key: cord-0903177-mi4t7b08
authors: Aquino, Liliam; Muniz, Juan Carlos; Laufer, Pablo Marcelo; Prieto, Lourdes R.
title: Gore Cardioform ASD device thrombus weeks after COVID‐19 infection
date: 2022-01-11
journal: Catheter Cardiovasc Interv
DOI: 10.1002/ccd.30067
sha: 8f72cf265cffcc387921d74fc6b3787a7bbf743f
doc_id: 903177
cord_uid: mi4t7b08

Device‐related thrombosis and device‐related endocarditis after atrial septal defect (ASD) transcatheter closure are extremely rare. It is known that COVID‐19 infection could lead to a thrombotic microangiopathy‐like phenomenon. We present the case of a 14‐year‐old female who developed fever and was found to have a thrombus on the right atrial side of the ASD closure device weeks after an asymptomatic COVID‐19 infection and negative COVID‐19 test 2 days before transcatheter ASD closure. Although there is no certainty that the thrombus was related to the prior COVID‐19 infection, the possibility of an ongoing COVID‐19‐related hypercoagulable state should be entertained.

Since the three blood cultures remained negative, in the context of the negative Karius test and an afebrile, nontoxic appearing patient during the entire hospitalization, she was not thought to have bacterial endocarditis, and antibiotics were discontinued. The patient was discharged home on Day 3 on daily aspirin 81 mg and warfarin 5 mg to keep INR between 2 and 3. On follow-up 1 week after discharge, she was well appearing with no symptoms and the echocardiogram was unchanged. Three months later, the thrombus had entirely resolved (Figure 4 , Supporting Information Video 4). She continues to be clinically stable with a well-positioned device. She will continue daily aspirin 162 mg to complete a total of 6 months of treatment.

Device thrombosis after ASD transcatheter closure is uncommon, with an estimated rate of 1.0%. 1 The incidence appears to be similar in the different available devices, although in some studies the Amplatzer device appears to confer a lower risk. 1,2 Atrial fibrillation vices. 3 Occasionally an earlier iteration of this device could develop a "bloated" appearance due to rapid expansion of the right atrial (RA) disc post-deployment caused by blood collecting within the Goretex membranes, for which a fenestration was placed in the RA disc to allow exiting of the blood. This phenomenon has also been seen to a lesser extent with the Gore Cardioform ASD occluder, which also has a fenestration in the RA disc, but has not been shown to result in a higher risk of thrombus formation to date. In this case, there was no evidence of rapid expansion of the RA disc immediately after deployment, but whether some amount of blood could have been trapped within the device and served as a nidus for thrombus formation cannot be absolutely excluded. Device-related endocarditis, which this patient did not exhibit, is exceedingly rare. A meta-analysis of 28,142 patients reported three patients with device-related endocarditis, one ASD, and 2 PFO patients. 1 pneumonia is 31%, with 27% venous and 3.7% arterial thrombotic events. 5 The procoagulant shift caused by COVID-19 is associated with the severity of the infection. 6 Our patient was asymptomatic with documented low viral load (CT of 34) 3 weeks before the procedure and tested negative on POC-PCR (Abbott Laboratories) 2 days before the procedure. On readmission post device ASD closure her RT-PCR showed persistent but lower viral load with a CT of 35.3.

In our practice patients with CT ≥ 34 are considered to have a low viral load, to be no longer infectious, and are cleared for elective surgical procedures.

COVID-19 triggers pro-inflammatory cytokines leading to hyper inflammation, which promotes endothelial dysfunction inducing a microangiopathy-like prothrombic state. Angiotensin-converting enzyme 2 (ACE2), a major component of the renin-angiotensinaldosterone system (RAAS), is the receptor used by COVID-19 to infect endothelial cells. Decreased ACE2 leads to an angiotensin II predominant state, increasing aldosterone, which augments angiotensinconverting enzyme expression, causing an enhanced breakdown of bradykinin, preventing the normal bradykinin-mediated increase in tPA.

RAAS imbalance ultimately exacerbates microthrombi development. 7 COVID-19 coagulopathy (CAC) is associated with a relatively modest decrease in platelet count, elevated lactate dehydrogenase, and most distinctively a high D-dimer level, 6, 8 all of which were found in our patient. However, these derangements in the clotting cascade can be seen in any patient with non-Covid related thrombosis. 9 Our patient's thrombophilia work-up did not reveal any abnormalities that would increase her risk of a device-related thrombus.

The cardiolipin Ab IgM is nonspecific and can be positive in response to any inflammatory process. The slight decrease in Protein C activity may represent its consumption due to the thrombus formation rather than thrombophilia.

Limited information has been reported regarding patients undergoing necessary or urgent procedures in the setting of a recent COVID-19 infection. A 4-month-old baby with a cardiac teratoma was reported to undergo heart surgery 2 weeks after testing positive for COVID-19 with no complications. 10 Berkhordari et al. reported that 21 out of 25 patients with COVID-19 who underwent heart surgery, mainly coronary artery bypass grafting, had smooth respiratory outcomes. 11 However, neither of these procedures required leaving a foreign body in the blood stream as with our patient. An international, multicenter, prospective cohort study among 140,231 patients undergoing all types of surgery found that operating at <7 weeks after COVID-19 diagnosis increased the risk of mortality, while a planned delay of ≥7 weeks was associated with similar mortality when compared with patients without preoperative COVID-19 infection. 12 Although there is no proof that the complication our patient experienced was Covid-related, the duration of the hypercoagulable state due to COVID-19 and the adequate follow-up studies needed for surgical clearance remain unknown. Elective cardiac catheterization with implantation of intravascular devices should perhaps be deferred until there is no evidence of any Covid-19 viral load in the system.

Thrombus formation on an ASD device is very uncommon. COVID-19 infection is known to confer a pro-thrombotic state. We describe a patient who developed a thrombus on an ASD device 7 weeks after an asymptomatic Covid-19 infection, with a very low viral load by RT-PCR with a CT of 35.3 two days after the procedure. Although a direct cause and effect cannot be established, it may be advisable to delay completely elective catheterization requiring implantation of intravascular devices for a longer time, and until there is no detectable Covid-19 viral load.

Short and long term complications of device closure of atrial septal defect and patent foramen ovale: meta-analysis of 28,142 patients from 203 studies

Incidence and clinical course of thrombus formation on atrial septal defect and patient foramen ovale closure devices in 1,000 consecutive patients

ASSURED Investigators. ASSURED clinical study: new GORE ® CARDIOFORM ASD occluder for transcatheter closure of atrial septal defect

Infective endocarditis after device closure of atrial septal defects: case report and review of the literature

Incidence of thrombotic complications in critically ill ICU patients with COVID-19

The unique characteristics of COVID-19 coagulopathy

Hyperinflammation and derangement of renin-angiotensin-aldosterone system in COVID-19: a novel hypothesis for clinically suspected hypercoagulopathy and microvascular immunothrombosis

Coagulation abnormalities and thrombosis in patients with COVID-19

Diagnosis and management of sepsis-induced coagulopathy and disseminated intravascular coagulation

Cardiothoracic surgery during the Covid-19 pandemic: perioperative care, safety, and surgical results

Early respiratory outcomes following cardiac surgery in patients with COVID-19

Timing of surgery following SARS-CoV-2 infection: an international prospective cohort study

SUPPORTING INFORMATION Additional supporting information may be found in the online version of the article at the publisher's website. How to cite this article

The authors declare that there are no conflict of interests.

Data sharing not applicable to this article as no data sets were generated or analyzed during the current study.

http://orcid.org/0000-0003-3519-7678