A 79-year-old male was admitted to the hospital for acute exacerbation of heart failure. The patient had history of atrial fibrillation and was planned for cardioversion. Preprocedure transesophageal echocardiogram (TEE) revealed a large multilobulated mobile thrombus in the left atrial appendage. The patient refused warfarin therapy and instead chose to take rivaroxaban. Upon outpatient follow-up, 3 months later, no visible thrombus was appreciated on repeat TEE. This case demonstrates successful resolution of left atrial and left atrial appendage thrombi with the use of rivaroxaban. At present time, limited data is available to support the use of rivaroxaban for treatment of intracardiac thrombi. This case highlights the need for further studies to investigate the outcomes and relative efficiency of use of direct oral anticoagulants (DOACs) in lysis of intracardiac thrombus. The benefits of DOACs compared to the standard of therapy could increase patient compliance, reduce length of stay, and improve treatment efficacy.

Background: Spontaneous coronary artery dissection (SCAD) is an important cause of myocardial infarction (MI) in women but rare in young healthy males. We report a case of a young male who presented with left hand tingling/numbness and was ultimately diagnosed with SCAD. Case Presentation: A 24-year-old male with history of asthma developed left hand tingling/numbness while playing basketball. This progressed to cold left upper extremity, prompting him to go to emergency room. Doppler ultrasound showed acute left brachial thrombus and emergent embolectomy of left brachial artery was done. Transesophageal echocardiogram, performed to investigate possible cardiac source of thrombus, showed normal ejection fraction, dyskinetic apex and biventricular thrombus (Figure 1A). Cardiac MRI revealed a large transmural MI in distribution of a wraparound left anterior descending artery (LAD) with associated regional akinesis of the left ventricular apex and an infarct in the right ventricular apex. Subsequent angiography revealed normal coronary arteries (Figure 1B) except a heterogenous linear filling defect in the apical LAD consistent with Type 1 SCAD (Figure 1C). No intervention was performed and the patient was treated conservatively. It was postulated that patient sustained an apical MI after SCAD of LAD, leading to formation of ventricular thrombi which then embolized to cause acute brachial artery thrombosis. Discussion: SCAD in young males is rare and can be a diagnostic challenge. Type 1 “pathognomic” angiographic finding in SCAD, is the classic appearance of multiple radiolucent lumens or arterial wall contrast staining. In case of inconclusive angiography, intravascular ultrasound or optical computed tomography can confirm diagnosis. Interventionalists should be familiar with angiographic appearance of SCAD as advanced imaging might not be available and in many cases, conservative management is preferred to percutaneous coronary intervention.

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Background: Intravenous unfractionated heparin (IV-UFH) has been the mainstay for bridging therapy, and for the treatment of suspected device hemolysis/thrombosis in patients with continuous-flow left ventricular assist devices (CF-LVADs). Significant levels of discordance between activated partial thromboplastin time (aPTT) and antifactor Xa (anti-FXa) levels have been reported in CF-LVAD patients. We sought to compare alternate monitoring protocols while on IV-UFH therapy in patients with CF-LVADs. Methods: Consecutive patients implanted with CF-LVAD and treated with IV-UFH had simultaneous measurement of aPTT, activated clotting time (ACT), R time (measured by thromboelastography), and anti-FXa. All patients were managed by targeting anti-FXa levels while on IV-UFH therapy. Results: 20 patients were enrolled. Poor relationship between anti-FXa and ACT was found (R 2 = 0.24); however, stronger relationship was found between aPTT and ACT (R 2 = 0.55). While Anti-FXa was in therapeutic range, aPTT was supra-therapeutic, thus ACT was <250 sec. The relationship between anti-FXa and R time was also limited (R 2 = 0.38); and it was similar to the relationship between aPTT and R time (R 2 = 0.45). Conclusion: Levels of aPTT and R time were disproportionately prolonged as compared to anti-FXa and ACT levels. Despite anti-FXa levels being in the therapeutic range, both aPTT and R time were supra-therapeutic, and the ACT <250 sec. Use of alternate monitoring protocols to guide IV-UFH therapy may lead to different estimates of heparin concentration in the same patient. In light of the early risk of device thrombosis, re-examination of bridging protocols while on IV-UFH therapy are necessary.