Journal of Postgraduate Medicine
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Year : 2002  |  Volume : 48  |  Issue : 4  |  Page : 312-3  

Coronary sinus thrombosis.

RC Parmar, S Kulkarni, S Nayar, A Shivaraman 
 Department of Paediatric Cardiology, Institute of Cardiovascular Diseases, Madras Medical Mission Hospital, Chennai - 600050, India. , India

Correspondence Address:
R C Parmar
Department of Paediatric Cardiology, Institute of Cardiovascular Diseases, Madras Medical Mission Hospital, Chennai - 600050, India.

How to cite this article:
Parmar R C, Kulkarni S, Nayar S, Shivaraman A. Coronary sinus thrombosis. J Postgrad Med 2002;48:312-3

How to cite this URL:
Parmar R C, Kulkarni S, Nayar S, Shivaraman A. Coronary sinus thrombosis. J Postgrad Med [serial online] 2002 [cited 2022 Aug 19 ];48:312-3
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A 63-days-old boy was evaluated for feeding difficulties, cyanosis and breathlessness. Examination revealed a cyanosed child (oxygen-saturation 48%) with left parasternal systolic murmur of grade 3/6. Echocardiography revealed transposition of great arteries, large subpulmonic ventricular septal defect (VSD), patent foramen ovale [PFO], small patent ductus arteriosus[PDA], malpositioned great arteries with unregressed left ventricle and severe pulmonary artery hypertension (PAH).

At 67 days, the patient underwent arterial-switch operation with closure of VSD with Lecompte manoeuvre. Pulmonary artery was reconstructed using pantaloon pericardial patch, and PDA was ligated and divided. At surgery superior and inferior venae cavae were cannulated using 26 FR polystan cannula and aortic cannulation was done using 10 FR polystan cannula. PFO was kept open and Swan Ganz catheter was put through the left internal jugular vein. The child was weaned from mechanical ventilation and was extubated on the 8th postoperative day. 36 hours after extubation, he developed sclerema and clinical signs of bacterial sepsis, which was confirmed by cultures that grew enterobacter. He was started on appropriate antibiotics along with intravenous immunoglobulin. Subsequently he developed PAH crisis with inadequate respiratory efforts and desaturation and needed reintubation. The child had persistent haemodynamic instability with metabolic acidosis, persistent hypoxaemia and low cardiac output. The patient continued to deteriorate and died on the 13th postoperative day.

At autopsy, the heart was markedly enlarged with moderate enlargement of both the ventricles and minimal enlargement of left atrium. VSD patch was intact; Lecompte repair was well-seen with normal coronary arteries. The coronary sinus (CS) was bulging in its terminal 1.5 cm [Figure:1] and was filled with a thrombus [Figure:2]. On microscopy, the thrombus was found to be made-up of platelets and some fibrin with various quantities of polymorphonuclear leucocytes and erythrocytes. It also showed fibroblasts and capillaries at the periphery (suggestive of organising thrombus). The cardiac veins showed widespread thrombosis. The coronary arteries were free of thrombus. An occlusive organising thrombus was also seen at the junction of superior vena cava and right atrium. The endocardium in the appendage also showed a small thrombus. Right ventricular (RV) cavity was moderately enlarged and myocardium showed moderate hypertrophy with focal area of haemorrhagic necrosis [Figure:3] and subepicardial vacuolation. RV endocardium showed moderate patchy fibroelastic thickening. Left ventricular myocardium showed minimal hypertrophy. Microscopy of the lungs showed, alveolar septae with patchy capillary dilatation and lymphocytic infiltration besides fresh and organising thrombi in arteries alongwith medial hypertrophy. The alveoli were filled with macrophages. The alveolar epithelial cells and macrophages showed occasional intracytoplasmic basophilic and intranuclear amphophilic inclusion. These changes were suggestive of coronary sinus thrombosis with haemorrhagic right myocardial necrosis and pulmonary thromboembolism.

  ::   DiscussionTop

Coronary sinus thrombosis (CST) is a rare acquired anomaly of the CS. Although cases of primary thrombosis of CS are reported,[1] most cases occur due to endothelial damage following invasive cardiac procedures. In cardiac procedures that use access to the right atrium, such as insertion of central venous lines, pacing wire, coronary sinus catheterisation for ventricular lead placement during cardiac resynchronisation therapy,[2],[3] the CS is at risk of accidental trauma and subsequent thrombosis. It has also been documented as a complication of fungal endocarditis, heart transplant and mitral valve replacement. Rare cases of CST resulting from the massive atrial thrombosis extending in to the CS have also been reported.[4] Similar to thrombosis at other sites, CST results from combination of vessel wall injury, stasis and alteration of coagulation profile.[5] Sepsis and disseminated coagulopathy, as in our case, may be an additional factor.

Clinical course of CST remains unpredictable. Most patients remain asymptomatic and escape from venous haemmorhagic myocardial infarction due to the presence of an adequate collateral circulation between coronary sinus system and anterior cardiac veins and Thebesian veins.[6] Our case had an organised thrombus (that escaped the initial recognition), which takes about seven days to develop and minimal right ventricular infarction again corroborating the presence of adequate collateral circulation. CST in these subjects is detected only at angiography done for other purposes or at autopsy. This may not be the case always; cases of CST with massive haemmorhagic necrosis, pericardial tamponade, left ventricular dysfunction and even sudden cardiac death have been reported.[3],[4],[7] In symptomatic patients an emergency thromboembolectomy may be rewarding.[4]

CS thrombosis is a rare but potentially fatal complication of cardiac invasive procedures and should be remembered as a cause of sudden deterioration inpatients undergoing invasive cardiac procedures.


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