Prosthetic valve thrombosis

Prosthetic valve thrombosis, valve thrombosis or leaflet thrombosis refers to thrombus formation of any component of a prosthetic heart valve and is a cause of prosthetic valve dysfunction and a potentially reversible complication of valvular surgery ^1,2.

Subclinical leaflet thrombosis is an entity of uncertain clinical significance without hemodynamic or thromboembolic consequences ².

Epidemiology

The exact incidence of valve thrombosis is not known and seem to be underestimated ^3-6 also because valve imaging is not widely performed on a routine basis ³. It is more common with mechanical than bioprosthetic valves, right-sided than left-sided and mitral than aortic prostheses ^3,6.

Risk factors

Predisposing factors include ³:

• mechanical heart valve
• right-sided prosthetic valves (tricuspid or pulmonary valve prosthesis)
• subtherapeutic anticoagulation
• early perioperative period

Associations

Valve thrombosis is frequently associated with the following ^3-6:

• subtherapeutic anticoagulation
• paroxysmal atrial fibrillation

Diagnosis

The diagnosis of valve thrombosis can be established by a combination of clinical and imaging features ^1,3:

• a short interval from valve replacement to valve dysfunction
• sudden symptom onset with regression after initiation of anticoagulation therapy
• presence of reduced leaflet motion and hypoattenuated leaflet thickening on cardiac CT
• direct visualization of valve thrombosis on echocardiography
• elevated trans prosthetic mean gradient with regression after initiation of anticoagulation

The diagnosis can be also proven pathologically either at autopsy or during cardiac surgery ³.

Clinical presentation

Clinical symptoms might depend on the extent and the presence of complications and include signs of heart failure, syncope, shock or signs of thromboembolism such as stroke or might be absent in the setting of subclinical valve thrombosis ^3,6-8.

Complications

Complications of prosthetic valve thrombosis include the following:

• thromboembolism including stroke
• valve obstruction with heart failure
• cardiac arrest
• sudden cardiac death

Pathology

Prosthetic valve thrombosis can occur even several years after surgery and is considered a complex multifactorial phenomenon involving different factors such as ^3,7,9,10.

• endothelial dysfunction or surface related factors
  • incomplete endothelialization
  • leaflet damage or deterioration
  • stent fracture
  • prosthesis malposition
• hemodynamic factors
  • low cardiac output or slow flow
  • incomplete apposition
  • flow turbulences
  • hyperviscosity
• hemostatic factors
  • hypercoagulable state
  • tissue injury
  • heparin-induced thrombocytopenia
  • suboptimal anticoagulation
  • platelet reactivity

Location

By definition, valve thrombosis can occur at any location or component of a prosthetic heart valve. However, compared to fibrotic pannus ingrowth as a result of structural valve deterioration, prosthetic valve thrombosis is more likely to occur in the following locations ³:

• aortic side in the setting of aortic valve prostheses
• atrial side in the setting of mitral valve prostheses

Radiographic features

Echocardiography

Transthoracic echocardiography (TTE) is the first-line modality for the evaluation of valvular function and trans-prosthetic gradients including serial changes over time ^1-3.

Transesophageal echocardiography (TEE) might be considered in the setting of suspected prosthetic valve dysfunction or in cases where transthoracic echocardiography or cardiac CT is technically suboptimal or findings are unclear ^2,3.

Echocardiographic features indicating valve thrombosis include ^3,6:

• increase in trans-prosthetic mean gradient (>10mmHg) with regression after oral anticoagulation
• large hyperechoic thrombotic mass with potential valvular obstruction
• increased leaflet thickness
• restricted leaflet motion
• location on the atrial side in mitral prostheses and the aortic side of the aortic prosthesis

CT

Cardiac CT can provide structural or anatomical information and aid in the early detection of valve thrombosis even in subclinical stages and seems to be the most sensitive and specific method for the evaluation of valve thrombosis ⁵. The following findings should be visible in two more multiplanar reconstructions ^1,8-11:

• hypoattenuated leaflet thickening (HALT)
• reduced leaflet motion (RELM)

It might also show other findings including ¹¹:

• impaired leaflet coaptation
• reduced or increased prosthesis orifice

The CT should be conducted on a CT scanner with a high spatial and temporal resolution with retrospective acquisition and no dose modulation ¹¹.

Radiology report

The radiological report should include a description of the following ^1,3,11:

• leaflet coaptation
• hypoattenuating leaflet thickening (HALT)
• reduced leaflet motion (RELM) with degree (<50%, 50-70%, >70%, immobile)
• leaflet thickening
• leaflet calcification
• prosthesis orifice area
• transvalvular gradient

Treatment and prognosis

Management depends on the extent of the valve thrombosis and options include anticoagulation with vitamin K antagonists ⁸ and unfractionated heparin as well as surgery or fibrinolysis, with the two latter carrying a considerable risk ^2,3.

Surgery should be considered in patients with obstructive valve thrombosis, large thrombi (>10mm) and/or with thromboembolic events and no contraindications or if pannus is considered ^2,6. Fibrinolysis can be considered in less severe cases with smaller thrombi ⁶ or in the setting of surgical contraindications and might be complicated by bleeding, thromboembolic events and recurrence ^2,3,5,12.

In patients, where subclinical leaflet thrombosis has been confirmed on imaging, the reflection about the use of oral anticoagulants has been recommended ².

Differential diagnosis

Conditions that might mimic the imaging appearance of valve thrombosis include structural valve deterioration with prosthetic valve degeneration and fibrotic pannus ingrowth.

Fibrotic pannus ingrowth is more likely in the following setting ^3,6:

• a longer interval from valve replacement to valve dysfunction
• slowly progressive onset
• less likely associated with suboptimal anticoagulation
• smaller hypoechoic or hyperdense mass >145 HU ¹³
• more commonly located on the ventricular side of aortic and mitral prostheses
• a lower degree of restricted leaflet motion