Case Report Cardiology 1992:81:384-388
Yoshifumi Tomitaa Takao Endoa Teruo Takanoa Hirokazu Havakawaa Koichi TamuraH0 Yuichi Sugisakib
Extensive Hemorrhagic Myocardial Infarction Associated with Left Atrial Myxoma
First Department o f Internal Medicine and Department o f Pathology. Nippon Medical School, Tokyo. Japan
Abstract We observed a case of a left atrial myxoma associated with extensive hemorrhagic myocardial infarction, most probably caused by occlusion of the main left coronary artery by the tumor embolus followed by reperfusion.
The clinical presentation of cardiac myxo ma, the most common primary tumor of the heart, includes nonspecific systemic findings, cardiac manifestations as well as embolic phe nomena [1], Embolization of the myxoma to the heart with resultant myocardial infarction is rare [2-4], and largely exists as healed infarcts with tumor emboli in the adjacent coronary arteries microscopically [4], We de scribe a case of left atrial myxoma associated with extensive hemorrhagic myocardial in farction, most probably due to reperfusion of the occluded main left coronary artery by the tumor embolus. Case Report A 19-year-old male college student was transferred to the coronary care unit o f Nippon Medical School Hospital on November 22, 1990, with a diagnosis o f
Received: August 26, 1992 Accepted after revision: September 1, 1992
acute myocardial infarction and the finding o f a left atrial mass. The patient had been in good health until the day of admission, when he suddenly experienced dyspnea after climbing five flights o f stairs and then collapsed. The patient was admitted to a nearby hospi tal. The systolic blood pressure was 74 mm Hg. Serum enzyme levels were normal. An electrocardiogram showed complete right bundle branch block, and Q waves with elevated ST segments in leads I, aVL and V 2 _4 . An échocardiographie study revealed a mass in the left atrium that prolapsed into the mitral orifice. N o thrombolytic therapy w'as performed, and he was medicated w'ith intravenous dopamine and lidocaine until the time o f transfer to our coronary care unit. His past and family histories were unremarkable. Body temperature was 35.1 °C, the pulse 108 and irregular, and respiration rate 20. Systolic blood pressure was 76 mm Hg. On physical examination, the patient was a well-developed, well-nourished young man who ap peared acutely ill. He had clammy skin with peripheral cyanosis. Heart sounds were clear without audible murmurs. The breath sounds were normal, and there were no crackles or wheezes. No peripheral edema in the extremities was observed. Results o f a neurological
Dr. Takao Endo First Department of Internal Medicine Nippon Medical School 1-1-5 Scndagi. Bunkyo-ku. Tokyo 113 (Japan)
© 1992 S. Karger AG. Basel 0008-6312/92/ 0816-0384S2.75/0
Downloaded by: UCL 144.82.238.225 - 6/15/2018 5:14:41 PM
KeyWords Left atrial myxoma Myocardial infarction Myocardial hemorrhage Coronary artery reperfusion
Fig. 1 . Parasternal long-axis two-dimensional echocardiograms in systole (a) and diastole mass in the left atrium (arrow heads). LV = Left ventricle; RV = right ventricle.
(b). showing a large mobile
slices o f the ventricular myocardium showed extensive, transmural, hemorrhagic myocardial infarct in the anteroseptal and lateral walls o f the left ventricle (fig. 2b). All major coronary arteries were normal and widely patent, and no tumor emboli or thrombi were found. The ostium o f the left coronary artery was slightly dis placed upward. Microscopically, the tumor had the characteristic histological findings of myxoma (fig. 3a). Microscopic sections o f the myocardium showed exten sive areas o f necrosis, contraction band formation and massive interstitial hemorrhage, with relatively little neutrophil infiltration (fig. 3b). At the periphery o f the infarct, extension o f the hemorrhage into areas o f noninfarcted myocardium was observed. Some tumor frag ments were observ ed within small intramural branches o f the left coronary artery. The kidneys had multiple fresh infarctions, and the small arteries adjacent to the infarcts contained tumor fragments.
Discussion Embolization from atrial myxoma is fre quently seen clinically, occurring in 32% of cases as a presenting symptom in one series [ l ]. Systemic emboli may be multiple and dis seminated to many sites, includng the brain, the kidneys and the extremities [2], The clini cal picture of acute myocardial infarction and the presence of left atrial tumor in our patient
385
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examination were negative. The urine gave a trace positive test for protein. The hematocrit was 42.0% the white cell count 20.700 and the platelet count 343,000. The urea nitrogen was 20 mg/dl and the creatinine 1.8 mg/dl. The serum enzyme levels were markedly ele vated: the creatine kinase was 2 .196 U /l, the CK-MB 160 U/l. the serum aspartate aminotransferase 2 9 1 IU/l and the lactic dehydrogenase 1.003 lU /l. An elec trocardiogram showed atrial fibrillation with complete right bundle branch block, and Q waves in leads I. aVL and V,_t with elevated ST segments. An X-ray film o f the chest revealed a heart o f normal size and signs of pulmonary congestion. An echocardiographic exami nation showed a large mobile mass in the left atrium attached to the interatrial septum, protruding into the mitral orifice during diastole (fig. I). The apex and anterior and lateral walls o f the left ventricle were severely hypokinetic, with an ejection fraction o f 20%. Right-sided cardiac catheterization with a Swan-Ganz catheter disclosed increased pulmonary arterial (41/30 mm Hg). mean pulmonary capillary wedge (33 mm Hg) and central venous pressures (20 cm LUO), and reduced cardiac index (l . 8l l/m in/m :). Despite treat ment which included use o f an intra-aortic balloon pumping system and vasopressors as well as ventila tory assistance, cardiogenic shock and oliguria per sisted. and the patient died on the 3rd hospital day in multiple organ system failure. At autopsy, the left atrium was found to hold a pol ypoid. gelatinous mass. 5 cm in diameter, containing foci o f hemorrhage, attached via a pedicle to the ante rior margin o f the fossa ovalis (fig. 2a). The transverse
suggested a diagnosis of coronary artery em bolization with resultant myocardial infarc tion. Although relatively rare, there have been reports in the literature of tumor emboli in epicardial or intramural coronary' arteries and healed infarcts being demonstrated at autopsy [4] as well as reports of unproven but possible clinical cases of coronary artery embolization from left atrial myxoma resulting in acute myocardial infarction [3], Coronary arteriog raphy performed early after the onset of acute myocardial infarction in those cases again revealed a complete obstruction or filling de fects caused by the embolus in the infarctrelated coronary' artery [3], However, our pa tient was completely different from those re ported previously in that the patient had a myocardial infarct that was extensively hem orrhagic. and no tumor emboli were found in the major coronary arteries. The extensive, transmural, hemorrhagic myocardial infarct observed in our patient was thought to be caused by occlusion of the
386
main left coronary artery by the tumor embo lus followed by reperfusion. The presence of tumor emboli and fresh infarcts in the kid neys as well as tumor fragments in the coro nary' artery suggested that the myocardial in farction in our patient was caused by coro nary' artery embolization from the left atrial myxoma. The extensiveness and transmural nature of the myocardial infarct, involving the whole anteroseptal and lateral walls of the left ventricle, indicated that the very proximal portion of the left coronary artery had been occluded for a relatively long period of time. Myocardial hemorrhage has been observed repeatedly in experimental animals subjected to coronary artery occlusion followed by re perfusion [5] and at necropsy in patients with acute myocardial infarction who underwent thrombolytic or surgical reperfusion [6], Thus, our finding of extensively hemorrhagic myocardial infarct with no tumor emboli in the major coronary arteries suggested that the coronary artery was reperfused after detach-
Tomita/Endo/Takano/Hayakawa/ Tamura/Sugisaki
Left Atrial Myxoma with Hemorrhagic Myocardial Infarction
Downloaded by: UCL 144.82.238.225 - 6/15/2018 5:14:41 PM
Fig. 2. a A polypoid gelatinous left atrial tumor (arrows) was found to be fixed via pedicle to the anterior margin o f the fossa ovalis. LV = Left ventricle, b Transverse section of the ventricular myocardium, showing extensive, transmural, hemorrhagic myocardial infarction. LV = Left ventricular cavity.
ment of the tumor embolus, most probably, from the ostium of the left coronary artery, the occurrence of which might relate to the upward displacement of the coronary ostium
observed in this patient. The timing of reper fusion could not be identified clinically from the analyses of enzymatic or electrocardio graphic changes.
387
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Fig. 3. a Microscopic section o f the tumor, showing polygonal cells with eosinophilic cytoplasm and hyperchromatic nuclei, sur rounded by myxomatous stroma. HE. b Histologic section of the cen tral infarct zone, showing myocar dial necrosis with contraction band formation and massive amounts o f extravasated erythrocytes in the in terstitial space. Few neutrophils in filtrated into the myocardium rela tive to the extent of myocardial ne crosis and hemorrhage. HE.
Whether reperfusion hemorrhage extends myocardial infarction or not is a controversial issue. In experimental animals, myocardial hemorrhage assessed grossly and microscopi cally has been reported to be within areas of necrosis in which severe vascular injury and irreversible myocardial damage have oc curred and is primarily located in the suben docardial portion [5], In necropsy patients, however, extension of the hemorrhage into areas of noninfarcted myocardium has been observed, and reperfusion hemorrhage may not be confined to the central necrotic zone [6], which is in accordance with the necropsy
findings of this patient. Recently, neutrophils have been suggested to have detrimental ef fects on the reperfused myocardium, causing myocardial reperfusion injury, although in our patient few neutrophils had infiltrated into the myocardium relative to the extent of myocardial necrosis and hemorrhage.
Acknowledgments We are grateful to Mrs. Tamiko Kikuchi for her secretarial assistance and Dr. Mari Watanabe for her advice in reviewing the manuscript.
References 4
388
Tomita/ Endo/Takano/Hayakawa/ Tamura/Sugisaki
5
Price DL. Harris JL. New PFJ. Cantu RC: Cardiac myxoma. A clinicopathologic and angiographic studv. Arch Neurol 1970:23:558— 567.' Endo T. Sato N. Hayakawa H. Maroko PR: Reduction of myocardial hemorrhage and the extent of necro sis by gallopamil (D600) in dogs with coronary artery reperfusion. J Cardiovasc Pharmacol 1991:18: 739-745.
6
Waller BE. Rothbaum DA. Pinker ton CA. Cowley MJ, LinnemeierTJ. Orr C. Irons M. Helmuth RA. Wills ER. Aust C: Status of the myocar dium and infarct-related coronary artery in 19 necropsy patients with acute recanalization using pharma cologic (streptokinase, r-tissuc plas minogen activator), mechanical (percutaneous transluminal coro nary angioplasty) or combined types of reperfusion therapy. J Am Coll Cardiol 1987:9:785-801.
Left Atrial Myxoma with Hemorrhagic Myocardial Infarction
Downloaded by: UCL 144.82.238.225 - 6/15/2018 5:14:41 PM
1 St. John Sutton MG. Mercier LA. Giuliani ER. Lie JT: Atrial myxo mas. A review of clinical experience in 40 patients. Mayo Clin Proc 1980:55:371-376. 2 Silverman J. Olwin JS. Graettinger JS: Cardiac myxomas with systemic embolization. Review of the litera ture and report of a case. Circulation 1962:26:99-103. 3 Rath S. Har-Zahav Y. Battler A, Agranat O. Neufeld HN: Coronary artery embolus from left atrial myx oma. Am J Cardiol 1984:54:1392— 1393.
Yoshifumi Tomitaa Takao Endoa Teruo Takanoa Hirokazu Havakawaa Koichi TamuraH0 Yuichi Sugisakib
Extensive Hemorrhagic Myocardial Infarction Associated with Left Atrial Myxoma
First Department o f Internal Medicine and Department o f Pathology. Nippon Medical School, Tokyo. Japan
Abstract We observed a case of a left atrial myxoma associated with extensive hemorrhagic myocardial infarction, most probably caused by occlusion of the main left coronary artery by the tumor embolus followed by reperfusion.
The clinical presentation of cardiac myxo ma, the most common primary tumor of the heart, includes nonspecific systemic findings, cardiac manifestations as well as embolic phe nomena [1], Embolization of the myxoma to the heart with resultant myocardial infarction is rare [2-4], and largely exists as healed infarcts with tumor emboli in the adjacent coronary arteries microscopically [4], We de scribe a case of left atrial myxoma associated with extensive hemorrhagic myocardial in farction, most probably due to reperfusion of the occluded main left coronary artery by the tumor embolus. Case Report A 19-year-old male college student was transferred to the coronary care unit o f Nippon Medical School Hospital on November 22, 1990, with a diagnosis o f
Received: August 26, 1992 Accepted after revision: September 1, 1992
acute myocardial infarction and the finding o f a left atrial mass. The patient had been in good health until the day of admission, when he suddenly experienced dyspnea after climbing five flights o f stairs and then collapsed. The patient was admitted to a nearby hospi tal. The systolic blood pressure was 74 mm Hg. Serum enzyme levels were normal. An electrocardiogram showed complete right bundle branch block, and Q waves with elevated ST segments in leads I, aVL and V 2 _4 . An échocardiographie study revealed a mass in the left atrium that prolapsed into the mitral orifice. N o thrombolytic therapy w'as performed, and he was medicated w'ith intravenous dopamine and lidocaine until the time o f transfer to our coronary care unit. His past and family histories were unremarkable. Body temperature was 35.1 °C, the pulse 108 and irregular, and respiration rate 20. Systolic blood pressure was 76 mm Hg. On physical examination, the patient was a well-developed, well-nourished young man who ap peared acutely ill. He had clammy skin with peripheral cyanosis. Heart sounds were clear without audible murmurs. The breath sounds were normal, and there were no crackles or wheezes. No peripheral edema in the extremities was observed. Results o f a neurological
Dr. Takao Endo First Department of Internal Medicine Nippon Medical School 1-1-5 Scndagi. Bunkyo-ku. Tokyo 113 (Japan)
© 1992 S. Karger AG. Basel 0008-6312/92/ 0816-0384S2.75/0
Downloaded by: UCL 144.82.238.225 - 6/15/2018 5:14:41 PM
KeyWords Left atrial myxoma Myocardial infarction Myocardial hemorrhage Coronary artery reperfusion
Fig. 1 . Parasternal long-axis two-dimensional echocardiograms in systole (a) and diastole mass in the left atrium (arrow heads). LV = Left ventricle; RV = right ventricle.
(b). showing a large mobile
slices o f the ventricular myocardium showed extensive, transmural, hemorrhagic myocardial infarct in the anteroseptal and lateral walls o f the left ventricle (fig. 2b). All major coronary arteries were normal and widely patent, and no tumor emboli or thrombi were found. The ostium o f the left coronary artery was slightly dis placed upward. Microscopically, the tumor had the characteristic histological findings of myxoma (fig. 3a). Microscopic sections o f the myocardium showed exten sive areas o f necrosis, contraction band formation and massive interstitial hemorrhage, with relatively little neutrophil infiltration (fig. 3b). At the periphery o f the infarct, extension o f the hemorrhage into areas o f noninfarcted myocardium was observed. Some tumor frag ments were observ ed within small intramural branches o f the left coronary artery. The kidneys had multiple fresh infarctions, and the small arteries adjacent to the infarcts contained tumor fragments.
Discussion Embolization from atrial myxoma is fre quently seen clinically, occurring in 32% of cases as a presenting symptom in one series [ l ]. Systemic emboli may be multiple and dis seminated to many sites, includng the brain, the kidneys and the extremities [2], The clini cal picture of acute myocardial infarction and the presence of left atrial tumor in our patient
385
Downloaded by: UCL 144.82.238.225 - 6/15/2018 5:14:41 PM
examination were negative. The urine gave a trace positive test for protein. The hematocrit was 42.0% the white cell count 20.700 and the platelet count 343,000. The urea nitrogen was 20 mg/dl and the creatinine 1.8 mg/dl. The serum enzyme levels were markedly ele vated: the creatine kinase was 2 .196 U /l, the CK-MB 160 U/l. the serum aspartate aminotransferase 2 9 1 IU/l and the lactic dehydrogenase 1.003 lU /l. An elec trocardiogram showed atrial fibrillation with complete right bundle branch block, and Q waves in leads I. aVL and V,_t with elevated ST segments. An X-ray film o f the chest revealed a heart o f normal size and signs of pulmonary congestion. An echocardiographic exami nation showed a large mobile mass in the left atrium attached to the interatrial septum, protruding into the mitral orifice during diastole (fig. I). The apex and anterior and lateral walls o f the left ventricle were severely hypokinetic, with an ejection fraction o f 20%. Right-sided cardiac catheterization with a Swan-Ganz catheter disclosed increased pulmonary arterial (41/30 mm Hg). mean pulmonary capillary wedge (33 mm Hg) and central venous pressures (20 cm LUO), and reduced cardiac index (l . 8l l/m in/m :). Despite treat ment which included use o f an intra-aortic balloon pumping system and vasopressors as well as ventila tory assistance, cardiogenic shock and oliguria per sisted. and the patient died on the 3rd hospital day in multiple organ system failure. At autopsy, the left atrium was found to hold a pol ypoid. gelatinous mass. 5 cm in diameter, containing foci o f hemorrhage, attached via a pedicle to the ante rior margin o f the fossa ovalis (fig. 2a). The transverse
suggested a diagnosis of coronary artery em bolization with resultant myocardial infarc tion. Although relatively rare, there have been reports in the literature of tumor emboli in epicardial or intramural coronary' arteries and healed infarcts being demonstrated at autopsy [4] as well as reports of unproven but possible clinical cases of coronary artery embolization from left atrial myxoma resulting in acute myocardial infarction [3], Coronary arteriog raphy performed early after the onset of acute myocardial infarction in those cases again revealed a complete obstruction or filling de fects caused by the embolus in the infarctrelated coronary' artery [3], However, our pa tient was completely different from those re ported previously in that the patient had a myocardial infarct that was extensively hem orrhagic. and no tumor emboli were found in the major coronary arteries. The extensive, transmural, hemorrhagic myocardial infarct observed in our patient was thought to be caused by occlusion of the
386
main left coronary artery by the tumor embo lus followed by reperfusion. The presence of tumor emboli and fresh infarcts in the kid neys as well as tumor fragments in the coro nary' artery suggested that the myocardial in farction in our patient was caused by coro nary' artery embolization from the left atrial myxoma. The extensiveness and transmural nature of the myocardial infarct, involving the whole anteroseptal and lateral walls of the left ventricle, indicated that the very proximal portion of the left coronary artery had been occluded for a relatively long period of time. Myocardial hemorrhage has been observed repeatedly in experimental animals subjected to coronary artery occlusion followed by re perfusion [5] and at necropsy in patients with acute myocardial infarction who underwent thrombolytic or surgical reperfusion [6], Thus, our finding of extensively hemorrhagic myocardial infarct with no tumor emboli in the major coronary arteries suggested that the coronary artery was reperfused after detach-
Tomita/Endo/Takano/Hayakawa/ Tamura/Sugisaki
Left Atrial Myxoma with Hemorrhagic Myocardial Infarction
Downloaded by: UCL 144.82.238.225 - 6/15/2018 5:14:41 PM
Fig. 2. a A polypoid gelatinous left atrial tumor (arrows) was found to be fixed via pedicle to the anterior margin o f the fossa ovalis. LV = Left ventricle, b Transverse section of the ventricular myocardium, showing extensive, transmural, hemorrhagic myocardial infarction. LV = Left ventricular cavity.
ment of the tumor embolus, most probably, from the ostium of the left coronary artery, the occurrence of which might relate to the upward displacement of the coronary ostium
observed in this patient. The timing of reper fusion could not be identified clinically from the analyses of enzymatic or electrocardio graphic changes.
387
Downloaded by: UCL 144.82.238.225 - 6/15/2018 5:14:41 PM
Fig. 3. a Microscopic section o f the tumor, showing polygonal cells with eosinophilic cytoplasm and hyperchromatic nuclei, sur rounded by myxomatous stroma. HE. b Histologic section of the cen tral infarct zone, showing myocar dial necrosis with contraction band formation and massive amounts o f extravasated erythrocytes in the in terstitial space. Few neutrophils in filtrated into the myocardium rela tive to the extent of myocardial ne crosis and hemorrhage. HE.
Whether reperfusion hemorrhage extends myocardial infarction or not is a controversial issue. In experimental animals, myocardial hemorrhage assessed grossly and microscopi cally has been reported to be within areas of necrosis in which severe vascular injury and irreversible myocardial damage have oc curred and is primarily located in the suben docardial portion [5], In necropsy patients, however, extension of the hemorrhage into areas of noninfarcted myocardium has been observed, and reperfusion hemorrhage may not be confined to the central necrotic zone [6], which is in accordance with the necropsy
findings of this patient. Recently, neutrophils have been suggested to have detrimental ef fects on the reperfused myocardium, causing myocardial reperfusion injury, although in our patient few neutrophils had infiltrated into the myocardium relative to the extent of myocardial necrosis and hemorrhage.
Acknowledgments We are grateful to Mrs. Tamiko Kikuchi for her secretarial assistance and Dr. Mari Watanabe for her advice in reviewing the manuscript.
References 4
388
Tomita/ Endo/Takano/Hayakawa/ Tamura/Sugisaki
5
Price DL. Harris JL. New PFJ. Cantu RC: Cardiac myxoma. A clinicopathologic and angiographic studv. Arch Neurol 1970:23:558— 567.' Endo T. Sato N. Hayakawa H. Maroko PR: Reduction of myocardial hemorrhage and the extent of necro sis by gallopamil (D600) in dogs with coronary artery reperfusion. J Cardiovasc Pharmacol 1991:18: 739-745.
6
Waller BE. Rothbaum DA. Pinker ton CA. Cowley MJ, LinnemeierTJ. Orr C. Irons M. Helmuth RA. Wills ER. Aust C: Status of the myocar dium and infarct-related coronary artery in 19 necropsy patients with acute recanalization using pharma cologic (streptokinase, r-tissuc plas minogen activator), mechanical (percutaneous transluminal coro nary angioplasty) or combined types of reperfusion therapy. J Am Coll Cardiol 1987:9:785-801.
Left Atrial Myxoma with Hemorrhagic Myocardial Infarction
Downloaded by: UCL 144.82.238.225 - 6/15/2018 5:14:41 PM
1 St. John Sutton MG. Mercier LA. Giuliani ER. Lie JT: Atrial myxo mas. A review of clinical experience in 40 patients. Mayo Clin Proc 1980:55:371-376. 2 Silverman J. Olwin JS. Graettinger JS: Cardiac myxomas with systemic embolization. Review of the litera ture and report of a case. Circulation 1962:26:99-103. 3 Rath S. Har-Zahav Y. Battler A, Agranat O. Neufeld HN: Coronary artery embolus from left atrial myx oma. Am J Cardiol 1984:54:1392— 1393.
