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Journal of the association of physicians of india • november 2013 • VOL. 61 Case Reports
Extreme Clinical Presentations of Venous
Stasis : Coronary Sinus Thrombosis
Amit Kachalia*, Panagiotis Sideras*, Mian Javaid*, Sethu Muralidharan*,
Pilar Stevens-Cohen**
Abstract
Sixty six year old male with history of heart failure was admitted for dysphagia, weight loss. CT scan chest
revealed diffuse oesophageal wall thickening. Upper endoscopy, oesophagogram confirmed diagnosis
of achalasia. TTE revealed severely reduced biventricular systolic function with LVEF 10%; PASP 75-80
mmHg. Parasternal long views showed dilated coronary sinus with a visible, mobile 2.0 cm thrombus.
Pro-thrombotic workup was negative.
Coronary sinus thrombosis has been identified as a rare complication to invasive cardiac procedures
causing damage to coronary sinus endothelium and in hypercoagulable states. Typically acute thrombosis
presents with chest pain, dynamic ECG changes, but chronic development does not present with ischaemic
signs due to formation of efficient collateral circulation. We present a case report of stable primary coronary
sinus thrombus incidentally diagnosed, secondary to chronic venous stasis in coronary circulation.
Currently, there are no guidelines to assist physicians in long term management of such patients and
thus warrants further investigations.
Introduction
C
oronary sinus thrombosis is a rare clinical entity with a very high fatality rate.
Invasive procedures of right heart including central venous line placements,
pacemaker wire insertion, coronary sinus catheterisation for ventricular lead placement
in resynchronisation therapy, heart surgeries can lead to damage of coronary sinus
endothelium and subsequent thrombosis. Coronary sinus thrombosis has also been
observed in patients with hyper-coagulable states. Primary thrombosis of coronary
sinus without any preceding cardiac interventions and in absence of hyper-coagulable
state very rarely reported in medical literature. We report the occurrence of primary
coronary thrombosis which was noted incidentally on an echocardiogram.
Case Report
Sixty six year old man with history of hypertension, stroke, and chronic
decompensated systolic heart failure since eight years prior to admission was admitted
with complaints of epigastric pain, dysphagia, dyspnoea Grade C, decreased exercise
tolerance and weight loss. Cardiac catheterisation done eight years prior to admission
did not show evidence of coronary artery disease. There is no history of any invasive
cardiac procedures or history of central venous line placement.
*
Department of Medicine,
Department of Cardiology,
Mount Sinai School of Medicine
at Queens Hospital Center,
Jamaica, NY
Received: 27.04.2012;
Revised: 27.11.2012;
Accepted: 19.11.2012
**
© JAPI • november 2013 • VOL. 61
Vitals recorded were Blood Pressure 116/86; Pulse 68/min, Breathing 18/min,
maintaining 97% saturation on two litres oxygen by nasal canula. Examination revealed
a well built individual lying comfortable in bed. Chest examination revealed bibasilar
crackles without any other abnormalities. Cardiac examination revealed tachycardia
with irregular rate, systolic murmur grade III loudest in the mitral area and all
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peripheral pulses were well felt. There was pitting
pedal oedema bilaterally extending till knee. Rest of
the examination was unremarkable.
Electrocardiogram showed sinus rhythm with
frequent premature atrial and ventricular contractions,
incomplete left bundle branch block and left axis
deviation. Trans-thoracic echocardiogram revealed
severely reduced left and right ventricular systolic
function with ejection fraction of 10%; Pulmonary
artery systolic pressure 75-80 mmHg, moderate
tricuspid regurgitation with moderate to severe mitral
regurgitation and moderate aortic regurgitation.
Parasternal long views revealed a markedly dilated
coronary sinus with a visible, mobile two cm
thrombus. Computed tomography of neck done for
evaluation of dysphagia indicated thickening of the
oesophageal 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 dyspnoea and able to tolerate medium
consistency oral feeds.
Discussion
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, 2-3
pacemaker wire placement, cardiac surgery, 4-5 heart
transplantation, coronary artery bypass grafting, 6
radiofrequency ablation around AV node. 1 Apart from
endothelial damage, hyper-coagulability (secondary
to malignancy) and venous stasis also play a role in
development of coronary sinus thrombosis although
very few incidents have been reported. 8-9 We present
a case of Coronary sinus thrombosis diagnosed
incidentally on an echocardiogram (Figure 1) in
a patient with no history indicative of damage to
coronary sinus endothelium or hyper-coagulability.
Journal of the association of physicians of india • november 2013 • VOL. 61
has never been reported as a sole aetiological factor
in formation of coronary sinus thrombus. The venous
system of heart consists of three separate systems. The
large bore coronary sinus and the anterior cardiac
veins both empty in the Right atrium and drain 60%
and 40% respectively of the total cardiac 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
all four chambers of heart. Wearn had described that
thebesian veins in full capacity can drain up to 50% of
cardiac venous return. 10 This explains how coronary
sinus thrombosis can present as a benign entity due
to efficient collateral circulation.
Typically acute thrombosis of coronary sinus
usually results in mortality and presents with chest
pain, dynamic electrocardiogram changes and signs
of acute cardiac decompensation. 1,5 This probably
results secondary to acute onset venous infarction
of myocardium. However chronic development of
thrombus does not present with ischaemic signs due
to formation of efficient collateral circulation between
coronary sinus, anterior cardiac and Thebesian
veins. Thus chronic development may go unnoticed
until it develops complications such as acute plaque
rupture causing myocardial infarction, 5-6 myocardial
dysfunction without infarction potentially reversible
with thrombectomy, 7 cardiac tamponade. 2 These cases
are usually fatal 2-5,8,9 and diagnosis is often made at
autopsy; thus limiting the evidence reported in such
instances.
Congestive heart failure is the leading cause
of mortality among geriatric population and it
is very important to focus on its potentially fatal
complications. It is important for physicians to be
alert and look for coronary sinus thrombosis in
long standing surviving cases of heart failure who
have chronic venous stasis in coronary circulation,
as missing diagnosis can lead to sudden death.
Currently, there are no long term guidelines to assist
physicians in diagnosis and long term management of
such patients. The role and efficacy of anticoagulation
is unclear and thus warrants further investigations.
Conclusion
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.
Venous stasis is long known to cause thrombosis
in deep venous system of legs; however this factor
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Journal of the association of physicians of india • november 2013 • VOL. 61 References
Fig. 1 : Parasternal long axis view during trans thoracic
echocardiography showing coronary sinus thrombus
(arrow) posterior to left atrium
Acknowledgement
No other acknowledgements other than the authors
and coauthors of manuscript.
No other financial sources or funding involved in
the formation of manuscript.
No potential financial conflicts of interest.
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