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Prenatal death from acute myocardial infarction and cardiac tamponade due to embolus from the placenta
Volume
109
Number
3, Part 1
Brief
The expected hemodynamic findings can be secondary to hemopericardium, constriction of the ventricles by the epicardial tumor, vena caval or tricuspid valvular obstruction, outflow obstruction, or a combination of mechanisms.In the present patient, elevated diastolic pressures in the ventricles, pulmonary artery wedge, and right atrium, along with angiographic findings, suggestedcon striction of the cardiac chambersby a tumor involving the right heart and raised the possibility of angiosarcoma subsequently confirmed on histopathology. Therapy of angiosarcomahas consistedof combinations of radiotherapy, chemotherapy, and surgery.5 To the best of our knowledge, this is the first casewhere hemodynamic and angiographic responseto resection surgery by means of cardiopulmonary bypass has been documented. The patient was on chemotherapy and survived for 8 months after surgery. REFERENCES
1. Glancy LD, Morales JB, Roberts WC: Angiosarcoma of the heart. Am J Cardiol 21:413, 1968. 2. Strohl KP: Angiosarcoma of the heart: A case study. Arch Intern Med 136:928, 1976. 3. Thompson DS, Westaby S, Lincoln JCR: Ventricular haemangioendothelioma diagnosed in life. Br Heart J 39:462, 1977. 4. Shackell M, Mitko A, Williams PL, Sulton GC: Angiosarcoma of the heart. Br Heart J 41:498, 1979. 5. Rossi NP, Kioschos JM, Aschenbrener CA, Ehrenhaft JL: Primary angiosarcoma of the heart. Cancer 37:891, 1976.
Prenatal death from acute myocardial infarction and cardiac tamponade due to embolus from the placenta Paul L. Wolf, M.D., Ken L. Jones, M.D., Sharon R. Longway, M.D., Kurt Benirschke, M.D., and Colin Bloor, M.D. San Diego, Calif.
Acute myocardial infarction is an infrequent cause of intrauterine fetal death. When present, it is virtually always associated with structurally abnormal coronary arteries. The purpose of this report is to document the occurrence of acute myocardial infarction secondary to coronary artery occlusion in a stillborn male infant of 37 weeks’ gestation. There were no congenital anomaliesof the coronary arteries. Microscopic evidence of fetal vascular occlusive diseasein multiple sections of the placenta suggeststhat occlusion of the coronary artery in this case was probably secondary to embolization from placental From the Departments nia Medical Center.
of Pathology
Reprint requests: Paul San Diego, CA 92103.
L. Wolf,
M.D.,
and Pediatrics, Pathology
University Dept.,
of Califor-
225 Dickinson
St.,
Communications
603
Fig. 1. Grossphotograph of heart and lungs demonstrating ruptured myocardial infarct (arrows).
vascular thrombi. The acute infarction resulted in myocardial rupture and fatal cardiac tamponade in utero. A stillborn male infant of 37 weeks’gestational agewas delivered near term to a 36-year-old gravida 3, para 2, mother. The pregnancy wasuneventful until a decreasein fetal movements was noted 2 days prior to delivery. The following day no fetal movements were noted by the mother. An ultrasound study performed on the day of delivery demonstrated absent fetal heart beats. The 2920 gm stillborn fetus was delivered by spontaneousvaginal delivery. At autopsy, no external congenital malformations were seen.Organ weights were normal, except for an enlarged thymus and congestedspleen. Thirty milliliters of clotted and unclotted blood were found in the pericardial sac, causing cardiac tamponade (Fig. 1). The heart and lungs weighed 84 gm (expected 68 gm). The anterior apical myocardium was dark red and soft, grossly consistent with an evolving acute myocardial infarct. There was a 3 x 2 mm perforation in the anterior right ventricular wall with a surrounding pale zone of myocardium. Anatomically normal coronary arteries were present. Both the foramen ovale and ductus arteriosus were patent. Heart valves were normal. The myocardium adjacent to the left anterior descendingcoronary artery was hemorrhagic. No other abnormalities were found in the heart or great vessels.The lungswere atelectatic, congested,and diffusely hemorrhagic. The brain was severely autolytic and weighed360gm. There wasacute passivecongestionof the liver, testicles,and spleen.Microscopic examination of the apex of the heart revealed necrotic myocardial muscle fibers with a few scattered neutrophils. The musclefibers showedlossof crossstriations and lossof nuclei. A section from the myocardium adjacent to the left anterior descending coronary artery also showed acute necrosis. These findings were consistent with a 2-day-old infarct. One section from the left ventricle showed a thromboembolus occluding a coronary artery branch. Microscopic examination of the lungs showedacute passivecongestion
March,
604
Brief Communications
American
Heart
1985 Journal
Fig. 2. Photomicrograph of thrombi in placental vessels.
and scattered areasof interstitial and subpleural hemorrhage. The umbilical cord contained three vesselsand measured 53 cm in length. The cord had an eccentric insertion. The placenta was found to be immature, pale, and edematouswith marginal infarcts. Microscopic examintion demonstrated multiple thrombi in the placental surface vesselsand umbilical vein (Fig. 2). The findings in this stillborn infant indicate that acute myocardial infarction can occur secondaryto intrauterine occlusion of a structurally normal coronary artery, and this is a rare phenomenon. Documentation of multiple thrombi in fetal placental surface vesselsas well as the umbilical vein suggeststhat systemic embolization must have occurred through the umbilical vein, ductus venosus, inferior vene cava, and patent foramen ovale paradoxically, leading to occlusionof a coronary artery. In a previous study by Hoyme et al.,’ it was demonstrated that some transverse limb reduction defects are probably due to occlusionof the brachial artery secondaryto embolization from microscopically similar placental vascular thrombi. Transverse limb reduction defect is a descriptive term used to characterize a specific type of limb abnormality involving reduction of one or more limbs distal to the elbow or knee. Gault and Usher2reported a caseof a premature infant who died at 18 hours of agefrom coronary thrombosisand myocardial infarction. Infantile intimal thickening subjacent to the coronary thrombosis waspresent. Bor3 classified acute myocardial infarction in infants and children into four categories:(1) embolisminto coronary arteries in eight patients; (2) inflammatory diseasesof coronary arteries in nine patients; (3) degenerative changes of coronary arteries in three patients; and (4) congenital abnormalities of coronary arteries in four patients. Of his 29 cases,8 (28%) were secondary to embolization to the coronary arteries. Most of these were associated with bacterial endocarditis, but one casewas causedby para-
doxical embolism of thrombi from a peripheral vessel. Arthur et a1.4reported a caseof acute myocardial infarction in a newborn that was secondary to coronary artery embolism,causingdeath at 23 hours. The ductus venosus contained an antemortem thrombus and these investigators concluded that the acute myocardial infarction was due to paradoxical embolization from ductus venosus thrombi to the anterior descending branch of the left coronary artery. Fletcher et, a1.5reported a case of acute myocardial infarction in a newborn infant associatedwith an umbilical cord hematoma.A thromboemboluswas found in the septal branch of the left anterior descendingartery, along with stasisthrombi in the umbilical vein. They suggested that the myocardial infarction wassecondary to paradoxical embolization from the umbilical vein to the septal branch of the left anterior descendingcoronary artery. Richart and Benirschke6describedtwo infants sustaining acute myocardial infarction in the perinatal period. In one neonate, infarction of a papillary musclehad occurred in utero with rupture shortly after birth. The findings in this caseindicate that an appropriate evaluation of the stillborn infant should include careful grossand microscopic evaluation of the coronary vasculature as well as the placenta for the presenceof fetal vascular occlusion.This unique situation also reemphasizesthe importance of performing autopsieson all stillborn fetuses.7 REFERENCES
1. Hoyme
HE,
Jones
KL,
Van
Allen
Ml,
Saunders
BS,
BenirschkeK: Vascularpathogenesis of transverselimb reduction defects. J Pediatr 101:&X39, 1982. 2. Gault MH, Usher R: Coronary thrombosis with myocardial infarction in a newborn infant: Clinical, electrocardiographic and post-mortem findings. N Engl J Med 263:379, 1960. 3. Bor I: Myocardial infarction and ischaemic heart disease in infants and children: Analysis of 29 cases and review of the literature. Arch Dis Child 44:268, 1969.
Volume Number
109 3. Part 1
4. Arthur A, Cottom D, Evans R, SpencerH: Myocardial infarction in a newborninfant. J Pediatr 73:110,1968. 5. FletcherMA, MeyerM, Kirkpatrick SE,PapelbaumS,Gluck L, BenirschkeK: Myocardial infarction associatedwith umbilicalcordhematoma.J Pediatr 89:806,1976. 6. Richart R, BenirschkeK: Myocardial infarction in the perinatal period: Report of two casesin newborninfants. J Pediatr 55:706,1959. 7. Mueller RF, Sybert VP, JohnsonJ, Brown ZA, ChenW-J: Evaluation of a protocol for post-mortemexaminationof stillbirths. N Engl J Med 309:587,1983.
Hydatid cyst of the heart: Diagnosis by two-dimensional echocardiography and computed tomography Joe Malouf, M.D., Faysal A. Saksouk, M.D., Samir Alam, M.D., GhassanK. Rizk, M.D., and Ibrahim Dagher, M.D. Beirut, Lebanon
Cardiac echinococcosisis characterized by a high incidence of intracardiac rupture and suddenlife-threatening complications.’ The rupture may be silent, with metastatic echinococcosisof the various organs being a late and often the only clue to the presence of an underlying From the Department of Internal Medicine, Division of Cardiology and the Department of Radiology, The American University of Beirut Medical Center. Reprint requests: Joe Malouf, M.D., Division of Cardiology, A.U.B.M.C., New York Office, 850 3rd Ave.. New York, NY 10022 (Attn: Maw Bajada).
Brief
Communications
606
cardiac involvement.’ To the best of our knowledge,there is no report of the use of computed tomography (CT) in cardiac echinococcosis, and very few reports have described the M-mode and two-dimensional echocardiographic (2DE) features in this disease.2*3 Herein we report a case of hydatid cyst of the heart detected by CT and 2DE. Y.S. is a 30-year-old man with a history sinceJuly, 1981, of hydatid cyst of the liver, maxillary sinus, baseof neck, chest wall, both kidneys, and recurrent hydatid diseaseof the brain. Whereasthe chest x-ray film remained normal, serial ECGs (Fig. 1) showedvarious abnormal patterns. In December,1983,he wasadmitted to the American University Medical Center becauseof orthopnea and dyspnea on exertion of 1 week duration. On physical examination the blood pressurewas110/70mm Hg, pulse waslOl/min, and temperature was 37’ C. The cardiovascular examination was normal. Auscultation of the lungs revealed bilateral basalcrackles. The chest x-ray film showedcardiomegaly with pulmonary congestion. M-mode and 2DE showed a large anterior and posterior echolucent space. The Mmode echocardiogram was otherwise normal. However, 2DE, in the apical four-chamber, “RAO equivalent,” and two-chamber views revealed two intramyocardial echolucent masseswith smooth contours (Figs 2, A and B) in the apex of the right ventricle (0.5 cm in diameter) and the left ventricular anterolateral apical segments(3.5 cm in diameter). The involved left ventricular segmentsproduced a diverticular-like deformity within the cavity and appeared dyskinetic (Fig. 2, B). Both cysts occupied most of the thickness of the affected walls, but neither appeared to communicatewith the ventricular cavity, and an echocontrast study through a peripheral vein wasnormal. A repeat echocardiogram5 days after admissionshowedcomplete resolution of the previously described effusion.
Fig. 1. Serial ECGs demonstrating the spectrum of abnormal ECG changesincluding RBBB and LAHB (September, 1983) seenin cardiac echinococcosis.
109
Number
3, Part 1
Brief
The expected hemodynamic findings can be secondary to hemopericardium, constriction of the ventricles by the epicardial tumor, vena caval or tricuspid valvular obstruction, outflow obstruction, or a combination of mechanisms.In the present patient, elevated diastolic pressures in the ventricles, pulmonary artery wedge, and right atrium, along with angiographic findings, suggestedcon striction of the cardiac chambersby a tumor involving the right heart and raised the possibility of angiosarcoma subsequently confirmed on histopathology. Therapy of angiosarcomahas consistedof combinations of radiotherapy, chemotherapy, and surgery.5 To the best of our knowledge, this is the first casewhere hemodynamic and angiographic responseto resection surgery by means of cardiopulmonary bypass has been documented. The patient was on chemotherapy and survived for 8 months after surgery. REFERENCES
1. Glancy LD, Morales JB, Roberts WC: Angiosarcoma of the heart. Am J Cardiol 21:413, 1968. 2. Strohl KP: Angiosarcoma of the heart: A case study. Arch Intern Med 136:928, 1976. 3. Thompson DS, Westaby S, Lincoln JCR: Ventricular haemangioendothelioma diagnosed in life. Br Heart J 39:462, 1977. 4. Shackell M, Mitko A, Williams PL, Sulton GC: Angiosarcoma of the heart. Br Heart J 41:498, 1979. 5. Rossi NP, Kioschos JM, Aschenbrener CA, Ehrenhaft JL: Primary angiosarcoma of the heart. Cancer 37:891, 1976.
Prenatal death from acute myocardial infarction and cardiac tamponade due to embolus from the placenta Paul L. Wolf, M.D., Ken L. Jones, M.D., Sharon R. Longway, M.D., Kurt Benirschke, M.D., and Colin Bloor, M.D. San Diego, Calif.
Acute myocardial infarction is an infrequent cause of intrauterine fetal death. When present, it is virtually always associated with structurally abnormal coronary arteries. The purpose of this report is to document the occurrence of acute myocardial infarction secondary to coronary artery occlusion in a stillborn male infant of 37 weeks’ gestation. There were no congenital anomaliesof the coronary arteries. Microscopic evidence of fetal vascular occlusive diseasein multiple sections of the placenta suggeststhat occlusion of the coronary artery in this case was probably secondary to embolization from placental From the Departments nia Medical Center.
of Pathology
Reprint requests: Paul San Diego, CA 92103.
L. Wolf,
M.D.,
and Pediatrics, Pathology
University Dept.,
of Califor-
225 Dickinson
St.,
Communications
603
Fig. 1. Grossphotograph of heart and lungs demonstrating ruptured myocardial infarct (arrows).
vascular thrombi. The acute infarction resulted in myocardial rupture and fatal cardiac tamponade in utero. A stillborn male infant of 37 weeks’gestational agewas delivered near term to a 36-year-old gravida 3, para 2, mother. The pregnancy wasuneventful until a decreasein fetal movements was noted 2 days prior to delivery. The following day no fetal movements were noted by the mother. An ultrasound study performed on the day of delivery demonstrated absent fetal heart beats. The 2920 gm stillborn fetus was delivered by spontaneousvaginal delivery. At autopsy, no external congenital malformations were seen.Organ weights were normal, except for an enlarged thymus and congestedspleen. Thirty milliliters of clotted and unclotted blood were found in the pericardial sac, causing cardiac tamponade (Fig. 1). The heart and lungs weighed 84 gm (expected 68 gm). The anterior apical myocardium was dark red and soft, grossly consistent with an evolving acute myocardial infarct. There was a 3 x 2 mm perforation in the anterior right ventricular wall with a surrounding pale zone of myocardium. Anatomically normal coronary arteries were present. Both the foramen ovale and ductus arteriosus were patent. Heart valves were normal. The myocardium adjacent to the left anterior descendingcoronary artery was hemorrhagic. No other abnormalities were found in the heart or great vessels.The lungswere atelectatic, congested,and diffusely hemorrhagic. The brain was severely autolytic and weighed360gm. There wasacute passivecongestionof the liver, testicles,and spleen.Microscopic examination of the apex of the heart revealed necrotic myocardial muscle fibers with a few scattered neutrophils. The musclefibers showedlossof crossstriations and lossof nuclei. A section from the myocardium adjacent to the left anterior descending coronary artery also showed acute necrosis. These findings were consistent with a 2-day-old infarct. One section from the left ventricle showed a thromboembolus occluding a coronary artery branch. Microscopic examination of the lungs showedacute passivecongestion
March,
604
Brief Communications
American
Heart
1985 Journal
Fig. 2. Photomicrograph of thrombi in placental vessels.
and scattered areasof interstitial and subpleural hemorrhage. The umbilical cord contained three vesselsand measured 53 cm in length. The cord had an eccentric insertion. The placenta was found to be immature, pale, and edematouswith marginal infarcts. Microscopic examintion demonstrated multiple thrombi in the placental surface vesselsand umbilical vein (Fig. 2). The findings in this stillborn infant indicate that acute myocardial infarction can occur secondaryto intrauterine occlusion of a structurally normal coronary artery, and this is a rare phenomenon. Documentation of multiple thrombi in fetal placental surface vesselsas well as the umbilical vein suggeststhat systemic embolization must have occurred through the umbilical vein, ductus venosus, inferior vene cava, and patent foramen ovale paradoxically, leading to occlusionof a coronary artery. In a previous study by Hoyme et al.,’ it was demonstrated that some transverse limb reduction defects are probably due to occlusionof the brachial artery secondaryto embolization from microscopically similar placental vascular thrombi. Transverse limb reduction defect is a descriptive term used to characterize a specific type of limb abnormality involving reduction of one or more limbs distal to the elbow or knee. Gault and Usher2reported a caseof a premature infant who died at 18 hours of agefrom coronary thrombosisand myocardial infarction. Infantile intimal thickening subjacent to the coronary thrombosis waspresent. Bor3 classified acute myocardial infarction in infants and children into four categories:(1) embolisminto coronary arteries in eight patients; (2) inflammatory diseasesof coronary arteries in nine patients; (3) degenerative changes of coronary arteries in three patients; and (4) congenital abnormalities of coronary arteries in four patients. Of his 29 cases,8 (28%) were secondary to embolization to the coronary arteries. Most of these were associated with bacterial endocarditis, but one casewas causedby para-
doxical embolism of thrombi from a peripheral vessel. Arthur et a1.4reported a caseof acute myocardial infarction in a newborn that was secondary to coronary artery embolism,causingdeath at 23 hours. The ductus venosus contained an antemortem thrombus and these investigators concluded that the acute myocardial infarction was due to paradoxical embolization from ductus venosus thrombi to the anterior descending branch of the left coronary artery. Fletcher et, a1.5reported a case of acute myocardial infarction in a newborn infant associatedwith an umbilical cord hematoma.A thromboemboluswas found in the septal branch of the left anterior descendingartery, along with stasisthrombi in the umbilical vein. They suggested that the myocardial infarction wassecondary to paradoxical embolization from the umbilical vein to the septal branch of the left anterior descendingcoronary artery. Richart and Benirschke6describedtwo infants sustaining acute myocardial infarction in the perinatal period. In one neonate, infarction of a papillary musclehad occurred in utero with rupture shortly after birth. The findings in this caseindicate that an appropriate evaluation of the stillborn infant should include careful grossand microscopic evaluation of the coronary vasculature as well as the placenta for the presenceof fetal vascular occlusion.This unique situation also reemphasizesthe importance of performing autopsieson all stillborn fetuses.7 REFERENCES
1. Hoyme
HE,
Jones
KL,
Van
Allen
Ml,
Saunders
BS,
BenirschkeK: Vascularpathogenesis of transverselimb reduction defects. J Pediatr 101:&X39, 1982. 2. Gault MH, Usher R: Coronary thrombosis with myocardial infarction in a newborn infant: Clinical, electrocardiographic and post-mortem findings. N Engl J Med 263:379, 1960. 3. Bor I: Myocardial infarction and ischaemic heart disease in infants and children: Analysis of 29 cases and review of the literature. Arch Dis Child 44:268, 1969.
Volume Number
109 3. Part 1
4. Arthur A, Cottom D, Evans R, SpencerH: Myocardial infarction in a newborninfant. J Pediatr 73:110,1968. 5. FletcherMA, MeyerM, Kirkpatrick SE,PapelbaumS,Gluck L, BenirschkeK: Myocardial infarction associatedwith umbilicalcordhematoma.J Pediatr 89:806,1976. 6. Richart R, BenirschkeK: Myocardial infarction in the perinatal period: Report of two casesin newborninfants. J Pediatr 55:706,1959. 7. Mueller RF, Sybert VP, JohnsonJ, Brown ZA, ChenW-J: Evaluation of a protocol for post-mortemexaminationof stillbirths. N Engl J Med 309:587,1983.
Hydatid cyst of the heart: Diagnosis by two-dimensional echocardiography and computed tomography Joe Malouf, M.D., Faysal A. Saksouk, M.D., Samir Alam, M.D., GhassanK. Rizk, M.D., and Ibrahim Dagher, M.D. Beirut, Lebanon
Cardiac echinococcosisis characterized by a high incidence of intracardiac rupture and suddenlife-threatening complications.’ The rupture may be silent, with metastatic echinococcosisof the various organs being a late and often the only clue to the presence of an underlying From the Department of Internal Medicine, Division of Cardiology and the Department of Radiology, The American University of Beirut Medical Center. Reprint requests: Joe Malouf, M.D., Division of Cardiology, A.U.B.M.C., New York Office, 850 3rd Ave.. New York, NY 10022 (Attn: Maw Bajada).
Brief
Communications
606
cardiac involvement.’ To the best of our knowledge,there is no report of the use of computed tomography (CT) in cardiac echinococcosis, and very few reports have described the M-mode and two-dimensional echocardiographic (2DE) features in this disease.2*3 Herein we report a case of hydatid cyst of the heart detected by CT and 2DE. Y.S. is a 30-year-old man with a history sinceJuly, 1981, of hydatid cyst of the liver, maxillary sinus, baseof neck, chest wall, both kidneys, and recurrent hydatid diseaseof the brain. Whereasthe chest x-ray film remained normal, serial ECGs (Fig. 1) showedvarious abnormal patterns. In December,1983,he wasadmitted to the American University Medical Center becauseof orthopnea and dyspnea on exertion of 1 week duration. On physical examination the blood pressurewas110/70mm Hg, pulse waslOl/min, and temperature was 37’ C. The cardiovascular examination was normal. Auscultation of the lungs revealed bilateral basalcrackles. The chest x-ray film showedcardiomegaly with pulmonary congestion. M-mode and 2DE showed a large anterior and posterior echolucent space. The Mmode echocardiogram was otherwise normal. However, 2DE, in the apical four-chamber, “RAO equivalent,” and two-chamber views revealed two intramyocardial echolucent masseswith smooth contours (Figs 2, A and B) in the apex of the right ventricle (0.5 cm in diameter) and the left ventricular anterolateral apical segments(3.5 cm in diameter). The involved left ventricular segmentsproduced a diverticular-like deformity within the cavity and appeared dyskinetic (Fig. 2, B). Both cysts occupied most of the thickness of the affected walls, but neither appeared to communicatewith the ventricular cavity, and an echocontrast study through a peripheral vein wasnormal. A repeat echocardiogram5 days after admissionshowedcomplete resolution of the previously described effusion.
Fig. 1. Serial ECGs demonstrating the spectrum of abnormal ECG changesincluding RBBB and LAHB (September, 1983) seenin cardiac echinococcosis.