Prosthetic Valve Malfunction
Lina Ya'qoub, Luai Tabaza
Definition
Over the past six decades valvular replacement and repair witnessed significant improvements in patient outcomes, this is largely due to development of new operative techniques, refinement of prosthetic valve design and advanced anesthesia cares. Malfunction of the mobile component of a prosthetic valve continues to be a challenge to the further improvements in these outcomes. Prosthetic valve dysfunction can be attributed to intrinsic or extrinsic causes; structural deterioration, pannus formation, thrombosis and thromboembolic complications, endocarditis, leaflet arrest/entrapment, patient-prosthesis mismatch, malfunction leading to hemolysis as well as valvular and paravalvular leakage [1,2,3,4,5].
Causes
Structural Degeneration
Like any device or viable organs, prosthetic valves can degenerate with time. It is known that degeneration occurs faster in bio prosthetic valves compared to mechanical valves [1]. The mitral valve is involved more frequently, presumably because of higher closing pressures. While bio prosthetic valves usually degenerate within the first 10 years and thus have higher reoperation rates, mechanical valves usually last more than 20 years [1,6,7,8]. The rate of structural valve failure is age-dependent and is significantly lower in patients older than 65 years [1,5]. Although degeneration is often associated with valve malfunction, mainly attributed to incomplete closure of the valve, it is important to note that degeneration does not always result in valve dysfunction [9].
Prosthetic valve obstruction caused by pannus formation
Pannus represents a bio reaction to the prosthetic valve and is mainly formed of collagen and elastic fibrous tissue [10]. Pannus can form on any prosthetic valve, but it is particularly common in mitral valve prosthesis as the chordae of mitral valves are usually spared in mitral valve replacement in order to preserve LV geometry and hemodynamic function, this in turn, accelerates the growth of host tissue resulting in the pannus formation [11].
Differentiating the cause of prosthetic valve obstruction (pannus versus thrombus) is crucial, as they are managed differently. While surgical management is required for cases of pannus formation, anticoagulation or thrombolytic agents can be used in selected cases of thrombus formation [12,13,14,15]. Multi-detector Computed Tomography (MDCT) may be helpful in differentiating thrombus from pannus as the former usually has lower attenuation [16]. The differentiation between these two entities on imaging can be challenging, especially if there was no response to anticoagulation or thombolytic agents, the definitive diagnosis is often made by histopathology [10].
Prosthetic valve obstruction caused by thrombus formation
Prosthetic valve thrombosis (PVT) and thromboembolic complications remain a major cause of morbidity and mortality following valve replacement. Several studies have shown that the risk of PVT is highest in the early post-operative period [17]. Unstable anti-coagulation appears to be the major risk factor predisposing to PVT [12].
Three basic mechanisms explain the tendency of thrombus formation in prosthetic valves; molecular interactions, influence of transprosthetic blood flow and local hypercoagulability [17]. Molecular interactions are those interactions that occur between the blood and any foreign body, leading to the initiation of the coagulation cascade. These interactions are more common in the early post-operative period when the endothelialization process of the prosthetic valves is still incomplete. Low blood flow states are associated with risk of thrombosis as well; this explains why mitral valves are associated with a higher risk of thrombosis compared to aortic valves. Moreover, heart failure patients with reduced ejection fraction are at increased risk of thrombosis given their relatively-low flow state. Lastly, hypercoagulability is associated with increased risk of thrombosis in general, and this is particularly important in prosthetic valves due to the presence of the factors discussed above [16,17].
Interestingly, some studies found increased incidence of PVT in the winter months; the authors attributed that to plasma viscosity [17] and increased fibrinogen levels during winter months [18].
The diagnosis and timely management of PVT is of significant importance as it is not only associated with local complications i.e. valve obstruction and malfunction but might also lead to systematic embolization, including coronary embolization [19,20,21].
The treatment of PVT can be broadly categorized into antiplatelet-based strategies (aspirin and/or a P2Y12 receptor inhibitor) and anticoagulant-based strategies (using VKAs or direct oral anticoagulants). These are outlined in the 2014 ACC/AHA Guidelines for Antithrombotic Therapy After Valve Replacement as follows [5]:
Transcatheter PVT has been increasing recognized and diagnosed [22]; with the advances in imaging modalities and the increasingly used transcatheter procedures. Studies have shown that there is increased incidence of PVT in TAVR patients compared to the general population; thus, regular follow up is warranted using echocardiogram and MDCT to detect PVT even in asymptomatic patient to prevent progression of the thrombus and subsequent complications. To date, there are no guidelines for antithrombotic treatment in patients with transcatheter PVT, and treatment strategies are individualized based on patient’s comorbidities and operator experience. Recent studies, however, have shown that antiplatelet therapy might not be sufficient for transcatheter PVT and anti-coagulation might be warranted in these patients. More studies are being conducted in the present time to assess the efficacy of the different antiplatelet and anticoagulation medications for transcatheter PVT [23].
Prosthetic Valve Endocarditis (PVE)
Prosthetic valve endocarditis (PVE) occurs when an endovascular microbial infection involves parts of a valve prosthesis or a reconstructed native heart valve [24]. Prostheses made from metal, pyrolyte or other materials do not allow adherence of microorganisms as long as they are free from thrombotic material. However the sewing cuff can act as nidus for thrombus formation near the sewing ring, which in turn can cause inflammatory peri-prosthetic leaks, ring abscesses, and invasion of the infective process into the adjacent tissue [24].
The pathogenesis of bio prosthetic infections may be similar to that of native valves. In these cases, the infection is restricted to the cusps, eventually initiating secondary bio prosthetic failure but with only a low tendency to invade the sewing cuff or to result in periprosthetic abscesses [24].
PVE is usually classified as early PVE (that is acquired perioperatively), and late PVE (resulting from infections unrelated to the valve operation, similar to community acquired native valve infective endocarditis). Time cut off point between early and late PVE is usually one year, with notable differences in microbiology. Staphylococci (especially novobiocin susceptible, coagulase negative staphylococci), bacteria of the HACEK group (Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella species), and fungi occur more frequently in early PVE, as these microorganisms have high affinity to foreign bodies and prosthesis, where Streptococci and enterococci are found more frequently in late PVE [24].
The basic principles of antimicrobial treatment in PVE do not differ much from those for native valve endocarditis (NVE), but some special aspects need to be considered. PVE is usually associated with larger vegetations. Consequently, longer duration of treatment at higher doses of antibiotics are needed to penetrate the total vegetation. When PVE is clinically apparent and blood cultures are not yet positive, empiric treatment should be initiated with Vancomycin, Gentamicin followed by Rifampin in 3-5 days after effective treatment with Vancomycin and Gentamicin and if the micro-organism is sensitive to Rifampin (ESC 2015 Guidelines, Class I, Level of Evidence B) [2,24,25]. Antibiotic therapy should be tailored based on the culture and susceptibility results of each organism.
PVE occurring in the post-operative period, PVE caused by Staphylococci, the presence of multiple comorbidities, severe heart failure, and new prosthetic dehiscence have all shown to be poor prognostic indicators [25].
Multi-disciplinary approach in managing PVE is of paramount importance. Both ACC/AHA 2014 and ESC 2015 guidelines recommend that patients with IE should be evaluated and managed with consultation of a multi-specialty heart valve team, including an infectious disease specialist, cardiologist, and cardiac surgeon. In Surgically managed patients, this team should also include a cardiac anesthesiologist (Class I, Level of Evidence: B) [2,3,5].
Early surgical intervention should be considered in most cases of PVE in order to prevent secondary complications. Indications for surgery include: heart failure, prosthesis dehiscence, recurrent embolization despite medical treatment, Staphylococcus, fungal infection, peri-valvular abscess, penetrating destructive lesions, and failure of medical treatment [AHA 2014 Guidelines ( Class I, Level of Evidence: B )] [5,26,27].
Leaflet Entrapment/Arrest
Leaflet entrapment is the inability of the leaflet to move properly leading to valve malfunction. It can occur both intra-operatively and postoperatively. It is hypothesized that it can occur due to the magnitude and direction of forces applied upon the valve annulus which can cause the hinge mechanism to become restricted. Another hypothesis attributes the entrapment to the presence of a sub-valvular apparatus which restricts the proper valve movement. The rate of leaflet entrapment can vary between different valves [28,29].
Patient-Prosthesis Mismatch (PPM)
Prosthesis‐patient mismatch (PPM) occurs when the effective orifice area (EOA) of the inserted prosthetic valve is too small in relation to the body surface area (BSA). Its main hemodynamic consequence is to generate higher than expected gradients through normally functioning prosthetic valves [30,31]. Assessment of PPM is complex and involves measurement of multiple variables on echocardiogram. In 2009, Zoghbi et al published the first comprehensive American Society of Echocardiography (ASE) guidelines for Doppler echocardiographic evaluation of prosthetic function. Quantitative parameters of valvular stenosis include: Transprosthetic flow velocity and pressure gradient, EOA, and Doppler Velocity Index (DVI) [32,33,34].
PPM seems to correlate well with the indexed EOA (EOA divided by BSA); Mild PPM occurs when iEOA is >0.9 cm2/m2, moderate PPM occurs when iEOA is between 0.6-0.9 cm2/m2, severe PPM occurs when iEOA is <0.6 cm2/m2 (These numbers are for the aortic valve which is the most studied valve). The iEOA can be measured using invasive catheterization as well as non-invasive measures, with echocardiogram being the most widely used method [35,36].
EOA of prosthetic valves are usually smaller than the native valves; thus, it is common to see a mild degree of PPM and this mild degree of mismatch is not associated with worse outcome. On the other hand, studies have shown that severe PPM acts similar to LV outflow tract obstruction with increased pressure gradient across the valve, and this typically is associated with worse outcomes, namely recovery of diastolic dysfunction, quality of life and in some studies it affected survival. The effect of PPM on mortality/survival has not been proven yet [35,36,37,38].
Interestingly, patients who had TAVR had lower incidence of PPM compared to surgical AVR. This could be attributed to the self-expanding prosthesis used in TAVR [35].
Hemolysis
Mild hemolysis after prosthetic valve implantation is not uncommon, but severe hemolysis is rare. The mechanism responsible for hemolysis most commonly involves a regurgitant jet and blood cell trauma, either at the valvular or paravalvular level [39, 40]. The degree of hemolysis appears to be independent of the regurgitation severity when assessed by echocardiography, as patients may experience severe hemolysis with only moderate regurgitant jets [41]. It is thought that subclinical hemolysis is rather influenced by valve position but not by valve size or effective orifice area index and remained stable through time [39].
In one report a malfunctioning prosthetic aortic valve, causing severe hemolytic anemia and requiring blood transfusions in an elderly female, was resolved by creating an extra-anatomic apico-aortic connection that created an alternative blood flow out of the left ventricle [42].
Valvular and Paravalvular Leakage (PVL)
Normal functioning heart valve prostheses are designed to have a certain degree of intrinsic structural regurgitation as a washout mechanism to avoid prosthetic thrombosis, however severe regurgitation can occur and lead to malfunction [41]. Similarly, prosthetic paravalvular leak (PVL) is a serious complication after valve replacement. This usually occurs as a result of inappropriate sealing of the prosthetic ring to the native cardiac tissue. Although most of the cases consist of mild and asymptomatic regurgitation that is usually detected incidentally on follow up echocardiography, a small percentage of patients show large and clinically significant regurgitations [43,44]. Paravalvular leak can have significant clinical consequence including congestive heart failure, hemolytic anemia, and infective endocarditis [43].
Studies looking at early generations of Transcatheter Aortic Valve Implantation (TAVI) showed higher incidence of PVL compared to surgical AVR [32]. However, latest generations of these valves show comparable rates of PVL as they are modified with an outer skirt designed to reduce leak by sealing gaps around the valve.
Although surgery has been the traditional treatment of choice in hemodynamically significant PVL, percutaneous transcatheter closure and transcatheter valve-in-valve implantation are emerging as novel and less invasive options for patients with high operative risk [32,44,45].
Clinical Presentation
The clinical presentation of patients with prosthetic valve malfunction varies widely depending on the nature of the complication, the valve involved and the type of the valve. Patients may be totally asymptomatic with incidental findings on blood tests or imaging suggestive of malfunction. They may present with fever and new onset murmur suggesting endocarditis. New-onset arrhythmia or conduction abnormalities caused by abscess formation, heart failure symptoms secondary to severe valvular regurgitation, stenosis or PVL can be the presenting symptom. A more critical presentation in the form of cardiogenic shock secondary to valve entrapment or obstruction by a thrombus or pannus formation can also happen.
Close attention should be made to cardiac auscultation during physical examination as diminution of the occluder clicks can suggest prosthetic valve thrombosis [17]. Furthermore, identifying murmurs of stenotic or insufficient valves can be the leading hint to the diagnosis of valve dysfunction.
Given the wide clinical presentations, prosthetic valve malfunction should be considered in any patient with a prosthetic cardiac valve who presents with any cardiac symptom or sign and further evaluation should be pursued to establish the diagnosis.
Workup
The diagnostic approach to prosthetic valve malfunction typically includes blood tests and imaging studies. Blood tests are performed to look for hemolysis, check the coagulation status of the patient and obtaining blood cultures if endocarditis is suspected [24].
Transthoracic echo (TTE) evaluation of the prosthesis may be challenging due to the acoustic shadowing. Thus, real time 3-D Transesophageal Echocardiography (TEE) is usually required to assess prosthesis malfunction as it provides better anatomical and functional assessment of prosthetic valves [46,47]. Moreover, TEE should be performed without delay in all patients with suspicion of PVE; as TEE can define the size of vegetation and peri-annular complications (abscesses, dehiscence, fistulas) more precisely than TTE. Both the size of vegetations and infection morphology significantly influence therapeutic decisions (namely duration of antimicrobial treatment and the need for urgent surgical intervention) [24].
If the routinely recommended echocardiography is inconclusive, other imaging studies (cinefluorography, CT, MRI) may be used to confirm the diagnosis [33,48,49,50,51,52,53,54]. Furthermore, CT provides accurate dimensions, which are important for prosthetic sizing. Compared to echocardiographic sizing, CT-based sizing may lead to better results [55]. Sound-pressure analysis and sound spectrography can detect clot formation at a very early stage. However, there is a limited number of centers worldwide that perform these highly-sophisticated studies [17].
It is important to note that prosthetic valve malfunction can be intermittent and may not be confirmed by imaging. In these cases, the diagnosis is very challenging and should be evaluated on case-by-case basis with experts in the field in order to determine the best management approach [56,57].
Management
The consequences of prosthetic valve dysfunction may be catastrophic, especially in cases of fixed obstruction and cardiogenic shock. Thus, diagnosis and management should be done simultaneously in these cases [11,12].
The initial approach to management is to make sure the patient is hemodynamically stable, with intravenous fluids, blood transfusions or using vasopressors and inotropic agents till the cause of dysfunction is identified. It is important to identify the etiology dysfunction, as it will define the management plan. A multidisciplinary team, including a cardiothoracic surgeon, an interventional cardiologist and an imaging cardiologist should be involved in the early course of management [2,3,5]. Medical, surgical and transcatheter management should be tailored to the individual case [2,3,5,15,25,42,43,58,59,60,61,62]. In patients with recurrent prosthetic malfunction or prior complex cardiac surgeries, the risk of reoperation should always be considered in the clinical decision making process [62,63,64].
Prevention
Although it is difficult to predict or prevent many causes of prosthetic valve malfunction, there are preventive measures to be considered including: Maintaining a therapeutic coagulation level to prevent valve thrombosis [11,17]. Guideline-directed PVE prophylaxis using antibiotics taken one hour before and six hours after the interventional procedure [24]. Using prospective strategies and calculations based on EOA and BSA to prevent PPM [35,36,38]. The use of transesophageal echocardiography-guided intra-operative techniques is used routinely to prevent or minimize early postoperative paravalvular leakage and PPM [37,43,58]. And lastly, new multi-imaging modalities including 3D echocardiography, cardiac CT and cardiac MRI are deployed to achieve better prosthetic valve sizing and early detection for prosthetic malfunction [55].
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1. Vongpatanasin W, Hillis L, Lange R. Prosthetic heart valves. N Engl J Med, 1996. 335(6): p. 407-16.
2. Habib G, Lancellotti P, Antunes M, et al., 2015 ESC Guidelines for the management of infective endocarditis: The Task Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM). Eur Heart J, 2015. 36(44): p. 3075-128.
3. Holmes D, Rich J, Zoghbi W, et al., The heart team of cardiovascular care. J Am Coll Cardiol, 2013. 61(9): p. 903-7.
4. Iung B, Baron G, Butchart E, et al., A prospective survey of patients with valvular heart disease in Europe: The Euro Heart Survey on Valvular Heart Disease. Eur Heart J, 2003. 24(13): p. 1231-43.
5. Nishimura R, Otto CM, Bonow RO, et al., 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol, 2014. 63(22): p. 2438-88.
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