Prosthetic heart valves

Article written and reviewed by Dr Luca Moretti

A prosthetic valve replaces a heart valve when repair, commissurotomy or conservative transcatheter therapy cannot provide adequate and durable function. The term includes mechanical devices, surgical bioprostheses, transcatheter-implanted valves, valved conduits and, in selected settings, homografts. All these solutions restore unidirectional flow, but they differ in material, hemodynamics, thrombogenicity, durability, antithrombotic requirements and the feasibility of future reinterventions.

Implantation does not end the history of valvular disease but opens a different phase in which the prosthesis interacts with the annulus, ventricles, rhythm, coagulation and other valves. Function that is perfectly normal for a specific model may appear abnormal if compared with a native valve, which is why follow-up must know the type, size, position, date and implantation technique, compare serial examinations and distinguish normal prosthetic phenomena from thrombosis, degeneration, endocarditis, leak or mismatch.

Device selection is an exercise in lifetime planning. A mechanical valve reduces the likelihood of structural deterioration but requires a vitamin K antagonist and carries bleeding or thrombotic risk, whereas a bioprosthesis often simplifies chronic anticoagulation management but may make a new procedure necessary. Age and life expectancy guide the decision without replacing preferences, pregnancy plans, access to monitoring, comorbidities and anatomy.

The expansion of transcatheter procedures has broadened options without eliminating trade-offs. TAVI and valve-in-valve can avoid sternotomy but introduce specific issues involving coronary access, residual gradient, leaflet thrombosis and planning of subsequent procedures. The best strategy therefore does not coincide with the newest device or the one that is theoretically most durable, but with the device most consistent with the patient’s goals, risk and foreseeable sequence of interventions.

Mechanical, biological and transcatheter prostheses

Modern mechanical prostheses are predominantly bileaflet: two pyrolytic carbon hemidiscs rotate within a ring and create a central orifice with two lateral orifices. Historical caged-ball or single-disc models remain in some patients and have different hemodynamic and thrombogenic profiles. The material resists degeneration, but artificial surfaces and vortices make effective anticoagulation indispensable.

Surgical bioprostheses use treated bovine or porcine tissue mounted on a stent, or stentless configurations; homografts are used for selected indications. The tissue provides more physiological flow and lower late thrombogenicity but undergoes calcification, fibrosis, tearing or loss of coaptation. Durability is not a fixed number: younger age, mineral metabolism, valve position, model and gradient influence deterioration.

Transcatheter aortic prostheses are bioprostheses mounted on balloon-expandable or self-expanding frames; in TAVI for native aortic stenosis they are positioned within the calcified valve but may also be used in other configurations such as valve-in-valve. Supra-annular or intra-annular implantation, frame height, sealing skirt and commissural orientation modify gradient, leak and coronary access. Transcatheter prostheses also exist for other valve positions, but the evidence, anatomies and indications are not interchangeable with TAVI.

A mechanical prosthesis physiologically produces opening and closing sounds and small washing jets that reduce stasis. These intraprosthetic regurgitant jets have characteristic location, direction and duration and should not be confused with dehiscence; bioprostheses may also show minimal central jets. Knowing the normal appearance is therefore essential to avoid misdiagnosis, while remembering that a new murmur or a change from baseline always requires further assessment.

Valve position modifies both thrombogenicity and hemodynamics. Faster flow in the aortic position reduces thrombotic risk compared with the mitral position, whereas a mechanical tricuspid prosthesis is particularly exposed to low flow velocity and is used more cautiously; moreover, the same nominal size does not necessarily correspond to the same effective area across manufacturers and models. The report should therefore state the manufacturer and size of the device rather than merely “aortic prosthesis”.

Every prosthesis retains some resistance to flow and no substitute perfectly reproduces a native valve. A moderate gradient may be normal in a small device and become pathological if it develops or increases over time; effective area also depends on correct measurement of the outflow tract and on hemodynamic state. Blood pressure, anemia, pregnancy, fever, fistulas and regurgitation may increase flow and gradient without true obstruction.

Sutureless and rapid-deployment valves are designed to shorten operative times and improve hemodynamics in some aortic valve replacements, but they are not equivalent to TAVI and remain devices used within a surgical pathway. Likewise, valved conduits and aortic root procedures require surveillance not only of the prosthesis but also of anastomoses, coronary arteries and aorta. The broad category of “prosthetic valve” therefore includes different anatomies that require specific protocols.

The patient should have a prosthetic valve identification document stating valve position, model, size, identification number, implantation date and center, therapy and INR target when relevant, while baseline images and the operative report should remain readily retrievable. In an emergency, this information accelerates distinction between normal hemodynamics and dysfunction and reduces the risk of prescribing treatment incompatible with the device.

Shared decision-making and lifetime planning

The choice between a mechanical and a biological prosthesis cannot be reduced to a single age cutoff. Guidelines use age ranges to express relative probabilities of durability and reintervention while leaving a broad area for shared decision-making: a young adult with long life expectancy may place greater value on durability, whereas a peer with high bleeding risk or inability to monitor INR may prioritize avoiding permanent anticoagulation.

An informed preference requires probabilities and consequences to be presented in understandable terms: bleeding and thromboembolism with a mechanical valve, deterioration and another procedure with a bioprosthesis, and differences between surgical reintervention and valve-in-valve. Describing a bioprosthesis as “drug-free” or a mechanical valve as “eternal” is misleading because both require follow-up and can be complicated by endocarditis, leak or other problems.

A person already taking a vitamin K antagonist for another indication may more readily accept a mechanical prosthesis, but this does not eliminate bleeding risk and the anticoagulation indication may change over time. Likewise, atrial fibrillation does not make a bioprosthesis pointless because the type of anticoagulant, possibility of future discontinuation and individual risk must be assessed separately. The decision therefore cannot be reduced to whether the patient “already takes anticoagulants”.

In people planning pregnancy, a mechanical prosthesis creates a high-risk pathway because VKAs, heparins and transitions between regimens expose mother and fetus to different risks. A bioprosthesis avoids permanent anticoagulation due solely to the valve, but in a young woman it may deteriorate more rapidly and require reintervention. Whenever possible, replacement should therefore be preceded by preconception counseling with a Pregnancy Heart Team.

Renal function, calcium-phosphate metabolism disorders and dialysis influence both bleeding risk and bioprosthetic calcification and do not automatically make one material preferable to another. Malignancy, liver disease, the need for invasive procedures and adherence in turn modify VKA tolerability; in very frail patients or those with limited life expectancy, theoretical durability beyond the expected benefit carries less weight and recovery and quality of life become priorities.

Anatomy and valve position can impose concrete limits on device selection. A small aortic annulus increases the risk of prosthesis-patient mismatch and may require enlargement, a supra-annular prosthesis or a transcatheter strategy, whereas extensive mitral calcification, destructive endocarditis or an infected root change the technique and reconstructive options. Patient preferences are therefore respected within what remains anatomically and clinically safe.

The possibility of future valve-in-valve has made bioprostheses more attractive, but it does not guarantee that the subsequent procedure will be simple or feasible. A small surgical annulus may leave a severe gradient after the second device, coronary arteries may be obstructed or become difficult to access, and a mitral prosthesis may create left ventricular outflow tract obstruction. A lifetime strategy therefore requires planning the first implant while envisioning at least the next intervention.

In younger patients with aortopathy, bicuspid valve or root dilatation, treatment of the aorta and the possibility of a Ross procedure, repair or composite replacement must enter the same decision because isolated TAVI does not correct an aorta at risk. In the mitral position, similarly, durable repair remains preferable to replacement when feasible, and discussion of prosthesis type should not forfeit a high-quality valve-preserving opportunity.

Antithrombotic therapy, endocarditis and daily life

Every mechanical prosthesis requires lifelong treatment with a vitamin K antagonist. The INR goal depends on model, valve position and prothrombotic factors and should be expressed as a target with its therapeutic range, not as a value to be reached occasionally; stability and time in range are as important as the average. DOACs do not replace VKAs in mechanical prostheses and their use exposes patients to an unacceptable risk of thrombotic events.

Education about dosing, stable dietary habits, interactions, acute illness and the monitoring schedule is an integral part of therapy. In selected, properly trained patients, INR self-monitoring and self-management can improve the quality of control, whereas a low INR should not be corrected with improvised rules and bleeding requires assessment of the balance between reversal and thrombotic risk. The center should therefore provide an explicit plan for emergencies and procedures as well.

Heparin bridging is not required for every VKA interruption and may increase bleeding risk. The strategy depends on prosthesis type and position, the patient’s thrombotic factors, duration of interruption and procedural risk; some minor procedures can be performed while maintaining the VKA within range. The decision should be planned in advance among the prescriber, anticoagulation clinic and proceduralist, avoiding unsupervised discontinuation.

After implantation of a surgical or transcatheter bioprosthesis, initial therapy depends on valve position, rhythm, any independent indications for anticoagulation and bleeding risk, and recommendations are not identical between aortic and mitral positions or between surgery and TAVI. A person with atrial fibrillation may require anticoagulation independently of the prosthesis, whereas adding antiplatelet therapy without a specific indication increases bleeding. The discharge plan should therefore state the drug, dose, duration and reason.

Persistent fever, chills, emboli, new heart failure or a change in murmur should raise suspicion of prosthetic valve endocarditis. When stability permits, blood cultures precede antibiotics and imaging may require transesophageal echocardiography, CT or nuclear techniques; a negative echocardiogram in the early stages does not exclude infection. Oral hygiene and treatment of infectious foci remain more important than indiscriminate antibiotic use.

According to guidelines, antibiotic prophylaxis is indicated for at-risk dental procedures in patients with prosthetic valves and should accompany regular dental health care. It does not protect against ordinary daily exposures and does not replace brushing and dental treatment; tattoos, piercings and other invasive procedures instead require attention to sterility and infection risk. Not every activity requires antibiotics, but unexplained fever always deserves prompt evaluation.

Physical activity is encouraged after recovery, adapted to ventricular function, other heart disease and any anticoagulation. Sports with a high risk of trauma increase bleeding hazard with VKA therapy, while mechanical valve sounds may be perceived and generally require only reassurance unless they change abruptly. Travel is also compatible with a normal life provided the patient has sufficient medication, documentation, access to INR monitoring and knowledge of interactions.

Pregnancy in the presence of a mechanical prosthesis should be planned and managed in an expert center beginning before conception because no regimen simultaneously eliminates maternal and fetal risk. Low-molecular-weight heparin requires rigorous anti-Xa monitoring, VKAs cross the placenta and transitions around delivery are critical phases. A significant or dysfunctional bioprosthesis also requires specific hemodynamic assessment: “biological” does not automatically mean low-risk pregnancy.

Baseline echocardiography and multimodality surveillance

After implantation, a reference transthoracic echocardiogram is obtained under stable hemodynamic conditions, generally within the first weeks or according to the procedural pathway. The report includes model and size, velocity and gradients, effective orifice area, Doppler velocity index, acceleration time when relevant, regurgitation, chamber dimensions, ventricular function and pulmonary pressure. This baseline fingerprint is more useful than a generic comparison with population values.

The gradient should be measured from multiple windows and interpreted together with heart rate, blood pressure, hemoglobin and stroke volume. Apical Doppler may underestimate aortic velocity if the jet is eccentric, and an incorrect outflow tract measurement alters area and volume; in mechanical prostheses, artifacts may also limit visualization of the discs. No single number confirms or excludes dysfunction in every valve position.

During follow-up, what matters most is the change from baseline. A persistent increase in gradient associated with a reduction in area or index suggests acquired obstruction, whereas a high but stable gradient from implantation points toward a small device or mismatch; high-flow states may instead increase velocity without reducing mobility. The diagnosis of prosthetic valve dysfunction should therefore specify cause, severity and consequences rather than simply use the label “high gradient”.

Transesophageal echocardiography is particularly useful for mitral prostheses, masses, leaks and endocarditis, and 3D imaging allows localization of defects and anatomical relationships. Cinefluoroscopy measures mechanical prosthesis opening angles with high temporal resolution but cannot distinguish tissues, whereas gated CT characterizes mobility, hypoattenuated thickening, thrombus, pannus, calcium and surrounding anatomy. The three modalities therefore answer different and complementary questions.

Cardiac magnetic resonance can quantify volumes and regurgitation when echocardiography is discordant and the device is compatible, although artifacts impose limitations, while PET/CT and leukocyte imaging are indicated in selected cases of suspected endocarditis. Each examination should answer a specific question such as mobility, mass, regurgitation, calcium, infection or chamber damage because multiplying modalities without a clinical question does not automatically increase accuracy.

Clinical follow-up should be lifelong. Bioprostheses require serial imaging to recognize deterioration before ventricular damage develops, whereas mechanical prostheses are reassessed when symptoms, signs or clinical changes suggest complications, in addition to the pathway established by the center; mitral position, small devices, new arrhythmias or disease of other valves may justify closer surveillance.

Dyspnea, syncope, chest pain, edema, palpitations, fever, embolism, anemia or a change in valve clicks require earlier evaluation. Chest radiography, ECG and laboratory testing may respectively provide information on device model and stability, rhythm and overload, and hemolysis or infection, but echocardiography remains the first step. A “non-diagnostic” transthoracic examination does not, however, close the case when clinical probability is high.

Surveillance should also include the other valves, the aorta and the ventricles because correcting one lesion does not prevent progression of associated disease. Tricuspid regurgitation, for example, may progress even when a left-sided prosthesis functions normally; follow-up focused only on the device therefore risks missing the physiology that actually determines symptoms and prognosis.

Dysfunction, reintervention and continuity of care

Complications should be classified by mechanism. Prosthetic valve thrombosis can restrict a mechanical occluder or thicken biological leaflets, endocarditis destroys tissue or anchoring, and structural degeneration instead represents a permanent intrinsic change of the bioprosthesis. Distinguishing them is not a terminological exercise because reversibility and treatment differ profoundly.

Non-structural dysfunction includes extrinsic or technical problems such as malposition, frame underexpansion, interference, hemolysis, paravalvular leak and mismatch. Some manifestations are present from implantation and remain stable, whereas others develop later because of dehiscence or remodeling; this taxonomy prevents an intact but simply undersized valve from being labeled “degenerated”.

A bioprosthesis may be dysfunctional without yet having reached clinical failure. International definitions distinguish morphological deterioration, hemodynamic worsening and bioprosthetic valve failure, which includes major clinical consequences, reintervention or prosthesis-related death. These stages are useful for research and surveillance, but in an individual patient the decision still depends on symptoms, ventricular response, trajectory over time and risk.

When reintervention is required, options may be surgical or transcatheter. Surgery allows removal of the prosthesis, pannus and infected tissue, annular enlargement and simultaneous treatment of other disease, but carries the risk of reoperation; valve-in-valve provides an alternative for selected degenerated bioprostheses but leaves the old ring in place and may worsen the gradient or obstruct the coronary arteries. A dysfunctional mechanical prosthesis is not treated with valve-in-valve.

Before valve-in-valve, CT should reconstruct the true internal diameter, coronary height, sinuses, frame and obstruction risk and, in the mitral position, estimate the neo-LVOT. Techniques such as ring fracture or coronary protection may be used in selected cases but add complexity and risk; the indication should therefore arise from the Heart Team and center experience, not simply from the availability of a catheter.

Endocarditis, extensive dehiscence or critical mechanical prosthetic thrombosis may require urgent surgery, whereas stable asymptomatic dysfunction can be followed over time. Delaying until shock or irreversible ventricular damage increases risk, but intervening on an isolated finding without consequences exposes the patient unnecessarily. The serial trajectory is what connects diagnosis with therapeutic timing.

Continuity of care requires cardiology follow-up, safe antithrombotic therapy, access to dental care, education about symptoms and the ability to contact a center promptly. Transfers, changes of physician and systems that do not communicate with one another can be as dangerous as a missed examination; a prosthetic valve passport and digital baseline report allow rapid reconstruction of what is normal for that patient.

A well-chosen and properly monitored prosthesis can restore functional capacity and survival, but it requires a permanent care partnership. The patient should neither live as a fragile carrier of a device nor regard themselves as definitively cured: knowing the therapy, INR target, signs of infection or heart failure and follow-up schedule transforms follow-up from passive surveillance into active prevention of complications.