Prosthetic heart valves
There are two main types of prosthetic heart valves, mechanical valves which are durable but require chronic anticoagulation
because of thrombogenicity and biological valves which are less durable, but also less thrombogenic. Biological valves do not require lifelong anticoagulation (unless there are other reasons for anticoagulation, such as atrial fibrillation).
Mechanical heart valves
Tilting disk valves: They are classified in single and double tilting disk (bileaflet) valves. Nowadays mainly double disk (bileaflet) valves are used.
Lillehei-Kaster) consist of a ring and a disk, that shifts between the opening position and the closing position, supported by metal struts. In the opening position the disc forms with the plane of the ring an angle of 60-80 degrees.
What do these two images show?
The top image shows a 3 dimensional (3D) echocardiogram of a mechanical bileaflet prosthetic valve in the mitral position viewed from the left atrial side in diastole with the leaflets in the open position. Normal opening of the valve can be seen. The lower image shows the same valve in systole (closed position). 1. sewing ring of the prosthesis/ 2. leaflets
Bioprosthetic heart valves (Biological tissue valves or bioprostheses)
porcine, bovine, or equine tissue (valvular or pericardial), or homografts, which are preserved human aortic valves. In cardiac auscultation, normally functioning bioprosthetic (biological) valves do not differ from normal native valves. There are several types of bioprosthetic valves: .
Heterografts are: 1) Porcine valves properly suited to a suture ring made of synthetic material. Such valves are: Carpentier-Edwards, Hancock II and Mosaic (Medtronic). With echocardiography, for the Carpentier-Edwards valve at the mitral position, the expected peak velocity is about 1.5-2 m /sec and the expected mean pressure gradient of 5-9 mmHg. In the aortic position, the expected peak velocity is 2-3 m /sec and the expected mean pressure gradient 8-20 mmHg.
Pericardial valves are also two valve types used in transcatheter aortic valve implantation (TAVI): SAPIEN XT (Edwards LifeSciences) made of bovine pericardium and CoreValve (Medtronic) made of porcine pericardium. The valves used for TAVI are trileaflet bioprosthetic valves mounted in a wire mesh stent. Delivery of the valve is performed over a catheter and the stent is expanded in the position of the aortic valve. TAVI can be performed with a catheter advanced from the femoral artery in retrograde fashion across the aortic valve, or from a small thoracotomy with the catheter passed through the apex of the left ventricle and advanced across the aortic valve. This procedure is used for calcific aortic stenosis with the native valve being compressed but remaining in place. TAVI is indicated in patients with severe symptomatic aortic stenosis who have a high risk of adverse surgical outcomes due to comorbidities. Possible complications include stroke, vascular complications (at the entrance site at the femoral artery), and paravalvular regurgitation
Usually taken 24 hours after the donor's death, they are sterilized by antibiotics and maintained at a temperature of -196 ° C. The recorded Doppler velocities are approximately the same as those of native aortic valves.
Autograft (Ross operation)
Pulmonary autograft is the patient's own pulmonary valve implanted to replace a pathologic aortic valve, during a Ross operation. The pulmonary autograft consists of the pulmonary valve with its ring and a small part of the main pulmonary artery. The aortic valve and the aortic root are replaced with the autograft, to which the coronary arteries are then implanted. Subsequently, a pulmonary allograft (cadaveric graft) is implanted in place of the pulmonary valve. Advantages of this operation are that the autograft placed in the aortic position has a very good hemodynamic behavior and better durability than other biological valves. The disadvantage is that it is a technically difficult procedure that requires a long duration of extracorporeal circulation and is only performed in a few cardio-surgical centers with experience.
Stentless prosthetic valves
Selection of the type of prosthetic heart valveThe patient should be informed about the advantages and disadvantages of each option and the desires of the well-informed patient are also taken into consideration, as well as the following important factors. Mechanical valves have greater durability, but need lifelong anticoagulation, whereas bioprostheses are less durable, but have the advantage of a lower thrombogenic potential and do not need lifelong anticoagulation.
In favor of a mechanical prosthetic valve are the following:
Age< 65 with a long life expectancy (> 10 years on the basis of age and the presence or absence of serious comorbidities),
No contraindications for anticoagulation, or a patient already receiving anticoagulation treatment (a patient that already has a mechanical prosthesis and needs a second prosthetic heart valve).
In favor of a biological prosthetic valve are the following:
Age >65, (more specifically for a valve in the aortic position age> 65 and for a valve in the mitral position age > 70) or a limited life expectancy,
a contraindication for anticoagulation,
or a woman of childbearing age who desires pregnancy.
Age limits are not absolute and they can be further refined, depending on the position if the prosthetic valve:
In the mitral position, a mechanical valve should be generally preferred in patients of age <65, and both valve types (mechanical or bioprosthetic) are acceptable in patients between 65-70 years.
In the aortic position, a mechanical valve should be generally preferred in patients of age <60, and both valve types (mechanical or bioprosthetic) are acceptable in patients between 60-65 years.
Antithrombotic treatment in patients with prosthetic heart valves
Bioprosthetic valves:Bioprosthetic (biological) valves are clearly less thrombogenic than mechanical ones, so they do not necessarily need anticoagulation. However, there is a risk of embolism during the initial postoperative period (mechanism: thrombus production on the prosthetic valve support ring). According to the guidelines in patients with a bioprosthetic valve in the mitral or tricuspid position, it is a good practice (with a category IIa-not absolute- indication) to administer anticoagulation with a vitamin K antagonist (acenocoumarol or warfarin) for the first 3 months after valve implantation. Postoperatively heparin (unfractionated or low molecular weight) is initially administered and treatment with a vitamin K antagonist (VKA) is also initiated. When the INR reaches therapeutic levels (2-3) heparin is discontinued and oral anticoagulant treatment is continued (with INR 2-3) for 3 months After 3 months, the risk of thromboembolism is much lower. (INR = international normalized ratio). Therefore, anticoagulation with VKA is discontinued, and permanent antithrombotic treatment with aspirin 80-100 mg (or clopidogrel 75 mg) per day is initiated.
Oral anticoagulation using a VKA should also be considered for the first 3 months after surgical mitral or tricuspid valve repair (a class IIa indication)
After surgical implantation of a bioprosthetic valve at the aortic position, because at this position there are higher blood flow velocities resulting in less risk of thrombosis, guidelines recommend administering only low dose aspirin (eg 80-100 mg daily) for the first 3 months after surgery. This has a Class IIa indication.
However, guidelines allow the option to give these patients (with an aortic bioprosthesis) in the first 3 months a VKA instead of aspirin but with a class IIb indication ( a "weak" indication).
Exception: In patients with a bioprosthetic valve that also have other risk factors for thromboembolism (such as: a previous embolic episode, atrial fibrillation, or severe left ventricular systolic dysfunction with an ejection fraction ≤ 35% or a hypercoagulable state), anticoagulation with INR 2-3 is administered lifelong (and not just for the first 3 months). This is an absolute (class I) indication for permanent anticoagulation.
After transcatheter aortic valve implantation (TAVI), dual antiplatelet therapy is administered for the first 3-6 months. This is followed by lifelong single antiplatelet therapy in patients who do not need oral anticoagulation for other reasons. In case of TAVI, where an additional thromboembolic risk factor (atrial fibrillation, left ventricular systolic dysfunction, hypercoagulability) is also present, a vitamin K antagonist (VKA) is permanently administered with target INR 2-3, while aspirin 80-100 mg, or clopidogrel 75 mg daily is given during the first year and then it is discontinued
Mechanical prosthetic heart valves
Thrombosis and thromboembolism risks are greater with a mechanical valve in the mitral than in the aortic position.
Mechanical valves of medium thrombogenicity are some other bileaflet valves with insufficient data.
Mechanical valves of high thrombogenicity are: the ball-cage valve (Starr-Edwards) and most single disk valves (with the exception of Medtronic Hall) such as Lillehei-Kaster, Omniscience, Bjork-Shiley and other single tilting-disc valves.
Good management of anticoagulation is important since a high variability of the INR is a strong independent predictor of
reduced survival after heart valve replacement with a mechanical prosthesis.
Patients with mechanical heart valves undergoing a percutaneous coronary intervention (PCI)
Initially triple antithrombotic treatment (VKA+aspirin+clopidogrel) is administered for 1 month (it may be given for up to a maximum duration of 6 months if the patient is considered to have a high thrombotic risk and a low bleeding risk). After the period of triple antithrombotic treatment, dual therapy (VKA+clopidogrel, or VKA+aspirin) follows until up to 12 months after coronary stent implantation. Then antiplatelet treatment is discontinued and the patient continues only VKA (anticoagulation). In patients with a high bleeding risk (when bleeding risk is considered as more important than ischemic risk), triple antithrombotic treatment is not given. Then treatment after PCI includes only a period of dual antithrombotic therapy (VKA+ clopidogrel) which can last up to 12 months. After that antithrombotic therapy continues only with the VKA. A high ischemic risk ( a high risk for a subsequent myocardial infarction) is considered to be present in patients presenting with an acute coronary syndrome or having certain characteristics of the coronary lesion (e.g. presence of thrombus, a complex lesion), whereas the bleeding risk is estimated by using the HAS-BLED score.
HAS-BLED stands for:
Hypertension (systolic >160 mmHg) or
Abnormal renal function (creatinine >2.2 or dialysis or renal transplant)
Abnormal liver function (Cirrhosis or Bilirubin >2x Normal or AST/ALT/ALP >3x Normal)
Stroke (history of previous stroke)
Bleeding (Prior major bleeding or predisposition to bleeding
Labile INR (unstable or high, remains in the therapeutic range for < 60% of the time)
Elderly (> 65 years)
Drugs (medication usage that predisposes to bleeding, such as NSAIDs or antiplatelet drugs) or
alcohol(≥ 8 drinks/week)
The presence of each of the above adds 1 point to the score.
A HAS-BLED score of ≥3 indicates high risk for major bleeding ( defined as intracranial hemorrhage, or bleeding requiring hospitalization, or hemoglobin decrease > 2 g/dL, and/or transfusion)
Clinical and echocardiographic follow-up of a patient with a prosthetic heart valveIn general, emphasis should be placed on informing the patient about proper adherence to anticoagulation and endocarditis prophylaxis.
According to the guidelines of the European Society of Cardiology (ESC) a patient who undergoes a valve replacement requires after 6-12 weeks a complete follow-up examination, including clinical examination (history of possible symptoms, cardiac auscultation to check for the expected auscultatory findings for the type of prosthetic valve and also to check for a possible new cardiac murmur), ECG, chest X-ray, transthoracic echocardiography (TTE) and blood tests.
Physical examination and cardiac auscultation of a patient with a prosthetic heart valveSignificant abnormal findings from the physical examination of a patient with a prosthetic heart valve may include a new or changed murmur, muffled valve sounds, or signs indicative of an embolic event (e.g. a neurological deficit in a case of an embolic stroke).
The expected auscultatory findings in patients with a prosthetic valve depend on the type of the valve prosthesis. Normally functioning biological prosthetic valves have the same auscultatory findings as normal native valves. Among the mechanical valves, the bileaflet mechanical valves, which are the type of mechanical valves currently implanted, do not produce an opening sound but only a metallic closing sound. Single-tilting disc mechanical valves produce an opening sound and a closing sound, while the cage-ball valves produce multiple opening sounds, due to the impact of the ball on the cage. On auscultation of the heart, the absence of the expected sounds produced by the prosthetic valves is a pathological finding indicative of limited valve mobility due to thrombosis or tissue hyperplasia.
All mechanical valves in the aortic position additionally produce a characteristic mild systolic ejection murmur. In contrast, the small normal regurgitation of blood (small physiological insufficiency) present in the mechanical valves does not produce a murmur. Therefore, in a patient with a mechanical aortic valve, the finding of a diastolic murmur is a pathological finding, indicating a paravalvular leak (paravalvular regurgitation).
Echocardiography of prosthetic heart valvesThe echocardiogram should include measurement of the transvalvular pressure gradient, color Doppler examination to search for a paravalvular regurgitation and assessment of ventricular function.
Echocardiographic findings and measurements within the first few weeks after surgery will serve as a reference for comparison with future findings. A basic parameter is the pressure gradient (pressure difference) across the valve when it is open. The measurement of the peak velocity and the calculation of the peak and mean transvalvular pressure gradient is performed with the continuous wave Doppler. All prosthetic valves have a peak transvalvular velocity which is higher than that of a normal, native valve. They also create a greater pressure gradient than a normal natural valve, given that the latter creates a negligible pressure gradient. As mentioned, depending on the type of prosthetic valve, there are some expected limits for the pressure gradient (some approximate limits have been given above).
Elevated transvalvular velocity and pressure gradient in a prosthetic valve, as compared to the expected values, is observed in cases of: 1) Valve malfunction causing stenosis (thrombus or pannus development, mechanical degeneration and stenosis due to degeneration and calcification of a bioprosthetic valve),
2) In cases of increased flow through of the valve with no narrowing of the valve (conditions with an increased cardiac output such as hyperthyroidism, anemia or a significant valvular or paravalvular regurgitation). In the case of significant regurgitation at the valve, there is a volume overload of the ventricular cavity located proximally to the valve, resulting in a larger volume of blood passing through the valve when it opens and thus in a higher velocity and pressure gradient.
3) In prosthesis-patient mismatch (PPM), where there is no valve dysfunction, but the valve is small for the patient's body size and circulatory needs.
Echocardiographic indications of prosthetic valve stenosisIn a prosthetic aortic valve (bioprosthetic or mechanical), indications of a significant stenosis are a peak flow velocity> 4 m / sec, a mean pressure gradient> 35 mmHg, an effective valve orifice <0.8 cm2, and an acceleration time > 100 msec. An indication for a possible stenosis or a moderate stenosis is a peak velocity between 3 and 4, a mean pressure gradient between 20 and 35, an effective orifice between 0.8 and 1.2 and an acceleration time between 80 and 100. The acceleration time is the time interval between the onset of blood flow through the valve and the peak flow velocity. Apart from the adequacy of valve opening, it is also affected by the heart rate and contractility of the left ventricle. When the shape of the flow signal obtained with the continuous Doppler is triangular with the peak velocity occurring early, this is a sign of normal flow, whereas when it is symmetrical and rounded, this is indicative of stenosis.
In a prosthetic mitral valve (biological or mechanical), a sign of significant stenosis is a peak flow velocity> 2.5 m / sec, a mean pressure gradient ≥ 10 mmHg,
an effective valve orifice<1 cm2 and a pressure half time (PHT) > 200 msec.
An indication of a possible stenosis, or moderate stenosis of a prosthetic mitral valve is a peak velocity is between 1.9 and 2.5 / a mean pressure gradient between 6 and 10 / an effective orifice area between 1 and 2 and a PHT between 130 and 200. Apart from valvular function, the PHT is also influenced by left ventricular diastolic function (compliance).
Calculation of the functional orifice area or effective orifice area (EOA) of prosthetic valvesThe functional orifice area or effective orifice area (EOA) of prosthetic valves is calculated with the continuity equation, which is based on the principle that flow in a heartbeat is the same through all areas of the circulation.
The EOA of a prosthetic valve in the mitral position is calculated as EOA = (CSA LVOT xVTI LVOT )/VTI PrMV,
CSA LVOT = 0.785 d2, where d is the diameter of the LVOT measured in the parasternal long axis echocardiographic view, just proximal to the aortic valve.
Prosthetic valve regurgitationFor the detection and grading of prosthesis regurgitation, the echocardiographic methods and measured parameters used are similar to those used for native cardiac valves.
It is important to distinguish pathologic prosthesis regurgitation from the small physiologic regurgitation usually present in prosthetic valves. Mechanical prosthetic valves have a normal small amount of regurgitation called leakage backflow which has a washing effect against blood stasis and thrombus formation. In contrast to the jets of pathologic regurgitation, the normal leakage backflow jets are short in duration, narrow, symmetric and have a small size. Also in bioprosthetic heart valves, a minor degree of central transvalvular regurgitation is often present.
In the case of pathologic regurgitation, the origin of the regurgitant jet should be located to distinguish paravalvular from transvalvular regurgitation.
Causes of pathologic prosthesis regurgitation include paravalvular regurgitation or pannus both in mechanical and biological valves, calcific degeneration and tear of valve leaflets in bioprosthetic valves, thrombus in mechanical valves. Paravalvular regurgitation is caused by infective endocarditis, calcification or fibrosis of the native valve annulus with poor contact with the suture ring, or suture detachment.Thrombus and pannus can also cause valve stenosis (this is their most usual presentation). The stentless prosthetic valve substitutes can also develop functional central aortic regurgitation as a result of continued dilation of the aortic root.
For the evaluation of prosthetic valve regurgitation, with transthoracic echocardiography (TTE) as well as with transesophageal echocardiography (TEE), obtaining color Doppler images in multiple views and multiple planes is essential.
Acoustic shadowing can obscure regurgitant jets and this is more an issue for prosthetic valves in the mitral than for those in the aortic position.
Grading of a mechanical or bioprosthetic aortic valve regurgitation (central or paravalvular)An indirect sign is left ventricular (LV) size which in the case of mild aortic regurgitation (AR) is expected to be normal, in moderate AR it will be either normal or mildly increased but in severe AR prominent LV dilation will be present.
Regurgitant color Doppler jet width at its origin expressed as % of the left ventricular outflow tract (LVOT) diameter: the wider the jet the more severe the regurgitation: Mild regurgitation ≤30 %, moderate between 30 and 60%, severe regurgitation >60%.
Vena contracta is another useful echocardiographic parameter used to grade valve regurgitation severity. Vena contracta is defined as the narrowest region of a flow jet that occurs at, or just downstream to, the regurgitant orifice (the orifice at the valve where regurgitation occurs).
Vena contracta width in mm:
mild regurgitation <4, moderate 4-6, severe regurgitation >6
Vena contracta area (measured with 3D color Doppler in mm2):
mild regurgitation <20 moderate 20-40, severe regurgitation >40
The density of the regurgitant jet examined with continuous wave (CW) Doppler: in mild regurgitation, the jet is incomplete or faint, whereas in moderate or severe regurgitation it appears dense.
The pressure half time (PHT measured in ms) of the regurgitant jet This is the time from the onset of the regurgitant flow to the point the pressure gradient (=4xvelocity2) between the aorta and the left ventricle becomes half of its initial value. It is calculated by the machine from the CW Doppler signal of the regurgitant flow when you trace the slope of the signal. The more severe the regurgitation the quicker the decline of the pressure difference (pressure gradient) between the two communicating cavities (aorta and left ventricle) and thus the smaller the value of the PHT: mild regurgitation PHT >500 ms, moderate regurgitation 200-500 ms, severe regurgitation <200 ms.
Another useful index is the diastolic flow reversal in the descending aorta, assessed with PW Doppler from the suprasternal echocardiographic view: In a mild regurgitation, this is absent or brief early-diastolic, whereas in severe regurgitation there is a prominent holodiastolic flow reversal with an end-diastolic velocity >20 cm/s. In moderate regurgitation, the findings are intermediate between those two situations.
Left ventricular outflow to right ventricular outflow ratio. This is calculated by obtaining the PW Doppler signal of the systolic flow in the left ventricular and right ventricular outflow tract and expressed as the ratio of the respective stroke volumes or velocity-time integrals. The greater the aortic regurgitation (AR), the greater the ratio of LV outflow/RV outflow. This happens because AR causes an increased stroke volume of the left ventricle due to volume overload of the ventricle, which has to eject not only the effective forward flow of blood that will reach the systemic circulation but also the volume of blood that regurgitates during diastole.
Thus in severe AR this ratio is increased (>1.8).
Grading of a mechanical or bioprosthetic mitral valve regurgitation (central or paravalvular)
The color flow jet area can also provide an indication but it underestimates regurgitation severity when the jet is not central but eccentric, impringing on the interatrial septum or the wall of the left atrium. When we are dealing with a relatively central jet, mild regurgitation is characterized by a small jet size (usually < 4 cm2 or
<20% of left atrial area), whereas severe mitral regurgitation (MR) is characterized by a large jet (usually >8 cm2 or >40% of left atrial area)
The size of the zone of flow convergence, which is viewed with color Doppler as a hemispheric area of blood at the left ventricular side, accelerating towards the regurgitant orifice: mild MR is characterized by a nonvisible or minimal zone of flow convergence, whereas severe MR is characterized by a large flow convergence zone.
MR jet density assessed with CW Doppler: mild MR is characterized by an incomplete or faint CW signal of the regurgitant jet, whereas severe MR by a dense CW signal.
MR Doppler signal contour assessed with CW Doppler: in mild MR it has a parabolic shape, whereas in severe MR the CW signal is triangular and early peaking.
The PW Doppler signal of pulmonary venous flow in mild MR demonstrates dominance of the systolic wave (versus the diastolic wave), in moderate MR there is systolic blunting (the height of the systolic wave is reduced), and in severe MR there is systolic flow reversal (a negative systolic flow wave).
A quantitative parameter is the effective regurgitant orifice area EROA (mm2 ), which in moderate MR is between 20 and 40 and in severe MR ≥40 mm2 (0.4 cm2)
Another quantitative parameter is the regurgitant volume RV (mL/beat) which in moderate MR is between 30 and 60 and in severe MR >60. These two quantitative parameters of MR severity are calculated by using the proximal isovelocity surface area (PISA) method (see chapter on mitral regurgitation, link Mitral regurgitation. Diagnosis, echocardiography and management.)
The regurgitant fraction= regugitant volume/stroke volume in moderate MR is 30-50 % and in severe MR >50 %
Indirect signs of the severity of MR that should not be neglected:
LV size : In mild MR it is expected to be normal, in moderate MR the LV is expected to be normal or mildly dilated and in severe MR it should be clearly dilated.
Left atrial (LA) size: in moderate MR it is usually normal or mildly dilated and in severe chronic MR left atrial dilation is prominent (but in cases of acute severe MR the LA size can be normal, because it did not have the time to enlarge).
Pulmonary hypertension is generally present in cases of severe MR
( systolic pulmonary arterial pressure SPAP ≥50 mm Hg at rest and ≥60 mm Hg at exercise).
Useful videos !! (LINKS)
Assessment of Prostheses in Echocardiography 123sonography (Prof Thomas Binder)
Prosthetic Valve Assessment (William A. Zoghbi, MD) DeBakey Institute For Cardiovascular Education & Training
Prosthetic valve echocardiography
A normally functioning bileaflet mechanical prosthetic valve in the mitral position (3D echo)
From you tube channel LondonCardioClinic
Prosthetic valve complications
Prosthetic valve thrombosisThere is an increased risk in case of inadequate anticoagulation in a patient with a mechanical prosthetic valve (INR significantly lower than target value) and mechanical prosthetic valves in the mitral position, or the older types of mechanical prosthetic valves (cage-ball, single leaflet). Clinical presentation can be with embolization, e.g. an embolic stroke, or acute limb ischemia, or acute valvular dysfunction causing acute pulmonary edema, or sudden death.
On physical examination diminished intensity of valve sounds may be present. On echocardiography or fluoroscopy, there is a reduced movement of the valve leaflets. There is also an increased transvalvular gradient on echocardiography.
Treatment: Anticoagulation with heparin. If the thrombus is <5 mm on echocardiography, then anticoagulation may suffice. If the thrombus is > 5 mm then apart from heparin, thrombolysis, thrombectomy or valve replacement will be required. Generally, for thrombosis of left-sided prosthetic heart valves, surgical treatment with valve replacement is indicated, unless there is a prohibitive surgical risk or a small thrombus. For thrombosis of a right-sided prosthetic valve, the treatment of choice is thrombolysis (fibrinolysis). Surgery is indicated if thrombolysis is unsuccessful 24 hours after discontinuation of the infusion.
In patients with prosthetic valves presenting with peripheral embolization, endocarditis should also be considered.
Risk factors include: atrial fibrillation, left ventricular systolic dysfunction, age > 70 years, mitral prostheses, cage-ball valves, the presence of more than 1 prosthetic heart valve. If there are clinical findings suggesting a stroke, a brain computed tomography (CT) should be performed immediately to exclude an intracranial hemorrhage ( in case of an intracranial hemorrhage anticoagulation is withheld and specialist help from a neurologist or neurosurgeon is also needed).
Patient-prosthesis mismatch (PPM)PPM is a situation where the problem is not prosthetic valve dysfunction, but a small prosthetic valve for patient needs. The effective orifice area (EOA) of the valve is indexed to body surface area (BSA), i.e. it is divided by the BSA. In a prosthetic valve in the aortic position when EOA / BSA> 0.85 cm2/m2, then there is only mild or no PPM. On the contrary, when EOA / BSA ≤ 0.65 cm2/m2 then there is considerable PPM and significant stenotic phenomena. Intermediate values below 0.85 but over 0.65 cm2/m2 suggest a moderate degree of patient-prosthesis mismatch (PPM).
In a case of a prosthetic valve at the mitral position, when
EOA / BSA >1.2 cm2/m2, there is only mild or no mismatch between prosthetic valve and patient. Conversely, when EOA / BSA ≤ 0.9 cm2/m2, then there is considerable PPM and significant stenosis. Intermediate values, below 1.2 but over 0.9 cm2/m2 indicate a moderate degree of PPM.
Several studies link PPM with a decreased postoperative cardiac index, a worse New York Heart Association (NYHA) functional class, a higher likelihood of late adverse events and shorter mean patient survival.
Haemolysis in patients with prosthetic heart valvesA mild haemolysis is common in patients with mechanical prostheses (even with normal prosthetic valve function). Severe haemolysis is not common and is usually a result of prosthetic valve dysfunction (regurgitation, dehiscence, infection).
Blood tests in case of haemolysis show anemia (decreased hemoglobin and hematocrit), increased levels of lactate dehydrogenase (LDH) and reticulocytosis.
Treatment: Administration of folic acid and ferrous sulphate may be needed to increase production of erythrocytes. In severe cases, blood transfusions will be required and identification and treatment of the underlying problem (including valve replacement for cases requiring frequent blood transfusions).
Prosthetic valve endocarditis
The imaging modality of choice is transesophageal echocardiography (TEE) which can detect vegetations, or complications of prosthetic valve endocarditis, such as valve dehiscence or an abscess.
Paravalvular leak or paravalvular regurgitation of prosthetic heart valves
Prosthetic valve dehiscenceDehiscence (detachment) of the prosthetic valve suture ring from the valve annulus may occur in the early postoperative period due to surgical errors, the presence of extensive calcification of the valve annulus, infection (endocarditis), fragile valve annular tissue due to previous surgery, or chronic corticosteroid use. Late dehiscence of a prosthetic valve is due to infectious endocarditis. An indication of valve dehiscence is an abnormal rocking motion of the prosthetic valve in echocardiography or fluoroscopic examination. Dehiscence is an indication for emergency surgery.
Prosthetic heart valve structural degeneration
Reoperation is required once symptoms develop (class I), or even in asymptomatic patients with severe regurgitation, or severe stenosis of the bioprosthesis because reoperation at a stable stage reduces the risk of this second operation and thus may be justified. The risk associated with reoperation in a stable patient is only slightly higher than the risk of the first operation. Bioprosthetic aortic valve failure in patients with a high surgical risk can be treated by transcatheter valve‐in‐valve implantation.
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BIBLIOGRAPHY AND LINKS
Zoghbi, WA, et al. Recommendations for Evaluation of Prosthetic Valves With Echocardiography and Doppler Ultrasound. Journal of the American Society of Echocardiography 2009;22: 075-1014.
Baumgartner H, et al. 2017 ESC/EACTS Guidelines for the management of valvular heart disease: The Task Force for the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS), European Heart Journal, ehx391, https://doi.org/10.1093/eurheartj/ehx391
Bajaj R, Karthikeyan G, et al.CSI consensus statement on prosthetic valve follow up. Indian Heart Journal 2012; 64: S3 -S11 LINK https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4244813/pdf/main.pdf
Huang G1, Schaff HV, et al. Treatment of obstructive thrombosed prosthetic heart valve.J Am Coll Cardiol. 2013 ;62:1731-1736.