Right atrial thrombus over eustachian valve — successful lysis with streptokinase

Right atrial thrombus over eustachian valve — successful lysis with streptokinase

354 International Joumal of Cardiology 30 (1991) 354-356 0 1991 Elsevier Science Publishers B.V. 0167-5273/91/$03.50 ADONIS 0167527391~87D CARD10 1...

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354 International Joumal of Cardiology 30 (1991) 354-356 0 1991 Elsevier Science Publishers B.V. 0167-5273/91/$03.50

ADONIS 0167527391~87D

CARD10

12163

Right atria1 thrombus over eustachian valve - successful lysis with streptokinase Neeraj Jolly, Upkar A. Kaul and M. Khalilullah Department of Cardiology, G.B. Pant Hospital, New Delhi, India (Received 17 September 1990; accepted 28 September 1990)

Patientf with pulmonary ~rn~rn~iisrn have occasionally been seen to have thrombi in the right atrium, either free floating or attached by a narrow pediele. An echocardiographic description of a thrombus attached to the eustachian valve has, however, never been made in the literature. One such case is described in which streptokinase successfully lysed the thrombus. Key words:

Thrombus;

Eustachian

valve; Streptokinase;

Introduction

Right atrial thrombuses may develop in situ or else are trapped in the heart during embohzation to the pulmonary vasculature [1,2]. Those embolized in transit are more often detected with the increasing use of cross-sectional echocardiography in patients with overt or suspected pulmonary thromboembolism [1,2]. Those arising initially from deep veins of the legs may be free floating in the atria1 cavity or may become adherent to any structure in the right atrium. We describe a case of pulmonary thromboembohsm in which streptokinase was successfully used to lyse a thrombus attached to the eustachian valve.

Echocardiography

the right infrascapular area, his chest examination unremarkable. A 12-lead surface electrocardiogram chest X-ray were normal.

was and

Case Report A 12-year-old boy was admitted with suspected pulmonary thromb~mbolism. He had chronic osteomyelitis of right tibia following blunt trauma sustained three months previously and was immobile on this account. Examination revealed a sick boy, tachypnoeic at rest. His pulse was 14O/min and regular, the respirations were 30/min, blood pressure 96/70 mmHg and temperature 38’ C. The mean jugular venous pressure was not raised and the cardiac examination was normal. Apart from diminished intensity of breath sounds over Correspondence to: Dr. U.A. Kaul, Dept. of Cardiology, G.B. Pant Hospital, New Delhi - 110 002. India.

c-4 Fig. 1. Cross-sectional frames of the modified apical 4-chamber view. A “bulbous” thrombus (white arrow) is attached to the eustachian valve (black arrow) (a, b). After intravenous streptokinase (c, d), the tbrombus has lysed. On follow up at 6 months (e, f). only a prominent eustachian valve is visible.

355

At discharge, 10 days after warfatin thereafter. admission, he was hemodynamically stable with a respiratory rate of 20 per minute. Six months later, he had gained weight, was asymptomatic and had a normal chest X-ray. A repeat echocardiogram revealed only a prominent eustachian valve in the right atrium. and

Discussion

Fig. 2. Digital subtraction image of right pulmonary artery and its branches. A thrombus (arrow) is seen partially obstructing flow to the right lower branch resulting in di-

minished vascularity.

A cross-sectional echocardiographic examination revealed normal sized cardiac chambers and normal heart valves. A mobile mass swaying freely in the right atria1 cavity was seen attached to the eustachian valve. Echocardiographic interrogation from different positions confirmed the prominent eustachian valve and also the freely mobile thrombus attached to it. The Doppler study was normal. Digital subtraction imaging of the pulmonary vasculature with Urografin injected in the superior caval vein revealed subtotal obstruction of the right lower lobe branch of pulmonary artery and markedly diminished blood flow in the right lower lobe of the lung. After an intravenous bolus of 200,000 units of streptokinase, he was maintained on a continuous infusion of streptokinase at a rate of 100,000 units per hour. Echocardiograms were repeated twelve hourly. A significant reduction in the size of the thrombus was apparent 72 hours after the initiation of the infusion of streptokinase. He was maintained on heparin initially

With the increasing use of echocardiography, right atria1 thrombuses are being detected more often [1,2]. Given the prevalence of pulmonary tluomboembolism, these lesions may soon become the most common right-sided cardiac masses detected. Their source from the peripheral venous system is borne out by their characteristic “finger like” configuration. They may be free-floating in the atria1 cavity or may become attached in the right atrium [1,2]. Previous accounts of right atria1 thrombus emphasize that certain areas in the right atrium appear predisposed to entrap clots, the leaflets of the tricuspid valve being a common site [3]. A eustachian valve is another potential area where an embolus may become attached [l]. This remnant of the right valve of the embryonic venous sinus is a structure of no clinical significance, although the increased facility for the formation of thrombus upon it was stressed in the review of the venous valves of the heart made by Yater [4]. Several autopsy reports have borne out this fact [1,4]. There is, however, to the best of our knowledge, no antemortem description of thrombus adherent to the eustachian valve. Echocardiography is an ideal modality for studying these cases and can clearly delineate the thrombus and the structure of the eustachian valve. There is enough evidence accumulating in the literature regarding the benefit of treating patients having right atria1 thrombi with surgery, thrombolytic agents or anticoagulants [5]. Treatment is essential, the more so in patients with pulmonary thromboembolism. In our patient, the decision to use streptokinase intravenously was taken in view of the occurrence of pulmonary embolism, the poor general condition of the child for surgery and the relatively small size of the thrombus.

References 1 Saner HE, Asinger RW, Daniel JA, Elsperger KJ. Two-dimensional echocardiographic detection of right-sided cardiac intracavitary thromboembolus with pulmonary embolism. J Am Co11 Cardiol 1984;7:1294-1301.

356 4 Yater WM. Variations and anomalies of the venous valves of the right atrium of the human heart. Arch Pathol 1929; 7:418-441. 5 Kinney EL, Wright RJ. Efficacy of treatment of patients with echocardiographically detected right-sided heart thrombi: a meta-analysis. Am Heart J 1989;118:569-573.

Farfel 2. Shechter M, Vered Z, Rath S, Goor D, Gafni J. Review of echocardiographically diagnosed right heart entrapment of pulmonary emboli-in-transit with emphasis on management. Am Heart J 1987;113:171-178. Covarrabias EA. Shekh MU, Fox LM. Echocardiography and pulmonary embolism. AM Intern Med 1977;87:720721.

International Journal of Cardiology, 30 (1990) 356-358 0 1991 Elsevier Science Publishers B.V. 0167-5273/91/$03.50 ADONIS 016752739100088Q

CARD10

12164

Congestive heart failure due to aortic incompetence with intestinal infarction due to endarteritis obiliterans J.A. Purvis ‘, A.A.J. Adgey 1 and M.D. O’Hara

2

’ Regional Medical Cardiology Centre, and ’ Queen’s University of Beljast. Department of Pathology, Royal Victoria Hospital, Belfast, N. Ireland (Received

8 September

1990; revision

accepted

28 September

1990)

A 27-year-old man with congestive heart failure due to aortic incompetence and subsequent intestinal infarction was found at laparotomy to have extensive necrosis of the bowel due to proliferative endarteritis. Symptoms resolved following treatment with prednisolone and cyclophosphamide, and replacement of the aortic valve. The sub-total occlusion produced by endarteritis obliterans may lead to acute end-organ infarction if cardiac output is reduced. Key words:

Congestive

heart failure;

Aortic incompetence;

Endarteritis

obliterans;

Intestinal

infarction

Introduction

Case Report

Polyarteritis nodosa can present as end-organ infarction due to thrombosis of medium-sized arteries, with acute inflammatory changes and fibrinoid necrosis of the internal elastic lamina. Our patient had classical prodromal symptoms and developed intestinal infarction during a period of diminished cardiac output secondary to congestive heart failure complicating significant aortic incompetence. Histologic examination of the culprit arteries revealed vessels compromised by fibro-intimal hyperplasia without acute vasculitis.

A 27-year-old man was admitted from a referring hospital with a 2-week history of increasing breathlessness and 2 days of pyrexia, malaise, vomiting, abdominal pain and blood-stained diarrhoea. He gave a 3-year history of progressive weight loss, myalgia and hypertension. Two years prior to admission he had had polyneuropathy. Medication on admission was atenolol 100 mg and enalapril 5 mg orally daily for hypertension. He was pyrexic, 38.5 “C, underweight 52 kg and tachypnoeic. The pulse was at the rate of lOO/min, regular, and collapsing in character. The blood pressure was 160/90 mmHg and the jugular venous pressure was elevated 6 cm. A harsh aortic systolic murmur was audible and a

Correspondence

to: Dr. A.A.J. Adgey M.D., Regional

Medi-

cal Cardiology Centre, Royal Victoria Hospital, Belfast BT12 6BA. N. Ireland.