Biomechanics of Transcatheter Aortic Valve Implant

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1		Francesco Nappi	--	5710	2022-09-24 06:40:15	\|
2	format	Jason Zhu	-4 word(s)	5706	2022-09-26 04:57:27	\|

This entry is adapted from the peer-reviewed paper 10.3390/bioengineering9070299

Transcatheter aortic valve implantation (TAVI) has grown exponentially within the cardiology and cardiac surgical spheres. It has now become a routine approach for treating aortic stenosis. Several concerns have been raised about TAVI in comparison to conventional surgical aortic valve replacement (SAVR). The primary concerns regard the longevity of the valves. Several factors have been identified which may predict poor outcomes following TAVI. To this end, the lesser-used finite element analysis (FEA) was used to quantify the properties of calcifications which affect TAVI valves. This method can also be used in conjunction with other integrated software to ascertain the functionality of these valves. Other imaging modalities such as multi-detector row computed tomography (MDCT) are now widely available, which can accurately size aortic valve annuli. This may help reduce the incidence of paravalvular leaks and regurgitation which may necessitate further intervention.

transcatheter aortic valve implantation surgical aortic valve replacement structural valve degeneration

1. Introduction

Transcatheter aortic valve implantation (TAVI) was first used by Cribier et al. 20 years ago ^[1]. Over the years, evidence has grown regarding the efficacy and safety of this novel modality, which has formed a major cornerstone in the treatment of structural heart disease. These minimally invasive procedures restore valve functionality in patients with calcific aortic valve stenosis (AVS) and have become routine approaches ^[2]^[3]^[4]^[5]^[6]^[7]^[8]^[9]^[10]^[11]^[12]^[13]^[14]^[15]^[16]^[17]^[18]. TAVI is recommended for symptomatic patients with severe AS who are 65 to 80 years of age and have no anatomic contraindications to the use of transcatheter aortic valve implantation via transfemoral access. TAVI is considered an adequate treatment option as an alternative to standard surgical aortic valve replacement (SAVR) after shared decision making, weighing the balance between expected patient longevity and valve durability ^[19]^[20]^[21]^[22]^[23]^[24]^[25]. Evidence suggested that TAVI (compared to standard medical and surgical options) had lower associated rates of death from any cause. Mid- and long-term follow-ups provided no evidence of restenosis or prosthesis dysfunction ^[6]^[9]^[10]^[11]^[18]^[26]^[27]^[28]^[29]^[30]. Moreover, recent randomized clinical trials (RCTs), meta-analyses, and propensity score analyses, confirming registry reports, revealed satisfactory outcomes of TAVI in terms of feasibility, long-term hemodynamics, and functional improvement ^[12]^[14]^[27]^[31]^[32]^[33]^[34]. However, the first and second generations of implanted transcatheter heart valves (THVs) had high related percentages of moderate to severe perivalvular aortic regurgitation ^[35], which is evidence that highlights the causes that determine one of the frequent complications associated with TAVI, which confers an increased rate of mortality ^[36]. During repeated follow-ups, the emerging data raised concerns about the incomplete apposition of prostheses related to calcification or annular eccentricity ^[37], the undersizing of the device, and the incorrect positioning of the valve, thus identifying the most common determinants of paravalvular aortic regurgitation ^[38].

Based on these observations, the criteria that are of utmost importance to avoid complications are the appropriate determination of the size of the annulus, the correct evaluation of the calcifications, and adequate sizing of the prosthetic valve. Pre-operative planning with biomechanical assessments should be completed for patients for whom TAVI is recommended, as suggested by international guidelines and by standardized endpoint definitions for transcatheter aortic valve implantation, dictated in the Valve Academic Research Consortium-2 (VARC-2) consensus document ^[19]^[20]^[38].

2. Evidence to Deploy Biomechanical Evaluation and to Definitively Accept the Use of Transcatheter Heart Valve Implantation as a New Paradigm Shift

Both cardiology and cardiovascular surgery have witnessed an era of consistently evolving change, and this new scenario has mainly been driven by the emergence of percutaneous coronary intervention, with novel options for the treatment of coronary heart disease. The new endovascular platforms have evolved rapidly and established themselves as vital cogs in the armamentarium available to address structural heart disease ^[39]. In the past ten years, the innovation has initially been primarily invested in the management of aortic valve stenosis and subsequently the pathological mitral valve with the progressive affirmation of transcatheter valve therapy (TVT) ^[22]^[24]^[40]. From the first experimental study by Bonhoeffer, who pioneered the transcatheter pulmonary valve implant, ^[41] the use of TVT to treat aortic valve stenosis progressed rapidly. In 2010, the first PARTNER (Placement of AoRTic TraNs cathetER Valve Trial) reported a series of high-risk patients who were treated using this novel technique as opposed to conventional aortic valve stenosis surgery ^[3]. In less than 10 years, PARTNER III affirmed the safety and efficacy of the transcatheter aortic valve replacement in low-risk patients ^[16]. It is conceivable that future generations of transcatheter valves with the advancement of device technology will herald improvements in the hemodynamic profile, longevity, and durability alongside reduced adverse events.

Thomas Kuhn, an American physicist and philosopher, introduced the term “paradigm shift” for the first time in The Structure of Scientific Revolutions in 1962 ^[42]. Researchers explained how a process can lead to a transition from the previously widely accepted worldview to a new model for demonstrating new emerging evidence. Cardiology and cardiovascular surgery have often faced paradigm shifts because these disciplines are constantly open to a transition that has, over time, progressively fostered the innovative spirit of those who practice them. Researchers can note that historically, numerous paradigm shifts emerged: coronary bypass grafting, heart transplantation, percutaneous coronary intervention, mechanical and bioprosthetic valves, generations of life-saving drugs for heart failure, and mechanical circulatory support ^[43]^[44]. The current summit of these advancements is the emergence of devices used for the replacement of the aortic valve with TVT.

Calcific aortic valve stenosis (AVS) is a pathoanatomic process of aortic valve leaflets that are affected by structural changes sustained by an inflammatory and atherosclerotic process associated with calcium deposition. The morphological changes generated at the level of the cusps alter the function of the valve with a consequent reduction in the opening of the variably narrow leaflets during systole. Aortic valve disease causes abnormal hemodynamics and increased mechanical stress on the left ventricle (LV) ^[45].

Prior to the advent of TAVI, surgical aortic valve replacement (SAVR) was considered the ideal treatment option for patients at risk of severe valve obstruction. However, new platforms for the treatment of structural heart diseases have fueled clinical attention that has shifted towards the use of new less invasive armamentarium represented by THV devices.

The PARTNER Ia study proved the superiority of the transcatheter balloon-expanded procedure in patients receiving TAVI over those who were managed with optimal medical therapy in short- and medium-term mortality (43.3% in the TAVI group and 68.0% in the standard-therapy group (p < 0.001, at 2 years, respectively) ^[5]. As for prohibitive/high-risk patients with severe AVS who were suitable to receive surgical treatment, the use of TAVI revealed the same mortality at 5 years as compared to SAVR (67.8% TAVR cohort vs. 62.4% SAVR). However, patients who received TAVI disclosed a rate of moderate to severe AVR of 14% as compared to 1% in those receiving SAVR ^[9]. Not least, evidence from the use of a first-generation CoreValve Self-Expanding System revealed that the 1-year all-cause death rate was higher in patients after SAVR as compared to recipients of TAVI ^[8].

THVT has proven to be a revolutionary and decisive procedure in the last decade thanks to the achievement of efficacy and safety. In fact, evidence from THVT offered a clear answer to the use of the only life-saving solution for high- and extreme-surgical-risk patients who cannot tolerate the open surgical option due to the presence of significant comorbidities ^[46]. Given the promising results associated with technological advancement which has undergone very rapid development, the use of TAVI has been approved for the treatment of intermediate-risk patients. The results reported by the pioneering RCTs suggested increased rates of residual aortic valve regurgitation and more pacemakers implanted in the population intended for the TAVI procedure; however, the use of THVT was directed toward the design of randomized trials involving the intermediate/low-surgical-risk population ^[9]^[10]^[13]^[15]^[16]^[17].

The SURTAVI trial enrolled 1660 patients who were eligible to receive either transcatheter aortic-valve bioprosthesis (n = 864) or SAVR with the standard procedure (n = 796). All patients were symptomatic of severe aortic stenosis at intermediate surgical risk. The primary objective was to demonstrate the non-inferiority, safety, and efficacy of the first and second generations of the CoreValve System ^[15].

In SURTAVI, 84% of patients were managed with the first-generation CoreValve System while 16% of recipients of TAVI had the second generation of Evolut R bioprosthesis. This cohort of individuals had an STS score Society for Predicted Risk of Mortality at 4.5 ± 1.6% ^[15].

At 2 years, the results revealed that the composite of death from any cause or disabling stroke was higher in the SAVR group as compared to the TAVI group (14% vs. 12.6%, respectively) ^[15]. The New York Heart Association values for clinical symptoms were significantly improved in both cohorts compared to pre-operative data and were consistent throughout the 24-month follow-up. In addition, the KCCQ summary score revealed a substantial and stable improvement in both populations at 2 years of follow-up, although patients managed with the TAVI procedure had a greater percentage of improvement at 1 month than those who received a standard aortic valve replacement ^[15].

Evidence of the non-inferiority of TAVI over SAVR recorded for intermediate and high-risk patients offered favorable points to undertake the randomized PARTNER 3 trial ^[16] and the multi-national randomized clinical Evolut Low Risk Trial Investigators 26 for patients presenting with severe AVS at low risk for death after surgical procedure ^[17]. In the third series of results reported from the two RCTs, the composite of death from any cause, stroke, or re-hospitalization at 1 year was less in TAVI recipients after the implantation of the device. Again, the investigators found shorter hospitalization rates for individuals undergoing TAVI, while there were no significant differences between groups in terms of major vascular complications, new permanent pacemaker insertions, or moderate or severe paravalvular regurgitation ^[16]^[17].

Certainly, a decisive impetus for the success of the large-scale TVT procedure has been linked to refined technological progress, which has seen the use of introducers of reduced diameter and an improvement in the use of stents which have proved to be safer and more effective. However, it is important to consider that the results must be confirmed by longer-term follow-ups.

3. Biomechanics Computational Modeling to Give Consistency to The Paradigm Shift

3.1. Paravalvular Aortic Regurgitation

Although there has been substantial initial growth in the use of TAVI confirmed by the success of the results, intra- and post-procedural clinical complications have questioned the paradigm shift, questioning the potential expansion of TVT in low-risk patients.

Researchers have learned that post-deployment PVAR, cardiac conduction abnormalities ^[47]^[48] (Bagur et al., 2012; Van der Boon et al., 2012), and coronary artery occlusion (Ribeiro) are among the most marked immediately recorded disadvantages ^[49]. Taken together, these complications revealed an increased rate of mortality and reoperation ^[23]^[47]^[48]^[49].

Surely the Achilles’ heel of the TAVI is constituted by the altered hemodynamics due to the occurrence of PVAR, in which the emergence of narrow gaps which are exposed to high gradients of systolic pressure can lead to an altered function of the platelets, which are therefore exposed to high flow shear stress. This pathoanatomic condition triggers platelet activation, perturbing the aggregation/coagulation balance, with the formation of microemboli. The latter are then expelled at the next systole and can remain trapped and/or deposited in the region of the Valsalva sinuses, which offer a suitable location for typical low-shear recirculation areas. Therefore, PVAR may be linked to the deposition of thrombi around the THV device as well as to the potential circulation of thromboembolic clots, which is followed by an increased risk of stroke. Several pieces of evidence have reported that thromboembolism is less common than the hypo-attenuated thickening of the leaflets; however, it is still a fairly common and dangerous phenomenon that requires adequate clinical treatment ^[50]. Another point to consider is the close association of leaflet thrombosis and the development of a structural degeneration of the valve incorporated in the device.

Several studies have suggested that the occurrence of PVAR in recipients of the TAVI procedure is directly correlated with higher late mortality, cardiac death, and repeated hospitalization even in the presence of traces of regurgitation ^[51]. Five-year results from Partner Ib RCT disclosed a rate of 14% moderate or severe aortic regurgitation in patients who received TAVI as compared to those who were managed with SAVR. This evidence caused an increased risk of mortality at 5 years for patients who developed moderate or severe aortic regurgitation after TAVI ^[9].

All the indicators testify that the mortality rate was proportional to the severity of the regurgitation, and in this regard, Generaux et al. ^[35] reported that even slight PVAR can lead to a doubling of the mortality rate after 1 year. However, Webb et al. ^[2] pointed out that the progression of PVAR can be unpredictable. The investigators observed that at 2 years, regurgitation increased by ≥ 1 grade in 22.4% of patients, remained unchanged in 46.2%, and improved by ≥ 1 grade in 31.5%.

In this context, substantial differences emerged after the installation of a balloon-expandable THV device or the use of the self-expandable valve. Two independent studies revealed that recipients of the Medtronic CoreValve self-expanding device experienced a higher PVL rate and worsening severity than patients who received an expandable Edwards SAPIEN balloon ^[52]^[53]. However, substantial improvements have been made in the new devices involving the low-profile delivery system and external skirt, thereby improving the sealing of the THV device and promoting more precise valve positioning. A lower rate of PVAR at short-term follow-up has been reported ^[54].

Patients who exhibit PVAR post-TAVI require clinical and imaging modality evaluation. The quantification of regurgitation is generally determined with the use of echocardiography.

In detail, methods such as transesophageal echocardiography, cineangiography, and hemodynamic measurements are commonly used during the procedure, while transthoracic echocardiography offers substantial support for the evaluation and follow-up of PVAR after TAVI ^[55]. Above all, the continuous wave echo is the most commonly used method to evaluate the overall hemodynamic performance of the valve, but with the disadvantage of not being able to obtain a spatial localization of leaks. The relative consequence is that aortic regurgitation is quantified as the ratio of reverse flow to direct flow. As reported by Hatoum et al. ^[56], the most obvious limitation is that the measurement and determination are experimental. However, a semi-quantitative description of jets by pulsed wave color Doppler can be used to obtain a precise localization and evaluation of the gravity of PVAR jets.

Concern related to the quantification of PVAR persists after TAVI due to a lack of standardization, leading to a challenging diagnosis. In fact, it is often qualitative, and different classification schemes are adopted (trace, mild, moderate, and severe) ^[55]^[57]. Several interventional alternatives to reduce paravalvular regurgitation have been put in place and include post-implantation balloon dilation, repositioning, entrapment maneuvers as well as the valve-in-valve (ViV) procedure ^[58]; all of these are not free from an increasing risk of vascular complications. A critical aspect of the procedure is represented by the positioning of the THV device with respect to the patient’s aortic annulus, which was directly associated with the degree of hemodynamic performance of TAVI as well as the rate of reintervention ^[59]. There is early evidence from Nombela Franco et al. ^[60] and Takagi et al. ^[61] who reported that balloon over-inflation is often used to reduce the degree of PVAR. The investigators revealed the post-balloon dilation decreases regurgitation in the preponderance of patients by at least one degree ^[60]^[61]. However, how crucial the post-dilation effect is on survival remains elusive. Again, an association with a higher incidence of cerebrovascular events was recorded ^[60]. The goal of a correctly performed transcatheter procedure necessarily involves minimizing the amount and incidence of PVAR in order to gain improved clinical outcomes in the long term.

The development of computational models was identified early as the correct method of studying the interaction between TAVI stents and native aortic tissue and predict the performance of the post-procedural device from the point of view of structural dynamics ^[62]^[63]^[64]^[65]^[66]. Recently, several studies have substantially quantified the degree of interaction between the device and the implantation site, as a surrogate measure of PVAR, by measuring the gap between the stent ^[67]^[68] or the skirt ^[69] from native tissue, considering the specific anatomical characteristics of the patient’s aortic root. Chang et al. reported ideal characteristics that offer better results in terms of PVAR occurrence ^[70]. Researchers compared the two most commonly used devices, documenting a better performance of the third generation of the balloon-expandable device compared to the third generation of the self-expandable device in adapting to the dynamics of the aortic root, reducing the risk of PVAR ^[52].

Similarly, great interest has been aroused in the creation of a maximum flow algorithm ^[71], producing a one-dimensional connected graph capable of representing the flow network based on the size of the gap existing between the stent and the aortic root. Although in the absence of PVAR the results showed a good correlation, nevertheless, the reliability was reduced with the development of models that lacked precision for patients with PVAR recurrence. A significant report was described by De Jaegere et al. ^[72], who referred to a large series of computational models that tested the predictability of 60 Medtronic CoreValve deployment cases in which the results were validated through angiographic and echocardiographic measurements. The limitation of the work lay in the lack of an adequate description of the reconstruction of the patient’s anatomy with respect to the modeling hypotheses. Finally, in a recent study, Mao et al. ^[73] evaluated the effect of CoreValve orientation and modeling assumptions, such as skirt shape and stent thickness, on post-deployment hemodynamics. However, the formation of post-TAVI thrombus only involved the generated clots on the valve leaflets following a ViV procedure. Vahidkhah et al. analyzed blood stasis by assessing and quantifying idealized ViV models with intra-annular and supra-annular TAVI positions ^[74].

3.2. Transcatheter Heart Valve Thrombosis

Evidence based on several reports displayed that recipients of TAVI experienced an unclear rate of bioprosthetic valve thrombosis (BPV-TH) and thromboembolic complications of the device. It is of note that both results from the RCTs and EU Partner Registry lack complete and satisfactory data. The PARTNER and CoreValve System randomized clinical trials did not note significant BPV-TH ^[9]^[10]^[25]. On the other hand, the EU Partner Registry ^[75] also revealed very poor data on thromboembolic events in patients who were managed with THV devices. The reported thromboembolic complication rate was only 1 case out of 130 patients undergoing TAVI. Latib et al. noted that from a large number of patients (n = 4266), only 27 cases of BPV-TH thrombosis (0.61%) occurred within a median of 181 days after TAVI procedure ^[75].

Importantly, Stortecky et al. observed that the risk of BPV-TH was higher in the first 3 months after device implantation. In addition, the risk curves showed a marked reduction in events in the subsequent months, which almost matched the curves of the general population ^[76]. A histopathological analysis from the CoreValve device thrombotic complication suggested that clot formation was completed approximately 3 months after the implantation of the THV device ^[77]^[78]^[79]^[80]^[81]. Makkar et al. ^[82] offered important data systematically using 4D computed tomography to prove bioprosthetic valve thrombosis events. Fifty-five patients included in the PORTICO Studio IDE (Portico Re-sheathable Transcatheter Aortic Valve System US IDE Trial) revealed the occurrence of BPV-TH at a median of 32 days after valve implantation with decreased leaflets movement in 40% of recipients. In total, 132 patients were included in the Savory study (subclinical aortic valve thrombosis assessed with 4D CT) and were eligible to receive either TAVI or SAVR, or were included in RESOLVE (surgical catheter and aortic evaluation of thrombosis of the bioprosthetic valve and its treatment with anticoagulation) and underwent 4D computed tomography within 3 months, recording reduced leaflet motion at a rate of 13% of recipients. Of these, 14% were treated with TVI, while 7% underwent SAVR with the use of a conventional bioprosthesis ^[82]^[83].

Pache et al. ^[84] corroborated the previous evidence ^[82]^[85] on 156 consecutive patients who were managed with TAVI using SAPIEN 3 (Edwards Lifesciences, Irvine, CA, USA). At a median of 5 days after the procedure, the investigators observed by the mean of multi-detector computed tomography that 10.3% of TAVI recipients disclosed leaflet thickening with hypo-attenuation. Although the absence of symptoms was considered a relevant point for a normal clinical evolution, individuals experienced a higher mean transvalvular gradient, and anticoagulant drug therapy led to the complete resolution of leaflet thickening ^[84]. Likewise, in patients who were treated with dual antiplatelet therapy (DAPT) less frequently than those who were managed with a single antiplatelet drug (37.5% and 50%, respectively) ^[84], a correlation between increased transvalvular gradient and uncontrolled neointimal proliferation was noted with thickening of the device leaflets ^[84]^[85].

Three recent studies reached significant relevance in BPV-TH and thromboembolic events ^[78]^[86]^[87]. Hansson et al. ^[78] monitored patients who underwent a TAVI procedure with the use of balloon-expandable valves (Edwards Sapien XT or Sapien 3 valves) by means of transthoracic or transesophageal echocardiography and multi-detector computed tomography to screen the incidence and predictors of BPV-TH at 1–3 months. The evidence of thrombosis was observed in a rate of 7% of patients with MDCT. In addition, 18% of individuals experienced bioprosthetic valve thrombosis events with clinical complications. Cox’s multi-variate regression analysis revealed that the two independent predictors of BPV-TH were related to the use of the TAVI and were the identified in the lack of warfarin administration and the larger size of the device measured at 29 mm ^[78].

Nührenberg et al. ^[86] studied hypo-attenuated leaflet thickening (HLAT) as a potential precursor of clot formation and thromboembolic events after TAVI. In all cohorts of patients, including those who underwent oral anticoagulation treatment, dual antiplatelet therapy with aspirin and clopidogrel was administered for at least 24 h before the procedure. In patients who had pre-existing indications for oral anticoagulation treatment, aspirin was discontinued, and the administration was pursued after TAVI for the rest of the cohort. Additionally, 18% of TAVI patients revealed hypo-attenuated leaflet thickening; however, lower complication rates were observed in patients receiving oral anticoagulation, suggesting that the administration of dual antiplatelet therapy (aspirin and clopidogrel) did not change the occurrence of early HLAT ^[86].

GALILEO 4D RCT ^[87] included 231 patients for antithrombotic strategy assessment, in which long-term anticoagulation was administered, either with the use of rivaroxaban (10 mg) associated with aspirin (75 to 100 mg) once daily or with the administration of a dual antiplatelet-based strategy with the use of (clopidogrel (75 mg) plus aspirin (75 to 100 mg) once daily. Four-dimensional CT was used after randomization to check all cohorts of individuals. Patients were successfully treated with TAVI with no indication for long-term anticoagulation therapy. The primary endpoint of the study comprehended the percentage of patients who experienced at least one prosthetic valve leaflet with grade 3 or higher motion reduction. Of note, this process involved substantially more than 50% of the leaflet as follows: 2.1% of patients with rivaroxaban administration revealed at least one prosthetic valve leaflet with grade 3 or higher motion reduction compared to 10.9% in the dual antiplatelet protocol. The thickening of at least one leaflet was recorded in 12.4% of patients in the rivaroxaban cohort compared to 32.4% in which the dual antiplatelet was administered. Lastly, concerns about the increased risk of death or thromboembolic events and the risk of life-threatening or disabling events, or greater bleeding were remarkably higher in patients who received the rivaroxaban administration ^[87].

One of the concerns affecting clot formation after the TAVI procedure is related both to the extent of bulky native valve calcification and its position with respect to the annulus of AV and the aortic root, as well as to stent deformation and the size of the patient’s annulus. Even more so, in these specific morphological features, the role of physiological blood dynamics plays a crucial role that has not been fully investigated ^[88].

Khalique et al. ^[89] noted that calcified blocks substantially affect the amount and asymmetry depending on the extent of aortic valve calcification. This condition led to the involvement of all regions of the aortic valve complex in predicting various grades of PVAR from greater than or equal to mild PAVR and the post-deployment performance of the device, thereby potentially evolving towards the bioprosthetic valve thrombosis of the THV device. The preexistent leaflet asymmetry was excluded so as to confirm the diagnosis of PAVR. The quantity of bulky calcification at the level of the junction between the annulus and LVOT, as well as the occurrence of leaflet calcification, independently predicted PVAR and the post-deployment of TAVI when taking into account the multi-detector row computed tomography area cover index ^[89].

For this reason, the use of computational biomodelling can lead to predicting both the extent of PVAR and the risk of clot formation ^[52]^[62]^[67]^[88]^[90]^[91]^[92]. Likewise, the bulky calcification penetrating the aortic annulus may have a different texture, thus raising some reflections about the ideal choice of device to implant ^[52]^[62]^[67]^[89]. So, the use of self- and balloon-expandable system prostheses can lead to different geometric alterations of the aortic annulus after deployment, with a greater or lesser risk of potential disturbance of the blood fluid dynamics that generate clot formation ^[5]^[62]^[67]^[90].

In this regard, researchers revealed that both balloon- and self-expandable devices were poorly effective in the presence of bulky native AV calcifications, and the different degrees of device deformation were studied. Two independent reports based on computational biomodelling suggested that both Sapien XT and Sapien 3 disclosed high values of the maximal principal stress in the aortic regions close to bulky calcification, resulting in a deformation of the stent that assumed an elliptical shape ^[67]^[92]. Accentuated geometric modification with incorrect post-deployment can lead to paravalvular leakage, leaflet mal-coaptation, and hypo-attenuated leaflet thickening. The extreme shape of elliptical deformation is likely to favor subclinical thrombosis due to the presence of residual calcifications that favor hypomobility ^[67]^[92].

Again, the core valve is based on the self-expansion mechanism that may succumb to the mechanical distortion phenomena. In self-expanding TAVI, the crucial role of positioning in determining valve anchorage is pivotal. The occurrence of non-uniform expansion related to extensive calcifications can lead to prosthetic device deformation that ranges from an increased eccentricity > 10%, resulting in the incomplete expansion of the nitinol frame at almost all levels and potentially causing clot formation ^[52]^[62]^[90].

No evidence has demonstrated a statistically significant correlation between the occurrence of moderate PVAR and abnormal flow patterns on the TAV implanted leaflets and in the left main coronary artery that could favor thrombosis of the THV device and the accelerated progression of the atherosclerotic process ^[93]. However, several observations suggest that clot formation has been hypothesized to be more directly related to PVAR with the clinical occurrence of a thrombotic embolism ^[78]^[82]^[83]^[84]^[85]^[86]^[87]^[92].

An explanation can be offered by the existence of localized flow at the PVAR level with the development of high-pressure gradients associated with the presence of small, tight, empty areas. This condition implies that the platelets are subjected to high flow shear stress ^[62]^[90]^[92]. This phenomenon, as Researchers have reported, has attracted ever-increasing clinical interest ^[62]^[92].

Bianchi et al. ^[90] evaluated the relationship between PVAR and platelet activation with a computational model to study the thrombogenic potential of three procedural configurations of TAVI, two of which were Sapien 3 and one was CoreValve Evolute. Investigators calculated the stress accumulation of platelets along particle trajectories in the PVAR region. All the probability density functions in the three simulations performed showed comparable patterns. For example, in one Sapien 3 with a valve measured 26 mm, in which an over-inflated aortic configuration was exhibited, the major stress accumulation of platelets was evident. This phenomenon can be related to the higher speed that can be recorded in PVAR jets, which leads to higher flow shear stress. In addition, HS values were observed to be in agreement with the largest overall regurgitation volumes. The information obtained from the probability density functions showed that the variation in the diameter of PVAR affects the activation potential of platelets. For example, in CoreValve Evolut 29, a reduction in PVAR grade led to slightly higher thrombogenic potential, as platelets were subjected to more shear stress which was related to their flow through smaller paravalvular spaces ^[90]. Finally, dynamic fluid has also shown people that when the volume of regurgitation is considerably higher, the cause–effect relationship established between PVAR reduction and susceptibility to platelet activation is supported by a more complicated interaction ^[62]^[90]^[92].

3.3. Structural Valve Degeneration

The term structural valve degeneration (SVD) implies an acquired anomaly of the valve bioprosthesis due to a substantial deterioration of the flaps and of the structural support that integrates the device. The correlated patho-anatomic consequence is the thickening, calcification, laceration, or rupture of the materials that make up the valve prosthesis. This context of the pathological disorder suggests the development of associated valvular hemodynamic dysfunction, such as the development of stenosis or regurgitation. To date, a thorough understanding of the precise mechanisms underlying SVD has not yet been substantially offered. However, the mechanisms that support SVD are multiple, both mechanical and related to fluid dynamics, which are responsible for tissue rupture or thickening over time ^[27]^[28]^[29]^[30]^[31]^[32]^[33]^[94]^[95]^[96]^[97]^[98]^[99]^[100]^[101]^[102]^[103]^[104]^[105]^[106]^[107]^[108]^[109]^[110]^[111]^[112]^[113]^[114]^[115]^[116]^[117].

Several factors cause SVD. First of all, a crucial role is provided by the mechanical stress levels associated with both flow anomalies and the occurrence of shear stresses on the surfaces of valve leaflets. These two factors are potentially responsible for the progression of SVD, leading to the breakdown of the collagen frame of the fibers and the calcification of the tissues ^[106]^[118]. Second, other clinical conditions, in which the pathological features of intrinsic structural deterioration of the valve tissue are not detectable, cannot be classified as SVD. However, they deserve to be taken into consideration. SVD may be related to the mismatch between prosthesis size and patient size, device malposition, paravalvular regurgitation, and abnormal frame expansion. Likewise, these abnormal situations attributable to the implanted bioprosthesis can lead to early SVD or be considered a cause of its development. Dysfunction involving the prosthesis implanted due to mismatch is difficult to distinguish from the structural degeneration of a valve. Therefore, it is not considered to be SVD as it exhibits normal leaflet morphology, but instead has a valve area that is relatively small with a high gradient ^[27]^[28]^[29]^[30]^[31]^[32]^[33]^[94]^[95]^[96]^[97]^[98]^[99]^[100]^[101]^[102]^[103]^[104]^[105]^[106]^[107]^[108]^[109]^[110]^[111]^[112]^[113]^[114]^[115]^[116]^[117].

A crucial point that characterizes the difference between the prosthetic mismatch and the SVD is related to the time during which the anomaly is established. The prosthetic maladjustment reveals hemodynamic anomalies of the valve which occur at the moment of the implantation of the prosthesis with the manifestation of the patient’s hemodynamic deterioration, which occurs in conjunction with an increase in gradients and a decrease in the valve area; these conditions reveal a progressive increase in the patient’s clinical conditions on repeated echocardiographic checks. In patients who develop SVD, associated stenosis develops progressively and is seen with the characteristics of a faded lesion during follow-up. Although both prosthetic valve thrombosis and infective endocarditis are not included in the definition of SVD, SVD may be noted despite having recorded therapeutic success. Intense debate currently surrounds SVD due to its potential to involve and therefore influence the TAVI procedure ^[94]^[95]^[96]^[97]^[98]^[99]^[100]^[101]^[102]^[103]^[104]^[105]^[106]^[107]^[108]^[109]^[110]^[111]^[112]^[113]^[114]^[115]^[116]^[117]. Indeed, since a less invasive transcatheter approach is available for patients presenting with comorbidities and at high risk with conventional surgical strategies, fewer cases of SVD were detected, possibly because the deceased patients were not included in the long-term follow-up. Cardiologists believe that SVD is not a reliable criterion for establishing true biological valve durability. They suggested that the actuarial freedom found by re-intervention is inherently lower than the freedom from SVD ^[94]^[95].

Only the NOTION RCT ^[31] with 6 years of follow-up disclosed SVD rates that were significantly greater after SAVR than the TAVI procedure (24.0% vs. 4.8%; p < 0.001). The investigators reported in post-procedural echocardiographic controls a mean gradient of >20 mm Hg in 22% of patients who experienced SVD compared to 2.9% for those who were managed with TAVI (p < 0.0001). This evidence was also corroborated at a 3-month post-procedure check where a modified definition of SVD was fixed and a mean gradient increase >10 mmHg was established (AVR-S 12.4% vs. TAVR 1.4%; p < 0.001) ^[31].

On the other end, patients who were checked at a 5-year follow-up in the PARTNER trial disclosed no structural valve deterioration with the preservation of low gradients and increased valve areas ^[9]^[10]. The results of the two randomized studies are encouraging, but a longer follow-up is necessary to confirm and give more solidity in terms of the safety and effectiveness of the transcatheter procedure ^[9]^[10].

The bioprosthesis designed as part of the Sapien THV balloon-expandable device consists of bovine pericardium as opposed to calf pericardium which characterizes the surgically implanted Edwards bioprosthesis. However, it should be noted that the treatment procedure is identical ^[118]. The use of the TAVR 22 Fr and 24 Fr systems has been adapted to the leaflets of the TAV, which are thinner than surgical bioprosthesis. Rapid technological advances have led to the development of delivery systems reduced to 18 Fr before and 4 Fr after for the second generation of Sapien XT and for the third-generation Sapien 3 (Edwards Lifesciences, Inc.), which accompanied the changes made to the stent in cobalt–chromium and thinner leaflets to obtain a lower crimped TAV profile.

The study by Xuan et al. ^[119] revealed that the major and minor stresses in the Sapien 26 mm valves are located proximally in the annulus, where the stent is deployed and narrowed. The investigators highlighted that maximum and minimum principal stresses were exhibited at the level of TAV leaflets that were attached to the stent located in close contact with the commissures. It is reasonable to suggest that these regions where the peak stress and the highest stress levels occur locally could result in the areas most prone to initiate degeneration. To date, researchers have no knowledge of studies that have shared a comparison on the relative duration of TAVI compared to surgical bioprosthesis. Evidence reported from studies on the degeneration of surgical bioprosthesis suggests that degeneration associated with calcification or tearing of the flaps correlates with areas of high tensile and compressive stresses ^[119].

Sun et al. ^[120] performed the first computational biomodelling using FEA on two bovine pericardial valves from Edwards Lifesciences Inc. The test was performed with quasi-static loading conditions set below 120 mm Hg, with leaflet material properties fixed from those valves and respecting the exact valve geometry 11. The investigators recorded a maximum in the plane stress that ranged from 544.7 kilopascals (kPa) to 663.2 kPa, reliant on the material properties of the leaflet were used. Of note, the degree of stress had different locations. In fact, they revealed that the stresses on the leaflets were greatest near the commissures and inferior near the free edge of the leaflet. In a subsequent study, the researchers reported the results of an FEA simulation performed on a 25 mm surgical bioprosthesis, which is the closest dimension to the size of the commonly implanted Sapien balloon-expandable device. Again, Xuan et al. ^[119] suggested levels of maximum principal stress for a 26 mm Sapien valve that were significantly higher than those recorded for a surgical bioprosthesis, offering an explanation due to the difference in the design of the leaflets or different interaction with the respective frame that constitutes the device ^[119]. Alavi et al. revealed that the crimping process physically damages TAV leaflets and may undermine leaflets, leading to increased leaflet stress ^[121].

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Francesco Nappi

Sanjeet Singh Avtaar Singh

Pierluigi Nappi

Antonio Fiore

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Update Date: 26 Sep 2022

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