a b s t r a c t

Left atrial thrombus after Acute pancreatitis is a rare clinical statement. Because of induction of systemic prothrombotic process by AP; some patients with underlying risk factors may develop an intra-cardiac thrombus. We present a 53 years-old-woman with moderate mitral stenosis and atrial fibrillation. However the patient was under Warfarin treatment, she developed a big left atrial big thrombus which was originated from left atrial ap- pendage after she was suffered from AP.

(C) 2016

Introduction

systemic inflammation is regarded as a strong prothrombotic stimu- lus [1]. In the natural course of inflammation; while procoagulant fac- tors increase natural anticoagulant factors and fibrinolytic activity decrease. We herein showed the contribution of systemic inflammation following acute pancreatitis (AP) to development of left atrial thrombus (LAT) in a patient under warfarin treatment.

Case report

A 53 years-old-woman was admitted to our emergency department with complaints of rest dyspnea (functional class II). She was under warfarin treatment because of Atrial fibrillation and rheumatic mi- tral stenosis (MS). She was hospitalized for AP a month ago and admin- istered with conservative treatment.

On present admission, the patient’s pulse rate was 102 per minute and irregular, her blood pressure was 130/70 mmHg. Body temperature was 37,1 ?C. The patient had 1+ edema in her lower limbs. Auscultation revealed fine crackles in both lungs bases and 3/6 pan-systolic murmur. Electrocardiogram (ECG) showed AF with rapid ventricular response. Laboratory parameters were unremarkable and her last five months’ in- ternational normalized ratios (INR) were in 2-3 range. Five months’ previous transthoracic echocardiogram showed: ejection fraction (EF) was 60%, rheumatic mitral valve (MV) moderate mitral stenosis (MS) and Mitral regurgitation (MR). Due to progression of dyspnea TTE was repeated: left ventricular ejection fraction was 60%, moderate

* Corresponding author at: Dr. Siyami Ersek Hospital, Tibbiye Str. No:25, Uskudar, Istanbul, Turkey.

E-mail address: drmuhammedkeskin@gmail.com (M. Keskin).

MS (MV peak/mean gradient were 9/6 respectively, MV area by planimetry was: 1.2 cm², by pressure half time (PHT) was: 1.12 cm²) moderate-severe MR (vena contracta: 0.6 cm) and biatrial dilation. A big homogenous mass (2.1 x 2.8 cm distance) (Fig. 1) which was hold on to left atrial lateral wall was observed. In order to better reveal the relations between the left atrial mass and left atrium, three dimensional transesophageal echocardiogram (3D TEE) was used. 3D TEE also showed a pedinculated, hypoechoic mass (5 cm²) which was compati- ble with thrombus was originating from left atrial appendage (Figs.s 2, 3). In a consultation with cardiovascular surgeon team; an urgent sur- gery decision was made subsequent to coronary angiogram (CAG). CAG revealed normal, patent coronary arteries. The patient underwent Urgent surgery through median sternotomy using cardiopulmonary by- pass. Left atrial mass was (Figs.s 4, 5) removed and Carbomedics(R) pros- thetic MV was placed. histologic examination was also compatible with thrombus. The patient’s course was uneventful and she was discharged at 16th day.

Discussion

MV disease leads to Atrial enlargement by elevated intraatrial pres- sure and volume. Pulmonary hypertension and edema occur as the re- sult of elevated intraatrial pressure and volume. In this context, it has been postulated that the valvular obstruction results in elevated atrial pressures and subsequent chamber enlargement. This dilation is be- lieved to lead to the thinning and fibrosis of myocardial and conducting fibers that have been demonstrated in pathological and histological studies and thereby result in disordered electrical activation and con- tractility. This observation and the evidence relating the duration of fi- brillation with left atrial size have led to the suggestion that atrial fibrillation per se leads to chamber enlargement [2]. Atrial fibrillation

http://dx.doi.org/10.1016/j.ajem.2016.11.034

0735-6757/(C) 2016

801.e2 M. Keskin et al. / American Journal of Emergency Medicine 35 (2017) 801.e1–801.e4

Fig. 1. Two-dimensional transthoracic echocardiogram shows the left atrial thrombus in dimensions 2.1 x 2.8 cm.

is the most common clinically significant cardiac arrhythmia. It is also a potent risk factor for ischemic stroke, increasing the risk of stroke 5-fold and accounting for approximately 15% of all strokes nationally [3]. Our patient had rheumatic MV and moderate MS. It is known that MR is de- creasing the development of atrial thrombus. Our patient was delibera- tive and she regularly measured her INR levels. She was taking warfarin treatment for five years and her previous echocardiograms did not show a thrombus or spontaneous echo contrast (SEC). No important event was happened in the meanwhile rather than AP.

Inflammation such as AP; initiates clotting, decreases the activity of natural anticoagulant mechanisms and impairs the fibrinolytic system. Inflammatory cytokines are the major mediators involved in coagula- tion activation. The natural anticoagulants function to dampen eleva- tion of cytokine levels. Furthermore, components of the natural anticoagulant cascades, like thrombomodulin, minimise endothelial cell dysfunction by rendering the cells less responsive to Inflammatory mediators, facilitate the neutralization of some inflammatory mediators

and decrease loss of endothelial barrier function. Hence, down regula- tion of anticoagulant pathways not only promotes thrombosis but also amplifies the Inflammatory process [1-3].

Intracardiac thrombus after acute pancreatitis is very rare. Splanch-

nic vein thrombosis (splenic, portal, and/or superior mesenteric veins) is incidentally found on imaging in 1 to 24% of patients with acute pan- creatitis, depending on the disease severity and the imaging modality [4]. Vinod et al. showed a right atrial thrombus after acute pancreatitis and it is the only case report about intracardiac thrombus after AP [5]. But there is not a report about the LAT in the literature.

Conclusion

This situation shows that acute inflammatory events such as AP could result in thrombogenic events. Patients with underlying risk fac- tor for thrombogenesis should be examined if they had these kinds of disorders. However warfarin is recommended and it prevents from

Fig. 2. Two-dimensional transesophageal echocardiography shows the left atrial thrombus.

M. Keskin et al. / American Journal of Emergency Medicine 35 (2017) 801.e1–801.e4 801.e3

Fig. 3. Three-dimensional transesophageal echocardiography shows the pedinculated thrombus is originating from left atrial appendage.

Fig. 4. Surgical view shows left atrial thrombus.

thromboembolism; we could see that warfarin is not an exact solution even though INR levels were in target therapeutic range. We suggest more frequent Echocardiographic examination after the patients had acute inflammatory disorders.

References

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2. Sanfalippo A, Abascal V, Sheehan M, Oertel LB, Harrigan P, Hughes RA, et al. Atrial en- largement as a consequence of atrial fibrillation. Circulation 1990;82:792-7.
3. Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV, et al. Prevalence of diag-

   nosed atrial fibrillation in adults national implications for rhythm management and Stroke prevention: the AnTicoagulation and Risk Factors In Atrial Fibrillation (ATRIA) Study. JAMA 2001;285(18):2370-5.

   Nadkarni NA, Khanna S, Vege SS. Splanchnic venous thrombosis and pancreatitis. Pan-

   creas 2013;42:924.

   Vinod KV, Arun K, Nisar KK, Dutta TK. Inferior vena caval thrombosis: a rare compli- cation of acute pancreatitis. J Assoc Physicians India 2014 May;62(5):430-2.

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   Fig. 5. Surgically removed left atrial thrombus.