Study of mechanical changes in the mitral-aortic coaptation in patients with chronic severe aortic valve closure insufficiency

doi:10.21203/rs.3.rs-1998153/v1

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Study of mechanical changes in the mitral-aortic coaptation in patients with chronic severe aortic valve closure insufficiency

https://doi.org/10.21203/rs.3.rs-1998153/v1

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Objective: Analysis of mechanical changes characteristic of the mitral-aortic valve commissure (MAC) in patients with chronic severe aortic valve closure insufficiency (AR) with preserved ejection left ventricular blood fraction.

Methods: A total of 40 patients with chronic severe AR and 40 normal individuals were included in this study. MAC parameters, such as angle, velocity, and displacement-related indicators, were estimated. Two-dimensional strain techniques were utilized to acquire Global longitudinal strain (GLS), Global transverse strain (GCS), Global circumferential strain (GRS), Anterolateral papillary muscle strain (ALPMS), Posterior medial papillary muscle strain (PMPMS) and Left ventricular torsion Angle (LV-Twist), Aortic ring torsion Angle (A-Twist), Mitral annulus orsion Angle (M-Twist).

Results: MAC displacement and angle were smaller in the AR group than in the control group (P<0.05). GLS, GCS, GRS, ALPMS, PMPMS, LV-Twist, A-Twist, and M-Twist were significantly lower in the AR group than the control group (P<0.05). MAC displacement, angle, and papillary muscle strain were correlated with GLS, and LV-Twist was positively correlated with A-Twist and M-Twist (P<0.05). The ROC curve showed that MAC displacement, angle, A-Twist, and M Twist had good diagnostic efficacy for severe AR.

Conclusion: Left ventricular papillary muscle strain and MAC angle, displacement, A-Twist, and M-Twist are reduced in patients with chronic severe AR, and a correlation was established among these and changes in the left ventricular (LV) systolic function and the underlying mechanics.

mitral-aortic coaptation

aortic regurgitation

strain

MAC is the anatomical association of the two valve annuli, the fibrous connections, and the surrounding left atrioventricular myocardial structures that form the two annuli and is a critical component of the cardiac fibrous skeleton^【^1】. The longitudinal motion is reflected by speed, angle, displacement, and other indicators, while transverse motion is reflected by the torsional angle of the aortic annulus and mitral annulus relative to the apex. Previous studies have been limited to one direction and a single index describing the movement pattern of the MAC, which does not provide a comprehensive and complete description of the overall movement pattern of the annulus. No studies have yet been performed on the MAC mechanics in patients with AR, while in normal subjects, the MAC motion pattern assists in the LV systolic function. Patients with chronic severe AR may have irreversible damage to myocardial structure and function due to enlarged left ventricle and the continually increasing LV wall stress and left heart mass^【^2】; this prevents the recovery of the postoperative LV function. MAC has an anatomical and functional correlation with the surrounding myocardial tissue and tendon papillary muscle during embryonic development, and any partial insufficiency or deficiency will affect the structure and function of the normal annular structure^【^3-4】. Thus, the MAC of AR patients who maintain normal ejection fraction will also undergo mechanical changes corresponding to the modified LV structure and function. Using ultrasound technology to measure MAC longitudinal and transverse motion indexes in patients with severe AR who maintain normal ejection fraction can describe MAC mechanical characteristics more completely.

1.1 Objective of the study

A total of 40 patients (23 males and 17 females, age 58.9 ± 8.1 years) with severe AR and 40 normal subjects (20 males and 20 females, mean age 59.3 ± 7.2 years) in the control group, between 2019 and 2021 in our hospital were included in this study. All the subjects signed an informed consent document.

1.1.1 Inclusion criteria

AR patients were evaluated by two experienced sonographers according to the 2017 American Society of Echocardiography Joint Cardiovascular Magnetic Resonance Society AR Guidelines^【^5】and the 2020 ACC/AHA Guidelines^【^6】 for the Management of Patients with Valvular Heart Disease for subjects who fulfilled the following criteria: regurgitant beam width (VCW) >6 mm; regurgitant beam width/outflow tract width (VCW/LVOTd) > 2/3; regurgitant beam cross-sectional area/outflow tract cross-sectional area (CSA/LVOT-CSA) >2/3; regurgitant spectrum (PHT) < 300 ms; high regurgitant spectrum concentration; return flow > 60 mL; regurgitant fraction (RF) > 50%; full diastolic flow in the proximal abdominal aorta; LVEF > 55%, LVDd > 50 mm; LVSd > 25 mm; significant severe clinical manifestations of AR; coronary angiography grade III-IV; diagnosis of severe AR during aortic valve replacement was performed.

1.1.2 Exclusion criteria

The following subjects were excluded from cardiomyopathy: infective endocarditis and cardiac insufficiency; mild or moderate AR; acute AR; coronary angiography grade I-II; diseases of other organs or systems; poor quality ultrasound images and missing imaging data.

1.2 Image retention and analysis methods

1.2.1 Image retention

Transthoracic echocardiography was performed by two experienced sonographers using the GE vivid E9 ultrasound diagnostic instrument and LV long-axis, apical four-chamber, three-chamber, two-chamber and aortic, mitral valve, papillary muscle, apical short-axis, two-dimensional (2D), and tissue Doppler imaging (TDI) images were obtained under synchronized electrocardiography. The papillary muscles were labeled as anterolateral papillary muscles (ALPM) and posterior medial papillary muscles (PMPM)^【^7】, according to their projection position relative to mitral valve coaptation. Apical 4-chamber and 3-chamber images showed ALPM and PMPM; local magnified 2D images of the aortic valve and mitral valve were obtained in the long axis of the subject’s left ventricle. The images showed that the aortic annulus plane included the fibrous junction and nadir of the right aortic annulus; the mitral annulus plane included the fibrous junction and nadir of the posterior mitral annulus (Figure 1A). The above ultrasound images were obtained for five consecutive cardiac cycles.

1.2.2 Image analysis

The ECHO PAC workstation was used to measure the relevant conventional ultrasound parameters Left atrium anteroposterior diameter (LAd), Left atrial volume(LAV), Left ventricular end-diastolic diameter (LVDd), Left ventricular end-shrinkage diameter (LVSd), Left ventricular mass (LVM), Left ventricular mass index (LVMI), and left ventricular ejection fraction (LVEF). The Doppler spectra of the mitral lateral annulus tissue in the apical 4-chamber view were used to determine the ECG time phases corresponding to the s, e, and a waves, and then the AMA magnitudes corresponding to these three time-phases were measured sequentially (s-AMA, e-AMA, and a-AMA) (Figure 1A). The sampling points were placed at the posterior mitral leaflet annulus point, mitral-aortic valve union point, and aortic right coronary annulus point under the TDI condition in the apical three-chamber view, and the software provided the displacement and velocity curves, measured and recorded the maximum displacement AEr (mm), MEp (mm), and FE (mm) at the three points (Figure 1B), and also recorded the annular point velocities V_AEr-s, V_AEr-e, V_AEr-a, V_MEp-s, V_MEp-e, V_MEp-a_， V_FE-s, V_FE-e, and V_FE-a at the three points in s-wave, e-wave, and a-wave (Figure 1C). The apical four-chamber, three-chamber, and two-chamber left ventricular images were traced using the 2D speckle tracking technique, and the software automatically calculated the strain values of each longitudinal segment of the heart. In addition, the left ventricular mitral short axis, papillary muscle short axis, and apical short-axis images were traced, and the software calculated the strain of each transverse, the circumferential segment of the left ventricle, and the left ventricular torsion angle LV-Twist (Figure 1F), and finally, the GLS, GCS, and GRS. The short axis of the aortic and mitral annulus was traced using the 2D speckle tracking technique, and the software provided the A-Twist and M-Twist (Figure 2a and b). The apical 4-chamber heart ALPM and apical 3-chamber heart PMPM were traced using the 2D speckle tracking technique, and the papillary muscle strain values ALPMS and PMPMS were read (Figure 1D, E). All data were measured more than twice in duplicate.

1.3 Statistical analysis

All data were analyzed using SPSS23.0 statistical software, and measurement data were expressed as mean ± standard deviation; t-test was applied for two independent samples for the comparison between the groups; Pearson correlation analysis; receiver operating characteristic (ROC) curves were plotted and the area under the curve (AUC) values were calculated. P < 0.05 indicated statistical significance.

Table 1 Difference analysis between control group and AR group
General information
	Normal	AR	t	P
Age (years)	59.3 ± 7.2	58.9 ± 8.1	0.22	0.827^a
Height (cm)	169.1 ± 5.32	168.5 ± 5.4	0.521	0.604^a
Height (kg)	66.1 ± 6.2	66.3 ± 6.8	-0.121	0.904^a
BMI	23.2 ± 1.3	23.3 ± 1.8	-0.389	0.698^a
Systolic pressure (mmHg)	115.35 ± 4.8	125.5 ± 8.8	-6.399	< 0.001^b
Diastolic blood pressure (mmHg)	75.8 ± 4.9	67.2 ± 7.1	6.335	< 0.001^b
Left ventricular cavity 2D ultrasound parameters
LAd (mm)	32.0 ± 2.8	39 ± 5.4	-7.692	< 0.001^b
LAV	29.0 ± 5.2	58.0 ± 14.7	-11.397	< 0.001^b
LVDd (mm)	47.0 ± 2.4	65.0 ± 8.7	-12.374	< 0.001^b
LVSd (mm)	31.0 ± 1.5	45.0 ± 8.7	-9.958	< 0.001^b
LVM	174.3 ± 20.3	346.9 ± 96.8	-11.04	< 0.001^b
LVMI	99.9 ± 12.2	188.7 ± 51.4	10.622	< 0.001^b
LVEF	63.5 ± 3.2	57.4 ± 2.8	-10.8	0.909^a
MAC parameters
AEr (mm)	12.5 ± 2.3	9.8 ± 2.8	4.618	< 0.001
MEp (mm)	13.8 ± 1.9	10.7 ± 3.0	5.537	< 0.001
FE (mm)	11.9 ± 1.6	9.4 ± 2.8	5.167	< 0.001
s-AMA (°)	136.2 ± 6.8	141.7 ± 8.6	-3.156	< 0.001
e-AMA (°)	116.3 ± 9.2	128.1 ± 9.9	-5.478	< 0.001
a-AMA (°)	128.9 ± 8.1	132.5 ± 13.1	-1.485	0.14
AMAmax-min	20.4 ± 4.8	15.4 ± 5.9	4.108	< 0.001
V_AEr-s (cm/s)	5.6 ± 1.4	4.9 ± 1.8	1.818	0.073
V_AEr-e (cm/s)	5.4 ± 1.81	4.7 ± 1.6	1.766	0.081
V_AEr-a (cm/s)	5.4 ± 1.5	4.8 ± 1.9	1.543	0.127
V_MEp-s (cm/s)	6.4 ± 1.2	5.6 ± 1.5	1.575	0.119
V_MEp-e (cm/s)	6.1 ± 1.6	5.6 ± 1.8	1.188	0.238
V_MEp-a (cm/s)	6.9 ± 1.3	6.2 ± 2.1	1.621	0.109
V_FE-s (cm/s)	4.6 ± 1.4	4.0 ± 1.5	1.704	0.092
V_FE-e (cm/s)	5.2 ± 1.7	4.7 ± 1.6	1.236	0.22
V_FE-a (cm/s)	6.0 ± 1.6	5.7 ± 2.3	0.551	0.583
left ventricular isotropic strain and papillary muscle strain
GLS	-25.1 ± 3.4	-13.7 ± 3.3	15.260	< 0.001
GCS	29.5 ± 3.3	19.6 ± 7.9	7.263	< 0.01
GRS	-25.0 ± 3.2	-16.4 ± 4.2	-10.306	< 0.001
ALPMS	-19.8 ± 3.2	-11.2 ± 4.4	9.171	< 0.001
PMPMS	-19.7 ± 3.5	-11.9 ± 6.0	7.108	< 0.001
annular torsion and left ventricular torsion angle
LV-Twist	16.8 ± 2.4	11.9 ± 4.5	6.107	< 0.001
A-Twist	9.4 ± 1.8	6.3 ± 1.6	8.023	< 0.001
M-Twist	10.0 ± 2.6	6.4 ± 1.9	7.059	< 0.001
Note: BMI body surface index; LAd, left atrial anteroposterior diameter; LAV, left atrial volume LVDd (mm) left ventricular end-diastolic internal diameter; LVSd (mm), left ventricular end-systolic internal diameter; LVM, left ventricular mass; LVMI, left ventricular mass index; MVd (mm), LVEF left ventricular ejection fraction; a. P < 0.05, difference is statistically significant; b. P > 0.05 differences are not statistically significant.AEr, aortic right coronary annular point; MEp, mitral posterior leaflet annular point; FE, mitral-aortic joint point; s-AMA, mitral-aortic annular angle at wave s; e-AMA, mitral-aortic annular angle at wave e; ∆θ-AMAmax-min, AMA difference between the maximum and minimum values; a-AMA, mitral-aortic annular angle at wave a; VAEr-s, VAEr-e, VAEr-a, velocities of the right coronary annulus of the aortic valve at waves s, e, and a, respectively; VMEp-s, VMEp-e, VMEp-a, velocities of the posterior mitral leaflet annulus at waves s, e, and a velocities, respectively; VFE-s, VFE-e, and VFE-a, velocities at the mitral-aortic annulus point at s, e, and a waves, respectively. P < 0.05 is statistically significant. P > 0.05 is not statistically significant. GLS, overall left ventricular longitudinal strain; GCS, overall left ventricular transverse strain; GRS, overall left ventricular circumferential strain; ALPMS, anterolateral papillary muscle strain value; PMPMS, posterior medial papillary muscle strain value; P < 0.05 is statistically significant; P > 0.05 is not statistically significant.LV-Twist, difference between basal and apical left ventricular torsion angles; A-Twist aortic annulus relative to apical torsion angle; M-Twist mitral annulus relative to apical torsion angle; P < 0.05 is statistically significant, P > 0.05 is not statistically significant.

Table 2 Correlation analysis between MAC longitudinal/transverse mechanics and left ventricular longitudinal/transverse mechanics
Correlation of papillary muscle strain and MAC displacement and angle indices with GLS in the AR and control groups
	Normal		AR
	r	P	r	P
AEr (mm)	0.412	0.008^b	0.459	0.003^a
MEp (mm)	0.376	0.017^b	0.537	< 0.001^a
FE (mm)	0.423	0.007^b	0.406	0.009^a
s-AMA (°)	-0.492	< 0.001^a	-0.32	0.044^b
e-AMA (°)	-0.581	< 0.001^a	-0.609	< 0.001^a
a-AMA (°)	-0.26	0.105^c	-0.494	0.001^a
△AMAmax-min	0.314	0.049^b	0.596	< 0.001^a
ALPMS	0.56	< 0.001^a	0.564	< 0.001^a
PMPMS	0.517	0.001^a	0.516	0.001^a
Correlation between A-Twist/M-Twist and LV-Twist in the AR group
A-Twist	0.772	< 0.001^a	0.574	< 0.001^a
M-Twist	0.577	< 0.001^a	0.739	< 0.001^a
Note: a at the 0.001 level (two-tailed), significant correlation; b at the 0.05 level (two-tailed), significant correlation; c P > 0.05, not statistically significant.

Table3 ROC curve analysis of MAC vertical and horizontal indicators’ diagnostic efficiency
Indicators	AUC	P	95% CI	Truncation value	Sensitivity	Specificity
AEr (mm)	0.769	< 0.0001	0.67–0.87	9.53	0.55	0.9
MEp (mm)	0.802	< 0.0001	0.70–0.90	12.75	0.78	0.75
FE (mm)	0.781	< 0.0001	0.67–0.89	11.49	0.775	0.75
s-AMA (°)	0.702	0.0019	0.59–0.82	138	0.725	0.6
e-AMA (°)	0.821	< 0.0001	0.73–0.92	123.2	0.725	0.875
△AMAmax-min	0.745	0.0002	0.64–0.85	16.9	0.675	0.775
A-Twist	0.895	< 0.0001	0.83–0.96	7.975	0.925	0.8
M-Twist	0.860	< 0.0001	0.78–0.94	8.57	0.85	0.725

No significant differences were detected in age, height, weight, and body surface index between the control and AR groups (P > 0.05). Systolic blood pressure in the AR group was significantly higher than that in the control group, and diastolic blood pressure was slightly lower than that in the control group (P < 0.05). LAd, LAV, LVDd, LVSd, LVM, and LVMI were significantly greater in the AR group than those in the control group (P < 0.001). LVEF was not significantly different between the control and AR groups (P > 0.05; Table 1).
Analysis of variance: ① Comparison of longitudinal parameters of mitral-aortic fibrous annulus union: Aer (mm), Mep (mm), FE (mm), s-AMA, e-AMA, ∆θAMA, and ∆θ/AMAmax were smaller in the AR group than those in the control group (P < 0.05). The values of VAer-s, VAer-e, VAer-a, VMep-s, VMep-e, VMep-a, VFE-s, VFE-e, VFE-a, and a-AMA did not differ significantly between the AR and control groups (P > 0.05; Table 1, Figure 2). ② Comparison of LV strain values in all directions and papillary muscle strain values: GLS, GCS, GRS, ALPMS, and PMPMS of LV strain values were lower in the AR group than in the control group (P < 0.05; Table 1, Figure 3). ③ Twist, A-Twist, and M-Twist were lower in the AR group than in the control group (P < 0.05; Table 1).
Correlation analysis: ① Correlation between MAC longitudinal indexes and GLS in the control and AR groups: AEr, MEp, FE (mm), △AMAmax-min, ALPMS, PMPMS, and GLS have a positive correlation (P < 0.05), while s-AMA, e-AMA (°), and GLS have a negative correlation (P < 0.05). On the other hand, no correlation was established between a-AMA (°) and GLS in the control group (P > 0.05; Table 2); ② Correlation between MAC transverse index and Twist in the control and AR groups: positive correlation was detected between A-Twist, M-Twist, and Twist (P < 0.05; Table 2).
In order to further explore the diagnostic value of MAC longitudinal and transverse indicators, the diagnostic efficacy of MAC longitudinal indicators (AEr, MEp, FE, s-AMA, e-AMA, and △AMAmax-min) and transverse indicators (A-Twist and M-Twist) was analyzed using the ROC curve. Also, the AUC values of each indicator were compared under the premise of P < 0.05, and was found to be 0.7. P < 0.05 indicated statistical significance and high diagnostic efficacy (Table 3,Figure 4).

Chronic AR develops slowly, and in order to maintain a normal ejection fraction, LV compensatory mechanisms are activated, leading to enlarged left atrial and left ventricular cavity. In addition, indicators, such as LV mass index increase and subtle changes in the cardiac function using traditional methods of assessment were difficult to detect^【8】 The LV strain responds to a decrease in LV systolic function before a decline in the ejection fraction^【9】 and can respond to LV in changing myocardial mechanical trends. GLS, GCS, and GRS are reduced in chronic severe AR compared to normal per capita when normal LVEF is maintained, which is consistent with previous studies^【10】. This phenomenon indicated that LV myocardium is a major player in cardiac compensatory mechanisms in patients with severe AR, wherein the normal cardiac function is maintained, and the changes in myocardial contractility are negative in both the long and short axis of the ventricle.

LVEF is maintained as a result of myocardial fiber contraction, while LV torsional motion also plays a critical role under normal conditions, the LV base rotates clockwise, and the LV apex rotates counterclockwise, resulting in towel-wringing motion^【11】 that can be used as a compensatory pathway to compensate for LVEF in normal subjects or patients with localized infarction^【12】. However, after the activation of compensatory mechanisms in patients with severe AR, torsional exercise did not contribute to LVEF, and Twist was significantly reduced in the AR group compared to controls. Broch et al.^【13】 also found reduced LV torsion in the same type of patients. This phenomenon might be related to the fact that LV torsion is influenced by the degree of myocardial contraction and diastole, the balance between endocardial and epicardial contractions, and the orientation of myocardial fibers^【14】. The present study also confirmed that LV enlargement/expansion in AR patients reduces the torsional angle.

MAC has a specific motion pattern during the cardiac cycle with cardiac torsion, systole, and diastole^【15】, and the MAC motion pattern and state can be divided into two directions: longitudinal and transverse. In the short-axis direction of the heart, along with the twisting of the left ventricle itself, the MAC coordinates the left ventricle via twisting. In this study, we used the speckle tracking technique to trace the short-axis of the aortic and mitral annulus and calculated the difference in the respective twisting angles relative to the apical part of the heart. The results showed that A-Twist and M-Twist were reduced in patients with severe AR who maintained normal ejection fraction and the control. An adequate correlation was established between A-Twist, M-Twist, and LV-Twist in both control and AR patients, indicating that the association between annular torsional mechanics and LV torsional mechanics not only exists in normal subjects but is also persistent when the LV structure and function are altered and that the annular torsion cooperates with LV torsion to complete the compensatory process of ventricular structure and function. The AUC values of A-Twist and M-Twist were 0.895 and 0.86, respectively, providing an adequate reference value for the diagnosis of AR while maintaining a normal ejection fraction.

In the direction of the long axis of the heart, the aortic and mitral valves move toward the apex during systole, both move toward the bottom of the heart during diastole, and this movement can be a part of the coordination of LV systolic function^【16–17. When the preserved ejection fraction AR turns on the compensatory mechanism, MAC is joined via an increase in AMA, a decrease in the magnitude of AMA changes, and a corresponding decrease in annular displacement, with the compensatory changes in LV strain and LV torsion. This phenomenon was consistent with the results of previous studies^【18】; because AR stimulates the compensatory mechanism of the LV, it enlarges the LV cavity and decreases the magnitude of ventricular bike-motion, which is consistent with the results of a previous study^[18]. This phenomenon could be attributed to the AR-stimulated compensatory mechanism of the left ventricle, resulting in an enlarged left cavity and reduced motion of the ventricular biscuit, which in turn affected the structure and motion of the MAC, resulting in a large AMA in the AR group. In addition, the displacement of the posterior mitral annulus was confirmed to be relatively large in animal experiments^【19】, which was consistent with the results of the present study. The mechanism might be that fibrous tissue constitutes the continuity of the aorta and that the right aortic annulus and posterior mitral annulus merge with muscle and fibrous tissue that has less peripheral restriction facilitating the posterior mitral annular motion. This correlation persists although the magnitude of AMA changes is reduced in severe AR with preserved LVEF, and the annular displacement is correspondingly reduced. The results of this study showed a good correlation between LV GLS and MAC angle, displacement, and other indices, indicating that the longitudinal mechanical changes of MAC and LV mechanics complement and influence each other. In patients with severe AR, the preoperative ultrasound assessment of longitudinal indices of MAC in response to its involvement in compensatory mechanisms serves as a reference for the selection of surgical timing.

In addition to the longitudinal motion of the mitral annulus, influenced by the surrounding myocardium, the papillary muscle also has an impact on it^【20】. The pulling force generated by the left ventricle contraction is transmitted to the mitral valve and annulus through the PM, which has a contractile function, pulling the tendon to transmit the force to the valve and annulus^{【21–23】}. In this study, we analyzed the longitudinal contractile function of the papillary muscle using strain techniques to observe the mechanical effects produced by the papillary muscle on the MAC. Previous studies demonstrated that reduced left ventricular systolic function is associated with reduced papillary muscle strain^【24】, which is consistent with the results of the present study. A good correlation was established between the AR group and control ALPMS, PMPMS, and GLS. Moreover, the reduced strain value of papillary muscle contraction, contractile force, and force on the annulus and valve contributed to the decreased displacement and angle of longitudinal motion of MAC in patients with severe AR.

In conclusion, the mechanical changes in MAC are correlated with the mechanical changes in the left ventricle. The mechanical system composed of the cardiac fibrous skeleton and myocardium is negatively affected in AR patients due to the secondary changes in the cardiac structure and function caused by hemodynamic alterations.

Statements & Declarations：The authors declare that no funds, grants, or other support were received during the preparation of this manuscript.

Competing Interests：The authors have no relevant financial or non-financial interests to disclose.

Author Contributions：All authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by Maierziya Abudireheman, Xueyi Li. The first draft of the manuscript was written by Xueyi Li and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

Consent to participate:Informed consent was obtained from all individual participants included in the study.

Ethics approval:This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of University B (Date：October 15, 2021/No：20211015-45).

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Study of mechanical changes in the mitral-aortic coaptation in patients with chronic severe aortic valve closure insufficiency

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