- Email: [email protected]
Coronary sinus dilatation in acute pulmonary embolism
1346
December
Brief Communications
American
3. Nerantzis C, Avgoustakis D. An S-shaped atria1 artery sul,plying the sinus node area. An anatomical study. Chest 1980;78:274-8. 4. Busquet J, Fontan F, Anderson RH, Ho YH, Davis MJ. ‘l’he surgical significance of the atria1 branches of the coronary arteries. Int J Cardiol 1984;6:P23-34. 5. Kennel AJ, Titus JL. The vasculature of the human sinus node. Mayo Clin Proc 1972;47:556-61.
Coronary sinus dilatation pulmonary embolism
in acute
Rolf L. Andersen, MD, and Allen H. Mogtader, MD. New York. N. Y.
The use of echocardiography in acute pulmonary embolism has been well described.lW6Some of the typical findings include dilatation of the pulmonary artery, dilatation and hypokinesis of the right ventricle, tricuspid regurgitation with systolic fluttering of the tricuspid valve, diminished E:F slope of the mitral valve, and abnormal septal configuration. Thrombolysis can rapidly reverse the hemodynamic and echocardiographic consequences of pulmonary embolism.6 In this report we describe an unusual echocar-
From The Division of Cardiology,Medical Service,St. Luke’+Roosevelt Hospital Center, and the Department of Medicine, Columbia University Collegeof Physiciansand Surgeons. Reprint requests:Allen H. MogtaderMD, Division of Cardiology,St. Luke’s Hospital, Amsterdam Avenueat 114th St., New York, NY 1002fi. 414115948
1989
Heart Journal
diographic finding in the setting of acute, massive pulmonary embolism. A 63.year-old man with a past history of venous insufticiency presented to the emergency department with 4 days of progressive dyspnea. Physical examination was notable for a blood pressure of 76/56 m m Hg, respiratory distress, jugular venous distention, and bibasilar rales. Chest, x-ray film showed cardiomegaly and decreased pulmonary vascular markings. The electrocardiogram displayed an S~-QII~ pattern, which progressed to a complete right bundle branch block. The patient’s hypotension responded to intravenous fluid administration. A ventilation-perfusion lung scan demonstrated multiple segmental perfusion defects consistent with pulmonary embolism. Swan-Ganz catheterization (Baxter Healthcare Corp., Edwards Division, Santa Ana, Calif.) revealed markedly elevated right heart pressures, with a right atria1 pressure of 28 m m Hg and a pulmonary artery pressure of 62/33 m m Hg. An echocardiogram was performed that showed a dilated right ventricle and right atrium, a prominent pulmonary artery, moderate t.ricuspid insufficiency, and abnormal systolic and diastolic septal flattening. In addition, an abnormally enlarged coronary sinus was noted (Figs. 1 and 2). The diameter of’ the sinus measured
I.1 cm. Intravenous
strep-
tokinase was administered at a dose of 100,000 units per hour because of progressive clinical deterioration. After I:! hours of thrombolytic therapy, significant clinical improvement was noted as well as a fall in pulmonary artery pressure to 40/20 m m Hg. Streptokinase was discontinued after 36 hours of infusion and heparin was reinstituted. A repeat lung scan demonstrated marked resolution of the perfusion defects. The patient was eventually discharged on warfarin sodium and has done well. Repeat echocardiographic stud-
Fig. 1. Parasternal long-axis view at end systole demonstrating a dilated coronary sinus (CS) 1.1 cm in diameter. A Swan-Ganz catheter (SGC) is present in the dilated right ventricle (RV). LV, Left ventricle; AO, aorta.
Volume
118
Number
6
Brief Communications 1347
Fig. 2. Parasternal short-axis view demonstrating a dilated coronary sinus. RA, Right atrium; IVS, interventricular septum; LVOT, left ventricular outflow tract; other abbreviations as in Fig. 1.
Fig. 3. Follow-up echocardiogram at end systole in the parasternal long-axis view. The coronary sinus is much smaller and measures 0.6 cm in diameter. It could not be visualized in the parasternal short-axis view. LA, Left atrium; other abbreviations as in Fig. 1.
ies 3 and 6 months later were identical to each other and demonstrated a decreasein the size of the right atrium and right ventricle, normalization of interventricular septal motion, and loss of tricuspid insufficiency. The coronary sinus was no longer dilated, measuring 0.6 cm in diameter on both studies (Fig. 3). The size of the normal coronary sinus has been evaluated in postmortem studies and by echocardiography. Potkin and Roberts7 found that the coronary sinus diameter ranged from 4.5 to 7.3 mm, with a mean of 6.2 m m in 19 normal male hearts. Using two-dimensional echocardiography, Ishimitsu et al8 found that the mean diameter of the coronary sinus in 25 normal patients was 6.7 mm, with
9 m m or greater considered abnormal. At the time of the initial echocardiographic examination, our patient’s coronary sinus was significantly enlarged, measuring 11 m m in diameter. Thrombolysis produced rapid hemodynamic improvement. Follow-up echocardiograms at 3 and 6 months documented resolution of the echocardiographic abnormalities seen in massive pulmonary embolism. The coronary sinus had decreasedby 46 % in diameter to 6 mm. Marked enlargement of the coronary sinus can be seen in certain congenital anomalies: persistent left superior vena cava draining into the coronary sinus, total anomalous pulmonary venous connection to the coronary sinus, and coronary arteriovenous fistula with drainage into the cor-
1348
December
Brief Communications
onary sinus. ‘9” The patient reported had no evidence of congenital heart disease. In addition, the fact that his car onary sinus was normal in size on follow-up echocardiographic examinations argues strongly against the presence of a congenital anomaly. Coronary sinus enlargement, has also been described in patients with right atria1 hypertension secondary to right ventricular dysfunction.1° Massive pulmonary embolism in our patient caused severe pulmonary hypertension with right ventricular failure. The resulting right atria1 pressure elevation presumably led to dilatation of the coronary sinus. Lysis of the patient’s pulmonary emboli produced a decrease in pulmonary artery pressure resulting in improved right ventricular function, As right ventricular function improved, right atria1 pressure fell and the coronary sinus diminished in size. Ishimitsu et a1.8found that coronary sinus dilatation was associated with volume overload of the right heart in patients with atria1 septal defect and tricuspid regurgitation. During his pulmonary embolism, our patient had moderate tricuspid regurgitation that later resolved. Tricuspid regurgitation could have exacerbated coronary sinus dilatation by further increasing right atria1 pressure, t,hereby increasing the distending pressure of the coronary sinus. Coronary sinus dilatation may be a useful marker of right ventricular failure and resultant right atria1 hypertension during acute pulmonary embolism, thus suggesting a massive or hemodynamically significant embolic event. Further studies are required to correlate changes in right atria1 pressure with the development of coronary sinus dilatation. REFERENCES
1. Jardin F, Dubourg 0, Gueret P, Delorme G, Bourdarias J. Quantitative two-dimensional echocardiography in massive pulmonary embolism: emphasis on ventricular interdependence and leftward septal displacement. J A m Co11 Cardiol 1987;10:1201-6. 2. Dianzumba SB, Monte110 NJ, Joyner CR. Systolic flutter of the tricuspid valve associated with massive pulmonary embolism. South Med J 1983;76:83-4. 3. Iwasaki T. Tanimoto M. Yamamoto T. Matikata S. Kawai Y. Yorifuji S.‘Echocardiographic abnormalities of tricuspid valve motion in pulmonary embolism. Br Heart J 1982;47:454-60. 4. Kasper W, Meinertz J, Jenkel B, Eissner D, Hahn K, Hofmann T, Zeiker A, Just H. Echocardiography findings in patients withprovedpulmonaryembolism.A~H~~~~J 1986; 112:128490. recognition of pulmonary arte5. Come PL. Echocardiographic rial disease and determination of its cause. A m J Med 1988;84:384-94. 6. Come PL, Ducksoo K, Parker JA, Goldhaber SZ, Braunwald E, Markis JE. Early reversal of right ventricular dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator. J A m Co11 Cardiol 1987;10:971-8. 7. Potkin BN, Roberts WC. Size of coronary sinus at necropsy in subjects without cardiac disease and in patients with various cardiac conditions. A m J Cardiol 1987;60:1418-21. 8. Ishimitsu T, Sakamoto T, Hada Y, Amano K, Yamaguchi T, Takenaka K, Takahashi M. Detection of coronary sinus by narasternal two-dimensional echocardiography and the clinla1 significance. J Cardiogr 1983;13:675-83. 9. Snider AR. Ports TA, Silverman NH. Venous anomalies of the coronary sinus: detection by M-mode, two-dimensional and contrast echocardiography. Circulation 1979;60:721-7. 10. Weyman AE. Cross-sectional echocardiography. Philadelphia: Lea & Febiger, 1982:209-11.
American
1989
Heart Journal
The differential diagnosis of partial absence of left pericardium and congenital left atrial aneurysm Jesus Vargas-Barron, MD, Tomas Sanchez-Ugarte, MD, Candace Keirns, MD, Jesus Vazquez-Sanchez, MD, Felipe Fernandez-Vazquez, MD, and Rodolfo Barragan, MD. Mexico City, Mexico
Congenital atriomegaly or1 congenital aneurysm of the left atrium (LAA) was first described by Semans and Taussig’ in 1938. This rare anomaly is sometimes associated with other congenital cardiovascular pathologic conditions (atria1 septal defect, persistent left superior vena cava, renal artery anomalies, and anomalous pulmonary venous return). Methods used to diagnose LAA include plain chest x-ray examination and lateral views, radionuclide blood pool imaging, two-dimensional echocardiography, and angiocardiography.2 In this article we report a case in which the correct diagnosis could not be made by any of these methods. The difficulty in establishing a differential diagnosis between LAA and partial congenital absence of the left pericardium and the advantage of computed axial tomography in distinguishing between the two is emphasized. A 19-year-old woman with no previous history of disease From the Department3 of Echocardiography, Radiology, and Surgery, the Institutl, National de Cardiologla “Ignacio Chavez.” Reprint requests: ,JesusVargas-Barrctn, MD, Department of Echocardiography, lnstituto National de Cardiologm “Ignacio Chavez,” Juan badiano No. 1, Mexico DF, 14080 Mexico. 414115949
Fig. 1. houette.
Plain chest x-ray showing abnormal cardiac silBulging
left border
is caused
by LAA
furrow).
December
Brief Communications
American
3. Nerantzis C, Avgoustakis D. An S-shaped atria1 artery sul,plying the sinus node area. An anatomical study. Chest 1980;78:274-8. 4. Busquet J, Fontan F, Anderson RH, Ho YH, Davis MJ. ‘l’he surgical significance of the atria1 branches of the coronary arteries. Int J Cardiol 1984;6:P23-34. 5. Kennel AJ, Titus JL. The vasculature of the human sinus node. Mayo Clin Proc 1972;47:556-61.
Coronary sinus dilatation pulmonary embolism
in acute
Rolf L. Andersen, MD, and Allen H. Mogtader, MD. New York. N. Y.
The use of echocardiography in acute pulmonary embolism has been well described.lW6Some of the typical findings include dilatation of the pulmonary artery, dilatation and hypokinesis of the right ventricle, tricuspid regurgitation with systolic fluttering of the tricuspid valve, diminished E:F slope of the mitral valve, and abnormal septal configuration. Thrombolysis can rapidly reverse the hemodynamic and echocardiographic consequences of pulmonary embolism.6 In this report we describe an unusual echocar-
From The Division of Cardiology,Medical Service,St. Luke’+Roosevelt Hospital Center, and the Department of Medicine, Columbia University Collegeof Physiciansand Surgeons. Reprint requests:Allen H. MogtaderMD, Division of Cardiology,St. Luke’s Hospital, Amsterdam Avenueat 114th St., New York, NY 1002fi. 414115948
1989
Heart Journal
diographic finding in the setting of acute, massive pulmonary embolism. A 63.year-old man with a past history of venous insufticiency presented to the emergency department with 4 days of progressive dyspnea. Physical examination was notable for a blood pressure of 76/56 m m Hg, respiratory distress, jugular venous distention, and bibasilar rales. Chest, x-ray film showed cardiomegaly and decreased pulmonary vascular markings. The electrocardiogram displayed an S~-QII~ pattern, which progressed to a complete right bundle branch block. The patient’s hypotension responded to intravenous fluid administration. A ventilation-perfusion lung scan demonstrated multiple segmental perfusion defects consistent with pulmonary embolism. Swan-Ganz catheterization (Baxter Healthcare Corp., Edwards Division, Santa Ana, Calif.) revealed markedly elevated right heart pressures, with a right atria1 pressure of 28 m m Hg and a pulmonary artery pressure of 62/33 m m Hg. An echocardiogram was performed that showed a dilated right ventricle and right atrium, a prominent pulmonary artery, moderate t.ricuspid insufficiency, and abnormal systolic and diastolic septal flattening. In addition, an abnormally enlarged coronary sinus was noted (Figs. 1 and 2). The diameter of’ the sinus measured
I.1 cm. Intravenous
strep-
tokinase was administered at a dose of 100,000 units per hour because of progressive clinical deterioration. After I:! hours of thrombolytic therapy, significant clinical improvement was noted as well as a fall in pulmonary artery pressure to 40/20 m m Hg. Streptokinase was discontinued after 36 hours of infusion and heparin was reinstituted. A repeat lung scan demonstrated marked resolution of the perfusion defects. The patient was eventually discharged on warfarin sodium and has done well. Repeat echocardiographic stud-
Fig. 1. Parasternal long-axis view at end systole demonstrating a dilated coronary sinus (CS) 1.1 cm in diameter. A Swan-Ganz catheter (SGC) is present in the dilated right ventricle (RV). LV, Left ventricle; AO, aorta.
Volume
118
Number
6
Brief Communications 1347
Fig. 2. Parasternal short-axis view demonstrating a dilated coronary sinus. RA, Right atrium; IVS, interventricular septum; LVOT, left ventricular outflow tract; other abbreviations as in Fig. 1.
Fig. 3. Follow-up echocardiogram at end systole in the parasternal long-axis view. The coronary sinus is much smaller and measures 0.6 cm in diameter. It could not be visualized in the parasternal short-axis view. LA, Left atrium; other abbreviations as in Fig. 1.
ies 3 and 6 months later were identical to each other and demonstrated a decreasein the size of the right atrium and right ventricle, normalization of interventricular septal motion, and loss of tricuspid insufficiency. The coronary sinus was no longer dilated, measuring 0.6 cm in diameter on both studies (Fig. 3). The size of the normal coronary sinus has been evaluated in postmortem studies and by echocardiography. Potkin and Roberts7 found that the coronary sinus diameter ranged from 4.5 to 7.3 mm, with a mean of 6.2 m m in 19 normal male hearts. Using two-dimensional echocardiography, Ishimitsu et al8 found that the mean diameter of the coronary sinus in 25 normal patients was 6.7 mm, with
9 m m or greater considered abnormal. At the time of the initial echocardiographic examination, our patient’s coronary sinus was significantly enlarged, measuring 11 m m in diameter. Thrombolysis produced rapid hemodynamic improvement. Follow-up echocardiograms at 3 and 6 months documented resolution of the echocardiographic abnormalities seen in massive pulmonary embolism. The coronary sinus had decreasedby 46 % in diameter to 6 mm. Marked enlargement of the coronary sinus can be seen in certain congenital anomalies: persistent left superior vena cava draining into the coronary sinus, total anomalous pulmonary venous connection to the coronary sinus, and coronary arteriovenous fistula with drainage into the cor-
1348
December
Brief Communications
onary sinus. ‘9” The patient reported had no evidence of congenital heart disease. In addition, the fact that his car onary sinus was normal in size on follow-up echocardiographic examinations argues strongly against the presence of a congenital anomaly. Coronary sinus enlargement, has also been described in patients with right atria1 hypertension secondary to right ventricular dysfunction.1° Massive pulmonary embolism in our patient caused severe pulmonary hypertension with right ventricular failure. The resulting right atria1 pressure elevation presumably led to dilatation of the coronary sinus. Lysis of the patient’s pulmonary emboli produced a decrease in pulmonary artery pressure resulting in improved right ventricular function, As right ventricular function improved, right atria1 pressure fell and the coronary sinus diminished in size. Ishimitsu et a1.8found that coronary sinus dilatation was associated with volume overload of the right heart in patients with atria1 septal defect and tricuspid regurgitation. During his pulmonary embolism, our patient had moderate tricuspid regurgitation that later resolved. Tricuspid regurgitation could have exacerbated coronary sinus dilatation by further increasing right atria1 pressure, t,hereby increasing the distending pressure of the coronary sinus. Coronary sinus dilatation may be a useful marker of right ventricular failure and resultant right atria1 hypertension during acute pulmonary embolism, thus suggesting a massive or hemodynamically significant embolic event. Further studies are required to correlate changes in right atria1 pressure with the development of coronary sinus dilatation. REFERENCES
1. Jardin F, Dubourg 0, Gueret P, Delorme G, Bourdarias J. Quantitative two-dimensional echocardiography in massive pulmonary embolism: emphasis on ventricular interdependence and leftward septal displacement. J A m Co11 Cardiol 1987;10:1201-6. 2. Dianzumba SB, Monte110 NJ, Joyner CR. Systolic flutter of the tricuspid valve associated with massive pulmonary embolism. South Med J 1983;76:83-4. 3. Iwasaki T. Tanimoto M. Yamamoto T. Matikata S. Kawai Y. Yorifuji S.‘Echocardiographic abnormalities of tricuspid valve motion in pulmonary embolism. Br Heart J 1982;47:454-60. 4. Kasper W, Meinertz J, Jenkel B, Eissner D, Hahn K, Hofmann T, Zeiker A, Just H. Echocardiography findings in patients withprovedpulmonaryembolism.A~H~~~~J 1986; 112:128490. recognition of pulmonary arte5. Come PL. Echocardiographic rial disease and determination of its cause. A m J Med 1988;84:384-94. 6. Come PL, Ducksoo K, Parker JA, Goldhaber SZ, Braunwald E, Markis JE. Early reversal of right ventricular dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator. J A m Co11 Cardiol 1987;10:971-8. 7. Potkin BN, Roberts WC. Size of coronary sinus at necropsy in subjects without cardiac disease and in patients with various cardiac conditions. A m J Cardiol 1987;60:1418-21. 8. Ishimitsu T, Sakamoto T, Hada Y, Amano K, Yamaguchi T, Takenaka K, Takahashi M. Detection of coronary sinus by narasternal two-dimensional echocardiography and the clinla1 significance. J Cardiogr 1983;13:675-83. 9. Snider AR. Ports TA, Silverman NH. Venous anomalies of the coronary sinus: detection by M-mode, two-dimensional and contrast echocardiography. Circulation 1979;60:721-7. 10. Weyman AE. Cross-sectional echocardiography. Philadelphia: Lea & Febiger, 1982:209-11.
American
1989
Heart Journal
The differential diagnosis of partial absence of left pericardium and congenital left atrial aneurysm Jesus Vargas-Barron, MD, Tomas Sanchez-Ugarte, MD, Candace Keirns, MD, Jesus Vazquez-Sanchez, MD, Felipe Fernandez-Vazquez, MD, and Rodolfo Barragan, MD. Mexico City, Mexico
Congenital atriomegaly or1 congenital aneurysm of the left atrium (LAA) was first described by Semans and Taussig’ in 1938. This rare anomaly is sometimes associated with other congenital cardiovascular pathologic conditions (atria1 septal defect, persistent left superior vena cava, renal artery anomalies, and anomalous pulmonary venous return). Methods used to diagnose LAA include plain chest x-ray examination and lateral views, radionuclide blood pool imaging, two-dimensional echocardiography, and angiocardiography.2 In this article we report a case in which the correct diagnosis could not be made by any of these methods. The difficulty in establishing a differential diagnosis between LAA and partial congenital absence of the left pericardium and the advantage of computed axial tomography in distinguishing between the two is emphasized. A 19-year-old woman with no previous history of disease From the Department3 of Echocardiography, Radiology, and Surgery, the Institutl, National de Cardiologla “Ignacio Chavez.” Reprint requests: ,JesusVargas-Barrctn, MD, Department of Echocardiography, lnstituto National de Cardiologm “Ignacio Chavez,” Juan badiano No. 1, Mexico DF, 14080 Mexico. 414115949
Fig. 1. houette.
Plain chest x-ray showing abnormal cardiac silBulging
left border
is caused
by LAA
furrow).