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Acute inferior myocardial infarction complicated by rupture into the coronary sinus: Diagnosis by two-dimensional echocardiography
Acute Inferior Myocardial Infarction Complicated by Rupture into the Coronary Sinus: Diagnosis by Two-Dimensional Echocardiography Wilson Evans Kemp, Jr., MD, William R. Shipley, MD, and Benjamin F. Byrd III, MD, Nashville, Tennessee
Ventricular rupture is a catastrophic, often fatal complication o f myocardial infarction. We present a unique case o f left ventricular rupture into the coronary sinus that was diagnosed by two-dimensional Doppler echocardiography in a patient with a recent inferior myo-
cardial infarction. The echocardiographic findings essential to diagnosis were subsequently confirmed at autopsy and are reviewed in detail. (J Am Soc Echocardiogr 1996;9:901-5.)
S u d d e n h e m o d y n a m i c decompensafion in the setring o f a recent myocardial infarction is often due to left ventricular, septal, or papillary muscle rupture. The exact cause must be determined immediately so that life-saving interventions may be undertaken. Ventricular free wall rupture complicates myocardial infarction in about 8% (range, 4% to 24%) o f all cases. 1 It is the third m o s t c o m m o n cause o f early post_infarction death after arrhythmia and cardiogenic shock, *'2 accounting for as m a n y as 31% o f such deaths, a Rapid diagnosis is critical because surgical repair can be successful. 4 e Two-dimensional D o p p ler echocardiography provides an excellent means for detecting ventricular rupture and allowing patients to u n d e r g o u r g e n t repair.
tion. Five days before admission at our institution, he was admitted to an outside hospital with prolonged chest pain. His electrocardiogram was 100% paced, and myocardial infarction was diagnosed when the creatinine phosphokinase level peaked at 628 units/L. Given his advanced age, hemodynamic stability, and comorbidities, it was decided to manage him medically. He was discharged 4 days later after an uncomplicated course but had recurrent chest pain the following day. On admission to our hospital, he complained of chest pain but was hemodynamically stable. His electrocardiogram was again 100% paced and he was taken emergently to the cardiac catheterization laboratory. Severe native vessel disease was found, with a patent, mildly diseased left internal mammary artery graft to the left anterior descending artery, a moderately diseased SVG to the second obtuse marginal artery, and patent SVG to the PDA. However, severe native right coronary artery disease just proximal and distal to the PDA vein graft insertion allowed very little flow to the inferior wall. This latter lesion was believed to be responsible for the acute event and no acute intervention was attempted. Several hours after catheterization, the patient became acutely dyspneic and hypotensive. An emergent two-dimensional echocardiogram revealed moderate aortic valve sclerosis, mild to moderate mitral and tricuspid valve regurgitation, and basal and midinferior and inferoseptal wall akinesis. There was abnormal septal motion compatible with elevated right ventricular end-diastolic pressure and sequential atrioventricular right-sided heart pacing. The left ventricular cavity was mildly enlarged with an estimated ejection fraction of 35% to 45%. The right ventricle was mildly enlarged with severe hypokinesis o f the inferior and lateral walls and mild hypoldnesis of the anterior wall consistent with global right ventricular systolic dysfunction and possible infarction. A well-defined inferior wall rupture was noted, with color Doppler flow passing from the left ventricle into the coronary sinus, the right atrium, and the
CASE R E P O R T An 82-year-old white man underwent coronary artery bypass grafting in 1980 with a left internal mammary artery to the left anterior descending artery, saphenous vein graft (SVG) to the second obtuse marginal artery, and SVG to the posterior descending artery (PDA). A dualchamber pacemaker was placed in ]985. Cardiac catheterization at the time of pacemaker placement revealed patent bypass grafts and a left ventricular ejection fraction of 35%. He also had a history of reactive airway disease, chronic renal insufficiency, and esophageal stricture requiring dila-
From the Division of Cardiology, Vanderbilt University School of Medicine. Reprint requests: W. Evans Kemp, Jr., MD, Division of Cardiology, 315 MRBII, Vanderbilt University School of Medicine, Nashville, TN 37232. Copyright © 1996 by the American Society of Echocardiography. 0894-7317/96 $5.00 + 0 27/4/72615
901
902
Kemp, Shipley, and Byrd
}'ournaIof the AmericanSocietyof Echocardiography November-December 1996
Figure 1 Parasternal long-axis view demonstrates a defect in inferopostcrior wall (A) (arrow) and as noted by the large arrow with color Doppler flow into the dilated coronary sinus (B). (LA, Left atrium; LV,, left ventricle; RA, right atrium; RV,, right ventricle; CS, coronary sinus; Ao, aorta.)
Journal of the AmericanSocietyof Echocardiography Volume 9 Number 6
Kemp, Shiptey, and Byrd
Figure 2 Color Doppler apical four-chamber view with posterior angulation demonstrates dramatic left-to-right shunting through the coronary sinus into the right atrium (arrow). (Abbreviations are given in Figure 1.)
Figure 3 Continuous-wave Dopplcr spcctrum dcmonstrates a 40 mm Hg gradient during systole and carly diastolc between coronary sinus and right atrium, consistent with left vcntricular rupture into coronary sinus.
903
Journal of the American Society of Echocardiography
904
Kemp, Shipley, and Byrd
November-December 1996
....~ f ~%IQ~¸
!
Figure 4 Autopsy specimen of heart viewed from opened left ventricle reveals a linear, circumferentially oriented defect in the inferopostcrior wall just below the posterior mitral valve anulus and leaflet. The mitral valve leaflet is rctracted into left atrium for bctter visualization. A small tube has been placed through the defect to demonstrate continuity with the coronary sinus (as seen in Figure 5).
Figure 5 Autopsy specimen of heart viewed from posterior base. The coronary sinus has been unroofed near its entry into the right atrium, and a defect is apparent in its anterior wall. A small tube has been passed through the defect, demonstrating continuity with the left ventricle (see Figure 4). A pulmonary artery catheter and pacing wire are seen within the right atrium.
right ventricle (Figures 1 and 2). Continuous-wave Doppler echocardiography revealed a 40 mm H g gradient during systole and early diastole between the coronary sinus and right atrium (Figure 3). No pericardial effusion was seen, both the coronary sinus and inferior vena cava (IVC) were dilated, and right atrial size was normal. The patient was taken emcrgently back to the cardiac catheterization laboratory. Right-sided heart catheterization revealed a significant oxygen stepup between the IVC and right atrium, as well as right atrimn and pulmonary artery. Single IVC, right atrial, and pulmonary artery oxygcn saturations were 39%, 63%, and 82%, respectively. Mean right atrial pressure was 22 mm Hg with V waves to 32 mm Hg, and the right ventricular pressure was 5 5 / 2 2 mm Hg. The patient developed pulseless electrical activity and could not be resuscitated in the catheterization laboratory. At autopsy a linear myocardial tear was found along the posterior vcntricular aspect of the mitral anulus. The disruption was 3 cm long, tapering to 8 mm at its entry into the coronary sinus 2 cm proximal to the right atrium (Figures 4 and S). This tear represented ventricular rupture within a region of an acute (6 to 12 hours duration) and
subacute (scveral days' duration) basal inferior wall infarction. An old right ventricular infarction was noted. No atrial or ventricular septal defect was noted. All native coronary arteries were occluded with patent bypass grafts.
DISCUSSION
In this case, left ventricular rupture into the coronary sinus resulted in dramatic left-to-right shunting as demonstrated by two-dimensional Doppler echocardiography and confirmed by catheterization and autopsy. This complication o f myocardial infarction has n o t been reported previously. Cardiac rupture occurs m o s t often within 7 days after infarction, with a peak incidence at days 0 to 5. 7'~ This patient had clinical and pathologic evidence o f subacute infarction 5 days before the acute infarction that resulted in ventricular rupture. Factors increasing the risk o f rupture after infarction include first infarction or extension o f a recent infarc-
~lournalof the AmericanSocietyof Echocardiography Kemp, Shipley, and Byrd
Volume 9 Number 6
tion, age greater than 60 years, female sex, and the use o f nonsteroidal inflammatory agents or steroids. H y p e r t e n s i o n has been suggested as a possible risk factor. Cardiac rupture m o s t c o m m o n l y involves the free wall, with rupture o f the septum and papillary muscle being less c o m m o n . T h e anterolateral wall o f the left ventricle is the m o s t c o m m o n site, with middle segments involved m o r e often than apical or basal segments. 8 As d e m o n s t r a t e d by this patient, other segments m a y rupture, leading to the same fatal consequences. This patient's advanced age m u s t have contributed to the rupture o f the infarcted inferior wall at its a t t a c h m e n t along the mitral anulus to the cardiac fibrous skeleton. Cardiac rupture m a y occur n o t abruptly but as a slow dissection o f b l o o d t h r o u g h the myocardium. With increased intramural pressure in systole, the dissection propagates and enlarges the defect. 9 Indeed, the endocardial opening is usually smaller than the epicardial defect, which ranges from 2 to 3 cm in length. 1° This early dissection m a y be d e m o n strated by two-dimensional echocardiography as an intramural h e m a t o m a with pericardial effusion or a p s e u d o a n e u r y s m , 1~ and early detection m a y allow e m e r g e n t repair. D o p p l e r echocardiography m a y demonstrate flow t h r o u g h this defect, strengthening the diagnosis. Ifpericardial fluid is also d e m o n s t r a t e d by echocardiography, e m e r g e n t pericardiocentesis should be p e r f o r m e d . I f the pericardial fluid is bloody, e m e r g e n t surgery should be undertaken. Two-dimensional echocardi0graphy allows distinction o f p s e u d o a n e u r y s m s from true aneurysms, In p s e u d o a n e u r y s m s there is a sudden discontinuity o f the ventricular free wall and a n a r r o w " n e c k " leading into a globoid fundus, whereas the opening into a true aneurysm is w i d e ) la2 This patient had no pericardial effusion or p s e u d o a n e u r y s m because the rupture entered the c o r o n a r y sinus rather than the pericardial space. Acute segmental wall dilation with thinning, t h o u g h t to represent infarct expansion, has also been described as an echocardiographic feature o f i m p e n d i n g free wall rupture 13 but was n o t present in this case. A l t h o u g h it is generally fatal, there are n u m e r o u s cases o f successful repair o f frec wall rupture and survival. 6a4 Survival depends on early detection and p r o m p t repair. In one large review, 84% o f 70 patients with free wall rupture after myocardial infarction had at least two o f the following three symptoms: pericardial pain, repetitive emesis, and restlessness or agitation. Only three o f 100 patients w i t h o u t
905
rupture manifest two o f these three symptoms.14 T h e unusual echocardiographic findings and absence o f pericardial effusion in this previously h e m o d y n a m i cally stable patient only recently returned from coronary arteriography led to his return to the cardiac catheterization laboratory. H o w e v e r , w h e n patients show the typical s y m p t o m s and echocardiographic signs o f cardiac rupture, surgical consultation should be obtained immediately. 1
REFERENCES
1. Bates RJ, Beutler S, Resnekov L, Anagnostopulos CE. Cardiac rupture-challenge in diagnosis and management. Am J Cardiol 1977;40:429-37. 2. Schuster EH, Bulkey BH. Expansion of transmural myocardial infarction: a pathophysiologic factor in cardiac rupture. Circulation 1979;60:1532-8. 3. Reddy SG, Roberts WC. Frequen W of rupture of the left ventricular free wall or ventricular septum among necropsy cases of fatal acute myocardial infarction since introduction of coronary care units. Am J Cardiol 1989;63:906-11. 4. Kitamura S, Mendex A, Kay J. Ventricular septal defect following myocardial infarction. I Thorac Cardiovasc Surg 1971;61:186-99. 5. Kopf G, Meshkov A, Laks H, Hammond G, Geha A. Changing patterns in the surgical management of ventricular septal rupture after acute myocardial infarction. Am J Surg 1982; 143:465-72. 6. Sinikk PS, Muller JE, Stone PH, et al. Ventricular septal and free wall rupture complicating acute myocardial infarction: experience in the Multicenter Investigation of Limitation of Infarct Size. Am Heart J 1989;117:809-16. 7. Rasmusseen S, Leth A, Kjoller E, Pedersen A. Cardiac rupture in acute myocardial infarction: a rex,iew of 72 consecutive cases. Acta Med Scand 1979;205:11-6. 8. Batts KP, Ackermann DM, Edwards WD. Postinfarction rupture of the left venn'icular free wall: clinicopathologic correlates in 100 consecutive autopsy cases. Hum Pathol 1990;21: 530-5. 9. Sarkar A, Krupadev HL. Myocardial rupture in acute myocardial infarction: case report and review of the literature. Heart Lung 1983;12:88-91. 10. Wessler S, Zoll PM, Schlesingrer MI. The pathogenesis of spontaneous rupture. Circulation ]952;6:334-51. 11. Catherwood E, Mintz GS, Kotler MN, Parry WR, Segal BL. Two-dimensional echocardiographic recognition of left ventricular psendoaneurysm. Circulation 1980;62:294-303. 12. Reeder GS, Seward JB, Tajik AJ. The role of two-dimensional echocardiography in coronary artery disease: a critical appraisal. Mayo Clin Proc 1982;57:247-58. 13. Hermoni Y, Engel I~J.Two-dimensional echocardiography in cardiac rupture. Am J Cardiol 1986;57:180-1. 14. Oliva PB, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. Am Coil Cardiol 1993;22:720-6.
Ventricular rupture is a catastrophic, often fatal complication o f myocardial infarction. We present a unique case o f left ventricular rupture into the coronary sinus that was diagnosed by two-dimensional Doppler echocardiography in a patient with a recent inferior myo-
cardial infarction. The echocardiographic findings essential to diagnosis were subsequently confirmed at autopsy and are reviewed in detail. (J Am Soc Echocardiogr 1996;9:901-5.)
S u d d e n h e m o d y n a m i c decompensafion in the setring o f a recent myocardial infarction is often due to left ventricular, septal, or papillary muscle rupture. The exact cause must be determined immediately so that life-saving interventions may be undertaken. Ventricular free wall rupture complicates myocardial infarction in about 8% (range, 4% to 24%) o f all cases. 1 It is the third m o s t c o m m o n cause o f early post_infarction death after arrhythmia and cardiogenic shock, *'2 accounting for as m a n y as 31% o f such deaths, a Rapid diagnosis is critical because surgical repair can be successful. 4 e Two-dimensional D o p p ler echocardiography provides an excellent means for detecting ventricular rupture and allowing patients to u n d e r g o u r g e n t repair.
tion. Five days before admission at our institution, he was admitted to an outside hospital with prolonged chest pain. His electrocardiogram was 100% paced, and myocardial infarction was diagnosed when the creatinine phosphokinase level peaked at 628 units/L. Given his advanced age, hemodynamic stability, and comorbidities, it was decided to manage him medically. He was discharged 4 days later after an uncomplicated course but had recurrent chest pain the following day. On admission to our hospital, he complained of chest pain but was hemodynamically stable. His electrocardiogram was again 100% paced and he was taken emergently to the cardiac catheterization laboratory. Severe native vessel disease was found, with a patent, mildly diseased left internal mammary artery graft to the left anterior descending artery, a moderately diseased SVG to the second obtuse marginal artery, and patent SVG to the PDA. However, severe native right coronary artery disease just proximal and distal to the PDA vein graft insertion allowed very little flow to the inferior wall. This latter lesion was believed to be responsible for the acute event and no acute intervention was attempted. Several hours after catheterization, the patient became acutely dyspneic and hypotensive. An emergent two-dimensional echocardiogram revealed moderate aortic valve sclerosis, mild to moderate mitral and tricuspid valve regurgitation, and basal and midinferior and inferoseptal wall akinesis. There was abnormal septal motion compatible with elevated right ventricular end-diastolic pressure and sequential atrioventricular right-sided heart pacing. The left ventricular cavity was mildly enlarged with an estimated ejection fraction of 35% to 45%. The right ventricle was mildly enlarged with severe hypokinesis o f the inferior and lateral walls and mild hypoldnesis of the anterior wall consistent with global right ventricular systolic dysfunction and possible infarction. A well-defined inferior wall rupture was noted, with color Doppler flow passing from the left ventricle into the coronary sinus, the right atrium, and the
CASE R E P O R T An 82-year-old white man underwent coronary artery bypass grafting in 1980 with a left internal mammary artery to the left anterior descending artery, saphenous vein graft (SVG) to the second obtuse marginal artery, and SVG to the posterior descending artery (PDA). A dualchamber pacemaker was placed in ]985. Cardiac catheterization at the time of pacemaker placement revealed patent bypass grafts and a left ventricular ejection fraction of 35%. He also had a history of reactive airway disease, chronic renal insufficiency, and esophageal stricture requiring dila-
From the Division of Cardiology, Vanderbilt University School of Medicine. Reprint requests: W. Evans Kemp, Jr., MD, Division of Cardiology, 315 MRBII, Vanderbilt University School of Medicine, Nashville, TN 37232. Copyright © 1996 by the American Society of Echocardiography. 0894-7317/96 $5.00 + 0 27/4/72615
901
902
Kemp, Shipley, and Byrd
}'ournaIof the AmericanSocietyof Echocardiography November-December 1996
Figure 1 Parasternal long-axis view demonstrates a defect in inferopostcrior wall (A) (arrow) and as noted by the large arrow with color Doppler flow into the dilated coronary sinus (B). (LA, Left atrium; LV,, left ventricle; RA, right atrium; RV,, right ventricle; CS, coronary sinus; Ao, aorta.)
Journal of the AmericanSocietyof Echocardiography Volume 9 Number 6
Kemp, Shiptey, and Byrd
Figure 2 Color Doppler apical four-chamber view with posterior angulation demonstrates dramatic left-to-right shunting through the coronary sinus into the right atrium (arrow). (Abbreviations are given in Figure 1.)
Figure 3 Continuous-wave Dopplcr spcctrum dcmonstrates a 40 mm Hg gradient during systole and carly diastolc between coronary sinus and right atrium, consistent with left vcntricular rupture into coronary sinus.
903
Journal of the American Society of Echocardiography
904
Kemp, Shipley, and Byrd
November-December 1996
....~ f ~%IQ~¸
!
Figure 4 Autopsy specimen of heart viewed from opened left ventricle reveals a linear, circumferentially oriented defect in the inferopostcrior wall just below the posterior mitral valve anulus and leaflet. The mitral valve leaflet is rctracted into left atrium for bctter visualization. A small tube has been placed through the defect to demonstrate continuity with the coronary sinus (as seen in Figure 5).
Figure 5 Autopsy specimen of heart viewed from posterior base. The coronary sinus has been unroofed near its entry into the right atrium, and a defect is apparent in its anterior wall. A small tube has been passed through the defect, demonstrating continuity with the left ventricle (see Figure 4). A pulmonary artery catheter and pacing wire are seen within the right atrium.
right ventricle (Figures 1 and 2). Continuous-wave Doppler echocardiography revealed a 40 mm H g gradient during systole and early diastole between the coronary sinus and right atrium (Figure 3). No pericardial effusion was seen, both the coronary sinus and inferior vena cava (IVC) were dilated, and right atrial size was normal. The patient was taken emcrgently back to the cardiac catheterization laboratory. Right-sided heart catheterization revealed a significant oxygen stepup between the IVC and right atrium, as well as right atrimn and pulmonary artery. Single IVC, right atrial, and pulmonary artery oxygcn saturations were 39%, 63%, and 82%, respectively. Mean right atrial pressure was 22 mm Hg with V waves to 32 mm Hg, and the right ventricular pressure was 5 5 / 2 2 mm Hg. The patient developed pulseless electrical activity and could not be resuscitated in the catheterization laboratory. At autopsy a linear myocardial tear was found along the posterior vcntricular aspect of the mitral anulus. The disruption was 3 cm long, tapering to 8 mm at its entry into the coronary sinus 2 cm proximal to the right atrium (Figures 4 and S). This tear represented ventricular rupture within a region of an acute (6 to 12 hours duration) and
subacute (scveral days' duration) basal inferior wall infarction. An old right ventricular infarction was noted. No atrial or ventricular septal defect was noted. All native coronary arteries were occluded with patent bypass grafts.
DISCUSSION
In this case, left ventricular rupture into the coronary sinus resulted in dramatic left-to-right shunting as demonstrated by two-dimensional Doppler echocardiography and confirmed by catheterization and autopsy. This complication o f myocardial infarction has n o t been reported previously. Cardiac rupture occurs m o s t often within 7 days after infarction, with a peak incidence at days 0 to 5. 7'~ This patient had clinical and pathologic evidence o f subacute infarction 5 days before the acute infarction that resulted in ventricular rupture. Factors increasing the risk o f rupture after infarction include first infarction or extension o f a recent infarc-
~lournalof the AmericanSocietyof Echocardiography Kemp, Shipley, and Byrd
Volume 9 Number 6
tion, age greater than 60 years, female sex, and the use o f nonsteroidal inflammatory agents or steroids. H y p e r t e n s i o n has been suggested as a possible risk factor. Cardiac rupture m o s t c o m m o n l y involves the free wall, with rupture o f the septum and papillary muscle being less c o m m o n . T h e anterolateral wall o f the left ventricle is the m o s t c o m m o n site, with middle segments involved m o r e often than apical or basal segments. 8 As d e m o n s t r a t e d by this patient, other segments m a y rupture, leading to the same fatal consequences. This patient's advanced age m u s t have contributed to the rupture o f the infarcted inferior wall at its a t t a c h m e n t along the mitral anulus to the cardiac fibrous skeleton. Cardiac rupture m a y occur n o t abruptly but as a slow dissection o f b l o o d t h r o u g h the myocardium. With increased intramural pressure in systole, the dissection propagates and enlarges the defect. 9 Indeed, the endocardial opening is usually smaller than the epicardial defect, which ranges from 2 to 3 cm in length. 1° This early dissection m a y be d e m o n strated by two-dimensional echocardiography as an intramural h e m a t o m a with pericardial effusion or a p s e u d o a n e u r y s m , 1~ and early detection m a y allow e m e r g e n t repair. D o p p l e r echocardiography m a y demonstrate flow t h r o u g h this defect, strengthening the diagnosis. Ifpericardial fluid is also d e m o n s t r a t e d by echocardiography, e m e r g e n t pericardiocentesis should be p e r f o r m e d . I f the pericardial fluid is bloody, e m e r g e n t surgery should be undertaken. Two-dimensional echocardi0graphy allows distinction o f p s e u d o a n e u r y s m s from true aneurysms, In p s e u d o a n e u r y s m s there is a sudden discontinuity o f the ventricular free wall and a n a r r o w " n e c k " leading into a globoid fundus, whereas the opening into a true aneurysm is w i d e ) la2 This patient had no pericardial effusion or p s e u d o a n e u r y s m because the rupture entered the c o r o n a r y sinus rather than the pericardial space. Acute segmental wall dilation with thinning, t h o u g h t to represent infarct expansion, has also been described as an echocardiographic feature o f i m p e n d i n g free wall rupture 13 but was n o t present in this case. A l t h o u g h it is generally fatal, there are n u m e r o u s cases o f successful repair o f frec wall rupture and survival. 6a4 Survival depends on early detection and p r o m p t repair. In one large review, 84% o f 70 patients with free wall rupture after myocardial infarction had at least two o f the following three symptoms: pericardial pain, repetitive emesis, and restlessness or agitation. Only three o f 100 patients w i t h o u t
905
rupture manifest two o f these three symptoms.14 T h e unusual echocardiographic findings and absence o f pericardial effusion in this previously h e m o d y n a m i cally stable patient only recently returned from coronary arteriography led to his return to the cardiac catheterization laboratory. H o w e v e r , w h e n patients show the typical s y m p t o m s and echocardiographic signs o f cardiac rupture, surgical consultation should be obtained immediately. 1
REFERENCES
1. Bates RJ, Beutler S, Resnekov L, Anagnostopulos CE. Cardiac rupture-challenge in diagnosis and management. Am J Cardiol 1977;40:429-37. 2. Schuster EH, Bulkey BH. Expansion of transmural myocardial infarction: a pathophysiologic factor in cardiac rupture. Circulation 1979;60:1532-8. 3. Reddy SG, Roberts WC. Frequen W of rupture of the left ventricular free wall or ventricular septum among necropsy cases of fatal acute myocardial infarction since introduction of coronary care units. Am J Cardiol 1989;63:906-11. 4. Kitamura S, Mendex A, Kay J. Ventricular septal defect following myocardial infarction. I Thorac Cardiovasc Surg 1971;61:186-99. 5. Kopf G, Meshkov A, Laks H, Hammond G, Geha A. Changing patterns in the surgical management of ventricular septal rupture after acute myocardial infarction. Am J Surg 1982; 143:465-72. 6. Sinikk PS, Muller JE, Stone PH, et al. Ventricular septal and free wall rupture complicating acute myocardial infarction: experience in the Multicenter Investigation of Limitation of Infarct Size. Am Heart J 1989;117:809-16. 7. Rasmusseen S, Leth A, Kjoller E, Pedersen A. Cardiac rupture in acute myocardial infarction: a rex,iew of 72 consecutive cases. Acta Med Scand 1979;205:11-6. 8. Batts KP, Ackermann DM, Edwards WD. Postinfarction rupture of the left venn'icular free wall: clinicopathologic correlates in 100 consecutive autopsy cases. Hum Pathol 1990;21: 530-5. 9. Sarkar A, Krupadev HL. Myocardial rupture in acute myocardial infarction: case report and review of the literature. Heart Lung 1983;12:88-91. 10. Wessler S, Zoll PM, Schlesingrer MI. The pathogenesis of spontaneous rupture. Circulation ]952;6:334-51. 11. Catherwood E, Mintz GS, Kotler MN, Parry WR, Segal BL. Two-dimensional echocardiographic recognition of left ventricular psendoaneurysm. Circulation 1980;62:294-303. 12. Reeder GS, Seward JB, Tajik AJ. The role of two-dimensional echocardiography in coronary artery disease: a critical appraisal. Mayo Clin Proc 1982;57:247-58. 13. Hermoni Y, Engel I~J.Two-dimensional echocardiography in cardiac rupture. Am J Cardiol 1986;57:180-1. 14. Oliva PB, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. Am Coil Cardiol 1993;22:720-6.