Bioprosthetic aortic valve haemodynamic deterioration secondary to a thrombus
- 1 Internal Medicine, Banner University Medical Center, Tucson, Arizona, USA
- 2 University of Arizona, Arizona Health Sciences Center, Tucson, Arizona, USA
- 3 Sarver Heart Center, Tucson, Arizona, USA
- Correspondence to Dr Martin A Chacon-Portillo; mchacon@deptofmed.arizona.edu
Abstract
A 77-year-old man with a history of coronary artery bypass grafting and surgical aortic valve replacement for severe aortic stenosis 2 years prior presented with exertional chest pain and shortness of breath. The patient underwent a thorough initial evaluation including a transthoracic echocardiogram and coronary angiogram without significant findings. One month later the patient presented with worsened symptoms and a repeat echocardiogram showed an increased mean aortic valve gradient of 87 mm Hg. The patient had to undergo reoperation for a surgical aortic valve replacement and was found to have an aortic bioprosthetic valve thrombus. This case suggests a mismatch between the aortic prosthesis and the patient’s aortic root size.
Background
This report describes the diagnosis and management of a man afflicted by an uncommon condition that required a multidisciplinary approach. Bioprosthetic valve (BPV) thrombosis is a rare but serious complication of surgical aortic valve replacement (SAVR). It is associated with significant morbidity and mortality and warrants rapid diagnostic evaluation and treatment.1 Due to its diverse clinical presentation from an asymptomatic imaging finding to haemodynamic collapse, it is important to always consider in the differential diagnosis. Its low incidence and the difficulty to visualise the thrombus, even with advanced imaging, made this case a diagnostic challenge.
We report a case of a BPV thrombosis that required surgery both for definitive diagnosis and treatment. The thrombus occurred within 2 years after the aortic valve (AV) had been replaced. Prosthesis-patient mismatch is known to increase the risk of thrombosis due to its influence on various rheological perturbations.2 The take-home message of this report is to consider thrombosis of the BPV in the differential diagnosis especially if it occurs within 3 years of the BPV placement.
Case presentation
A 77-year-old man who underwent coronary artery bypass grafting and SAVR for severe aortic stenosis 2 years ago with a 21 mm Edwards Magna-Ease BPV (stented pericardial valve) presented with intermittent episodes of exertional chest pain and shortness of breath for 5 months. The patient also reported associated intermittent dizziness and lightheadedness during this period. Due to his significant history of coronary artery disease, the patient was evaluated with a coronary angiogram that did not show any significant new coronary lesions and was discharged home. The patient presented 1 month later with worsening exertional chest pain and shortness of breath.
On examination, the patient was slightly hypertensive with a blood pressure of 141/74 mm Hg, heart rate of 78 bpm and respiratory rate of 16 rpm. Cardiovascular examination revealed a holosystolic murmur in the aortic area. General examination was unremarkable. The body surface area of the patient was 2.37 m2.
Investigations
On initial presentation, the patient was found to have an elevated troponin-I of 0.6 ng/mL (peak of 0.94 ng/mL). A CT ruled out the presence of a pulmonary embolism. Blood cultures drawn on the day of admission were positive for Enterococcus faecalis. During cardiac workup, a transthoracic echocardiogram (TTE) showed severe bioprosthetic AV stenosis with a mean gradient of 87 mm Hg and AV area of 0.7 cm2 compared with a mean AV gradient of 25 mm Hg 1 month earlier. A three-dimensional transesophageal echocardiogram was performed to further evaluate the AV stenosis in the context of bacteremia and it revealed a mean AV gradient of 66 mm Hg (figure 1) and a potential thrombus of the right aortic coronary cusp (figure 2). Thus, the differential diagnosis of aortic stenosis secondary to bacterial endocarditis or thrombosis of the aortic leaflet was considered.
Colour wave Doppler of the aortic valve gradient.
Three-dimensional transesophageal echocardiogram showing the occlusive thrombus.
Of note, the patient’s initial mean AV gradient across the AV 2 days after the initial surgery was 24 mm Hg. On the initial presentation to the hospital 1 month prior the patient had a similar mean AV gradient of 25 mm Hg with only trace aortic regurgitation.
Treatment
The patient was started on intravenous ampicillin and ceftriaxone and a heparin drip for possible endocarditis and valve thrombosis, respectively. There was no significant improvement in the BPV gradient on repeat TTE performed after 4 days, thus more concerning for endocarditis. Furthermore, the patient developed worsening conduction system disease with Mobitz type II atrioventricular block and sinus pauses. The worsening dyspnoea and progression of electrocardiographic abnormalities were concerning for involvement of the aortic root by the infectious process and cardiothoracic surgery was consulted.
The patient was taken to the operating room for an urgent SAVR. Intraoperatively, the ascending aorta was opened just superior to the previous aortotomy closure site, down into the non-coronary sinus. Surgeons did not find any sign of active infection of the BPV during the surgery. However, there was a large thrombus obstructing flow across the right coronary cusp (figure 3). There seemed to be some super-added infection of the thrombus without active infection of the aortic root. The previously placed pledgets and BPV were removed and new 25 mm stentless Edwards Intuity BPV was placed into position. An intraoperative TTE confirmed that the newly placed valve was well positioned without any significant perivalvular leakage and mean AV gradient across the valve was 8 mm Hg. He was discharged on 3 months of warfarin and 6 weeks of intravenous antibiotics.
Bioprosthetic valve with thrombus obstructing the right coronary cusp.
Outcome and follow-up
The patient was seen in the clinic 5 months after the BPV replacement. The patient denied recurrent episodes of chest pain, shortness of breath, orthopnea or palpitations. The patient completed his course of 3 months of anticoagulation and 6 weeks of intravenous antibiotics. The patient was instructed to continue his daily intake of 81 mg of aspirin and would be followed-up in clinic in the future.
Discussion
There has been a gradual shift from mechanical toward BPV implantations in the USA. This phenomenon is most likely secondary to their lower thrombogenicity, improved valve haemodynamics, no need for lifelong anticoagulation and the introduction of transcatheter AV replacement.2 3
The most common cause of valve haemodynamic deterioration is structural degeneration, followed by pannus ingrowth and thrombosis.4 BPV thrombosis can have a diverse clinical presentation ranging from asymptomatic to gradual worsening dyspnoea, systemic or pulmonary embolisms and even cardiogenic shock.2 5 The incidence of subclinical valve thrombosis on CT scan is found to be 4% in surgical valves compared with 13% in transcatheter valves.6 A recent study by Salaun et al reported how the haemodynamic deterioration of bioprosthetic AVs is often echocardiographically evident approximately 7 years postoperatively and is a strong predictor of adverse clinical outcomes.3 Known predictors of AV deterioration are younger age at implantation, concomitant cardiovascular risk factors and valve-related factors (eg, prosthetic-patient mismatch).7
Brown et al reported their experience with BPV thrombosis within 2 years of placement that required reoperation. Stented porcine valves had an overall incidence of 0.55%, however, stented pericardial valves did not have thrombosis. This is interesting since our patient had a stented pericardial valve in place.8 Makkar et al analysed data from 187 patients after AV replacement and found a high incidence (20.9%) of reduced leaflet motion on CT scans responsive to anticoagulation therapy.9 Puri et al recently reported an incidence of BPV thrombosis in surgically placed valves at 1 year to be up to 14% and ≤1% in subclinical and symptomatic cases, respectively. In surgically placed BPVs, the peak incidence is within 2 years of implantation.2 Egbe et al proposed early reoperation could be avoided by screening patients for early BPV thrombosis with the following echocardiographic criteria: >50% increase in transvalvular gradient, increase in cusp thickness >2 mm and abnormal cusp mobility.10 This is relevant since operative mortality associated with reoperation can be significantly high (6%–13%).7
The mechanisms that have been associated with BPV thrombosis include perturbations in blood flow (ie, wall shear stress and blood stasis), patient-related factors (ie, renal insufficiency, obesity, diabetes mellitus (DM), smoking and anaemia), low cardiac output states and peri-procedural trauma leading to exposure to tissue factor and activation of the coagulation cascade. We believe that the BPV thrombosis in our patient occurred most likely secondary to elevated transvalvular gradients, coagulation factor alterations and altered flow patterns seen in prosthetic-patient mismatch.2
The treatment of choice for patients with minimally obstructive and/or small (<5 mm) thrombi is anticoagulation.2 Valve replacement surgery should be considered if valve thrombus fails to resolve with anticoagulation such as the case we presented. Systemic fibrinolysis of the BPV thrombosis is not an effective option due to high mortality (10%–15%) and increased risk of systemic embolism (12%) with such procedure.2 Further research to determine appropriate methods to identify and manage subclinical BPV leaflet thrombosis before an open valve replacement is warranted.
Learning points
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Bioprosthetic valve thrombosis should be part of the differential diagnosis in any patient with a history of an aortic valve replacement.
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Prosthetic-patient mismatch can predispose patients to future thrombosis.
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A multidisciplinary approach to these cases is necessary in order to achieve good outcomes.
Footnotes
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Contributors All authors were involved in the conception and design of the case report. All authors were involved in the drafting of the article. All authors approved the final version of the article. MAC-P conceptualised and designed the case report, interpreted the laboratory results, drafted the initial manuscript and approved it for publication. BD conceptualised and designed the study, interpreted the data, drafted the initial manuscript and approved it for publication. RJ interpreted the data, critically revised the manuscript and approved it for publication.
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Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
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Competing interests None declared.
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Patient consent for publication Obtained.
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Provenance and peer review Not commissioned; externally peer reviewed.
- © BMJ Publishing Group Limited 2020. No commercial re-use. See rights and permissions. Published by BMJ.
References
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