Volume
120
Number
2
Brief Communications
visualization of coronary abrupt occlusion.
collaterals
in response to an
REFERENCES
1. Braunwald E, ed. Heart disease: A textbook of cardiovascular medicine. 3rd ed. Philadelphia: WB Saunders Co, 1988: 1193-4. 2. Levin D. Pathways and functional significance of the coronary collateral circulation. Circulation 1974;40:831-7. 3. Gensini GG, Bruto Da Costa BC. The coronary collateral circulation in living man. Am J Cardiol 1969;24:393-400. 4. Elavda MA. Mathur VS. Hall RJ. Massum GA. Garcia EG, Castro CM.‘Collateral circulation in coronary artery disease: Am J Cardiol 1985;55:58-60. 5. Gregg DE, Patterson RE. Functional importance of the coronary collaterals. N Engl J Med 1980;303:1404-6. 6. Rentrop KP, Thornton JC, Feit F, VanBuskirk M. Determinants and protective potential of coronary arterial collaterals as assessed by an angioplasty model. Am J Cardiol 1988;61: 677-84.
7. Takeshita A, Koiwaya Y, Nakamura M, Yamamoto K, Torii S. Immediate appearance of coronary collaterals during ergonovine-induced arterial spasm. Chest 1982;82:319-22.
Right atrial infarction and cardiogenic shock complicating acute myocardial infarction: Diagnosis by transesophageal echocardiography Thomas C. Hilton, MD, Anthony C. Pearson, MD, Harvey Serota, MD, Frederick A. Dressler, MD, and Morton J. Kern, MD. St. Louis, MO. From
the Division
of Cardiology,
Reprint requests: Morton tory, St. Louis University Louis, MO 63110.
414121339
J. Kern, Hospital,
St. Louis
University
MD, Cardiac 3635 Vista
Medical
Catheterization Ave. at Grand
Center. LaboraBlvd., St.
Atria1 infarction, first described in 1925,’ occurs in up to 42% of fatal myocardial infarctions.2 Electrocardiography and surface echocardiography are of limited use in establishing the diagnosisof atria1 infarction.3, 4 Transesophageal echocardiography has superior ability to image the atria and may prove to be useful in the diagnosisof this condition. We report a caseof acute myocardial infarction with clinical and hemodynamic characteristics of right ventricular infarction in which transesophagealechocardiography confirmed right atria1 infarction asa contributing causeof cardiogenic shock. An 81-year-old man, with no previous cardiac history, experienced chestpain progressingto complete cardiac arrest on the day of admission.The initial electrocardiogram showedventricular fibrillation from which he wassuccessfully resuscitated. He subsequently developed high-grade atrioventricular block requiring temporary pacing. Cardiac catheterization on the day of admissionrevealed a 95% narrowing of the proximal right coronary artery, 50% diffuse narrowing of the left anterior descending,and a 50% narrowing of the proximal circumflex artery. Left ventriculography revealed moderate hypokinesis of the posterobasaland diaphragmatic left ventricular segments,with an ejection fraction of 55% and no mitral regurgitation. The patient underwent emergency percutaneoustransluminal coronary angioplasty of the right coronary artery. Although the proximal right coronary artery was successfully dilated, the originally patent right atria1 artery was occluded (Fig. 1). Following right coronary angioplasty, he had persistent hypotension requiring vasopressor and intraaortic balloon pump support. Electrocardiography showedan ectopic atria1 rhythm with runs of atria1 tachycardia, a right bundle branch block, and anterior ST segment changesconsistentwith acute anterior ischemia(Fig. 2). No PTA segment depression (atria1 repolarization abnormality) was observed. Subsequent electrocardiogramsrevealedfirst-degree atrioventricular block and right
1A. Right coronary artery in the left anterior oblique projection is shown with critically narrowed proximal segment (small arrows) with a visualized patent atria1 branch (large arrow).
Fig.
427
428
Brief Communications
American
August 1990 Heart Journal
Fig. 1 B. Right coronary artery following angioplasty isshown,with a typical hazy appearanceto the patent angioplasty segmentwith lossof the atria1 branch.
Fig. 2. Electrocardiogram demonstrating features consistentwith right bundle branch block and inferior wall myocardial infarction.
precordial lead ST segmentelevation consistentwith right ventricular infarction. The pulmonary artery pressurewas 38/Z! mm Hg (mean 27 mm Hg), the mean pulmonary capillary wedgepressurewas18mm Hg, cardiac output was 3.5 L/min, and cardiac index was 1.8 L/min/m2. The patient was treated for right ventricular infarction and shockwith large bolusesof saline,intraaortic balloon pump support, and positive inotropic agents. After 48 hours, the patient remained hypotensive, despite optimal ventricular filling pressureswith pharmacologic and intraaortic balloon pump support. Although the transthoracic echocardiogramwastechnically difficult, the
left ventricle appeared to function normally. There was right ventricular enlargementand a small pericardial effusion.A transesophagealechocardiogramwasperformed 24 hourslater during a period of ectopic atria1rhythm and revealed a large akinetic right atrium with spontaneousecho contrast consistent with a low flow state. The mitral and aortic valves were normal. There wasposterior akinesisof the left and right ventricles. The right ventricular ejection fraction and left ventricular ejection fraction were estimated to be 20% and >40 %, respectively. Of note, Doppler interrogation of the mitral valve revealed normal early and atria1 filling waves.However, only an early filling wave was
Volume Number
120 2
Brief Communications
429
Fig. 3. The Doppler echocardiogramof the mitral (left panel) and tricuspid (right panel) valves demonstrating preserved E and A waves in the mitral Doppler velocity tracings with only an E wave in the tricuspid velocity flow consistent with lossof atria1 activity of the right atrium.
Fig.
4A. Grosspathologic specimenshowing extensive myocardial necrosisinvolving the right atrium.
seenacrossthe tricuspid valve, consistent with absenceof effective right atrial contraction (Fig. 3). Color flow Doppler echocardiographicexamination revealed severetricuspid regurgitation and mild aortic regurgitation. The patient gradually deteriorated with persistent hypotension despite maximal therapy. Sepsisof undetermined etiology developed and the patient died on the sixteenth hospital day. At necropsy, the heart weighed460 gm. There wassevere atherosclerotic narrowing of the right coronary artery (95%), left anterior descendingartery (70%), and circumflex artery (70%). There wastransmural necrosisof the left and right ventricular posterior walls extending from the apex to the base.The right atrium was markedly dilated
and histologic specimensrevealed extensive transmural necrosis(Fig. 4). Also, there wasseverepassivecongestion of the liver, spleen,and lungs. The persistent and refractory hypotension leading to death in the present caseappearsto have been secondary to an inferoposterior myocardial infarction with right atria1 and right ventricular involvement, as confirmed by transesophagealechocardiography. Atria1 infarction has been previously described and probably occurs in 15% to 20% of all myocardial infarctions.4*7Right atria1 infarction is more common than left atria1 infarction, presumably becausethe higher oxygen concentration of left atrial blood is sufficient to prevent ischemiain the thin left atrial wall.
August
430
Brief
Communications
Fig. 48. wall.
Histologic
American
specimen
demonstrating
extensive
Previous studieshave reported difficulty in localizing the site of atria1 infarction electrocardiographically.4 Electrocardiographic diagnosis of atria1 infarction requires PTA segment depression in the inferior limb leads6 or in leads Vz to V4.l A previous report8 has described the diagnosis of
right atria1infarction by gated cardiac blood pool scanthat demonstrated a noncontracting right atrium. Also, transesophagealechocardiography has been usedto document right atrial infarction in one previous casereport.g However, no previous reports describe a diagnosis of right atria1 infarction by transesophagealechocardiography in acute myocardial infarction. Although right atria1 infarction was not clinically suspected, transesophageal echocardiographic examination establishedthe diagnosisby three independent features. This previously undescribed triad consistsof (1) a visually akinetic right atria1 free wall, despite left atria1 contraction; (2) right atria1 spontaneous echocontrast; and (3) absenceof Doppler A waveacrossthe tricuspid valve with normal mitral A waves.The akinesis and low flow state of the right atrium may be partially attributable to right ventricular failure. Also, the absenceof a Doppler A wave acrossthe tricuspid valve doesnot preclude the possibility of effective right atria1 contraction with retrograde flow into the great veins. However, we believe that the constellation of echocardiographicand Doppler findings, confirmed by histologic studies,make the diagnosisof right atria1infarction certain. The importance of right atrial function to maintain cardiac output in patients with right ventricular infarction has been previously described.5The hemodynamic and clinical consequences of right ventricular infarction in this casewere undoubtedly exacerbated by the loss of effective right atria1 contraction. Right atria1infarction, contributing to the hemodynamic collapseof patients with acute myocardial infarction, may be under-reported becauseof the difficulty in making this diagnosis.Correct diagnosisof right atria1 infarction may be of particular importance in patients with presumed right ventricular infarction who are being consideredfor atrioventricular sequential pacing. We believe that right atria1 infarction may be clinically indistinguishable from right ventricular infarction without the use of either transesophagealechocardiography or angiography.
myocardial
necrosis
(arrows)
Heart
1990 Journal
of right atria1 free
REFERENCES
Clerc A, Levy R. Infarctus auriculaire: tachyarrhythmie terminale. Bull Mem Sot Med Hop Paris 1925;41:1603. 2. Lazar EJ, Goldberger J, Peled H, Sherman M, Frishman WH. Atria1 infarction: diagnosis and management. AM HEART J 1.
1988;116:1058. 3. 4. 5.
6. 7.
8.
9.
Burch GE. Of the P-R segment depression and atria1 infarction. AM HEART J 1976;91:129. Gardin JM, Singer DH. Atria1 infarction: importance, diagnosis and localization. Arch Intern Med 1981;141:1345. Top01 EJ, Goldschulser N, Ports TA. Hemodynamic benefit of atria1 pacing in right ventricular myocardial infarction. Ann Intern Med 1982;96:594. Langendorf R. Electrokardiogramm bei vorhof-infarkt. Acta Med Stand 1939;100:136. Cushing EH, Feil HS, Stauton EJ, et al. Infarction of the cardiac auricles (atria): clinical, pathological and experimental studies. Br Heart J 1942;4:17. Gordon S, Finck DR, Perera RD, et al. Atria1 infarction complicating an acute inferior myocardial infarction. Arch Intern Med 1984;114:193. Sasaki T, Matauzaki M, Anno Y, Tohma Y, Hiroyama N, Uchida T. Tamitani M. Yonezawa F. Oaawa H. Matsuda Y. Kumada T, Murata T. Diagnosis of righi atria1 infarction by transesophageal echocardiography. J Cardiogr 1982;12:595.
Aspergillus myocardial block
myocarditis presenting as infarction with complete heart
Joseph G. Rogers, MD, John R. Windle,
MD,
Bruce M. McManus, MD, PhD, and Arthur R. Easley, Jr., MD. Omaha, Nebr.
A 69-year-old
man with two previous
myocardial
infarc-
tions and recurrent ventricular tachycardia (VT) was referred for electrophysiologic (EPS) evaluation following multiple failed trials with different antiarrhythmic agents. From the Section of Cardiology and the Department of Pathology and Microbiology, University of Nebraska Medical Center. Reprint requests: John R. Windle, MD, Section of Cardiology, University of Nebraska Medical Center, 600 South 42nd St., Omaha, NE 68198-2265. 414121333
120
Number
2
Brief Communications
visualization of coronary abrupt occlusion.
collaterals
in response to an
REFERENCES
1. Braunwald E, ed. Heart disease: A textbook of cardiovascular medicine. 3rd ed. Philadelphia: WB Saunders Co, 1988: 1193-4. 2. Levin D. Pathways and functional significance of the coronary collateral circulation. Circulation 1974;40:831-7. 3. Gensini GG, Bruto Da Costa BC. The coronary collateral circulation in living man. Am J Cardiol 1969;24:393-400. 4. Elavda MA. Mathur VS. Hall RJ. Massum GA. Garcia EG, Castro CM.‘Collateral circulation in coronary artery disease: Am J Cardiol 1985;55:58-60. 5. Gregg DE, Patterson RE. Functional importance of the coronary collaterals. N Engl J Med 1980;303:1404-6. 6. Rentrop KP, Thornton JC, Feit F, VanBuskirk M. Determinants and protective potential of coronary arterial collaterals as assessed by an angioplasty model. Am J Cardiol 1988;61: 677-84.
7. Takeshita A, Koiwaya Y, Nakamura M, Yamamoto K, Torii S. Immediate appearance of coronary collaterals during ergonovine-induced arterial spasm. Chest 1982;82:319-22.
Right atrial infarction and cardiogenic shock complicating acute myocardial infarction: Diagnosis by transesophageal echocardiography Thomas C. Hilton, MD, Anthony C. Pearson, MD, Harvey Serota, MD, Frederick A. Dressler, MD, and Morton J. Kern, MD. St. Louis, MO. From
the Division
of Cardiology,
Reprint requests: Morton tory, St. Louis University Louis, MO 63110.
414121339
J. Kern, Hospital,
St. Louis
University
MD, Cardiac 3635 Vista
Medical
Catheterization Ave. at Grand
Center. LaboraBlvd., St.
Atria1 infarction, first described in 1925,’ occurs in up to 42% of fatal myocardial infarctions.2 Electrocardiography and surface echocardiography are of limited use in establishing the diagnosisof atria1 infarction.3, 4 Transesophageal echocardiography has superior ability to image the atria and may prove to be useful in the diagnosisof this condition. We report a caseof acute myocardial infarction with clinical and hemodynamic characteristics of right ventricular infarction in which transesophagealechocardiography confirmed right atria1 infarction asa contributing causeof cardiogenic shock. An 81-year-old man, with no previous cardiac history, experienced chestpain progressingto complete cardiac arrest on the day of admission.The initial electrocardiogram showedventricular fibrillation from which he wassuccessfully resuscitated. He subsequently developed high-grade atrioventricular block requiring temporary pacing. Cardiac catheterization on the day of admissionrevealed a 95% narrowing of the proximal right coronary artery, 50% diffuse narrowing of the left anterior descending,and a 50% narrowing of the proximal circumflex artery. Left ventriculography revealed moderate hypokinesis of the posterobasaland diaphragmatic left ventricular segments,with an ejection fraction of 55% and no mitral regurgitation. The patient underwent emergency percutaneoustransluminal coronary angioplasty of the right coronary artery. Although the proximal right coronary artery was successfully dilated, the originally patent right atria1 artery was occluded (Fig. 1). Following right coronary angioplasty, he had persistent hypotension requiring vasopressor and intraaortic balloon pump support. Electrocardiography showedan ectopic atria1 rhythm with runs of atria1 tachycardia, a right bundle branch block, and anterior ST segment changesconsistentwith acute anterior ischemia(Fig. 2). No PTA segment depression (atria1 repolarization abnormality) was observed. Subsequent electrocardiogramsrevealedfirst-degree atrioventricular block and right
1A. Right coronary artery in the left anterior oblique projection is shown with critically narrowed proximal segment (small arrows) with a visualized patent atria1 branch (large arrow).
Fig.
427
428
Brief Communications
American
August 1990 Heart Journal
Fig. 1 B. Right coronary artery following angioplasty isshown,with a typical hazy appearanceto the patent angioplasty segmentwith lossof the atria1 branch.
Fig. 2. Electrocardiogram demonstrating features consistentwith right bundle branch block and inferior wall myocardial infarction.
precordial lead ST segmentelevation consistentwith right ventricular infarction. The pulmonary artery pressurewas 38/Z! mm Hg (mean 27 mm Hg), the mean pulmonary capillary wedgepressurewas18mm Hg, cardiac output was 3.5 L/min, and cardiac index was 1.8 L/min/m2. The patient was treated for right ventricular infarction and shockwith large bolusesof saline,intraaortic balloon pump support, and positive inotropic agents. After 48 hours, the patient remained hypotensive, despite optimal ventricular filling pressureswith pharmacologic and intraaortic balloon pump support. Although the transthoracic echocardiogramwastechnically difficult, the
left ventricle appeared to function normally. There was right ventricular enlargementand a small pericardial effusion.A transesophagealechocardiogramwasperformed 24 hourslater during a period of ectopic atria1rhythm and revealed a large akinetic right atrium with spontaneousecho contrast consistent with a low flow state. The mitral and aortic valves were normal. There wasposterior akinesisof the left and right ventricles. The right ventricular ejection fraction and left ventricular ejection fraction were estimated to be 20% and >40 %, respectively. Of note, Doppler interrogation of the mitral valve revealed normal early and atria1 filling waves.However, only an early filling wave was
Volume Number
120 2
Brief Communications
429
Fig. 3. The Doppler echocardiogramof the mitral (left panel) and tricuspid (right panel) valves demonstrating preserved E and A waves in the mitral Doppler velocity tracings with only an E wave in the tricuspid velocity flow consistent with lossof atria1 activity of the right atrium.
Fig.
4A. Grosspathologic specimenshowing extensive myocardial necrosisinvolving the right atrium.
seenacrossthe tricuspid valve, consistent with absenceof effective right atrial contraction (Fig. 3). Color flow Doppler echocardiographicexamination revealed severetricuspid regurgitation and mild aortic regurgitation. The patient gradually deteriorated with persistent hypotension despite maximal therapy. Sepsisof undetermined etiology developed and the patient died on the sixteenth hospital day. At necropsy, the heart weighed460 gm. There wassevere atherosclerotic narrowing of the right coronary artery (95%), left anterior descendingartery (70%), and circumflex artery (70%). There wastransmural necrosisof the left and right ventricular posterior walls extending from the apex to the base.The right atrium was markedly dilated
and histologic specimensrevealed extensive transmural necrosis(Fig. 4). Also, there wasseverepassivecongestion of the liver, spleen,and lungs. The persistent and refractory hypotension leading to death in the present caseappearsto have been secondary to an inferoposterior myocardial infarction with right atria1 and right ventricular involvement, as confirmed by transesophagealechocardiography. Atria1 infarction has been previously described and probably occurs in 15% to 20% of all myocardial infarctions.4*7Right atria1 infarction is more common than left atria1 infarction, presumably becausethe higher oxygen concentration of left atrial blood is sufficient to prevent ischemiain the thin left atrial wall.
August
430
Brief
Communications
Fig. 48. wall.
Histologic
American
specimen
demonstrating
extensive
Previous studieshave reported difficulty in localizing the site of atria1 infarction electrocardiographically.4 Electrocardiographic diagnosis of atria1 infarction requires PTA segment depression in the inferior limb leads6 or in leads Vz to V4.l A previous report8 has described the diagnosis of
right atria1infarction by gated cardiac blood pool scanthat demonstrated a noncontracting right atrium. Also, transesophagealechocardiography has been usedto document right atrial infarction in one previous casereport.g However, no previous reports describe a diagnosis of right atria1 infarction by transesophagealechocardiography in acute myocardial infarction. Although right atria1 infarction was not clinically suspected, transesophageal echocardiographic examination establishedthe diagnosisby three independent features. This previously undescribed triad consistsof (1) a visually akinetic right atria1 free wall, despite left atria1 contraction; (2) right atria1 spontaneous echocontrast; and (3) absenceof Doppler A waveacrossthe tricuspid valve with normal mitral A waves.The akinesis and low flow state of the right atrium may be partially attributable to right ventricular failure. Also, the absenceof a Doppler A wave acrossthe tricuspid valve doesnot preclude the possibility of effective right atria1 contraction with retrograde flow into the great veins. However, we believe that the constellation of echocardiographicand Doppler findings, confirmed by histologic studies,make the diagnosisof right atria1infarction certain. The importance of right atrial function to maintain cardiac output in patients with right ventricular infarction has been previously described.5The hemodynamic and clinical consequences of right ventricular infarction in this casewere undoubtedly exacerbated by the loss of effective right atria1 contraction. Right atria1infarction, contributing to the hemodynamic collapseof patients with acute myocardial infarction, may be under-reported becauseof the difficulty in making this diagnosis.Correct diagnosisof right atria1 infarction may be of particular importance in patients with presumed right ventricular infarction who are being consideredfor atrioventricular sequential pacing. We believe that right atria1 infarction may be clinically indistinguishable from right ventricular infarction without the use of either transesophagealechocardiography or angiography.
myocardial
necrosis
(arrows)
Heart
1990 Journal
of right atria1 free
REFERENCES
Clerc A, Levy R. Infarctus auriculaire: tachyarrhythmie terminale. Bull Mem Sot Med Hop Paris 1925;41:1603. 2. Lazar EJ, Goldberger J, Peled H, Sherman M, Frishman WH. Atria1 infarction: diagnosis and management. AM HEART J 1.
1988;116:1058. 3. 4. 5.
6. 7.
8.
9.
Burch GE. Of the P-R segment depression and atria1 infarction. AM HEART J 1976;91:129. Gardin JM, Singer DH. Atria1 infarction: importance, diagnosis and localization. Arch Intern Med 1981;141:1345. Top01 EJ, Goldschulser N, Ports TA. Hemodynamic benefit of atria1 pacing in right ventricular myocardial infarction. Ann Intern Med 1982;96:594. Langendorf R. Electrokardiogramm bei vorhof-infarkt. Acta Med Stand 1939;100:136. Cushing EH, Feil HS, Stauton EJ, et al. Infarction of the cardiac auricles (atria): clinical, pathological and experimental studies. Br Heart J 1942;4:17. Gordon S, Finck DR, Perera RD, et al. Atria1 infarction complicating an acute inferior myocardial infarction. Arch Intern Med 1984;114:193. Sasaki T, Matauzaki M, Anno Y, Tohma Y, Hiroyama N, Uchida T. Tamitani M. Yonezawa F. Oaawa H. Matsuda Y. Kumada T, Murata T. Diagnosis of righi atria1 infarction by transesophageal echocardiography. J Cardiogr 1982;12:595.
Aspergillus myocardial block
myocarditis presenting as infarction with complete heart
Joseph G. Rogers, MD, John R. Windle,
MD,
Bruce M. McManus, MD, PhD, and Arthur R. Easley, Jr., MD. Omaha, Nebr.
A 69-year-old
man with two previous
myocardial
infarc-
tions and recurrent ventricular tachycardia (VT) was referred for electrophysiologic (EPS) evaluation following multiple failed trials with different antiarrhythmic agents. From the Section of Cardiology and the Department of Pathology and Microbiology, University of Nebraska Medical Center. Reprint requests: John R. Windle, MD, Section of Cardiology, University of Nebraska Medical Center, 600 South 42nd St., Omaha, NE 68198-2265. 414121333
