We present a case of Coronary sinus
thrombosis diagnosed incidentally on an echocardiogram (Fig. 1) in a patient with no
Coronary sinus thrombosis is a rare clinical entity with a very high history indicative of damage to coronary sinus fatality rate. Invasive procedures of right heart including central endothelium or hyper-coagulability. Venous venous line placements, pacemaker wire insertion, coronary sinus stasis is long known to cause thrombosis in catheterization for ventricular lead placement in resynchronization deep venous system of legs; however this therapy, heart surgeries can lead to damage of coronary sinus factor has never been reported as a sole endothelium and subsequent thrombosis. Coronary sinus etiological factor in formation of coronary sinus thrombosis has also been observed in patients with hyperthrombus. The venous system of heart consists coagulable states. Primary thrombosis of coronary sinus without of three separate systems. The large bore any preceding cardiac interventions and in absence of hypercoronary sinus and the anterior cardiac veins coagulable state has been very rarely reported in medical both empty in the Right atrium and drain 60% literature. We report the occurrence of primary coronary and 40% respectively of the total cardiac thrombosis which was noted incidentally on an echocardiogram
.
.
venous return.
There are many anastomotic connections between tributaries of these two venous systems. Finally, the heart is also drained by minor Thebesian veins into
66 y/o man with history of HTN, stroke, and systolic heart failure since all four chambers of heart
.
This explains how coronary sinus thrombosis can
8 years prior to admission was admitted with complaints of epigastric present as a benign entity due to efficient collateral circulation. pain, dysphagia, dyspnea Grade C, decreased exercise tolerance and Typically acute thrombosis of coronary sinus usually results in mortality and weight loss. Cardiac catheterization done eight years prior to presents with chest pain, dynamic electrocardiogram changes and signs of admission did not show evidence of coronary artery disease. No acute cardiac decompensation 1 . This probably results secondary to acute onset history of any invasive cardiac procedures or history of central venous venous infarction of myocardium. However chronic development of thrombus line placement.
does not present with ischemic signs due to formation of efficient collateral
Vitals recorded were Blood Pressure 116/86; Pulse 68/min, Breathing circulation between coronary sinus, anterior cardiac and Thebesian veins. Thus
18/min, maintaining 97% saturation on two liters oxygen by nasal chronic development may go unnoticed until it develops complications such as canula. Examination revealed a well built individual lying comfortable acute plaque rupture causing myocardial infarction 4 , myocardial dysfunction in bed. Chest examination revealed bibasilar crackles. Cardiac without infarction potentially reversible with thrombectomy 5 , cardiac examination revealed tachycardia, irregular rate, systolic murmur tamponade 2 . These cases are usually fatal 2,5 and diagnosis is often made at grade III loudest in the mitral area and all peripheral pulses were well autopsy; thus limiting the evidence reported in such instances.
felt. There was pitting pedal edema bilaterally extending till knee. Rest Congestive heart failure is the leading cause of mortality amongst geriatric of the examination was unremarkable.
population and it is very important to focus on its potentially fatal complications.
EKG showed sinus rhythm with frequent premature atrial and It is important for physicians to be alert and look for coronary sinus thrombosis ventricular contractions, incomplete LBBB and left axis deviation. TTE in long standing surviving cases of heart failure who have chronic venous stasis revealed severely reduced biventricular ventricular systolic function in coronary circulation, as missing diagnosis can lead to sudden death. with EF 10%; PASP 75-80mmHg, moderate TR, moderate to severe
MR and moderate AR. Parasternal long views revealed a markedly
dilated coronary sinus with a visible, mobile 2 cm thrombus. CT neck done for evaluation of dysphagia indicated thickening of the esophageal wall suggesting an infiltrative process. Upper endoscopy and barium studies followed which confirmed the diagnosis of achalasia and ruled out any infiltrative process. Coagulation profile was normal and all prothrombotic factors were negative.
During the admission patient was treated for acute on chronic decompensated systolic heart failure, coronary sinus thrombosis and achalasia. Patient responded to furosemide and improved symptomatically. Patient was recommended Coumadin with
Enoxaparin bridging for his coronary sinus thrombosis but he declined
Coumadin, hence was anti-coagulated with Enoxaparin alone during inhospital stay. Patient was recommended defibrillator placement but he refused the same. Patient was continued and discharged on
Aspirin, clopidogrel, lisinopril, carvedilol and furosemide with follow up in GI and cardiology clinic. At discharge patient was symptomatically stable with Grade C dyspnea and able to tolerate medium consistency oral feeds.
The most common mechanism to initiate thrombus formation in coronary sinus is endothelial damage, usually occurring as a secondary complication of procedures such as central venous line placement 2 , pacemaker wire placement, cardiac surgery 3 , heart transplantation, coronary artery bypass grafting 4 , radiofrequency ablation around AV node 1 . Apart from endothelial damage, hypercoagulability (secondary to malignancy) and venous stasis also play a role in development of coronary sinus thrombosis although very few incidents have been reported 6 .
Considering the fact that coronary sinus thrombosis is a potential, though rare complication of invasive cardiac procedures; it is important to look for such an event in cases of chronic coronary venous stasis also. The evidence for the role of long term anticoagulation and diagnostic standards is unclear and further guidelines are warranted.
1. K K Yeo, J Davenport, G Raff and JR. Laird. Life-threatening coronary sinus thrombosis following catheter ablation: case report and review of literature.
, October-
December 2010, Pages 262.e1-262.e5
2. Figuerola M, Tomas MT, Armengol J, Bejar A, Adrados M, Bonet A. Pericardial tamponade and coronary sinus thrombosis associated with central venous catheterization. Chest. 1992;101(4):1154-1155.
3. Parmar RC, Kulkarni S, Nayar S, Shivaraman A: Coronary sinus thrombosis. J
Postgrad Med 2002, 48:312-313.
4. Salim Dabbah MD, Shimon A. Reisner MD, Zvi Adler MD, Simcha Milo MD,
Yoram Agmon MD: Intermittent Coronary Sinus Occlusion Complicating
Coronary Sinus Cannulation During Coronary Artery Bypass Operation;
, August 2005,
Pages 882
5. Neri E, Tripodi A, Tucci E, Capannini G, Sassi C. Dramatic improvement of LV function after coronary sinus thromboembolectomy. Ann Thorac Surg.
2000;70(3):961-963.
6. Kitazawa, S., Kitazawa, R., Kondo, T., Mori, K., Matsui, T., Watanabe, H.,
Watanabe, M.: Fatal cardiac tamponade due to coronary sinus thrombosis in acute lymphoblastic leukemia; Cases Journal. 2009; 2:9095