients with a prior myocardial infarction confirmed by abnormal Q waves in the electrocardiogram. End-diastolic short axis outlines of the ventricle at both mitral valve and papillary muscle levels were traced with a light pen digitizing system using the onset of the electrocardiographic QRS complex as a marker of end-diastole. Similarly, end-systolic frames were traced using the first high frequency component of the second heart sound as an indicator of end systole. At each tomographic level the mid point of the interventricular septum on the left ventricular endocardia!l surface was identified by the observer. From this starting point an initial axis (Fig. 3, axis SL) was constructed using a computer algorithm to that point on the lateral left ventricular wall that allowed the diastolic image to be divided into anterior and posterior halves of equal area. The mid point of this initial diastolic axis is systematically bisected by a series of radii 45” apart. This, then creates a diastolic radial axis system of eight ch.ords and their enclosed areas. Maintaining this reference system fixed in space and superimposing the systolic endocardial outline permits segmental evaluation of the ventricle, either by chordal shortening or regional area shrinkage. Thirty-two patients were evaluated once the normal range of contraction was established from 10 normal volunteers. Twenty patients with coronary artery disease but without remote infarction had no difference in contraction pattern from that of the volunteers. Twelve patients had remote transmural infarction evidenced by abnormal Q waves. Six patients with anterior infarction showed impaired regional motion in anterior and anteroseptal regions, and six patients with inferior infarction showed impaired motion in posterior and lateral regions (Fig. 4 and 5). In conducting a parallel computer analysis of angiocardiograms in these 12 patients, two dimensional echocardiography proved as sensitive as angiography for detection of regional contraction defects: Each technique identified 10 of 12 patients correctly. These further observations confirm that two dimensional echocardiography can be used systematically to study regional wall motion abnor-
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malities in patients with remote as well as acute myocardial infarction. Surgical implications: The use of two dimensional echocardiography to characterize regional areas of abnormal contraction is in its nascent stage. Information gleaned from M mode techniques such as diastolic thinning, failure of appropriate systolic thickening and change of echocardiographic character within the wall producing acoustically “hard” areas, have only begun to be explored by two dimensional echocardiography (Fig. 6). The technique ultimately has the potential not only for identifying the presence of wall motion abnormalities, but also for quantifying their extent on a global basis and for assessing their reversibility. Thus, the unusually thinned echo-dense noncontractile region, which is probably composed of scar tissue, is unlikely to have its function restored by bypass surgery, whereas a poorly contracting area of myocardium of normal diastolic thickness and wall character may indeed recover its function after the blood supply is restored. The potential of echocardiography in this regard will be the subject of many further explorations within the next few years.
Special Complications of Myocardial Infarction Ventricular aneurysm: Ventricular aneurysm (defined as an abnormal diastolic outpouching of the normal ventricular cavity) has long been recognized by M mode echocardiography. In a typical examination with the transducer in a standard location, a scan of the left ventricle from base to apex shows that the cavity expands or fails to taper as the region of the papillary muscles is approached. This finding is highly associated with the presence of left ventricular aneurysm. Many, but not all, left ventricular aneurysms fall within the path of a standard M mode scan. Thus, Weyman et a120 noted that in a series of 31 patients with angiographitally proved left ventricular aneurysm, two dimensional echocardiography detected 100 percent of these defects whereas M mode studies were successful in detecting this abnormality 47 percent of the time. Typical examples of left ventricular aneurysm detected with two dimensional echocardiographic examinations are shown in Figure 7. Ventricular pseudoaneurysm: In contrast to a true left ventricular aneurysms which is an abnormal outpouching of the infarcted left ventricular myocardium, a false aneurysm consists of cavitated clots that communicate with the left ventricular body through an area of myocardial rupture. In the patient who has not had antecedent cardiac trauma or surgery, myocardial infarction is the leading cause of pseudoaneurysm formation. Unlike the orifice to a true aneurysm, which is wide and patent, the orifice to a false aneurysm is narrow. By virtue of this anatomic feature a false aneurysm is often detectable by echocardiography. Although the narrow orifice leading to the false aneurysm cavity was originally reported in M mode echocardiographic studies, two dimensional echocardiography greatly facilitates its recognition22*23 (Fig. 8). Detection of a false aneurysm is more than an academic question
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FIGURE 4. End-diastolicand end-systolic short axis images and computer regenerated outlines from a normal subject (top), a patient with anteroseptal myocardial infarction (middle) and a patient with inferior myocardial infarction (bottom).
SEGMENT FIGURE 5. Plots of regional area shrinkage in 20 patients with no antecedent myocardial infarction and in two patient subgroups who had anterior or inferior myocardial infarction (see text). Abbreviations as in Figure 3.
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because a false aneurysm is prone to fatal myocardial rupture, a complication very rarely encountered in a true left ventricular aneurysm. Moreover, it is readily amenable to surgery, which remains the treatment of choice. Thus, echocardi.ography, particularly with the two dimensional technique, is a key examination in the patient with an abnormally bulging radiographic cardiac silhouette after myocardial infarction. Because the
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primary clue to distinguishing true and false aneurysm depends on recognition of the narrowed orifice, a false aneurysm will not be suspected using standard chest roentgenograms. Papillary muscle dysfunction and rupture: Mitral regurgitation may arise from anatomic or functional derangements of the papillary muscles. Papillary muscle dysfunction is most commonly caused by ischemia or
FIGURE 6. Short axis view oi the left ventricle shown schematically and the actual image showing unusually hard echoes from the posteroseptal region in a patient with remote inferior myocardial infarction. These hard echoes correspond to the echo densities previously reported on M mode echocardiography. It would be difficult to gain access to the echodense region in this figure with the standard M mode approach. LV = left ventricle; PM = papillary muscles.
FIGURE 7. Examples of left ventricular aneurysm. Left, aneurysm of the interventricular septum in a patient with remote anterior myocardiil infarction. This type of aneurysm is more likely to be missed on M mode scanning than is an apical aneurysm. Right, apical left ventricular aneurysm seen with an apical view on two dimensional echocardiography. The cloud of echoes within the aneurysmal chamber suggests a possible left ventricular thrombus. A = aneurysm; LA = atrium; LV = left ventricle; MV = mitral valve; RV = right ventricle.
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infarction which leads to asynergic contraction of the muscles, or by ventricular dilatation or aneurysm that produces sufficient malalignment to result in mitral regurgitation. In a series of 14 patients with papillary muscle dysfunctionz4 two abnormal patterns of mitral valve closure were identified with two dimensional echocardiography: Three patients showed mitral valve prolapse associated with inferoposterior wall akinesia and increased tissue echo density consistent with papillary muscle fibrosis; nine patients with ventricular enlargement or aneurysm had apically displaced mitral leaflet coaptation, and the remaining two patients had both of these patterns. Papillary muscle rupture is a devastating complication of acute myocardial infarction. It produces mitral regurgitation, which acutely imposes a volume overload on the left heart chambers. The magnitude of the vol-
ume load depends on the exact location of papillary muscle rupture. It is usually suspected from the sudden appearance of a loud systolic murmur, which may be impossible to distinguish at the bedside from the murmur of a ruptured interventricular septum (see later). If a head of a papillary muscle rather than an entire papillary muscle ruptures, it is possible that the patient can survive and undergo diagnostic evaluation that will allow its detection. As with ruptured chordae tendineae, this condition will lead to a flail anterior or posterior mitral leaflet; a flail valve can be readily appreciated on two dimensional echocardiography because one of the mitral leaflets swings freely into the left atria1 cavity during ventricular systole25 (Fig. 9). Ventricular septal rupture: A ruptured flap of interventricular septum, showing an unusual pattern of motion, has been detected with M mode echocardiography in a patient with acute anteroseptal myocardial infarction.26 Patients with this problem have also been reported to have, on average, an enlarged right ventricular internal dimension.27 Direct visualization of loss of septal continuity is unlikely to be detected with M mode echocardiography because the septal rent may be irregular and obliquely located relative to the echographic beam passage from a parasternal or precordial transducer location. Nevertheless one such case has been reported. 2s In one instance2g of a patient with documented postinfarction ventricular septal defect, the septum appeared split into two layers separated by an echo-free zone, which represented an obliquely passing communication from the left to the right ventricle. Two dimensional echocardiography allows more complete inspection of the interventricular septum. With use of an apical four chamber view in which the length of the septum was delineated, three consecutive patients with ventricular septal rupture in the course of acute anterior infarction were identified.30 In two of the three this was imaged as an oblique rent from the distal left ventricle to the proximal right ventricle, while in the third patient a large orifice was evident in the distal septum. Although postinfarction ventricular septal defect has not been frequently reported, it is anticipated that additional reports will appear as two dimensional equipment becomes more widely used in coronary care units and greater sophistication develops in exploring the integrity of the interventricular septum from different transducer locations. Other complications of myocardial infarction: Two dimensional echocardiography offers the potential for making diagnostic decisions regarding other complications of myocardial infarction. Clots can be detected in relation to immobile areas of infarcted myocardial wall; pericardial effusion can be documented in the postinfarction patient with pericarditis. The latter is one of the applications in which M mode echocardiography is still quite valuable. In patients with inferior myocardial infarction in whom a pericardial friction rub and elevated neck veins develop, the distinction between right ventricular infarction and postinfarction pericarditis with cardiac tamponade accounting for
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FffilJRE 8. Top, two dimensional echocardiogram in apical two chamber projection of a patient with a pseudoaneurysm of the left ventricle. Rottom, schematic drawing of the orientation of the cardiac chambers and the pseudoaneqsm (PA). Ao = aorta: I = inferior; LA = left atrium; LV = left ventricle; S = superior. (Figure kindly supplied by Dr. M. Kotler and reprinted from Catherwood et al.23 by permission of the American Heart Association, Inc.)
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impaired right ventricular filling can be aided by echocardiography. Not. all patients who manifest a pericardial friction rub in the course of myocardial infarction have significant pericardial effusion. In the absence of detectable effusion cardiac tamponade would be a very unlikely complication of acute myocardial infarction. Patients with. tamponade not only show signs of effusion, but also are very likely to show signs of right ventricular compression. In contrast, regional dilatation of the right ventricle has been reported in right ventricular infarction if the involved area is traversed by the echographic beam.2*1~32
Advantages and Limiitations of Two Dimensional Echocardiography in Myocardial Infarction Two dimensional echocardiography offers distinct advantages for evaluating myocardial structure and function in myocardial infarction not currently available by other methods. First and foremost, if offers the most comprehensive information of any noninvasive imaging technique. One can appreciate from a single bedside examination not only myocardial structure and func-
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tion, but also the area around the heart and the function of the cardiac valves. In addition, the resolution of detail obtainable with echocardiography is superior to that of any other noninvasive imaging modality. The relatively high degree of resolution is particularly useful in detecting special complications of infarction that can affect small and highly localized anatomic regions of the ventricle, such as papillary muscle dysfunction and formation of intramural thrombi. Another advantage of echocardiography in this setting is that it can be repeated, if necessary, multiple times on a daily basis without the concern of exposing the patient to ionizing radiation. The principal limitation of echocardiography is its inability to obtain high quality images more than 60 to 80 percent of the time, depending on the investigator and the patient population. Although this difficulty is in part being overcome through improved techniques of examination using different approaches to imaging of the heart, further development of instrumentation will be necessary to achieve a success rate with ultrasound comparable with that of radionuclide imaging techniques.
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References 1. Tennant R, Wiggers CJ. The effect of coronary occlusion on myocardial contraction. Am J Physiol 1935; 112:35 1. 2. Heyndrkkx G, Millard RW. McRitchie RJ, Maroko PR, Vatner SF. Regional myocardial function and electrophysiological alterations after briif coronary artery occlusion in conscious dogs. J Clin Invest 1975;56:978-85. 3. Kerber RE, Abboud FM. Echocardiographic detection of regional myocardial infarction: an experimental study. Circulation 1973; 47:997-1005. 4. Kerber RE, Marcus ML, Wilson R, Erhardt J, Abboud FM. Effects of acute coronary occlusion on the motion and perfusion of the normal and ischemic interventricular septum: an experimental echocardiographic study. Circulation 1976;54:928-35. 5. Meltzer RS, Woythaler JN. Buda AJ, et al. Two dimensional echocardiographic quantification of infarct size alteration by pharmacologic agents. Am J Cardiol 1979;44:257-62. 6. Vlsser CA, Lle KI, Durrer JD, van Capelle F, Durrer D. Quantification and localization of uncomplicated acute myocardial infarction by cross-sectional echocardiography (abstr). Circulation 1979;6O:Suppl ll:ll-152. 7. Bauwens D, O’Donnell 1111, Miller JG. Mlrnbs JW. Detection of acute myocardiil ischemia in vivo with quantitative ultrasonic backscatter (abstr). Circulation 1979;6O:Suppl ll:ll-152. 8. Dines KA, Weyman AE, Franklin TD, et al. Quantitation of changes in myocardial fiber bundle spacing with acute infarction, using pulse-echo ultrasound signals (abstr). Circulation 1979;6O:Suppl ll:ll-17. 9. K&lo J, kteker R, Harrison L, et al. Serial wall changes after acute myocardial infarction by two-dimensional echo (abstr). Circulation 1979:6O:Suppl ll:ll-151. 10. Wldlansky S, McHenry PL, Corya BC, Phllllps JF. Coronary angiographic, echocardiographic, and electrocardiographic studies on a patient with variant angina due to coronary artery spasm. Am Heart J 1975;90:631-5. 11. Corya BC, Rasmussen S, Knoebel SB, Felgenbaum H, Black MJ. Echocardiography in acute myocardial Infarction. Am J Cardiol 1975;36:1-10. 12. Helkklla J, Nlemlnen M. Echoventriculographic detection, localization and quantification of left ventricular asynergy in acute myocardial infarction. Br Heart J 1975;37:46-59. 13. Corya BC, Rasmussen S, Felgenbaum H, Knoebel SB, Black MJ. Systolic thickening and thinning of the septum and posterior wall in patients with coronary artery disease, congestive cardiomyopathy and atrial septal defect. Circulation 1977;55:109-14. 14. Rasmussen S, Corya BC, Felgenbaum H, Knoebel SB. Detection of myocardial scar tissue by M-mode echocardiography. Circulation 1978;57:230-7. 15. Klsslo JA, Robertson D, Gllberl BW, von Ramm 0, Behar VS. A comparison of real-time two-dimensional echocardiography and cineangiography in detecting left ventricular asynergy. Circulation 1977;55:134-41. 16. Heger JJ, Weyman AE, Wann LS, Dlllon JC, Felgenbaum H. Cross-sectional echocardiography in acute myocardial infarction: detection and localization of regional left ventricular asynergy.
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Circulation 1979;60:531-8. 17. Eaton LW, Weiss JL, Bulkley BH, Garrison JB, Welsfeldl ML. Regional cardiic dilatation after acute rnyocardiil infarction. N Engl J Med 1979;300:57-62. 18. Parlsl AF, Moynlhan PF, Folland ED, Feldman CL. Assessment of regional wall motion in coronary artery disease by twodirnensional echocardiography. In: Lancee CT, ed. Echocardiology. The Hague: Martinus Nijhoff, 1979;125-9. 19. Moynlhan PF, Feldman CL, Parlsl AF. Comparison of methods for quantitative evaluation of left ventricular function with twodimensional echocardiography (abstr). Clin Res 1979;27:566A. 20. Weyman AE, Peskoe SM, Williams ES, Dillon JC, Felgenbaum H. Detection of left ventricular aneurysms by cross-sectional echocardiography. Circulation 1976;54:936-44. 21. Davidson KH, Parlsl AF, Harrlngton JJ, Barsamlan EM, Flshbeln MC. Pseudoaneurysms of the left ventricle: an unusual echocardiographic presentation. Ann Intern Med 1977;86:430-3. 22. Sears TD, Ong YS, Starke H, Forker AD. Left ventricular pseudoaneurysm identified by cross-sectional echocardiography. Ann Intern Med 1979;90:935-6. 23. Catherwood E, Mlntz GS, Kotler MN, Perry W. Two-dimensional echocardiographic differentiation of true and false ventricular aneurysms. Circulation, in press. 24. Dgawa S, Hubbard FE, Mardelll TJ, Drelfus LS. Cross-sectional echocardiographic spectrum of papillary muscle dysfunction. Am Heart J 1979;97:312-21. 25. Child JS, Skorton DJ, Taylor RD, Abbasl AS, Wong M, Shah PM. Cross-sectional and M-mode echocardiographic features of flail mitral leaflets (abstr). Am J Cardiol 1979;43:411. 26. DeJoseph RL, Seldes SF, Llndner A, Damato AN. Echocardio graphic findings of ventricular septal rupture in acute myocardial infarction. Am J Cardiol 1975:36:346-6. 27. Chandraratna PAN, Balacbandran PK, Shah PH, Hodges M. Echocardiographic observations on ventricular septal rupture complicating acute myocardial infarction. Circulation 1975;51: 506-10. 28. Kerln NZ, Edelstein J, DeRue RG. Ventricular septal defect complicating acute myocardial infarction. Chest 1976:70:5803. 29. Egeblad H, Haunso S. Echocardiographic findings in ventricular septal rupture and anterior wall aneurysm complicating myocardial infarction (abstr). Acta Medica Stand Suppl 1977;627:224. 30. Farcot JC, Bolsantl L, Rlgand M, Bardet J, Bourdarlas JP. Twodimensional echocardiographic visualization of ventricular septal rupture after acute myocardial infarction. Am J Cardiol 1980:45: 370-7. 31. Lorell B, Welnbach RC, Pohosl GM, Gold HK, et al. Right ventricular infarction: clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction. Am J Cardiol 1979;43: 465-71. 32. Elkayam U, Halprln SL, Frlshman W, Strom J, Cohen MN. Echocardiographic findingsJn cardiiic shock due to right ventricular myocardial infarction. Cath Cardiovasc Diag 1979;5:289-94.
Volume 48
ALFRED F. PARISI, PAUL F. MOYNIHAN EDWARD
MD,
D. FOLLAND,
WILLIAM
E. STRAUSS,
G.V.R.K.
SHARMA,
ARTHUR
A.
Two dimensional echocardiography is just beginning to be used to char-
FACC MD,
FACC
MD
MD
SASAHARA,
MD,
FACC
Boston, Massachusetts
acterize cardiac damage in patients with acute myocardial infarction. The two dimensional approach allows for a more comprehensive evaluation of cardiac anatomy and is able to detect with high sensitivity changes in regional wall motion that previously were sometimes missed or only found with difficulty using M mode echocardiography. Two dimensional echocardiography appears to offer a basis for quantifying the extent of myocardial damage in acute myocardial infarction and thus may permit objective assessment of therapeutic modalities and prognosts. In addition, the technique facilitates recognition of specific complications in acute myocardial infarction. In particular, the technique offers the ability to distinguish true from false ventricular aneurysm, postinfarction ventricular septal defect from papillary muscle dysfunction and rupture, and right ventricular infarction from cardiac tamponade.
By its nature clinical coronary artery disease is a process that impairs coronary blood flow in one or more segments of the coronary arterial tree. When coronary flow is reduced to a point inadequate to meet the demands of metabolism in a given area of the heart, tissue ischemia leads to regional myocardial dysfunction. Experimental and clinical characterization of the regional myocardial dysfunction, which occurs in coronary artery disease, has been the subject of continued investigation over the past half century. This review will outline some of the experimental background pertaining to regional myocardial dysfunction in coronary artery disease and will describe in detail observations made during the past decade using both M mode and two dimensional echocardiography in patients with acute and remote myocardial infarction. Observations
From the Cardiology Section and Department of Medicine, West Roxbury Veterans Administration Medical Center, Peter Sent Brigham Hospital and Harvard Medical School, Boston, Massachusetts. This study was supported by the Medical Research Service of the U.S. Veterans Administration, Washington, D.C. Manuscript received April 14, 1980, accepted April 18, 1980. Address for reprints: Alfred F. Parisi, MD, Veterans Administration Medical Center, 1400 VFW Parkway, West Roxbury, Massachusetts 02132.
in Experimental Animals
Over the past five decades a number of acute animal experiments using differing techniques have shown abnormalities of regional contraction to occur in the distribution of an acutely ligated coronary artery shortly after its occlusion. Most frequently cited are the original studies of Tennant and Wiggersl in which epicardial myographic recordings showed within seconds after coronary occlusion new systolic aneurysmal bulging of the acutely ischemic distal area. M mode echocardiography in experimental coronary occlusion: During the past 10 years, ultrasonic methods have been used to study the effects of acute and sustained ischemia further. Appreciation of regional contraction abnormalities within, rather than on the surface of the heart has been possible by implanting ultrasonic sonomicrometers in pairs in control subendocardial regions preserved from and in test areas subiected to exnerimental ischemia.2 Conventional single crystal M mode echocardiograms have also been used to study endocardial motion during induced acute ischemia either by placing the transducer on the wall of the closed chest dog or more commonly on the surface of
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TABLE I Regional Wall Motion Abnormalities Detected in Experimental Animals With Ultrasonic Techniques
opposite wall, will show compensatory hyperactivity; that is, the septum will show increased velocity and amplitude of motion when the posterior wall is ischemic and the posterior wall will show similar changes when the septum is ischemic. The abnormalities of left ventricular wall motion commonly detected with echocardiography in acute animal experiments are recapitulated in Table I. Two dimensional echocardiography in acute myocardial infarction: This method is beginning to be used to observe the effects of acute myocardial infarction in closed chest dogs. The two dimensional technique enables the investigator to examine the extent of abnormal wall motion associated with acute coronary occlusion; in one recent study the amount of wall motion abnormality correlated with infarct size determined with technetium pyrophosphate scintigraphy.5 Wall motion abnormalities have also been positively correlated with peak rise in serum creatine kinase values.6 Attention is also being paid to analysis of changes in A mode echocardiographic signals backscattered from the acutely ischemic myocardium. Acute ischemia and injury increase the amplitude and change the frequency distribution of backscattered signals; computer-aided signal analysis can distinguish such evidence of injury from normal myocardium.7*8 Using two dimensional echocardiography, Kisslo et al9 reported a qualitatively echo-dense “speckle” pattern appearing in acutely infarcted canine myocardial walls. These hard echoes appear in the first few days of infarction and perhaps represent an evolution of the increased amplitude A mode signals seen shortly after acute coronary ligation.
lschemic or Injured Area Abnormal bulging during isovolumic systole Decreased amplitude of motion during systolic ejection Decreased velocity of motion during systolic ejection Impaired systolic wall thickening Normally Perfused
Area
Compensatory hyperactivity in healthy remote areas Transitional wall motion abnormalities in adjacent areas
the heart of the open chest dog. By passing the ultrasonic beam through the interventricular septum and left ventricular posterior wall, the behavior of opposite sides of the heart can be observed when one or the other wall is made ischemic.3*4 Abnormalities of contraction as seen in the transmyocardial view rendered by M mode echocardiography are also apparent within seconds after experimental coronary occlusion. During isovolumic systole there is aneurysmal bulging of the ischemic segment away from the center of the left ventricular cavity; during the ejection phase of systole the amplitude and velocity of motion of the ischemic wall are reduced compared with control values; the wall fails to thicken and may even be observed to become thinner. Regions adjacent to the ischemic area can show transitional forms of motion abnormalities between normal and ischemic regions. Often remote regions, particularly the
mode echocardic+ grams from normal patient (A), patient with acute inferoposterior myocardial infarctiin (B) and patient with remote anteroseptal myocardial infarction (C). The amplitude of left ventricular posterior wall motion and its systolic thickening are diminished in the patient with acute infarction (B). Also, there is hyperactivity of the interventricular septum which can be conceptualized as compensating for the poor posterior wall motion. In the patient with remote anterior infarction (C) the same features affecting the interventricular septum are evident. In addition, the septum is relatively echo-dense compared with the posterior wall end Is thin in d&stole (approximately 6 mm).
FIGURE 1. M
A.
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TABLE II Wall Motion Amplitude in Normal Subjects and Patients With Acute Myocardial Infarction*
Observations
1111 Mode Echocardiography One of the earlier observations made with M mode echocardiography in a patient with acute myocardial ischemia is directly analogous to the results of the animal experiments cited. ‘These occurred in a patient with Prinzmetal’s angina who had angiographically documented coronary arterial spasm but no fixed obstructions in the distribution of the left anterior descending coronary artery.lO This patient had a striking loss of the amplitude of systolic septal motion during ischemic episodes characterized1 by chest pain and associated with S-T segment elevation and T wave peaking in mid precordial electrocardiographic leads. The amplitude of septal motion returned to normal as the clinical episodes abated and electrocardiographic manifestations of the ischemic process resolved. This observation underscores the appropriateness of the animal models discussed because co:mparable regional myocardial dysfunction is seen with clinical episodes of ischemic pain and the changes appear immediately with evidence of onset of the ischemic process. Abnormal left ventricular wall motion: Several systematic studies performed in patients admitted to coronary care units with the diagnosis of acute myocardial infarction have further confirmed the observation that impaired amplitude of wall motion is a finding highly associated with regional myocardial damage. A typical example is shown in Figure 1. In a series of 64 patients with acute transmural myocardial infarction, Corya et al.ll reported abnormal left ventricular wall motion in the echocardiogram corresponding to the electrocardiographic s.ite of infarction in 84 percent of the group. Thirty percent of these patients had exaggerated motion in noninfarcted areas, an observation consistent with the compensatory hyperactivity noted in the animal experim’ents cited. Table II summarizes the echocardiographic measurements of the amplitude of motion compared with the normal range in those patients in the series of Corya et al.ll with well localized anterior and inferior myocardial infarction. Detection of wall motion abnormalities with M mode echocardiography is critically dependent on traversing the abnormally contracting myocardial segment with the echographic beam. Because some myocardial infarcts are not necessarily in the path of the standard M mode study, further techniques have been developed with this study and successfully used particularly to detect abnormal anterior wall motion in patients with anterior infarction. These techniques usually involve further lateral exploration of the left precordium at multiple sites in a search for a “window” through which the anterior left ventricular wall can be directly imaged. When this approachl:! is used, absent or paradoxical anterior left ventricular wall motion is a frequent finding in patients with anterior infarction, whereas anterior wall motion abnormalities are rarely seen in patients with inferior infarction. Dynamic changes in wall thickness: Because ab-
Normal Septal amplitude Range (cm) Mean % decreased % increased Posterior wall amplitude Range (cm) Mean % decreased % increased l
Site of Infarction Anterior Inferior
0.3-0.8
O-O.6
O-2.0
0.63 -
0.08 80% 0%
0.81
0.8-2.1 1.40 0% 16%
O-l.7 0.66 57% 7%
0.8-1.6 1.29 -
393;
Adapted from Cotya et al. 11
normalities of wall motion, particularly of the interventricular septum, are nonspecific findings and occur in patients with other conditions, notably right ventricular volume overload and chronic cardiomyopathy, closer scrutiny has been devoted to other local properties of the myocardium in the affected region in patients with acute infarction. In this regard, dynamic changes in wall thickness in transition from diastole to systole have received a great deal of attention as a manifestation of impaired regional function in contraction caused by myocardial ischemia. In a series of 40 patients with acute myocardial infarction (composed of equal numbers with anterior and inferior infarcts),13 18 of the 20 with an anterior infarct had abnormally decreased septal systolic thickening, 19 had abnormally decreased septal motion and 18 had both decreased septal thickening and abnormal wall motion. Interestingly, 11 of these patients had systolic septal thinning. Of the 20 patients with inferior infarction, 65 percent had abnormally decreased posterior wall thickening, 18 abnormally decreased posterior wall motion and 13 both the thickening and motion abnormalities. Systolic thinning of the posterior wall was infrequently recorded, being seen in only one patient. Abnormalities of wall motion and systolic thickening can be seen, although less frequently, in patients with chronic coronary artery disease, particularly if there has been an antecedent myocardial infarction. However, systolic thinning is highly suggestive of acute injury since it is an unusual finding outside of the setting of acute myocardial infarction. Changes in myocardial scarring: Further observations have resulted in the emergence of criteria that identify myocardial scar tissue as a residual of previous myocardial infarction. In a series of 182 patients Rasmussen et a1.14 showed that scar tissue was very likely to be present if (1) the myocardium was less than 7 mm thick in diastole and more echo-producing than the adjacent or opposing wall, or (2) an area of myocardium was 30 percent less thick than an adjacent area in the same scan (Fig. 10 These observations were confirmed in all instances by surgical observations and in 34 cases by histologic examination of either autopsy or surgical
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FIGURE 2. Epicardial and endocardial diastolic outlines of short axis views of the left ventricle at the level of the papillary muscles in a patient with an acute transmural anterior infarction and evidence of infarct expansion over the course of serial studies. The development of regional dilatation and thinning in the infarcted areas is apparent from the tracing of day 7. (Reprinted by permission, from Eaton et al.“)
PL
resection specimens. Ninety percent of these patients had a clinical history of antecedent myocardial infarction and most had consistent electrocardiographic findings as well. Two Dimensional Echocardiography Acute myocardial infarction: Two dimensional echocardiography offers the ability to evaluate regional abnormalities of myocardial motion with much greater facility than M mode examination since the field of the examination is not restricted to the narrow M mode beam and the spatial orientation of the tomographic sections can be appreciated. As early as 1977 Kisslo et a1.15 reported that two dimensional echocardiograms lent themselves as readily to qualitative examination of regional wall motion abnormalities as did left ventricular cineangiograms. More recently several observers have looked specifically at two dimensional echocardiography for its ability to detect wall motion abnormalities that are associated with acute myocardial infarction. Most observers have depended on one or more short axis views that allow evaluation of departures from the normally concentric contraction of the left ventricle around its perimeter. Heger et a1.r6 devised a nine segment subdivision of the left ventricle that included anterior, medial, posterior and lateral quadrants at the mitral and papillary muscle levels and an apical segment recorded by placing the transducer directly over the apex and obtaining a long axis scan. Complete studies, allowing evaluation of these nine segments, was accomplished in 37 of 44 attempts. Nineteen of 20 patients with inferior infarction had asynergy in posterior segments, 14 patients with anterior infarction had asynergy in anterior segments and 3 patients with both anterior and inferior infarction had appropriately localized wall motion abnormalities. In four patients pathologic lo-
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end diastole end systole
FIGURE 3. Schematic drawing illustrating short axis views of the left ventricle obtained with two dimensional echocardiography. The insert shows diastolic and systolic outlines of the left ventricle at either level as a pair of outlines that approximate concentric circles. The axis system used for analysis is superimposed. Regional function of the left ventricle can be characterized with use of either segmental areas or chords (see text). A = anterior; AL = anterolateral; AS = anteroseptal; L = lateral; P = posterior; PL = posterolateral; PS = posteroseptal; S = septal.
calization of infarction corresponded to the asynergic areas detected on two dimensional echocardiography, thus confirming that this technique is a reliable method of detecting and localizing regional contraction abnormalities that occur in acute myocardial infarction. Eaton et a1.17 performed serial two dimensional echocardiographic examinations in 28 patients during the first 2 weeks after myocardial infarction. Diastolic short axis two dimensional echocardiograms at the level of the papillary muscle tips were evaluated serially in this study in patients whose first echocardiogram had been obtained within 60 hours of the acute event. Endocardial and epicardial outlines were traced; segment lengths and wall thickness were calculated using a computer-aided semiautomated contouring system. Eight of the patients showed evidence of infarct expansion with disproportionate transmural thinning of the infarcted zone and associated left ventricular dilatation, whereas the remaining 20 patients had no evidence of these findings. Patients with anterior and anteroseptal infarction seemed particularly prone to infarct expansion (Fig. 2). At 8 weeks after infarction 4 of the 8 patients who showed infarct expansion had died, whereas all 20 patients without infarct expansion were
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living. On the basis of this study these investigators contended that infarct expansion, rather than further extension of the’ischemic process with further necrosis of myocardial tissue, might play a more important role than had previously been appreciated in patients surviving acute myocardial infarction. This study demonstrates that two dimensional echocardiography can be used as an indicator of topographic changes that occur in the evolution of an acute myocardial infarction and may have considerable clinical importance, not only in assessing survival but potentially in assessing interventions that may influence survival of such patients. Remote myocardia.1 infarction: Using a computer-aided approach in our laboratory, wel*Jg have also been interested with the ability of two-dimensional echocardiography to define and quantify regional wall motion abnormalities. We obtained cross-sectional short axis views of the left ventricle in a series of normal volunteers, patients with coronary artery disease without remote myocardlial infarction as well as patients with a prior myocardial infarction confirmed by abnormal Q waves in the electrocardiogram. End-diastolic short axis outlines of the ventricle at both mitral valve and papillary muscle levels were traced with a light pen digitizing system using the onset of the electrocardiographic QRS complex as a marker of end-diastole. Similarly, end-systolic frames were traced using the first high frequency component of the second heart sound as an indicator of end systole. At each tomographic level the mid point of the interventricular septum on the left ventricular endocardia!l surface was identified by the observer. From this starting point an initial axis (Fig. 3, axis SL) was constructed using a computer algorithm to that point on the lateral left ventricular wall that allowed the diastolic image to be divided into anterior and posterior halves of equal area. The mid point of this initial diastolic axis is systematically bisected by a series of radii 45” apart. This, then creates a diastolic radial axis system of eight ch.ords and their enclosed areas. Maintaining this reference system fixed in space and superimposing the systolic endocardial outline permits segmental evaluation of the ventricle, either by chordal shortening or regional area shrinkage. Thirty-two patients were evaluated once the normal range of contraction was established from 10 normal volunteers. Twenty patients with coronary artery disease but without remote infarction had no difference in contraction pattern from that of the volunteers. Twelve patients had remote transmural infarction evidenced by abnormal Q waves. Six patients with anterior infarction showed impaired regional motion in anterior and anteroseptal regions, and six patients with inferior infarction showed impaired motion in posterior and lateral regions (Fig. 4 and 5). In conducting a parallel computer analysis of angiocardiograms in these 12 patients, two dimensional echocardiography proved as sensitive as angiography for detection of regional contraction defects: Each technique identified 10 of 12 patients correctly. These further observations confirm that two dimensional echocardiography can be used systematically to study regional wall motion abnor-
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malities in patients with remote as well as acute myocardial infarction. Surgical implications: The use of two dimensional echocardiography to characterize regional areas of abnormal contraction is in its nascent stage. Information gleaned from M mode techniques such as diastolic thinning, failure of appropriate systolic thickening and change of echocardiographic character within the wall producing acoustically “hard” areas, have only begun to be explored by two dimensional echocardiography (Fig. 6). The technique ultimately has the potential not only for identifying the presence of wall motion abnormalities, but also for quantifying their extent on a global basis and for assessing their reversibility. Thus, the unusually thinned echo-dense noncontractile region, which is probably composed of scar tissue, is unlikely to have its function restored by bypass surgery, whereas a poorly contracting area of myocardium of normal diastolic thickness and wall character may indeed recover its function after the blood supply is restored. The potential of echocardiography in this regard will be the subject of many further explorations within the next few years.
Special Complications of Myocardial Infarction Ventricular aneurysm: Ventricular aneurysm (defined as an abnormal diastolic outpouching of the normal ventricular cavity) has long been recognized by M mode echocardiography. In a typical examination with the transducer in a standard location, a scan of the left ventricle from base to apex shows that the cavity expands or fails to taper as the region of the papillary muscles is approached. This finding is highly associated with the presence of left ventricular aneurysm. Many, but not all, left ventricular aneurysms fall within the path of a standard M mode scan. Thus, Weyman et a120 noted that in a series of 31 patients with angiographitally proved left ventricular aneurysm, two dimensional echocardiography detected 100 percent of these defects whereas M mode studies were successful in detecting this abnormality 47 percent of the time. Typical examples of left ventricular aneurysm detected with two dimensional echocardiographic examinations are shown in Figure 7. Ventricular pseudoaneurysm: In contrast to a true left ventricular aneurysms which is an abnormal outpouching of the infarcted left ventricular myocardium, a false aneurysm consists of cavitated clots that communicate with the left ventricular body through an area of myocardial rupture. In the patient who has not had antecedent cardiac trauma or surgery, myocardial infarction is the leading cause of pseudoaneurysm formation. Unlike the orifice to a true aneurysm, which is wide and patent, the orifice to a false aneurysm is narrow. By virtue of this anatomic feature a false aneurysm is often detectable by echocardiography. Although the narrow orifice leading to the false aneurysm cavity was originally reported in M mode echocardiographic studies, two dimensional echocardiography greatly facilitates its recognition22*23 (Fig. 8). Detection of a false aneurysm is more than an academic question
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FIGURE 4. End-diastolicand end-systolic short axis images and computer regenerated outlines from a normal subject (top), a patient with anteroseptal myocardial infarction (middle) and a patient with inferior myocardial infarction (bottom).
SEGMENT FIGURE 5. Plots of regional area shrinkage in 20 patients with no antecedent myocardial infarction and in two patient subgroups who had anterior or inferior myocardial infarction (see text). Abbreviations as in Figure 3.
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because a false aneurysm is prone to fatal myocardial rupture, a complication very rarely encountered in a true left ventricular aneurysm. Moreover, it is readily amenable to surgery, which remains the treatment of choice. Thus, echocardi.ography, particularly with the two dimensional technique, is a key examination in the patient with an abnormally bulging radiographic cardiac silhouette after myocardial infarction. Because the
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primary clue to distinguishing true and false aneurysm depends on recognition of the narrowed orifice, a false aneurysm will not be suspected using standard chest roentgenograms. Papillary muscle dysfunction and rupture: Mitral regurgitation may arise from anatomic or functional derangements of the papillary muscles. Papillary muscle dysfunction is most commonly caused by ischemia or
FIGURE 6. Short axis view oi the left ventricle shown schematically and the actual image showing unusually hard echoes from the posteroseptal region in a patient with remote inferior myocardial infarction. These hard echoes correspond to the echo densities previously reported on M mode echocardiography. It would be difficult to gain access to the echodense region in this figure with the standard M mode approach. LV = left ventricle; PM = papillary muscles.
FIGURE 7. Examples of left ventricular aneurysm. Left, aneurysm of the interventricular septum in a patient with remote anterior myocardiil infarction. This type of aneurysm is more likely to be missed on M mode scanning than is an apical aneurysm. Right, apical left ventricular aneurysm seen with an apical view on two dimensional echocardiography. The cloud of echoes within the aneurysmal chamber suggests a possible left ventricular thrombus. A = aneurysm; LA = atrium; LV = left ventricle; MV = mitral valve; RV = right ventricle.
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infarction which leads to asynergic contraction of the muscles, or by ventricular dilatation or aneurysm that produces sufficient malalignment to result in mitral regurgitation. In a series of 14 patients with papillary muscle dysfunctionz4 two abnormal patterns of mitral valve closure were identified with two dimensional echocardiography: Three patients showed mitral valve prolapse associated with inferoposterior wall akinesia and increased tissue echo density consistent with papillary muscle fibrosis; nine patients with ventricular enlargement or aneurysm had apically displaced mitral leaflet coaptation, and the remaining two patients had both of these patterns. Papillary muscle rupture is a devastating complication of acute myocardial infarction. It produces mitral regurgitation, which acutely imposes a volume overload on the left heart chambers. The magnitude of the vol-
ume load depends on the exact location of papillary muscle rupture. It is usually suspected from the sudden appearance of a loud systolic murmur, which may be impossible to distinguish at the bedside from the murmur of a ruptured interventricular septum (see later). If a head of a papillary muscle rather than an entire papillary muscle ruptures, it is possible that the patient can survive and undergo diagnostic evaluation that will allow its detection. As with ruptured chordae tendineae, this condition will lead to a flail anterior or posterior mitral leaflet; a flail valve can be readily appreciated on two dimensional echocardiography because one of the mitral leaflets swings freely into the left atria1 cavity during ventricular systole25 (Fig. 9). Ventricular septal rupture: A ruptured flap of interventricular septum, showing an unusual pattern of motion, has been detected with M mode echocardiography in a patient with acute anteroseptal myocardial infarction.26 Patients with this problem have also been reported to have, on average, an enlarged right ventricular internal dimension.27 Direct visualization of loss of septal continuity is unlikely to be detected with M mode echocardiography because the septal rent may be irregular and obliquely located relative to the echographic beam passage from a parasternal or precordial transducer location. Nevertheless one such case has been reported. 2s In one instance2g of a patient with documented postinfarction ventricular septal defect, the septum appeared split into two layers separated by an echo-free zone, which represented an obliquely passing communication from the left to the right ventricle. Two dimensional echocardiography allows more complete inspection of the interventricular septum. With use of an apical four chamber view in which the length of the septum was delineated, three consecutive patients with ventricular septal rupture in the course of acute anterior infarction were identified.30 In two of the three this was imaged as an oblique rent from the distal left ventricle to the proximal right ventricle, while in the third patient a large orifice was evident in the distal septum. Although postinfarction ventricular septal defect has not been frequently reported, it is anticipated that additional reports will appear as two dimensional equipment becomes more widely used in coronary care units and greater sophistication develops in exploring the integrity of the interventricular septum from different transducer locations. Other complications of myocardial infarction: Two dimensional echocardiography offers the potential for making diagnostic decisions regarding other complications of myocardial infarction. Clots can be detected in relation to immobile areas of infarcted myocardial wall; pericardial effusion can be documented in the postinfarction patient with pericarditis. The latter is one of the applications in which M mode echocardiography is still quite valuable. In patients with inferior myocardial infarction in whom a pericardial friction rub and elevated neck veins develop, the distinction between right ventricular infarction and postinfarction pericarditis with cardiac tamponade accounting for
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FffilJRE 8. Top, two dimensional echocardiogram in apical two chamber projection of a patient with a pseudoaneurysm of the left ventricle. Rottom, schematic drawing of the orientation of the cardiac chambers and the pseudoaneqsm (PA). Ao = aorta: I = inferior; LA = left atrium; LV = left ventricle; S = superior. (Figure kindly supplied by Dr. M. Kotler and reprinted from Catherwood et al.23 by permission of the American Heart Association, Inc.)
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impaired right ventricular filling can be aided by echocardiography. Not. all patients who manifest a pericardial friction rub in the course of myocardial infarction have significant pericardial effusion. In the absence of detectable effusion cardiac tamponade would be a very unlikely complication of acute myocardial infarction. Patients with. tamponade not only show signs of effusion, but also are very likely to show signs of right ventricular compression. In contrast, regional dilatation of the right ventricle has been reported in right ventricular infarction if the involved area is traversed by the echographic beam.2*1~32
Advantages and Limiitations of Two Dimensional Echocardiography in Myocardial Infarction Two dimensional echocardiography offers distinct advantages for evaluating myocardial structure and function in myocardial infarction not currently available by other methods. First and foremost, if offers the most comprehensive information of any noninvasive imaging technique. One can appreciate from a single bedside examination not only myocardial structure and func-
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tion, but also the area around the heart and the function of the cardiac valves. In addition, the resolution of detail obtainable with echocardiography is superior to that of any other noninvasive imaging modality. The relatively high degree of resolution is particularly useful in detecting special complications of infarction that can affect small and highly localized anatomic regions of the ventricle, such as papillary muscle dysfunction and formation of intramural thrombi. Another advantage of echocardiography in this setting is that it can be repeated, if necessary, multiple times on a daily basis without the concern of exposing the patient to ionizing radiation. The principal limitation of echocardiography is its inability to obtain high quality images more than 60 to 80 percent of the time, depending on the investigator and the patient population. Although this difficulty is in part being overcome through improved techniques of examination using different approaches to imaging of the heart, further development of instrumentation will be necessary to achieve a success rate with ultrasound comparable with that of radionuclide imaging techniques.
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Circulation 1979;60:531-8. 17. Eaton LW, Weiss JL, Bulkley BH, Garrison JB, Welsfeldl ML. Regional cardiic dilatation after acute rnyocardiil infarction. N Engl J Med 1979;300:57-62. 18. Parlsl AF, Moynlhan PF, Folland ED, Feldman CL. Assessment of regional wall motion in coronary artery disease by twodirnensional echocardiography. In: Lancee CT, ed. Echocardiology. The Hague: Martinus Nijhoff, 1979;125-9. 19. Moynlhan PF, Feldman CL, Parlsl AF. Comparison of methods for quantitative evaluation of left ventricular function with twodimensional echocardiography (abstr). Clin Res 1979;27:566A. 20. Weyman AE, Peskoe SM, Williams ES, Dillon JC, Felgenbaum H. Detection of left ventricular aneurysms by cross-sectional echocardiography. Circulation 1976;54:936-44. 21. Davidson KH, Parlsl AF, Harrlngton JJ, Barsamlan EM, Flshbeln MC. Pseudoaneurysms of the left ventricle: an unusual echocardiographic presentation. Ann Intern Med 1977;86:430-3. 22. Sears TD, Ong YS, Starke H, Forker AD. Left ventricular pseudoaneurysm identified by cross-sectional echocardiography. Ann Intern Med 1979;90:935-6. 23. Catherwood E, Mlntz GS, Kotler MN, Perry W. Two-dimensional echocardiographic differentiation of true and false ventricular aneurysms. Circulation, in press. 24. Dgawa S, Hubbard FE, Mardelll TJ, Drelfus LS. Cross-sectional echocardiographic spectrum of papillary muscle dysfunction. Am Heart J 1979;97:312-21. 25. Child JS, Skorton DJ, Taylor RD, Abbasl AS, Wong M, Shah PM. Cross-sectional and M-mode echocardiographic features of flail mitral leaflets (abstr). Am J Cardiol 1979;43:411. 26. DeJoseph RL, Seldes SF, Llndner A, Damato AN. Echocardio graphic findings of ventricular septal rupture in acute myocardial infarction. Am J Cardiol 1975:36:346-6. 27. Chandraratna PAN, Balacbandran PK, Shah PH, Hodges M. Echocardiographic observations on ventricular septal rupture complicating acute myocardial infarction. Circulation 1975;51: 506-10. 28. Kerln NZ, Edelstein J, DeRue RG. Ventricular septal defect complicating acute myocardial infarction. Chest 1976:70:5803. 29. Egeblad H, Haunso S. Echocardiographic findings in ventricular septal rupture and anterior wall aneurysm complicating myocardial infarction (abstr). Acta Medica Stand Suppl 1977;627:224. 30. Farcot JC, Bolsantl L, Rlgand M, Bardet J, Bourdarlas JP. Twodimensional echocardiographic visualization of ventricular septal rupture after acute myocardial infarction. Am J Cardiol 1980:45: 370-7. 31. Lorell B, Welnbach RC, Pohosl GM, Gold HK, et al. Right ventricular infarction: clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction. Am J Cardiol 1979;43: 465-71. 32. Elkayam U, Halprln SL, Frlshman W, Strom J, Cohen MN. Echocardiographic findingsJn cardiiic shock due to right ventricular myocardial infarction. Cath Cardiovasc Diag 1979;5:289-94.
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