BRIEF COMMUNICATIONS
Biventricular apical rupture and formation of pseudoaneurysm: Unique flow patterns by Doppler and color flow imaging Ramesh C. Bansal, MD, Ramdas G. Pai, MD, Arthur J. Hauck, MD, and Dale M. Isaeff, MD Loma Linda, Calif.
Myocardial rupture accounts for 4 30 to 24 PC of in-hospital deaths from acute myocardial infarction.’ Rupture of the left ventricular free wall is generally fatal because of acute From the Departments of Cardiology Laboratory, Loma Linda University
and Pathology and Echocardiography Medical Center.
Reprint requests: Ramesh C. Bansal, Room 4420, Loma Linda University Loma Linda. CA 92354.
MD, Echocardiography Medical Center, 11234
4/4/37955
Laboratory, Anderson St..
cardiac tamponade. Some patients, however, may survive as a result of containment of rupture by overlying pericardium and the development of a pseudo or false aneurysm.2 A variety of techniques has been utilized for the diagnosis of pseudoaneurysm. These include radioisotope gated blood pool imaging,3 left ventricular angiography,4 and echo-Doppler techniques.5-g All the published echo-Doppler reports describe findings in patients with isolated left ventricular pseudoaneurysm. 5-g In this communication, we describe the unique color-flow and continuous wave Doppler findings in a patient with a postinfarction apical pseudoaneurysm that communicated with both ventricles through biventricular apical rupture. A 64-year-old white man with a previous history of hypertension and diabetes mellitus was hospitalized with increasing shortness of breath of 1 week’s duration. He denied history of chest pain or prior myocardial infarction. Findings on admission included: heart rate of 90 beats/min, blood pressure of 120/75 mm Hg, respiration 30/min, temperature 97.6” F, normal jugular venous pressure, lack of pulsus paradoxus, expiratory wheezing in the lung fields,
Fig. 1. Apical five-chamber two-dimensional echocardiographic views with color flow imaging. A bounded echo-free space or false aneurysm (FA) communicates with the left ventricular (LV) cavity through a small defect in the region of the apex (arrow). Panels A and D show the two-dimensional freeze frame and its schematic taken during presystole following atria1 contraction. Panels B and E are taken during systole, and panels C and F are taken during mid-diastole. Presystolic images show low-velocity red color flow from the left ventricle to the false aneurysm. Systolic images show high-velocity mosaic-colored flow from the left ventricle to the false aneurysm. The diastolic images show blue color reversed flow from the false aneurysm to the left ventricle. A small amount of pericardial effusion (PE) is noted around the right ventricle fl?V). AV, Aortic valve; LA, left atrium. 497
498
Brief
C‘ommunications
American
August 1992 Hem Journal
Fig. 2. Top panel shows the schematic of an apical five-chamber view with the left ventricular (LV) apical rupture site (arrow) and the false aneurysm (FA). Bottom panel shows the continuous wave Doppler flow velocity across the left ventricular rupture site. During presystole after atria1 {A) contraction, flow is toward the false aneurysm with a low velocity of 0.8 m/set. During systole (S), flow is from the left ventricle to the false aneurysm, but the velocity is increased to 2.5 m/set. During early to mid-diastole (D), the pressure gradient favors flow from the false aneurysm to the left ventricle, with an early peaking velocity of 1.3 m/set. AO, Aorta; LA, left atrium; PE, pericardial effusion; RV, right ventricle.
normal first and second heart sounds, and grade II/VI ejection systolic murmur at the base. The electrocardiogram showed ST segment elevation from leads Vz to VI;, findings consistent with recent anterior myocardial infarction. Highest creatine phosphokinase (CPK) level at the time of admission was 227, with a 5.8”;’ MB fraction. Coronary angiography showed proximal occlusion of the left anterior descending artery, and 90”; stenosis of superior and 80% stenosis of inferior obtuse marginal arteries. Left ventricular angiography was not performed. Two weeks after admission, he developed a loud grade III/VI systolic murmur in the apical region. Two-dimensional echocardiography revealed a large area of left ventricular apical dyskinesis and localized akinesis of the right ventricular apex. A small pericardial effusion was also noted (Fig. I). This study also revealed a bounded echo-free space around the cardiac apex and this space (false aneurysm) appeared to communicate with both ventricles through defects in the apex of each ventricle (Figs. 1 to 3). Color flow imaging across the left ventricular apical rupture site showed a
low-velocity red color flow from the left ventricle into the false aneurysm during presystole at the time of atria1 conflow t~raction (Fig. 1, A and D); high velocity mosaic-colored from the left ventricle into the false aneurysm during systole (Fig. 1, B and E); and blue color reversed flow from the false aneurysm into the left ventricle during early to mid diastole (Fig. 1, C and F). Continuous wave Doppler examination of this flow revealed a low velocity (0.8 m/set) flow from the left ventricle into the pseudoaneurysm during presystole and a high velocity flow (2.5 m/set) during systole. There was reverse flow in early to mid diastole of 1.3 m/set (Fig. 2). Using a simplified Bernoulli equation, instantaneous pressure gradients between the left ventricle and pseudoaneurysm can be calculated during different portions of the cardiac cycle. From the apical transducer position, posterior tilt of the transducer was helpful in visualization of the rupture site of the right ventricular apex. Color flow imaging and Doppler interrogation of this flow showed flow from the pseudoaneurysm into the right ventricle throughout the cardiac cycle (Fig. 3). The flow veloc-
Volume
124
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2
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Fig. 3. Top panel shows a schematic of the short-axis view at the apex of the heart by angulating the transducer posteriorly from the apical four-chamber recording position. A mosaic-colored flow pattern is noted from the false aneurysm (FA) to the right ventricular chamber (RV). Bottom panel shows the continuous wave Doppler flow pattern across the false aneurysm to right ventricular communication. The velocity of flow is lowest at 1 m/set in diastole CD), and increases slightly to 1.5 m/set during presystole, and markedly to 3.6 m/set during systole (S). A, Anterior; L, left; LV, left ventricle; P, posterior: R, right. itg was high during systole (3.6 m/set), indicating a high pressure gradient from pseudoaneurysm to right ventricle. The velocities were lower during diastole (1 m/set) and presystole (1.5 m/set). Biventricular apical rupture with formation of false aneurysm was diagnosed. While he was awaiting surgery, the patient developed hypotension, bradycardia, and electromechanical dissociation and could not be resuscitated. Postmortem examination of the heart confirmed the infarction and rupture of both ventricular apices with formation of apical pseudoaneurysm (Fig. 4). Furthermore, there was evidence of rupture of the pseudoaneurysm with 600 ml of blood in the pericardial space. Left ventricular pseudoaneurysms usually develop as a complication of acute myocardial infarction.‘-” Two-dimensional echocardiography, in conjunction with Doppler and color flow imaging, is uniquely suited to provide the anatomic, hemodynamic, and flow information in these aneurysms. Two-dimensional echocardiographic studies demonstrate the narrow neck or communication orifice t,ypical of false aneurysms.” The restrictive communication (narrow neck) between the pseudoaneurysm and the main ventricular cavity establishes pressure gradients that favor flow of blood from the main left ventricular chamber into the pseudoaneurysm during systole. In early to mid-diastole, the pressure in the pseudoaneurysmal chamber is higher and this generates a gradient favoring flow from the false aneurysm to the left ventricle. However. t.he pressure
in the left ventricle may be higher during presystole following atria1 contraction, and this may favor flow from left ventricle to the pseudoaneurysm. This finding was noted in our case as well as in the one reported by Roelandt et a1.7 The magnitude of velocity and the duration of these flows will most likely depend on complex interaction of the size of the communication, the force of left atria1 contraction, left ventricular systolic and diastolic pressures, and compliance of both left ventricle and pseudoaneurysmal chamber. The presystolic flow velocity may be absent in the presence of normal left ventricular compliance and a moderately large communication between the pseudoaneurysm and the left ventricle. The case reported by Nate110 et al8 had a relatively large communication orifice and the presystolic flow velocity was absent. The unique finding in our case was the pseudoaneurysm to right ventricle communication. Our patient developed small right ventricular apical damage in association with a left ventricular apical infarct because of left anterior descending arterial occlusion, as has been reported previously.“’ The pseudoaneurysm communicated with the right ventricular cavity through a small posteriorly located perforation in the right ventricular apex. The pressure in the pseudoaneurysm was higher than that in the right ventricle throughout the cardiac cycle, and this accounted for a continuous flow from the pseudoaneurysm to the right ventricle. The higher systolic flow velocity represents
500
Brief Communications
Fig. 4. Anatomic section of the heart corresponding with apex oriented downward, with the left ventricle is noted communicating with both ventricles.
increased pressure gradient between these two chambers (Fig. 3). These color flow and continuous wave Doppler findings suggest that the pseudoaneurysm filled in systole and presystole from the left ventricle and emptied into the left ventricle in diastole and continuously into the right ventricle because of unique pressure gradients between the pseudoaneurysm and the two ventricles.
American
to the echocardiographic apical five-chamber plane to the viewer’s right. A large apical pseudoaneurysm
5.
6.
7.
REFERENCES
1. Bates R, Beutler S, Resnekov L, Anagnostopoulos C. Cardiac rupture-challenge in diagnosis and management. Am J Cardiol 1977;40:429-37. 2. Vlodaver Z, Coe JI, Edwards JE. True and false aneurysms. Propensity for the latter to rupture. Circulation 1975;51:56772. 3. Botvinick EH, Shames D, Hutchinson JC, Benson HR, Fitzpatrick M. Noninvasive diagnosis of false ventricular aneurysm with radioisotope gated cardiac blood pool imaging. Am J Cardiol 1976;37:1089-93. 4. Higgins CB, Lipton MJ, Johnson AD, Peterson KL, Vieweg
August 1992 HearI Journal
8.
9.
10.
WVR. False aneurysm of the left ventricle. Radiology 1978; 127:21-7. Gatewood RP, Nanda NC. Differentiation of left ventricular pseudoaneurysm from true aneurysm with two-dimensional echocardiography. Am J Cardiol 1980;46:869-77. Tunick PA, Slater W, Kronzon I. The hemodynamics of left ventricular pseudoaneurysm: color Doppler echocardiographic study. AM HEARTJ 1989;117:1161-5. Roelandt JRTC, Sutherland GR, Yoshida K, Yoshikawa J. Improved diagnosis and characterization of left ventricular pseudoaneurysm by Doppler color flow imaging. J Am Co11 Cardiol 1988;12:807-11. Nate110 GW, Nanda NC, Zachariah ZP. Color Doppler recognition of left ventricular pseudoaneurysm. Am J Med 1988: 85:432-4. Bach M, Berger M, Hecht SR, Strain JE. Diagnosis of left ventricular pseudoaneurysm using contrast and Doppler echocardiography. AM HEART J 1989;118:854-6. Andersen HD, Falk E, Nielsen D. Right ventricular infarction: frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Co11 Cardiol 1987;10:1223-32.
Biventricular apical rupture and formation of pseudoaneurysm: Unique flow patterns by Doppler and color flow imaging Ramesh C. Bansal, MD, Ramdas G. Pai, MD, Arthur J. Hauck, MD, and Dale M. Isaeff, MD Loma Linda, Calif.
Myocardial rupture accounts for 4 30 to 24 PC of in-hospital deaths from acute myocardial infarction.’ Rupture of the left ventricular free wall is generally fatal because of acute From the Departments of Cardiology Laboratory, Loma Linda University
and Pathology and Echocardiography Medical Center.
Reprint requests: Ramesh C. Bansal, Room 4420, Loma Linda University Loma Linda. CA 92354.
MD, Echocardiography Medical Center, 11234
4/4/37955
Laboratory, Anderson St..
cardiac tamponade. Some patients, however, may survive as a result of containment of rupture by overlying pericardium and the development of a pseudo or false aneurysm.2 A variety of techniques has been utilized for the diagnosis of pseudoaneurysm. These include radioisotope gated blood pool imaging,3 left ventricular angiography,4 and echo-Doppler techniques.5-g All the published echo-Doppler reports describe findings in patients with isolated left ventricular pseudoaneurysm. 5-g In this communication, we describe the unique color-flow and continuous wave Doppler findings in a patient with a postinfarction apical pseudoaneurysm that communicated with both ventricles through biventricular apical rupture. A 64-year-old white man with a previous history of hypertension and diabetes mellitus was hospitalized with increasing shortness of breath of 1 week’s duration. He denied history of chest pain or prior myocardial infarction. Findings on admission included: heart rate of 90 beats/min, blood pressure of 120/75 mm Hg, respiration 30/min, temperature 97.6” F, normal jugular venous pressure, lack of pulsus paradoxus, expiratory wheezing in the lung fields,
Fig. 1. Apical five-chamber two-dimensional echocardiographic views with color flow imaging. A bounded echo-free space or false aneurysm (FA) communicates with the left ventricular (LV) cavity through a small defect in the region of the apex (arrow). Panels A and D show the two-dimensional freeze frame and its schematic taken during presystole following atria1 contraction. Panels B and E are taken during systole, and panels C and F are taken during mid-diastole. Presystolic images show low-velocity red color flow from the left ventricle to the false aneurysm. Systolic images show high-velocity mosaic-colored flow from the left ventricle to the false aneurysm. The diastolic images show blue color reversed flow from the false aneurysm to the left ventricle. A small amount of pericardial effusion (PE) is noted around the right ventricle fl?V). AV, Aortic valve; LA, left atrium. 497
498
Brief
C‘ommunications
American
August 1992 Hem Journal
Fig. 2. Top panel shows the schematic of an apical five-chamber view with the left ventricular (LV) apical rupture site (arrow) and the false aneurysm (FA). Bottom panel shows the continuous wave Doppler flow velocity across the left ventricular rupture site. During presystole after atria1 {A) contraction, flow is toward the false aneurysm with a low velocity of 0.8 m/set. During systole (S), flow is from the left ventricle to the false aneurysm, but the velocity is increased to 2.5 m/set. During early to mid-diastole (D), the pressure gradient favors flow from the false aneurysm to the left ventricle, with an early peaking velocity of 1.3 m/set. AO, Aorta; LA, left atrium; PE, pericardial effusion; RV, right ventricle.
normal first and second heart sounds, and grade II/VI ejection systolic murmur at the base. The electrocardiogram showed ST segment elevation from leads Vz to VI;, findings consistent with recent anterior myocardial infarction. Highest creatine phosphokinase (CPK) level at the time of admission was 227, with a 5.8”;’ MB fraction. Coronary angiography showed proximal occlusion of the left anterior descending artery, and 90”; stenosis of superior and 80% stenosis of inferior obtuse marginal arteries. Left ventricular angiography was not performed. Two weeks after admission, he developed a loud grade III/VI systolic murmur in the apical region. Two-dimensional echocardiography revealed a large area of left ventricular apical dyskinesis and localized akinesis of the right ventricular apex. A small pericardial effusion was also noted (Fig. I). This study also revealed a bounded echo-free space around the cardiac apex and this space (false aneurysm) appeared to communicate with both ventricles through defects in the apex of each ventricle (Figs. 1 to 3). Color flow imaging across the left ventricular apical rupture site showed a
low-velocity red color flow from the left ventricle into the false aneurysm during presystole at the time of atria1 conflow t~raction (Fig. 1, A and D); high velocity mosaic-colored from the left ventricle into the false aneurysm during systole (Fig. 1, B and E); and blue color reversed flow from the false aneurysm into the left ventricle during early to mid diastole (Fig. 1, C and F). Continuous wave Doppler examination of this flow revealed a low velocity (0.8 m/set) flow from the left ventricle into the pseudoaneurysm during presystole and a high velocity flow (2.5 m/set) during systole. There was reverse flow in early to mid diastole of 1.3 m/set (Fig. 2). Using a simplified Bernoulli equation, instantaneous pressure gradients between the left ventricle and pseudoaneurysm can be calculated during different portions of the cardiac cycle. From the apical transducer position, posterior tilt of the transducer was helpful in visualization of the rupture site of the right ventricular apex. Color flow imaging and Doppler interrogation of this flow showed flow from the pseudoaneurysm into the right ventricle throughout the cardiac cycle (Fig. 3). The flow veloc-
Volume
124
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2
RriPf Communications
Fig. 3. Top panel shows a schematic of the short-axis view at the apex of the heart by angulating the transducer posteriorly from the apical four-chamber recording position. A mosaic-colored flow pattern is noted from the false aneurysm (FA) to the right ventricular chamber (RV). Bottom panel shows the continuous wave Doppler flow pattern across the false aneurysm to right ventricular communication. The velocity of flow is lowest at 1 m/set in diastole CD), and increases slightly to 1.5 m/set during presystole, and markedly to 3.6 m/set during systole (S). A, Anterior; L, left; LV, left ventricle; P, posterior: R, right. itg was high during systole (3.6 m/set), indicating a high pressure gradient from pseudoaneurysm to right ventricle. The velocities were lower during diastole (1 m/set) and presystole (1.5 m/set). Biventricular apical rupture with formation of false aneurysm was diagnosed. While he was awaiting surgery, the patient developed hypotension, bradycardia, and electromechanical dissociation and could not be resuscitated. Postmortem examination of the heart confirmed the infarction and rupture of both ventricular apices with formation of apical pseudoaneurysm (Fig. 4). Furthermore, there was evidence of rupture of the pseudoaneurysm with 600 ml of blood in the pericardial space. Left ventricular pseudoaneurysms usually develop as a complication of acute myocardial infarction.‘-” Two-dimensional echocardiography, in conjunction with Doppler and color flow imaging, is uniquely suited to provide the anatomic, hemodynamic, and flow information in these aneurysms. Two-dimensional echocardiographic studies demonstrate the narrow neck or communication orifice t,ypical of false aneurysms.” The restrictive communication (narrow neck) between the pseudoaneurysm and the main ventricular cavity establishes pressure gradients that favor flow of blood from the main left ventricular chamber into the pseudoaneurysm during systole. In early to mid-diastole, the pressure in the pseudoaneurysmal chamber is higher and this generates a gradient favoring flow from the false aneurysm to the left ventricle. However. t.he pressure
in the left ventricle may be higher during presystole following atria1 contraction, and this may favor flow from left ventricle to the pseudoaneurysm. This finding was noted in our case as well as in the one reported by Roelandt et a1.7 The magnitude of velocity and the duration of these flows will most likely depend on complex interaction of the size of the communication, the force of left atria1 contraction, left ventricular systolic and diastolic pressures, and compliance of both left ventricle and pseudoaneurysmal chamber. The presystolic flow velocity may be absent in the presence of normal left ventricular compliance and a moderately large communication between the pseudoaneurysm and the left ventricle. The case reported by Nate110 et al8 had a relatively large communication orifice and the presystolic flow velocity was absent. The unique finding in our case was the pseudoaneurysm to right ventricle communication. Our patient developed small right ventricular apical damage in association with a left ventricular apical infarct because of left anterior descending arterial occlusion, as has been reported previously.“’ The pseudoaneurysm communicated with the right ventricular cavity through a small posteriorly located perforation in the right ventricular apex. The pressure in the pseudoaneurysm was higher than that in the right ventricle throughout the cardiac cycle, and this accounted for a continuous flow from the pseudoaneurysm to the right ventricle. The higher systolic flow velocity represents
500
Brief Communications
Fig. 4. Anatomic section of the heart corresponding with apex oriented downward, with the left ventricle is noted communicating with both ventricles.
increased pressure gradient between these two chambers (Fig. 3). These color flow and continuous wave Doppler findings suggest that the pseudoaneurysm filled in systole and presystole from the left ventricle and emptied into the left ventricle in diastole and continuously into the right ventricle because of unique pressure gradients between the pseudoaneurysm and the two ventricles.
American
to the echocardiographic apical five-chamber plane to the viewer’s right. A large apical pseudoaneurysm
5.
6.
7.
REFERENCES
1. Bates R, Beutler S, Resnekov L, Anagnostopoulos C. Cardiac rupture-challenge in diagnosis and management. Am J Cardiol 1977;40:429-37. 2. Vlodaver Z, Coe JI, Edwards JE. True and false aneurysms. Propensity for the latter to rupture. Circulation 1975;51:56772. 3. Botvinick EH, Shames D, Hutchinson JC, Benson HR, Fitzpatrick M. Noninvasive diagnosis of false ventricular aneurysm with radioisotope gated cardiac blood pool imaging. Am J Cardiol 1976;37:1089-93. 4. Higgins CB, Lipton MJ, Johnson AD, Peterson KL, Vieweg
August 1992 HearI Journal
8.
9.
10.
WVR. False aneurysm of the left ventricle. Radiology 1978; 127:21-7. Gatewood RP, Nanda NC. Differentiation of left ventricular pseudoaneurysm from true aneurysm with two-dimensional echocardiography. Am J Cardiol 1980;46:869-77. Tunick PA, Slater W, Kronzon I. The hemodynamics of left ventricular pseudoaneurysm: color Doppler echocardiographic study. AM HEARTJ 1989;117:1161-5. Roelandt JRTC, Sutherland GR, Yoshida K, Yoshikawa J. Improved diagnosis and characterization of left ventricular pseudoaneurysm by Doppler color flow imaging. J Am Co11 Cardiol 1988;12:807-11. Nate110 GW, Nanda NC, Zachariah ZP. Color Doppler recognition of left ventricular pseudoaneurysm. Am J Med 1988: 85:432-4. Bach M, Berger M, Hecht SR, Strain JE. Diagnosis of left ventricular pseudoaneurysm using contrast and Doppler echocardiography. AM HEART J 1989;118:854-6. Andersen HD, Falk E, Nielsen D. Right ventricular infarction: frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Co11 Cardiol 1987;10:1223-32.
