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Totally anomalous pulmonary venous connection in an infant with tricuspid atresia
113
mittent obstruction to the left ventricular inflow and resultant pulmonary oedema. Sudden development of a large free-floating thrombus within 10 days of successful closed mitral valvotomy was unusual and cross-sectional echocardiography helped in this rare diagnosis, which could have been life-threatening. References 1 Fraser AG, Angelini
GD, Ikram S, Butchart EC. Left atria1 ball thrombus: echocardiographic features and clinical implications. Eur Heart J 1988;9:672-677.
International Elsevier
CARD10
Journal of Cardiology,
2 Maltaghati
A, Pepi M. Fiorentini C. Doppler and echocardiographic diagnosis of a free-floating left atrial thrombus. Int J Cardiol 1989;25:131-134. 3 Heller SJ, Carleton RA. Abnormal left ventricular contraction in patients with mitral stenosis. Circulation 1970:42: 1099-1110. 4 Silverstein DM, Hansen DP, Ojiambo HP, Griswold HE. Left ventricular function in severe mitral stenosis as seen at the Kenyatta National Hospital. Am Heart J 1980;99:727733. 5 Mohan JC, Reddy KS, Mukhopadhaya S. Bhatia ML. Left ventricular aneurysm following closed mitral valvotomy: report of two cases. Ind Heart J 1985;37:62-65.
28 (1990) 113-117
10904
Totally anomalous pulmonary venous connection in an infant with tricuspid atresia Monica
L. Garrick,
Ralph D. Siewers and Frederick
S. Sherman
Division of Pediatric Cardiology, Children’s Hospital of Pittsburgh, University of Pittsburgh Pennsylvania, 0: S.A. (Received
23 October
1989; revision
accepted
2 February
School of Medicine, Pittsburgh,
1990)
The occurrence of tricuspid atresia in association with totally anomalous pulmonary venous connection is a rare one. This combination has been described in the literature only twice previously. Such a case is presented with special regard to the therapeutic options and the need for cardiac catheterization. Key words:
Tricuspid
atresia;
Anomalous
pulmonary
venous connection
Introduction Tricuspid atresia comprises 2-3% of all cases of congenital heart disease [l]. A ventricular septal defect is an essential component of the lesion for survival. Other common associated defects include atria1 septal defect, pulmonary stenosis and discordant ventriculo-
arterial connections 121. Tricuspid atresia with totaliy anomalous pulmonary venous connection has been described in the literature, to the best of our knowledge, only twice previously [3,4]. There is no example of such a heart in the 2100 specimens in the Children’s Hospital of Pittsburgh Cardiac Museum. In this report, we describe a further example of the rare association of these lesions. Case Report
Correspondence to: M.L. Garrick, M.D., Children’s Hospital of Pittsburgh, 3705 Fifth Avenue at DeSoto St.. Pittsburgh, PA 15213. U.S.A.
O167-5273/90/$03.50
0 1990 Elsevier Science
Publishers
A 6-day-old. 3800-gram infant was transferred to the Children’s Hospital of Pittsburgh for treatment of con-
B.V. (Biomedical
Division)
gestive heart failure. The 34-week gestation was complicated by maternal gestational diabetes. An ultrasonic study at 30 weeks gestation had demonstrated the anatomy of tricuspid atresia, a large ventricular septal defect and normally related great arteries with a concordant ventriculo-arterial connection. The baby was stable during the first 5 days of life. The initial chest radiograph showed cardiomegaly and normal pulmonary vascular markings. An echocardiogram done on the first day of life without the use of color Doppler demonstrated the same anatomy. The infant was transferred to this institution for pulmonary arterial banding. On examination he was acyanotic but tachycardic and tachypneic. There was a grade II/VI systolic ejection murmur at the upper left sternal border and the second heart sound was single. A chest radiograph showed cardiomegaly and bilaterally increased interstitial pulmonary markings. Repeat echocardiography demonstrated tricuspid atresia but showed, in addition, totally anomalous pulmonary venous connection to the brachiocephalic vein (Fig. 1A. B). Prominent echo densities lined the left ventricle and the posteromedial papillary muscle suggestive of endomyocardial fibroelastosis. Ventricular function was normal. The anatomy of tricuspid atresia and unobstructed anomalous pulmonary venous connection was confirmed at catheterization (Fig. lC, D). Unrestricted atria1 and ventricular septal defects were documented, and the pulmonary arterial pressure was systemic. There was no obstruction to left ventricular output. After catheterization, the condition of the neonate deteriorated. Hypotension, metabolic acidosis and respiratory insufficiency required resuscitative treatment. High levels of positive end-expiratory pressure partially stabilized the baby and improved systemic blood pressure, although the acidosis persisted. Fourteen hours after the catheterization, a band was placed on the pulmonary trunk. The intra- and immediate postoperative courses required maximum support. Within 24 hours, cardiopulmonary stability had been established and inotropic support reduced. Ultrasonic examination of the head, however, demonstrated bilateral severe hemorrhages and electroencephalography showed diffuse slowing and widespread seizure activity. Support was withdrawn and the infant died on the ninth day, 36 hours after the operative procedure. Postmortem examination was limited to the thorax. The only finding other than the anticipated totally anomalous pulmonary venous connection (Fig. 2) was left ventricular hypertrophy. There was no evidence for endomyocardial fibroelastosis.
Discussion This case promotes consideration of several issues concerning management. Excessive pulmonary blood flow was the result of decreasing pulmonary vascular resistance in the face of an unrestrictive ventricular septal defect and the absence of pulmonary stenosis (the latter, seen more frequently with a concordant ventriculoarterial connection, was not present in our patient). These children should be maintained on minimal concentrations of inspired oxygen and ventilated to produce slightly elevated arterial levels of carbon dioxide to vasoconstrict the pulmonary bed. The low systemic output and metabolic acidosis after cardiac catheterization are not readily explained. Lowionic contrast was used within the recommended volume limits. Evidence for obstruction to left ventricular outflow was not found echocardiographically. angiographitally nor at autopsy. The deleterious effect of the catheterization on this infant was thought, possibly, to have been due to endomyocardial fibroelastosis, which was suspected echocardiographically. This was not confirmed at autopsy. The echocardiographic aspects of this case are important. Anomalous pulmonary venous connections are difficult to diagnose during fetal life due to decreased pulmonary blood flow. This results in small, non-distended venous structures which are difficult to image, and detection by color Doppler is limited (even when a low-velocity profile is employed). Postnatally, the retroatria1 confluence may be difficult to image for the same especially in the absence of obstructed reason, pulmonary venous return. Color Doppler has proven to be a necessary adjunct to cross-sectional imaging for distinction of both normal and abnormal vascular structures [5]. The low velocity profile must be used for optimal color resolution of these low flow states. The therapeutic options consisted of banding of the pulmonary trunk combined with repair of the anomalous venous connection, or banding alone as a palliative procedure with subsequent repair of the anomalous venous return at the time of a modified Fontan procedure. Excessive pulmonary blood flow and decreased systemic cardiac output were the primary problems in our patient. We chose banding alone, therefore, as the safest and most direct palliative procedure. Early restriction of pulmonary blood flow by means of a band might offer excellent palliation for this rare cardiac anomaly. Failure in this case was caused by the sequels of hypotension, low systemic cardiac output and profound acidosis following catheterization and prior to placement of the band. Avoiding the stress of cardiac
Fig. 1. A. Echocardiogram in the suprastemal notch projection demonstrating bilateral anomalous pulmonary venous drainage to the venous confluence (C) and brachiocephalic vein (BV), via a vertical vein (W). B. Echocardiogram in the apical four-chamber projection. The absent right atrioventricular connection (solid arrow) and the opened mitral leaflet are well seen. The right ventricle is hypoplastic and a large ventricular septal defect (open arrow) is present. The pulmonary venous confluence (C) is seen behind the left atrium (LA). LV = left ventricle; RA = right atrium. CD. Cineangiogram of the pulmonary venous confluence in the anterior-posterior projection. Early phase (C) demonstrates anomalous venous connection of the right pulmonary veins to the brachiocephalic vein (BV) via the vertical vein (VV) and thence to the superior caval vein (XV). Later phase (D) demonstrates the absent right atrioventricular connection (solid arrows) and the interatrial communication (open arrows).
116
Fig . 2. Pathologic specimen demonstrating the absent right atrioventricular connection (large arrow), and anomalous connection oi the vertical vein (small arrows) to the bracbiocephalic vein (BV). Superior caval vein (SCV).
cat.heterization is an attractive retrospective consideration. It seemed essential to establish that the interatrial communication and pulmonary venous return were unobstructed. Since anomalous connection to a left vertical vein which courses anteriorly to the left bronchus is rarely, if ever, obstructive, and since echocarcliographic evaluation established the true position of the vertical vein, one may argue that catheterization could have been avoided. If later the interatrial communication was
found to be restrictive, a septostomy could have been performed. We would recommend avoidance of catheterization, therefore, if confronted with such a case in the future.
References 1 Report of the New England Regional Infant Cardiac Program. Pediatrics 1980;65(suppl):388:392-403. 2 Zuberbubler JR. Valvular atresia. In: Zuberbubler, JR, ed. Clinical diagnosis in pediatric cardiology. New York: 1981;107-108. 3 Guller B, Ritter DG, Kincaid OW. Tricuspid atresia with pulmonary atresia and total anomalous pulmonary venous connection to the right superior vena cava. Mayo Clin Proc 1972;45:105-109. 4 Pieri D, Rubino A, Pipitone S, Grill0 R, LaMonaca P, Sperandeo V. Tricuspid atresia and total anomalous pulmonary venous return of supracardiac type. Report of a
117
case associated with extracardiac Cardiol 1987;17:613-616. 5 Van Hare GF, Schmit KG, Cassidy
International Journal of Cardiology, Elsevier CARD10
malformations. SC, Gooding
G
Ital
CA, Silver-
man NH. Color Doppler flow mapping in the ultrasound diagnosis of total anomalous pulmonary venous connection. J Am Sot Echo 1988;1:341-347.
28 (1990) 117- 119
10905
Coronary
arterial aneurysm after percutaneous transluminal coronary recanalization with streptokinase Ming-Fong
Department
Chen, Chiau-Suong
Liau and Yuan-Teh
Lee
of Internal Medicine (Cardiology, National Taiwan University Hospital, Taipei, Taiwan. R. 0. C. (Received
20 November
1989; revision accepted
2 February
1990)
A 49-year-old man developed an aneurysm of the right coronary artery after successful thrombolytic therapy with streptokinase following an acute inferior wall myocardial infarction. He was free from symptoms despite the existence of the aneurysm. The possible mechanisms for the formation of the aneurysm are discussed. Key words:
Coronary
arterial
aneurysm;
Acute myocardial
Introduction The most frequent cause of coronary arterial aneurysms as studied in Japan is Kawasaki disease [l]. In Western countries, it is usually related to atherosclerosis [2], or is a complication of percutaneous transluminal coronary angioplasty [3]. In this report, we present a case of acute myocardial infarction in which a coronary arterial aneurysm occurred one month after successful recanalization using intracoronary streptokinase. This is, to date, a very rare complication after thrombolytic therapy. Case Report A 49-year-old man was sent to the emergency room on 17 August 1985, because of an angina1 attack lasting
Correspondence to: Yuan-Teh Lee., M.D., Ph.D., Dept. of Internal Medicine (Cardiology), National Taiwan University Hospital, 1, Chang-Teh Street, Taipei, Taiwan, Republic of China. This report was included in the “Multi-Hospital Cooperative Study on Acute Myocardial Infarction in Taiwan”. The study was supported by a grant from the National Science Council and the Department of Health, the Executive Yuan, R.O.C. 0167-5273/90/$03.50
0 1990 Elsevier Science Publishers
infarction;
Thrombolytic
therapy
half an hour. Similar pains had waxed and waned in the previous week. His coronary risk factors included hypertension, smoking, a family history of cardiovascular disease, type A personality and sedentary life. Physical examination revealed a man looking acutely ill. The blood pressure was 158/86 mm Hg, and the heart rate was 72 beats/m.in with regular beats. The breathing sound was clear. There was a normal S, and an audible S, without a heart murmur. The chest X-ray revealed cardiomegaly and mild congestion of the lungs. The electrocardiogram showed ST segment elevation in leads II, II and aVF with reciprocal changes in precordial leads. Intracoronary streptokinase was given within 2 hours of the onset of the pain at the dose of 4000 units per min, for a period of 50 minutes. Prior to that. selective coronary arteriograms showed a total occlusion with a thrombus visible in the middle portion of the right coronary artery (Fig. la). The arteriograms were repeated at 10 minute intervals during the infusion of streptokinase, showing a gradual visualization of the distal part and total recanalization at the 40th minute. yet leaving an 80% residual stenosis at the middle portion (Fig. lb). A maintenance dose of intravenous streptokinase 750,000 units was given for 24 hours. Anticoagulation and antiplatelet therapies were given later. There was no other complication. Follow-up
B.V. (Biomedical
Division)
mittent obstruction to the left ventricular inflow and resultant pulmonary oedema. Sudden development of a large free-floating thrombus within 10 days of successful closed mitral valvotomy was unusual and cross-sectional echocardiography helped in this rare diagnosis, which could have been life-threatening. References 1 Fraser AG, Angelini
GD, Ikram S, Butchart EC. Left atria1 ball thrombus: echocardiographic features and clinical implications. Eur Heart J 1988;9:672-677.
International Elsevier
CARD10
Journal of Cardiology,
2 Maltaghati
A, Pepi M. Fiorentini C. Doppler and echocardiographic diagnosis of a free-floating left atrial thrombus. Int J Cardiol 1989;25:131-134. 3 Heller SJ, Carleton RA. Abnormal left ventricular contraction in patients with mitral stenosis. Circulation 1970:42: 1099-1110. 4 Silverstein DM, Hansen DP, Ojiambo HP, Griswold HE. Left ventricular function in severe mitral stenosis as seen at the Kenyatta National Hospital. Am Heart J 1980;99:727733. 5 Mohan JC, Reddy KS, Mukhopadhaya S. Bhatia ML. Left ventricular aneurysm following closed mitral valvotomy: report of two cases. Ind Heart J 1985;37:62-65.
28 (1990) 113-117
10904
Totally anomalous pulmonary venous connection in an infant with tricuspid atresia Monica
L. Garrick,
Ralph D. Siewers and Frederick
S. Sherman
Division of Pediatric Cardiology, Children’s Hospital of Pittsburgh, University of Pittsburgh Pennsylvania, 0: S.A. (Received
23 October
1989; revision
accepted
2 February
School of Medicine, Pittsburgh,
1990)
The occurrence of tricuspid atresia in association with totally anomalous pulmonary venous connection is a rare one. This combination has been described in the literature only twice previously. Such a case is presented with special regard to the therapeutic options and the need for cardiac catheterization. Key words:
Tricuspid
atresia;
Anomalous
pulmonary
venous connection
Introduction Tricuspid atresia comprises 2-3% of all cases of congenital heart disease [l]. A ventricular septal defect is an essential component of the lesion for survival. Other common associated defects include atria1 septal defect, pulmonary stenosis and discordant ventriculo-
arterial connections 121. Tricuspid atresia with totaliy anomalous pulmonary venous connection has been described in the literature, to the best of our knowledge, only twice previously [3,4]. There is no example of such a heart in the 2100 specimens in the Children’s Hospital of Pittsburgh Cardiac Museum. In this report, we describe a further example of the rare association of these lesions. Case Report
Correspondence to: M.L. Garrick, M.D., Children’s Hospital of Pittsburgh, 3705 Fifth Avenue at DeSoto St.. Pittsburgh, PA 15213. U.S.A.
O167-5273/90/$03.50
0 1990 Elsevier Science
Publishers
A 6-day-old. 3800-gram infant was transferred to the Children’s Hospital of Pittsburgh for treatment of con-
B.V. (Biomedical
Division)
gestive heart failure. The 34-week gestation was complicated by maternal gestational diabetes. An ultrasonic study at 30 weeks gestation had demonstrated the anatomy of tricuspid atresia, a large ventricular septal defect and normally related great arteries with a concordant ventriculo-arterial connection. The baby was stable during the first 5 days of life. The initial chest radiograph showed cardiomegaly and normal pulmonary vascular markings. An echocardiogram done on the first day of life without the use of color Doppler demonstrated the same anatomy. The infant was transferred to this institution for pulmonary arterial banding. On examination he was acyanotic but tachycardic and tachypneic. There was a grade II/VI systolic ejection murmur at the upper left sternal border and the second heart sound was single. A chest radiograph showed cardiomegaly and bilaterally increased interstitial pulmonary markings. Repeat echocardiography demonstrated tricuspid atresia but showed, in addition, totally anomalous pulmonary venous connection to the brachiocephalic vein (Fig. 1A. B). Prominent echo densities lined the left ventricle and the posteromedial papillary muscle suggestive of endomyocardial fibroelastosis. Ventricular function was normal. The anatomy of tricuspid atresia and unobstructed anomalous pulmonary venous connection was confirmed at catheterization (Fig. lC, D). Unrestricted atria1 and ventricular septal defects were documented, and the pulmonary arterial pressure was systemic. There was no obstruction to left ventricular output. After catheterization, the condition of the neonate deteriorated. Hypotension, metabolic acidosis and respiratory insufficiency required resuscitative treatment. High levels of positive end-expiratory pressure partially stabilized the baby and improved systemic blood pressure, although the acidosis persisted. Fourteen hours after the catheterization, a band was placed on the pulmonary trunk. The intra- and immediate postoperative courses required maximum support. Within 24 hours, cardiopulmonary stability had been established and inotropic support reduced. Ultrasonic examination of the head, however, demonstrated bilateral severe hemorrhages and electroencephalography showed diffuse slowing and widespread seizure activity. Support was withdrawn and the infant died on the ninth day, 36 hours after the operative procedure. Postmortem examination was limited to the thorax. The only finding other than the anticipated totally anomalous pulmonary venous connection (Fig. 2) was left ventricular hypertrophy. There was no evidence for endomyocardial fibroelastosis.
Discussion This case promotes consideration of several issues concerning management. Excessive pulmonary blood flow was the result of decreasing pulmonary vascular resistance in the face of an unrestrictive ventricular septal defect and the absence of pulmonary stenosis (the latter, seen more frequently with a concordant ventriculoarterial connection, was not present in our patient). These children should be maintained on minimal concentrations of inspired oxygen and ventilated to produce slightly elevated arterial levels of carbon dioxide to vasoconstrict the pulmonary bed. The low systemic output and metabolic acidosis after cardiac catheterization are not readily explained. Lowionic contrast was used within the recommended volume limits. Evidence for obstruction to left ventricular outflow was not found echocardiographically. angiographitally nor at autopsy. The deleterious effect of the catheterization on this infant was thought, possibly, to have been due to endomyocardial fibroelastosis, which was suspected echocardiographically. This was not confirmed at autopsy. The echocardiographic aspects of this case are important. Anomalous pulmonary venous connections are difficult to diagnose during fetal life due to decreased pulmonary blood flow. This results in small, non-distended venous structures which are difficult to image, and detection by color Doppler is limited (even when a low-velocity profile is employed). Postnatally, the retroatria1 confluence may be difficult to image for the same especially in the absence of obstructed reason, pulmonary venous return. Color Doppler has proven to be a necessary adjunct to cross-sectional imaging for distinction of both normal and abnormal vascular structures [5]. The low velocity profile must be used for optimal color resolution of these low flow states. The therapeutic options consisted of banding of the pulmonary trunk combined with repair of the anomalous venous connection, or banding alone as a palliative procedure with subsequent repair of the anomalous venous return at the time of a modified Fontan procedure. Excessive pulmonary blood flow and decreased systemic cardiac output were the primary problems in our patient. We chose banding alone, therefore, as the safest and most direct palliative procedure. Early restriction of pulmonary blood flow by means of a band might offer excellent palliation for this rare cardiac anomaly. Failure in this case was caused by the sequels of hypotension, low systemic cardiac output and profound acidosis following catheterization and prior to placement of the band. Avoiding the stress of cardiac
Fig. 1. A. Echocardiogram in the suprastemal notch projection demonstrating bilateral anomalous pulmonary venous drainage to the venous confluence (C) and brachiocephalic vein (BV), via a vertical vein (W). B. Echocardiogram in the apical four-chamber projection. The absent right atrioventricular connection (solid arrow) and the opened mitral leaflet are well seen. The right ventricle is hypoplastic and a large ventricular septal defect (open arrow) is present. The pulmonary venous confluence (C) is seen behind the left atrium (LA). LV = left ventricle; RA = right atrium. CD. Cineangiogram of the pulmonary venous confluence in the anterior-posterior projection. Early phase (C) demonstrates anomalous venous connection of the right pulmonary veins to the brachiocephalic vein (BV) via the vertical vein (VV) and thence to the superior caval vein (XV). Later phase (D) demonstrates the absent right atrioventricular connection (solid arrows) and the interatrial communication (open arrows).
116
Fig . 2. Pathologic specimen demonstrating the absent right atrioventricular connection (large arrow), and anomalous connection oi the vertical vein (small arrows) to the bracbiocephalic vein (BV). Superior caval vein (SCV).
cat.heterization is an attractive retrospective consideration. It seemed essential to establish that the interatrial communication and pulmonary venous return were unobstructed. Since anomalous connection to a left vertical vein which courses anteriorly to the left bronchus is rarely, if ever, obstructive, and since echocarcliographic evaluation established the true position of the vertical vein, one may argue that catheterization could have been avoided. If later the interatrial communication was
found to be restrictive, a septostomy could have been performed. We would recommend avoidance of catheterization, therefore, if confronted with such a case in the future.
References 1 Report of the New England Regional Infant Cardiac Program. Pediatrics 1980;65(suppl):388:392-403. 2 Zuberbubler JR. Valvular atresia. In: Zuberbubler, JR, ed. Clinical diagnosis in pediatric cardiology. New York: 1981;107-108. 3 Guller B, Ritter DG, Kincaid OW. Tricuspid atresia with pulmonary atresia and total anomalous pulmonary venous connection to the right superior vena cava. Mayo Clin Proc 1972;45:105-109. 4 Pieri D, Rubino A, Pipitone S, Grill0 R, LaMonaca P, Sperandeo V. Tricuspid atresia and total anomalous pulmonary venous return of supracardiac type. Report of a
117
case associated with extracardiac Cardiol 1987;17:613-616. 5 Van Hare GF, Schmit KG, Cassidy
International Journal of Cardiology, Elsevier CARD10
malformations. SC, Gooding
G
Ital
CA, Silver-
man NH. Color Doppler flow mapping in the ultrasound diagnosis of total anomalous pulmonary venous connection. J Am Sot Echo 1988;1:341-347.
28 (1990) 117- 119
10905
Coronary
arterial aneurysm after percutaneous transluminal coronary recanalization with streptokinase Ming-Fong
Department
Chen, Chiau-Suong
Liau and Yuan-Teh
Lee
of Internal Medicine (Cardiology, National Taiwan University Hospital, Taipei, Taiwan. R. 0. C. (Received
20 November
1989; revision accepted
2 February
1990)
A 49-year-old man developed an aneurysm of the right coronary artery after successful thrombolytic therapy with streptokinase following an acute inferior wall myocardial infarction. He was free from symptoms despite the existence of the aneurysm. The possible mechanisms for the formation of the aneurysm are discussed. Key words:
Coronary
arterial
aneurysm;
Acute myocardial
Introduction The most frequent cause of coronary arterial aneurysms as studied in Japan is Kawasaki disease [l]. In Western countries, it is usually related to atherosclerosis [2], or is a complication of percutaneous transluminal coronary angioplasty [3]. In this report, we present a case of acute myocardial infarction in which a coronary arterial aneurysm occurred one month after successful recanalization using intracoronary streptokinase. This is, to date, a very rare complication after thrombolytic therapy. Case Report A 49-year-old man was sent to the emergency room on 17 August 1985, because of an angina1 attack lasting
Correspondence to: Yuan-Teh Lee., M.D., Ph.D., Dept. of Internal Medicine (Cardiology), National Taiwan University Hospital, 1, Chang-Teh Street, Taipei, Taiwan, Republic of China. This report was included in the “Multi-Hospital Cooperative Study on Acute Myocardial Infarction in Taiwan”. The study was supported by a grant from the National Science Council and the Department of Health, the Executive Yuan, R.O.C. 0167-5273/90/$03.50
0 1990 Elsevier Science Publishers
infarction;
Thrombolytic
therapy
half an hour. Similar pains had waxed and waned in the previous week. His coronary risk factors included hypertension, smoking, a family history of cardiovascular disease, type A personality and sedentary life. Physical examination revealed a man looking acutely ill. The blood pressure was 158/86 mm Hg, and the heart rate was 72 beats/m.in with regular beats. The breathing sound was clear. There was a normal S, and an audible S, without a heart murmur. The chest X-ray revealed cardiomegaly and mild congestion of the lungs. The electrocardiogram showed ST segment elevation in leads II, II and aVF with reciprocal changes in precordial leads. Intracoronary streptokinase was given within 2 hours of the onset of the pain at the dose of 4000 units per min, for a period of 50 minutes. Prior to that. selective coronary arteriograms showed a total occlusion with a thrombus visible in the middle portion of the right coronary artery (Fig. la). The arteriograms were repeated at 10 minute intervals during the infusion of streptokinase, showing a gradual visualization of the distal part and total recanalization at the 40th minute. yet leaving an 80% residual stenosis at the middle portion (Fig. lb). A maintenance dose of intravenous streptokinase 750,000 units was given for 24 hours. Anticoagulation and antiplatelet therapies were given later. There was no other complication. Follow-up
B.V. (Biomedical
Division)