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Ann Thorac Surg 2000;70:961-963
© 2000 The Society of Thoracic Surgeons

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Case report

Dramatic improvement of LV function after coronary sinus thromboembolectomy

^a Thoracic and Cardiovascular Department, University Hospital, Siena, Italy

Address reprint requests to Dr Neri, Istituto di Chirurgia Toracica e Cardiovascolare Universita’ degli Studi di Siena, Policlinico le Scotte, Viale M. Bracci, 53100 Siena, Italy
e-mail: euxneri{at}tin.it

	Abstract

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We present the case of a 79-year-old man suffering from chronic atrial fibrillation, severe left ventricular dysfunction, massive right atrial thrombosis, and pulmonary hypertension. Complete coronary sinus thrombosis was found incidentally during preoperative screening. Successful coronary sinus, right atrial, and pulmonary operative embolectomy was followed soon after by a dramatic improvement of cardiac performance; the patient’s left ventricular function recovery, in particular, suggests that cardiac venous system played an important role in the genesis of myocardial impairment.

	Introduction

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We present a case of a patient with severe left ventricular (LV) dysfunction associated with complete coronary sinus (CS) thrombosis, chronic atrial fibrillation, massive atrial thrombosis, and pulmonary hypertension. Successful operative thromboembolectomy of the coronary sinus, right atrium, and pulmonary artery was followed by a dramatic improvement of cardiac performance early in the postoperative course.

A 79-year-old man suffering from atrial fibrillation for 10 years who was under treatment with digitalis, angiotensin converting enzyme inhibitors, and furosemide for chronic cardiac failure was admitted to the hospital for a worsening of dyspnea. On examination he was peripherally cyanosed, with a blood pressure of 140/75 mm Hg with an irregular pulse at 108 beats/min. His jugular venous pressure was elevated, and peripheral edema was evident. Arterial blood gas analysis showed severe hypoxia (PaO₂ of 42 mm Hg) with compensatory alkalosis. The chest roentgenogram showed enlargement of the cardiac silhouette with signs of congestive heart failure and bilateral pleural effusion. Transesophageal echocardiography revealed the presence of a severely dilated right atrium with extensive mural thrombosis and a snake-like mass that had prolapsed through the tricuspid valve (Fig 1). Severely dilated right ventricle with septal flattening was compatible with pulmonary hypertension. Severe LV dysfunction (ejection fraction, 0.25), without segmental wall motion abnormalities, and global LV dilatation (LV end-diastolic volume, 79 ml) were present. Minimal mitral regurgitation caused by annulus dilatation was also detected. Contrast computed tomographic scanning excluded the presence of renal tumors or other neoplastic processes and showed both the superior and inferior vena cava to be perfectly patent without mural thrombus. Color-coded Doppler examination excluded peripheral sources of emboli. A ventilation/perfusion scan confirmed multiple ventilation/perfusion mismatched defects, compatible with the computed tomography findings of extensive pulmonary artery branches obliteration. In preparation for surgical thromboembolectomy, a cardiac catheterization was performed, which revealed normal coronary artery vessels and no opacification of the CS.

View larger version (118K): [in this window] [in a new window]   Fig 1. Transesophageal echocardiogram revealed the presence of a snake-like mass that had prolapsed through the tricuspid valve.

View larger version (168K): [in this window] [in a new window]   Fig 2. The coronary sinus was obliterated by an extension of the mural thrombus; the cast of the coronary sinus is seen in the retrieved thrombus.

A marked reduction of systolic pulmonary artery pressure, from 95 to 30 mm Hg, and the reestablishment of sinus rhythm were observed at the end of the procedure. The postoperative course was unremarkable Transthoracic echocardiography in postoperative day 7 demonstrated, in spite of a poor acoustic window, a reduction of right ventricular and LV diameters and a sensible recovery of LV function. The patient was discharged home on oral anticoagulants. At one month postoperative follow-up, the patient’s condition were good; he maintained sinus rhythm and he was in New York Health Association functional class II. Transesophageal echocardiography demonstrated a dramatic recovery of LV function, with an estimated ejection fraction of 0.48 and a reduction of LV end-diastolic volume from 79 to 51 mL. Mitral regurgitation and septal flattening were absent, and the CS was patent. Estimated systolic pulmonary artery pressure was 38 mm Hg.

	Comment

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CS thrombosis is a rare occurrence, and in all reported cases the cause was endothelial damage following invasive cardiac procedures [1–4].

Primary CS thrombosis is not a described entity, and the present case is probably not an exception, although the mechanism of onset is not attributable to the previously described cause. The likely cause of the condition was an extension of the massive atrial thrombosis to the thebesian valve of the CS. Right atrial fibrillation along with chronic pulmonary embolism and consequent right heart failure contributed to aggravate CS thrombus formation. Right-sided thrombi may arise locally or may be trapped on the right side of the heart during transit. It is generally thought that parietal thrombi arise locally; they are found in conditions associated with an enlarged right atrium, decreased cardiac output, and relative stasis of blood [5].

The association of CS thrombosis and severe cardiac dysfunction in the absence of coronary artery disease is intriguing. Although in this case severe right ventricular dysfunction, chronic atrial fibrillation, pulmonary hypertension, and embolism contributed to clinical deterioration, they could not have caused LV failure and dilatation. Patient history and laboratory findings allow exclusion of toxic, metabolic, or infective myocarditis, and an idiopathic dilated cardiomyopathy would not have allowed such favorable recovery after operation.

Not much is known about the venous circulation of the heart and the consequences of the thrombosis of the CS on the hemodynamics of the coronary system. Stasis in the coronary venous system may not cause venous myocardial infarction if the patients has adequate collateral circulation with anterior cardiac veins and thebesian veins [1]. This may not always be the case: as reported in the literature CS thrombosis may produce myocardial infarction [1–3] and fatal cardiac complications [4].

In the patient described, CS thrombosis may have led to severe deterioration of the LV function through chronic CS system venous stasis. The diffuse areas of subendocardial necrosis localized in the inner third of the ventricular wall may represent regions of the myocardium that are in particularly jeopardy from venous obstruction. Outer and inner regions of the myocardium, less affected by this process because of collateral venous circulation, could have contributed to the observed myocardial recovery.

Cavernous sinus thrombosis, a rare condition, is a known cause of acute ventricular deterioration, but less is known about the role of CS system venous obstruction in chronic cardiac failure. Assessment of CS patency in patients with congestive cardiac insufficiency may help to elucidate this issue and possibly help define a subgroup that may benefit, as our patient did, from surgical CS embolectomy.

	References

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1. Wells C.A., Senior A.J. Coronary sinus thrombosis and myocardial infarction secondary to ventriculoatrial shunt insertion. J Pediatr Surg 1990;25:1214-1215.[Medline]
2. Philips J.B., Ruiz-Castanada N., Setzer E.S. Coronary sinus thrombosis. J Pediatr Surg 1981;16:733-734.[Medline]
3. Vinayak N., et al. Coronary sinus thrombosis after cannulation during cardiopulmonary bypass. Ann Thorac Surg 1996;62:1506-1507.[Abstract/Free Full Text]
4. Figuerola M., Tomas M.T., Armengol J., Bejar A., Adrados M., Bonet A. Pericardial tamponade and coronary sinus thrombosis associated with central venous catheterization. Chest 1992;101:1154-1155.[Abstract/Free Full Text]
5. Cameron J., Pohiner P.G., Stafford K.G., et al. Right heart thrombus recognition, diagnosis, and management. J Am Coll Cardiol 1985;5:1239-1243.[Abstract]

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Eugenio Neri Carlo Sassi Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Neri, E. Articles by Sassi, C. Search for Related Content PubMed PubMed Citation Articles by Neri, E. Articles by Sassi, C.