Failure properties of ascending thoracic aortic aneurysms with dysfunctional tricuspid aortic valves

Abstract

 

OBJECTIVES

Ascending thoracic aortic aneurysms (ATAAs) often coexist with dysfunctional tricuspid aortic valves (TAVs). How valvular pathology relates to the aortic wall mechanical properties requires detailed examination.

METHODS

Intact-wall and layer-specific mechanical properties from 40 and 21 patients with TAV-ATAAs, respectively, were studied using uniaxial tensile testing, longitudinally and circumferentially. Failure stress (tensile strength), failure stretch (extensibility) and peak elastic modulus (stiffness) measurements, along with histological assays of thickness and elastin/collagen contents, were compared among patients with no valvular pathology (NVP), aortic stenosis (AS) or aortic insufficiency (AI).

RESULTS

Intact-wall stiffness longitudinally and medial strength and stiffness, in either direction, were significantly lower in AI patients than in AS and NVP patients. Intact-wall/medial thickness and extensibility in either direction were significantly lower in AS patients than in AI and NVP patients. In contrast, intact-wall/medial stiffness circumferentially was significantly higher in AS patients than in NVP patients, consistent with the significantly increased medial collagen in AS patients. Failure properties and medial thickness and elastin/collagen contents were significantly lower (more impaired) in females. The left lateral was the thickest quadrant in NVP patients, but the 4 quadrants were equally thick in AS and AI patients. There were significant differences in strength and stiffness among quadrants, which varied however in the 3 patient groups.

CONCLUSIONS

The aortic wall load-bearing capacity was impaired in patients with ATAA in the presence of TAV stenosis or insufficiency. These findings lend biomechanical support to the current guidelines suggesting lower thresholds for elective ascending aorta replacement in cases of aortic valve surgery.

Ascending thoracic aortic aneurysms (ATAAs) are potentially lethal, with a linearized mortality rate of 1.99% per patient-year [1].

INTRODUCTION

Ascending thoracic aortic aneurysms (ATAAs) are potentially lethal, with a linearized mortality rate of 1.99% per patient-year [1]. Current guidelines indicate that asymptomatic patients with tricuspid aortic valves (TAVs), no connective tissue syndromes and degenerative ATAAs whose diameter exceeds 55 mm should be evaluated for surgical repair to avoid aortic dissection or rupture [2]. For patients with an indication for aortic valve (AV) surgery, a lower diameter threshold (>45 mm) can be applied for concomitant ascending aorta replacement, based on clinical judgement [2]. Nevertheless, aortic diameter, albeit a valuable tool, appears inadequate per se to guide decision-making for elective ATAA repair. Most patients before acute dissection reportedly have aortic diameters below the recommended cut-off values [3]. From the biomechanical viewpoint, wall stress and strength are major contributing factors to the ATAA risk of rupture or dissection [4]. Thus, the information on the aneurysmal aortic wall's ability to sustain stress and strain could enhance the identification of at-risk patients and allow optimal surveillance and therapeutic strategies.

To this end, several studies have reported an association of the strength and histology of the ATAA wall with abnormal AV morphology, predominantly bicuspid AV (BAV) [5–9]. On the other hand, aneurysmal disease regularly coexists and may be aetiologically related to valvular dysfunction, i.e. aortic stenosis (AS) or aortic insufficiency (AI), in the absence of morphological alterations. The aetiological relation of ATAA and valve pathology may be complex and bidirectional (e.g. AI may initially result from rather than trigger ATAA development). In any case, the mechanical properties of the ATAA wall have not been adequately characterized in these conditions. In an effort towards filling this gap, we aimed to identify the failure properties of the ATAA wall in the presence of stenotic or insufficient TAVs compared to the functionally normal AV. To study how the strength, stiffness and extensibility of intact-wall and layered tissue varied among patient groups, we constructed an extensive dataset from some patients examined in our previous studies, adding failure-property data exclusively performed for the present objective. These were complemented with our prior histological estimates of layer-specific thickness and elastin/collagen contents whenever available, determining an association with the functional state of the AV.

MATERIALS AND METHODS

Patient groups

The study population encompassed TAV patients subjected to elective (i) ascending aorta tube graft replacement with or without AV surgery or (ii) modified Bentall procedure. Although proper classification into TAV or BAV may occasionally be challenging due to severe valve calcification and morphology distortion, the valves were confidently classified as TAV intraoperatively by 2 experienced surgeons based on their morphological characteristics. Patients with aortic dissection and known familial syndromic or non-syndromic aortopathies were excluded. Written informed consent was obtained from all patients regarding tissue handling and protected health information use for research purposes in accordance with the hospital Ethics Committee guidelines. Supplementary Material, Table S1 lists some clinical parameters according to the experiment type. The severity of AI and AS was graded I–III (mild to severe) during preoperative echocardiography.

Intact-wall failure-property and thickness measurements from 40 patients [11 presented with no valvular pathology (NVP), 13 with AS and 16 with AI] were analysed. We used data from 34 patients presented before [5, 10], and for whom the type and degree of valvular pathology were available in our database; 6 patients were new. Data from 21 patients (7 with NVP, 7 with AS and 7 with AI) concerning layer-specific failure property and thickness measurements were evaluated. Twelve patients were new, and 9 patients had been presented before [5]; both layer-specific and intact-wall properties were examined in those 9 patients. Histological assays of thickness and elastin/collagen contents in 30 patients from our previous studies were also included and re-analysed after classification per valvular pathology status (8 with NVP, 9 with AS and 13 with AI).

Tissue handling and testing

Details of specimen harvesting and handling were thoroughly presented in our previous studies [5, 10–13]. All ATAAs were collected as short cylinders, starting at the level of the sinotubular junction. Periadventitial tissues were detached, and the cylinders were immersed in refrigerated (4°C) normal saline until mechanical testing within 24 h after harvesting. Multiple strip specimens with circumferential/longitudinal direction were cut from the anterior, posterior and 2 lateral quadrants referring to the greater and lesser curvature of the aorta; these were marked with different numbers of proximal cuts immediately after resection. A circumferential specimen from every quadrant was kept for histology. It was formalin-fixed, paraffin-embedded and stained with haematoxylin–eosin, orcein and Sirius red to determine thickness, elastin content and collagen content, respectively. The experimental system used to evaluate failure properties has been described in detail elsewhere [5, 10]. Briefly, intact-wall and layer strips underwent an increasing tensile load until failure, and the following parameters were evaluated: failure stress (viz. strength), failure stretch (extensibility) and peak elastic modulus (maximum stiffness).

Statistical analysis

The mechanical and histological data were not always representative of a normal distribution, as demonstrated by the Shapiro–Wilk test. Given also the relatively small patient numbers examined, the median and interquartile range are reported as statistical measures of all continuous parameters' central tendency and distribution. The non-parametric Kruskal–Wallis one-way analysis of variance was used to compare failure properties, thickness and compositional parameters among patient groups (NVP versus AS versus AI) and quadrants (anterior versus right lateral versus posterior versus left lateral). In case of significance, data were evaluated in pairs by the non-parametric Mann–Whitney test. The Mann–Whitney test was also used to assess directional (circumferential versus longitudinal) and AS or AI grade (i.e. I versus II versus III) differences. Categorical parameters are presented as numbers, and Fisher's exact test was used to compare patient groups. Understanding that the failure properties could depend on patient age, gender and diameter, comparisons were only performed among matched groups. When a group was not age-matched, its data were linearly regressed as a function of age to calculate a new set of properties at the other groups’ average age. The results were regarded as significant when P < 0.05. Statistical evaluation was conducted in OriginPro 2018 (OriginLab Corp, Northampton, MA, USA).

RESULTS

Effect of valvular pathology

The patient groups, wherefrom intact-wall failure properties and thickness were measured, did not differ significantly in ATAA diameter [Supplementary Material, Table S1; NVP: 5.1 (4.5–5.4); AS: 5.5 (5.0–6.0); AI: 5.6 (5.0–6.0) cm; P > 0.1]. However, there was dissimilar gender prevalence among groups (NVP male/female ratio: 7/4; AS: 12/1; AI: 8/8; P < 0.05) and the patients of the AS group were older [NVP: 60 (52–71); AS: 71 (68–74); AI: 64 (55–69) years; P < 0.05]. To facilitate patient group comparisons, the data of AS patients that were not age-matched were extrapolated through correlations with age to the average age of NVP and AI patients. The comparison of the extrapolated results of AS patients with the other groups is presented in Fig. 1 only for males, as the AS group contained 1 female patient (Supplementary Material, Table S1). There were altogether no failure stress differences among males (Fig. 1A), but males with AS exhibited significantly increased peak elastic modulus compared to those with NVP circumferentially and those with AI longitudinally (Fig. 1B). The opposite trend was noted for failure stretch, namely males with AS exhibited significantly decreased failure stretch compared to those with NVP longitudinally and those with AI in both directions (Fig. 1C). Significantly smaller wall thickness was additionally noted in males with AS than in those with NVP and AI (Fig. 1D).

Figure 2:

Box plots of (A and B) failure stress, (C and D) peak elastic modulus, (E and F) failure stretch and (G) thickness for intact-wall strips from ascending thoracic aortic aneurysm patients with mild, moderate and severe degrees of aortic stenosis and aortic insufficiency. Failure parameters are shown with circumferential/longitudinal direction, while wall thickness is pooled from both directions. No data are shown for grade I (mild) of aortic stenosis and grade III (severe) of aortic insufficiency including <4 patients. ‡ denotes grade differences (P < 0.05); * and **, directional differences (P < 0.05, P < 0.001).

Effect of stenosis and insufficiency severity

Grade I of AS (mild) and grade III of AI (severe) were not examined, as relevant groups consisted of only 1 patient. Patients in the remaining AS and AI grades were matched by ATAA diameter, age and male/female ratio (Supplementary Material, Table S1), permitting valid comparisons. With an increasing grade of AS, thickness significantly increased (Fig. 2G), failure stress decreased (yet significantly so only circumferentially; Fig. 2A), while peak elastic modulus and failure stretch did not vary with the grade of AS (Fig. 2C–F). In contrast, all 3 failure parameters significantly decreased from grade I to grade II of AI (Fig. 2A–F), and thickness significantly increased (Fig. 2G).

Figure 3:

Box plots of (A and B) failure stress, (C and D) peak elastic modulus and (E and F) failure stretch for intact-wall strips of (left) circumferential and (right column) longitudinal direction from ascending thoracic aortic aneurysm patients with no valvular pathology, aortic stenosis and aortic insufficiency according to quadrant (anterior, right lateral, posterior, left lateral). * and ** above the whiskers denote statistically significant directional differences (P < 0.05, P < 0.001); @ and @@, versus right lateral (P < 0.05, P < 0.001); #, versus posterior (P < 0.05).

Figure 1:

(A) Failure stress, (B) peak elastic modulus, (C) failure stretch and (D) thickness for intact-wall strips of circumferential/longitudinal direction from all quadrants of male ascending thoracic aortic aneurysm patients with no valvular pathology, aortic stenosis and aortic insufficiency. Box plots show median (horizontal line), 25% and 75% quartiles (top and bottom borders) and minimal and maximal values (whiskers). s denotes significant differences versus aortic stenosis (P < 0.05); i and ii, versus aortic insufficiency (P < 0.05, P < 0.001); * and **, directional differences (P < 0.05, P < 0.001).

Regional differences

There were significant differences in intact-wall failure stress and peak elastic modulus among quadrants. These regional differences patterns also varied among patient groups (Fig. 3). Significant differences in wall thickness among quadrants were only observed in NVP patients (Fig. 4). See Supplementary Material, S3.3 for a detailed exposition of the regional and directional differences in intact-wall properties.

Figure 4:

Box plots of thickness for intact-wall strips of both directions from ascending thoracic aortic aneurysm patients with no valvular pathology, aortic stenosis and aortic insufficiency according to quadrant. $ above the whiskers denotes significant differences versus left lateral (P < 0.05).

Figure 5:

Box plots of (A and B) failure stress, (C and D) peak elastic modulus, (E and F) failure stretch and (G) thickness for intimal, medial and adventitial strips from ascending thoracic aortic aneurysm patients with no valvular pathology, aortic stenosis and aortic insufficiency. Failure parameters are shown with circumferential/longitudinal direction and thickness is pooled from both directions. s and ss denote significant differences versus aortic stenosis (P < 0.05, P < 0.001); i and ii, versus aortic insufficiency (P < 0.05, P < 0.001); * and **, directional differences (P < 0.05, P < 0.001).

Layer-specific properties

The layer-specific data were mostly obtained from males (Supplementary Material, Table S1) and were thus comparable to the intact-wall data from males in Fig. 1. As a first note, intimal/medial failure stress and peak elastic modulus resembled the respective intact-wall properties, whereas medial/adventitial failure stretch resembled the intact-wall property (cf. Fig. 1A–C with Fig. 5A–F). Second, the significantly decreased intimal failure stress and peak elastic modulus circumferentially in NVP compared to AI patients counteracted the reverse trend found in the medial parameters in both directions (Fig. 5A–D), reflecting the non-varying intact-wall parameters for males circumferentially and the significantly decreased peak elastic modulus longitudinally (Fig. 1A and B). Third, the increased intimal/medial peak elastic modulus circumferentially in AS compared to NVP patients (Fig. 5C) mirrored the respective intact-wall differences between those patient groups that were only noted circumferentially (Fig. 1B). Fourth, the decreased medial failure stress and peak elastic modulus in AI compared to AS patients mirrored the decreased intact-wall peak elastic modulus longitudinally. Fifth, the decreased medial failure stretch in both directions in AS compared to NVP and AI patients (Fig. 5E and F) was in analogy to the differences found in intact-wall data (Fig. 1C). Sixth, the significantly greater intimal thickness in AS and AI than in NVP patients, the smaller medial thickness and the constant adventitial thickness (Fig. 5G) substantiated the intact-wall thickness data (Fig. 1D).

Figure 6:

Box plots of (A) failure stress, (B) peak elastic modulus, (C) failure stretch and (D) thickness for intact-wall strips of circumferential/longitudinal direction from all quadrants of male and female ascending thoracic aortic aneurysm patients with no valvular pathology and aortic insufficiency. f and ff denote significant differences versus females (P < 0.05, P < 0.001); * and **, directional differences (P < 0.05, P < 0.001).

Gender differences

These were examined in the NVP and AI groups including ≥4 patients, noting that males and females in each patient class were matched by age and ATAA diameter (Supplementary Material, Table S1). Compared to males, failure stress and peak elastic modulus were significantly lower in females though only circumferentially (Fig. 6A and B), while failure stretch was lower in both directions (Fig. 6C). There were non-significant gender differences in thickness (Fig. 6D).

Histological data

Table 1 summarizes layer-specific thickness and elastin/collagen contents. The patient groups differed in their male/female ratio and were sub-grouped by gender to permit valid comparisons. Medial thickness was significantly lower in male patients with AS than in those with NVP and AI. On the other hand, intimal and adventitial thickness did not show significant group differences. There were no females with AS for comparison, but no layer thickness varied significantly between female patients with NVP and AI. Medial thickness was significantly greater in male patients with AI than in female patients with AI.

Table 1:

Histological parameters of intimal, medial and adventitial layers of the ascending thoracic aortic aneurysm wall in patients with no valvular pathology, aortic stenosis and aortic insufficiency

	NVP males	AS males	AI males	NVP females	AS females	AI females
Thickness (μm)
Intima	70 (54–94)	105 (35–438)	68 (47–104)	96 (41–127)	–	87 (49–283)
Media	1383 (1127–1628)s	1089 (955–1306)i	1427 (1274–1699)f	1364 (994–1610)	–	1177 (626–1507)
Adventitia	303 (162–441)	202 (115–452)	257 (211–319)	237 (95–585)	–	264 (135–315)
Elastin content (%)
Intima	12.8 (9.7–21.6)	15.9 (9.5–22.8)	15.4 (11.0–33.1)f	19.1 (8.5–32.3)	–	12.2 (7.9–20.3)
Media	19.5 (17.1–24.5)	18.4 (13.8–25.5)	19.0 (14.6–27.5)f	19.1 (15.0–26.8)	–	16.0 (11.8–19.1)
Adventitia	9.5 (6.9–12.8)	8.9 (7.2–11.7)	9.7 (7.8–12.4)f	10.8 (6.8–16.7)i	–	6.3 (4.0–8.0)
Collagen content (%)
Intima	19.4 (9.8–32.4)	15.9 (11.4–34.5)	16.7 (11.9–22.3)	20.5 (16.4–30.3)	–	18.8 (11.8–31.3)
Media	22.7 (18.4–25.9)sf	28.1 (24.2–33.9)i	25.8 (18.7–30.3)	17.1 (14.3–19.5)	–	22.6 (14.5–27.5)
Adventitia	36.5 (22.3–44.7)f	38.9 (31.8–45.8)	44.2 (36.8–51.0)	45.5 (37.7–59.4)	–	44.8 (40.0–56.6)

Median and IQR are listed. Superscripts s and i indicate significant difference versus AS and AI, respectively (P < 0.05); superscript f, versus females (P < 0.05).

AI: aortic insufficiency; AS: aortic stenosis; IQR: interquartile range; NVP: no valvular pathology.

Concerning our compositional data, elastin content of all layers did not display significant group differences, except for that of the adventitia that was higher in females with NVP than those with AI. Yet, elastin content of all layers was significantly higher in male than female patients with AI. In contrast, medial collagen content was significantly increased in male patients with AS than those with NVP and AI, whereas intimal and adventitial collagen contents did not vary among patient groups. Nonetheless, significantly higher medial collagen content was observed in male than female patients with NVP.

DISCUSSION

Whereas much attention has been paid to the influence of BAV morphology on the mechanical remodelling of the ascending thoracic aorta, the relation of dysfunctional TAVs to ATAA biomechanics has been overlooked. To address this issue, we evaluated the mechanical properties and composition of fresh human ATAA tissue, comparing them among TAV patients with AS, AI, or NVP. Extensive uniaxial tensile testing of intact aortic wall and layer (intima, media, adventitia) strips, both longitudinally and circumferentially, disclosed significant differences in the failure properties of the ATAA wall related to valvular dysfunction. We found inferior medial strength in AI patients and increased stiffening and thinning of the aneurysmal wall in AS patients compared to ATAA patients with normally functioning valves (Figs. 1 and 5). All these conditions correspond to an overall reduced load-bearing capacity, related to variations in elastin/collagen contents as established by quantitative histology (Table 1). Moreover, distinct variations in wall properties were observed as a function of anatomical location both for AS and AI patients (Figs. 3 and 4). These findings support the role of haemodynamics in ATAA remodelling.

Contrary to our findings, Okamoto et al. [14] concluded that valvular pathology had a non-significant effect on wall thickness, distensibility and in vivo wall stresses, examining patients with TAV (3 NVP, 0 AS, 3 AI, 1 mixed), BAV (3 NVP, 5 AS, 7 AI, 5 mixed) and Marfan syndrome (5 NVP, 0 AS, 3 AI, 0 mixed). However, the heterogeneous underlying aortic pathology and the small patient number per valvular pathology group may have hindered the significance of possible differences.

Benedik et al. [15] reported on radial tensile strength, referring to the strength of the bonds holding the media together, in patients with AS and AI. They removed a single sample from the margin of the aortic incision in patients undergoing AV surgery. Examining a large population with mixed valve morphology, they disclosed that AI patients exhibited increased tendency to aortic media degeneration and disruption but a thicker wall than AS patients [15]. Although inspecting different loading directions, their findings are in line with ours, namely the decreased medial strength (Fig. 5), decreased collagen content and increased media thickness in AI patients (Table 1).

The role of AV dysfunction in ATAA pathogenesis has been extensively examined in BAV patients. Several studies have demonstrated that aortic dilatation and reduced distensibility, as assessed in vivo by transthoracic echocardiograms or magnetic resonance imaging, are related to the severity of BAV AI but not AS [8, 9, 16]. Clinical and histological observations have also implicated AI (but not AS) as a risk factor for adverse aortic events [17, 18]. Hence, according to the consensus guidelines on BAV-related aortopathy of the American Association for Thoracic Surgery, predominant AI or root dilatation (the so-called root phenotype) should prompt elective repair of ATAA at a lower diameter (≥50 mm) [19]. On the other hand, Kalinowski et al. [20] demonstrated that the severity of BAV stenosis and insufficiency was associated with ascending tubular aorta and aortic root dilatation, respectively, implying that both valve lesions induce haemodynamic impact on the aortic wall.

Pertinent research in TAV patients is sparse. Our findings indicated that similarly to BAV patients, TAV insufficiency may have detrimental effects on all 3 measured aortic wall failure properties (representing strength, extensibility and stiffness), which deteriorate with increasing AI severity from mild to moderate (severe AI was not examined). Notably, our data established that stenotic TAVs were also associated with compromised mechanical behaviour, while to a lesser degree, as only impaired strength was demonstrated (Fig. 2). Although this impairment was aggravated with increasing AS (from moderate to severe), this finding should be interpreted with caution as grade I (mild) AS patients were not included in the analysis, and a partial view of the phenomenon is presented. In 118 AS patients (at least 87% TAV), Crawford and Roldan [21] failed to show a relation of the echocardiographically assessed aortic diameter to the severity of AS. Regardless, the wall thickening we observed with increasing severity of both AI and AS may be an adaptive response to the aortic wall's reduced load-bearing capacity compensating for the impaired wall strength.

Gender differences in the failure properties of ATAAs, specifically a weaker wall in females, have been reported by our group [10], yet the patients were not categorized by valvular pathology. The same gender-related differences were underscored herein in NVP and AI patients (Fig. 6). Conclusions could not be drawn for AS patients as there was just 1 female AS patient registered in our database.

The spatial variation in the local thickness and failure properties of ATAAs has also been previously identified by our group [12, 13] and others [6]. This study similarly reported non-uniform thickness and longitudinal failure properties along the circumference (Figs. 3 and 4), in relation to valvular haemodynamic status. The left lateral was the thickest of all quadrants but only in NVP patients, implicating haemodynamics for the non-significant thickness variation in AS and AI patients, but also for the different strength and stiffness variation among quadrants in the 3 patient groups.

Quantitative microscopy confirmed the medial thickness differences found on fresh tissue ATAAs with valvular dysfunction undergoing mechanical testing (cf. Table 1 and Fig. 5). It also revealed significant group differences in layer-specific collagen but not elastin content, indicating that the significantly higher medial collagen content in male AS patients related to their stiffer media and intact-wall compared to AI and NVP patients (Figs. 1 and 5), as well as for their stronger media compared to AI patients (Fig. 5). Moreover, loss of medial collagen and intimal/medial/adventitial elastin in female patients with AI may be linked with the reduced strength, maximum stiffness and extensibility in females compared to males (Fig. 6).

There are some limitations to the current study. First, contrasting intact-wall data shown for distinct quadrants, there were fewer layer-specific data. They were presented as pooled data from all quadrants, precluding us from making safe statistical inferences about regional differences, but still managed to explain intact-wall properties. Second, our data interpretation was complicated by the lack of age-matching among patient groups. Nevertheless, the mechanisms compensating for the age effects were considered and based on the significant variations in ATAA wall failure properties and composition, we believe that sound conclusions were made regarding the effects of valvular dysfunction. Third, comparisons among the patient groups were restricted to male patients that became mostly available during the study period. While changes in the measured failure and histological properties between NVP, AS and AI patients represent true patient group differences and not gender differences, future studies should confirm the current trends in females. Fourth, our study lacks data from non-aneurysmal tissue for comparison; these would help us appreciate if the reported changes with valve dysfunction were specific to ATAAs. Fifth, we were unable to adjust our results for other demographic parameters or comorbidities theoretically affecting aortic biomechanics. However, Benedik et al. [15] failed to demonstrate any relation of such parameters with aortic wall medial cohesion after using multivariate analysis in 229 patients. A larger group of patients may be required to avoid potential type II error but, bearing in mind our extensive mechanical testing protocol, this would have rendered the study exceedingly complicated and resource consuming.

In summary, tensile tests disclosed impaired failure properties of the ATAA wall in patients with valvular dysfunction (AS or AI) despite normal valve morphology (TAV), explained by alterations in elastin/collagen contents, as revealed by quantitative histology. Distinct variations in the failure properties and thickness as a function of anatomical location both for AS and AI patients highlight the role of haemodynamics in ATAA remodelling. Although partially examined, it seems that the severity of valvular dysfunction relates to the degree of aortic wall weakness.

Our findings have 2 considerable implications. First, they raise uncertainty about the validity of prior pertinent comparisons of aortic wall mechanical behaviour among groups non-matched for AV dysfunction; a weaker wall may reflect a higher prevalence of patients with valvular pathology in one group over another and not actual material differences. Second, in the clinical setting, our data suggest that patients with ATAA and coexisting AV pathology are probably at greater risk for an aortic event. Although reverse aortic remodelling and mitigation of this risk after AV surgery is a theoretical possibility, our results endorse current therapeutic guidelines suggesting a rather aggressive ATAA replacement strategy for patients with an indication for AV surgery [2].

SUPPLEMENTARY MATERIAL

Supplementary material is available at ICVTS online.

 

Conflict of interest: none declared.

Author contributions

Dimitrios P. Sokolis: Conceptualization; Data curation; Formal analysis; Investigation; Methodology; Software; Validation; Visualization; Writing—original draft; Writing—review & editing. Dimitrios C. Angouras: Conceptualization; Data curation; Investigation; Methodology; Project administration; Supervision; Validation; Visualization; Writing—original draft; Writing—review & editing.

Reviewer information

Interactive CardioVascular and Thoracic Surgery thanks Alessandro Della Corte and the other, anonymous reviewer(s) for their contribution to the peer review process of this article.

ABBREVIATIONS

AI

Aortic insufficiency

AS

Aortic stenosis

AV

Aortic valve

ATAAs

Ascending thoracic aortic aneurysms

BAV

Bicuspid AV

NVP

No valvular pathology

TAVs

Tricuspid aortic valves