Academic Editors: Carmela Rita Balistreri and Calogera Pisano
Background: Secondary mitral regurgitation (SMR) has been related to
left ventricular (LV) remodeling and geometric deformation of the mitral
apparatus after myocardial infarction (MI), and proved to be associated with
adverse cardiac events. We assessed the proportion of mild SMR before and after
isolated coronary artery bypass grafting (CABG) surgery, and further study to
evaluate dynamic changes of MR and the determinants of such process on 1 year
follow-up. Methods: From 2019 to 2021, cohort study of 171 consecutive
hospitalized patients who underwent selective isolated CABG surgery were included
and divided into the control group and mild MR group according to whether mild MR
occurred at baseline. Univariate analysis and multivariate logistic regression
analysis were used to test the associations of changes in MR after CABG, and
p
Secondary mitral regurgitation (SMR) is often induced by coronary artery disease, especially myocardial infarction (MI), and a powerful predictor of adverse prognosis with increased risk for death and heart failure [1, 2]. SMR is associated with a higher prevalence of comorbidities and adverse cardiovascular outcomes in subjects with previous cardiovascular events [3, 4] and progression of MR after MI promotes an increased likelihood of cardiovascular morbidity [5, 6, 7]. Moreover, left ventricular (LV) remodeling causes left atrial (LA) enlargement which is common in chronic moderate to severe MR [8, 9], and LA remodeling and dysfunction can be considered as indicators of underlying LA myopathy and might also contribute to low-grade functional MR [10, 11].
In order to reduce the risk of sudden cardiac death and improve myocardial function, coronary artery bypass grafting (CABG) is an effective revascularization treatment [12], and concomitant mitral valve surgery at the time of CABG is recommended patients with symptoms of severe MR and promotes to eliminate moderate MR [13, 14]. However mild MR is often neglected in clinical practice, which has been shown to be associated with mortality in a diabetic population even in the presence of normal ejection fraction [15]. The present study design excluded moderate or severe MR to evaluate percentage of patients with mild MR before CABG, and observe dynamic changes in MR and explored clinical related risk factors and echocardiographic derived parameters as a potential predictor of dynamic changes in MR on 1-year follow-up.
This study was conducted in Fuwai Hospital, National Center for Cardiovascular Diseases (Beijing, China) from January 2019 to January 2021 and the medical records of consecutive patients who underwent selective isolated CABG were screened. The protocol was consistent with the principles of the Declaration of Helsinki and approved by the institutional ethics committee of Fuwai hospital and all participants provided written informed consent.
Preoperative echocardiography was performed within 1 week before surgery to determine the etiology and severity of MR and patients with trivial to mild MR were enrolled. Exclusion criteria were absence of sinus rhythm, moderate or severe valve stenosis or insufficiency, mitral valve organic pathology (prolapse, rheumatic, endocarditis, leaflet perforation, annular or leaflet calcification), valve prosthesis, the history of CABG or other cardiac surgery, unstable clinical conditions and poor quality of echocardiographic images (Fig. 1).
Flow chart of study inclusion. Flow chart of study enrollment to illustrate the inclusion and exclusion criteria. CABG, coronary artery bypass graft.
Echocardiography was performed by an experienced sonographer in accordance with American Society Echocardiography guidelines [16], preoperative (1 week before surgery), postoperative (1 week after surgery) period and 1 year follow-up. Comprehensive 2-dimensional (2D) echocardiography studies were performed with commercial equipment (EPIQ7 and iE33, Philips, Andover, MA), 3.5-MHz transducer and stored in DICOM format and transferred to TOMTEC image system (TOMTEC IMAGE SYSTEMS GMBH).
MR was assessed using a multiparametric approach in accordance with ASE and
European Society of Cardiology valvular regurgitation guidelines, and defined as
no or trace, mild (central jet area
LV ejection fraction (LVEF) was obtained by the Simpson’s biplane method. LV end-diastolic dimension (LVEDd), end-systolic dimension (LVESd), wall thickness (LVPW), LA dimension and right ventricular dimension (RVD) were obtained in 2-dimensional or M-mode images, and relative wall thickness (RWT = 2 * LVPW/LVEDd) derived. LV end-diastolic volume (LVEDV) and end-systolic volume (LVESV) and LA volume (LAV) measured from the apical 2-chamber and 4-chamber views, calculated stroke volume (SV = LVEDV – LVESV). The LV mass (LVM) was calculated from formula. Parameters were normalized to body surface area (BSA). Peak velocities of early (E) and late (A) diastolic filling were obtained from Doppler recordings of mitral inflow, and peak early (e’) velocities were measured by tissue Doppler imaging recordings of mitral valve movement. The mitral E/A and E/e’ ratios were also calculated. In addition, mitral annulus (MA) diameter was measured in parasternal long-axis view and the interpapillary muscle distance (IPMD) was measured at parasternal short-axis view.
Speckle-tracking echocardiography (STE) was performed on the apical 4-chamber, 3-chamber and 2-chamber views, and calculated LV global longitudinal strain (LVGLS) by averaging the peak value of 3 apical views. LA function showed by three strain components on the same apical 4-chamber, respectively LA reservoir function (LASr), LA pump function (LASct) and LA conduit function (LAScd). The right ventricular global longitudinal strain (RVGLS) was measured similarly with LVGLS, and RV free wall strain (RVFWS) was the mean value recorded for basal, mid, and apical segments, both performed on the apical focused RV-4-chamber. All Strain measurements were analyzed by the TOMTEC image system (TOMTEC IMAGE SYSTEMS GMBH). The myocardium border detection was automated to ensure optimal tracking throughout cardiac cycle by the software, and the operator confirmed that the true boundaries were traced.
Reproducibility in measurement of strain was evaluated in 30 randomly selected patients using the interclass correlation coefficient. The results of intra- and interobserver variabilities for strain measurements were showed in Appendix Table 6.
The study analyzed MR at baseline and 1 year follow-up, to assess the proportion of individuals who remained in the same category or changed on follow-up.
(1) Reference group: individuals without MR or less than mild MR at baseline, who remained in the same pattern;
(2) Persistence group: individuals with mild MR at baseline who persisted;
(3) Improvement group: individuals who reverted to none or less than mild MR from mild MR at baseline;
(4) Worsening group: individuals who developed to mild MR from none or less than mild MR at baseline.
Statistical calculations were performed using IBM SPSS Statistics version 23.0
(IBM SPSS Statistics, IBM Corporation, Armonk, NY, USA). Continuous variables
were performed by Kolmogorov-Smirnov tests to check for a
normal distribution and are expressed as mean
The clinical characteristics of 171 patients are summarized in Table 1, the mean
age of the total study population was 61.31
Variable | Total | Control group | Mild MR group | p | |
(n = 171) | (n = 128) | (n = 43) | |||
Age, yrs | 61.31 |
60.80 |
62.81 |
0.191 | |
Female | 36 (21.05%) | 26 (20.31%) | 10 (23.26%) | 0.682 | |
Body surface area, m |
1.78 |
1.78 |
1.76 |
0.557 | |
Systolic blood pressure, mmHg | 124.43 |
125.55 |
121.07 |
0.198 | |
Diastolic blood pressure, mmHg | 73.18 |
73.16 |
73.23 |
0.967 | |
Basic heart rate, beats/min | 68.70 |
67.43 |
72.47 |
0.007 | |
NYHA functional classification | 2.26 |
2.20 |
2.42 |
0.047 | |
Smoking | 94 (54.97%) | 69 (53.91%) | 25 (58.14%) | 0.629 | |
Underlying disease | |||||
Hypertension | 112 (65.50%) | 90 (70.31%) | 22 (51.16%) | 0.022 | |
Diabetes mellitus | 61 (35.67%) | 46 (35.94%) | 15 (34.88%) | 0.901 | |
Stroke | 29 (16.96%) | 21 (16.41%) | 8 (18.60%) | 0.740 | |
Peripheral artery disease | 27 (15.79%) | 21 (16.41%) | 6 (13.95%) | 0.703 | |
Chronic kidney disease | 21 (12.28%) | 12 (9.38%) | 9 (20.93%) | 0.046 | |
Old myocardial infarction | 59 (34.50%) | 42 (32.81%) | 17 (39.53%) | 0.422 | |
Percutaneous intervention | 26 (15.20%) | 17 (13.28%) | 9 (20.93%) | 0.227 | |
Preoperative angina pectoris | 154 (90.06%) | 113 (88.28%) | 41 (95.35%) | 0.180 | |
Medications at baseline | |||||
Beta-blockers | 99 (57.89%) | 75 (58.59%) | 24 (55.81%) | 0.749 | |
ACEI/ARB | 44 (25.73%) | 30 (23.44%) | 14 (32.56%) | 0.237 | |
Antiplatelets | 94 (54.97%) | 71 (55.47%) | 23 (53.49%) | 0.821 | |
Diuretics | 15 (8.77%) | 9 (7.03%) | 6 (13.95%) | 0.165 | |
Laboratory exam | |||||
White blood cell count, 10 |
6.61 |
6.70 |
6.34 |
0.270 | |
Hemoglobin, g/dL | 138.12 |
139.59 |
133.72 |
0.069 | |
Platelet count, 10 |
216.00 (175.00–257.00) | 219.50 (174.75–261.25) | 205.00 (175.00–246.00) | 0.139 | |
Creatinine, |
86.29 |
86.18 |
86.62 |
0.883 | |
Glucose, mmol/L | 5.46 (3.59–13.24) | 5.46 (3.59–13.24) | 5.41 (4.04–8.20) | 0.205 | |
Glycated hemoglobin | 6.61 |
6.65 |
6.50 |
0.510 | |
High-density lipoprotein, mmol/L | 1.10 |
1.09 |
1.11 |
0.897 | |
Low-density lipoprotein, mmol/L | 2.13 (0.93–5.71) | 2.20 (0.93–5.71) | 1.96 (1.12–4.36) | 0.261 | |
Total cholesterol, mmol/L | 3.95 |
4.01 |
3.76 |
0.204 | |
NT-proBNP, pg/mL | 153.90 (58.40–543.95) | 118.50 (49.63–329.47) | 578.95 (211.55–1233.40) | ||
Angiographic findings | |||||
LM | 59 (34.50%) | 44 (34.38%) | 15 (34.88%) | 0.952 | |
LAD | 135 (78.95%) | 100 (78.12%) | 35 (81.40%) | 0.649 | |
LCX | 147 (85.96%) | 107 (83.59%) | 40 (93.02%) | 0.124 | |
RCA | 153 (89.47%) | 113 (88.28%) | 40 (93.02%) | 0.381 | |
Intraoperative off-pump | 74 (43.27%) | 56 (43.75%) | 18 (41.86%) | 0.829 | |
Number of grafts, n | 3.19 |
3.16 |
3.28 |
0.472 | |
POAF | 29 (16.96%) | 20 (15.62%) | 9 (20.93%) | 0.423 | |
In-hospital day, n | 16.08 |
15.60 |
17.49 |
0.097 | |
Medication at discharge | |||||
Beta-blockers | 114 (66.67%) | 85 (66.41%) | 29 (67.44%) | 0.901 | |
ACEI/ARB | 50 (29.24%) | 37 (28.91%) | 13 (30.23%) | 0.869 | |
Antiplatelets | 168 (98.25%) | 126 (98.44%) | 42 (97.67%) | 0.742 | |
Diuretics | 57 (33.33%) | 39 (30.47%) | 18 (41.86%) | 0.170 | |
NYHA, New York Heart Association; ACEI/ARB, angiotensin-converting enzyme inhibitors/angiotensin II receptor antagonists; NT-proBNP, N-terminal pro-brain natriuretic peptide; LM, left main coronary artery; LAD, left anterior descending branch; LCX, left circumflex branch; RCA, right coronary artery; POAF, postoperative atrial fibrillation. |
The mean LVEF was 58.38
Variable | Total | Control group | Mild MR group | p | ||
(n = 171) | (n = 128) | (n = 43) | ||||
LVEF, % | 58.38 |
61.21 |
49.96 |
|||
LVGLS, % | –11.82 |
–12.58 |
–9.49 |
0.005 | ||
iLVEDd, mm/m |
28.47 |
27.59 |
31.10 |
|||
iLVESd, mm/m |
20.54 |
19.00 |
24.08 |
|||
iLVEDV, mL/m |
69.32 |
64.55 |
88.15 |
|||
iLVESV, mL/m |
30.62 |
25.60 |
50.44 |
|||
iSV, mL/m |
38.69 |
38.94 |
37.70 |
0.570 | ||
IVSd, mm | 9.89 |
10.04 |
9.44 |
0.035 | ||
LVPW, mm | 9.17 |
9.22 |
9.02 |
0.354 | ||
RWT | 0.37 |
0.38 |
0.34 |
|||
LVMI, g/m |
98.96 |
95.48 |
109.32 |
0.005 | ||
E/A | 1.19 |
1.28 |
1.17 |
0.401 | ||
E/e’ | 10.89 |
10.54 |
10.91 |
0.932 | ||
Mitral apparatus | ||||||
MA diameter, mm | 19.32 |
19.04 |
20.18 |
|||
IPMD, mm | 22.38 |
22.10 |
23.21 |
0.001 | ||
Aortic values | ||||||
Ao Ann, mm | 22.13 |
22.14 |
22.12 |
0.973 | ||
Ao Asc, mm | 32.99 |
32.65 |
34.00 |
0.118 | ||
Ao SV, mm | 32.78 |
32.71 |
32.98 |
0.711 | ||
AR | 0.072 | |||||
155 (90.64%) | 119 (92.97%) | 36 (83.72%) | ||||
mild | 16 (9.36%) | 9 (7.03%) | 7 (16.28%) | |||
Left atrial values | ||||||
LA dimension, mm | 36.82 |
36.06 |
39.07 |
|||
LAVi, mL/m |
31.34 |
29.73 |
37.49 |
0.013 | ||
LASr, % | 22.70 |
24.44 |
17.45 |
0.008 | ||
LAScd, % | –14.32 |
–15.16 |
–11.76 |
0.027 | ||
LASct, % | –9.23 (–15.75 to –0.79) | –9.50 (–16.56 to –1.09) | –6.06 (–13.23 to –0.75) | 0.049 | ||
Right ventricular values | ||||||
RVD, mm | 22.97 |
23.05 |
22.74 |
0.537 | ||
MPA, mm | 23.24 |
23.20 |
23.37 |
0.707 | ||
RVGLS, % | –12.43 |
–12.78 |
–11.37 |
0.264 | ||
RVFWS, % | –15.47 |
–15.80 |
–14.45 |
0.410 | ||
TR | ||||||
149 (87.13%) | 120 (93.75%) | 29 (67.44%) | ||||
mild | 22 (12.87%) | 8 (6.25%) | 14 (32.56%) | |||
LVEF, left ventricular ejection fraction; LVGLS, LV global longitudinal strain; iLVEDd, indexed LV end-diastolic dimension; iLVESd, indexed LV end-systolic dimension; iLVEDV, indexed LV end-diastolic volume; iLVESV, indexed LV end-systolic volume; iSV, indexed stroke volume; LVMI, indexed LV mass; RWT, relative wall thickness; IVSd, interventricular septum thickness; LVPW, LV posterior wall thickness; MA, mitral annular; IPMD, interpapillary muscle distance; LA, left atrial; LAVi, LA volume index; LASr, LA reservoir strain; LAScd, LA conduit strain; LASct, LA contraction strain; RVD, right ventricular dimension; MPA, main pulmonary artery; RVGLS, RV global longitudinal strain; RVFWS, RV free wall strain; TR, tricuspid regurgitation. |
LVGLS, LASr, LAScd and LASct were lower in the mild MR group (p
Of the 128 patients in the control group, MR had progressed in 16 patients (12.50%) at one year after surgery. Of the 43 patients, MR had regressed in 21 patients (48.84%) and persisted in 22 patients (51.16%).
In this study, there were 37 individuals describing the change in MR after 1-year follow-up (Tables 3,4). 112 individuals (white form) remained without MR (reference group), 16 participants (red form) progressed to mild MR from the control group (worsening group), and 21 individuals (green form) who regressed from mild MR (improvement group). Furthermore, 22 individuals (yellow form) who remained in the mild MR (persistence group).
Preoperative MR | MR 1-year after surgery | |
None | Mild | |
None (n = 128) | 87.50% (n = 112) | 12.50% (n = 16) |
Mild (n = 43) | 48.84% (n = 21) | 51.16% (n = 22) |
White form: individuals without MR or less than mild MR at baseline, who
remained in the same pattern (reference group); Yellow form: individuals with mild MR at baseline who persisted (persistence group); Green form: individuals who reverted to no MR or less than mild MR from mild MR at baseline (improvement group); Red form: individuals who developed to mild MR from no MR or less than mild MR at baseline (worsening group). |
Variables | Reference group | Worsening group | Persistence group | Improvement group | p | ||
(n = 112) | (n = 16) | (n = 22) | (n = 21) | ||||
LVEF, % | 60.78 |
55.88 |
54.33 |
56.10 |
0.001 | ||
LVGLS, % | –13.88 |
–9.35 |
–11.64 |
–11.61 |
0.013 | ||
iLVEDd, mm/m |
27.07 |
28.22 |
30.85 |
27.36 |
|||
iLVESd, mm/m |
18.04 |
19.43 |
22.16 |
17.45 |
0.027 | ||
iLVEDV, mL/m |
61.65 |
72.36 |
76.85 |
72.64 |
0.014 | ||
iLVESV, mL/m |
24.93 |
32.74 |
36.27 |
34.72 |
0.018 | ||
iSV, mL/m |
37.04 |
39.62 |
42.13 |
39.37 |
0.008 | ||
IVSd, mm | 9.94 |
9.21 |
9.85 |
10.25 |
0.239 | ||
LVPW, mm | 9.15 |
8.65 |
8.83 |
9.29 |
0.282 | ||
RWT | 0.38 |
0.36 |
0.34 |
0.38 |
0.120 | ||
LVMI, g/m |
90.95 |
99.57 |
105.76 |
97.27 |
0.021 | ||
E/A | 1.21 |
1.47 |
1.44 |
1.33 |
0.322 | ||
E/e’ | 9.36 |
12.42 |
12.18 |
11.89 |
0.597 | ||
Mitral apparatus | |||||||
MA diameter, mm | 18.91 |
19.82 |
20.53 |
19.67 |
|||
IPMD, mm | 21.87 |
23.16 |
23.38 |
22.84 |
|||
Aortic values | |||||||
Ao Ann, mm | 21.68 |
20.76 |
21.48 |
21.69 |
0.311 | ||
Ao Asc, mm | 33.00 |
33.18 |
32.05 |
34.06 |
0.396 | ||
Ao SV, mm | 32.76 |
30.81 |
32.05 |
33.69 |
0.138 | ||
AR | 0.008 | ||||||
106 (94.64%) | 13 (81.25%) | 16 (72.73%) | 21 (100.00%) | ||||
mild | 6 (5.36%) | 3 (18.75%) | 6 (27.27%) | - | |||
Left atrial values | |||||||
LA dimension, mm | 37.92 |
41.76 |
40.94 |
39.86 |
0.005 | ||
LAVi, mL/m |
28.58 |
36.19 |
41.10 |
31.18 |
0.020 | ||
LASr, % | 23.89 |
15.81 |
18.51 |
20.38 |
0.033 | ||
LAScd, % | –14.22 |
–11.58 |
–11.56 |
–12.21 |
0.280 | ||
LASct, % | –9.81 (–15.60 to –4.29) | –5.20 (–8.68 to –2.54) | –8.74 (–13.38 to –2.01) | –10.54 (–13.70 to –0.03) | 0.187 | ||
Right ventricular values | |||||||
RVD, mm | 22.31 |
22.66 |
21.02 |
22.53 |
0.254 | ||
MPA, mm | 22.54 |
22.59 |
22.37 |
23.28 |
0.645 | ||
RVGLS, % | –10.05 |
–10.03 |
–11.29 |
–10.37 |
0.892 | ||
RVFWS, % | –9.90 |
–9.11 |
–9.76 |
–9.28 |
0.921 | ||
TR | |||||||
105 (93.75%) | 6 (37.50%) | 10 (45.45%) | 19 (90.48%) | ||||
mild | 7 (6.25%) | 10 (62.50%) | 12 (54.55%) | 2 (9.52%) |
Table 5 reported the results from the univariate and multivariate logistic
regression analysis. In multivariate analysis, LVEF (OR = 0.91 [95% CI:
0.84–1.00]; p = 0.042) and LAVi (OR = 1.17 [95% CI: 1.00–1.37];
p = 0.045) were associated with an increased risk of developing MR
(worsening group) (p
Variable | Worsening group (n = 16) | Improvement group (n = 21) | ||||||
Univariate analysis | Multivariate analysis | Univariate analysis | Multivariate analysis | |||||
OR (95% CI) | p | OR (95% CI) | p | OR (95% CI) | p | OR (95% CI) | p | |
Age, yrs | 1.13 (1.04, 1.22) | 0.003 | 0.99 (0.91, 1.06) | 0.693 | ||||
Female | 2.76 (0.90, 8.47) | 0.076 | 0.75 (0.17, 3.31) | 0.707 | ||||
NYHA functional class | 1.71 (0.70, 4.13) | 0.237 | 0.75 (0.27, 2.15) | 0.598 | ||||
LM occlusion | 2.11 (0.73, 6.08) | 0.166 | 0.26 (0.06, 1.03) | 0.056 | 0.03 (0.00, 0.55) | 0.018 | ||
LVEF, % | 0.94 (0.87, 1.00) | 0.064 | 0.91 (0.84, 1.00) | 0.042 | 1.02 (0.97, 1.07) | 0.474 | ||
iLVEDD, mm/m |
1.03 (0.87, 1.22) | 0.716 | 0.89 (0.77, 1.02) | 0.094 | 0.87 (0.70, 1.08) | 0.214 | ||
LAVi, mL/m |
1.16 (1.01, 1.32) | 0.030 | 1.17 (1.00, 1.37) | 0.045 | 0.89 (0.74, 1.05) | 0.170 | ||
RVD, mm | 0.75 (0.60, 0.94) | 0.013 | 0.83 (0.65, 1.07) | 0.153 | 1.03 (0.80, 1.34) | 0.813 | 0.84 (0.56, 1.28) | 0.428 |
MA diameter, mm | 1.43 (1.01, 2.02) | 0.043 | 1.55 (1.01, 2.38) | 0.043 | 0.90 (0.67, 1.22) | 0.512 | 0.54 (0.25, 1.19) | 0.128 |
IPMD, mm | 1.78 (1.19, 2.64) | 0.005 | 2.06 (1.32, 3.21) | 0.001 | 0.79 (0.53, 1.17) | 0.238 | 0.71 (0.31, 1.60) | 0.404 |
This study showed that regurgitation disappeared in the 48.84% patients with mild MR, while 12.50% progressed to mild MR from no or trace regurgitation one year after surgery. Consistent with previous studies, MA diameter and IPMD were associated with development of mild MR. Furthermore, LAVi has the potential for predicting the change of MR on follow-up, meanwhile preoperative left main coronary artery occlusion may impede the improvement from mild MR.
The post MI remodeling in LV composition, geometry and function is accompanied with inflammatory changes within the MI region and followed by myocardial hypertrophy, progressive cavity dilation and contractile dysfunction [17, 18]. The extent of ventricular dilation is directly related to the magnitude of the initial myocardial damage, but subsequent changes in ventricular geometry may also be associated with the effect of the tissue healing process, leading to further hemodynamic consequences, including more ischemic MR [19]. A mild degree of ischemic MR is often concerned for its progression to heart failure and increases short- or long-term mortality [20]. The study observed more than a quarter individual with mild MR at baseline, with significant lower LVEF and LVGLS. Previous studies have shown that baseline MR is associated with worse LV function, greater LV enlargement and chamber distortion after high-risk MI [21]. Otsuji et al. [22] found that global contractile dysfunction leads to functional MR especially in presence of a dilated left ventricle. Kim et al. [23] reported IPMD were increased significantly in patients with FMR than in those without FMR, and was the major determinant of mitral tenting volume and FMR severity. Consistent with previous studies, we observed significant increases in LV end-systolic and end-diastolic volumes and more TR occurred, with greater MA diameter and IPMD in patients with mild MR.
LV and LA function are tightly interdependence, and LV remodeling affects LA structure and function, which plays a key role in maintaining optimal cardiac performance [24, 25]. Previous studies showed that subtle LV remodeling and dysfunction lead to progression of regurgitation and LA remodeling, meanwhile MR is a cause of progressive LA impairment and eventually LV dysfunction [26, 27]. Consistent with these studies, we observed increased LA dimension and volume, and impaired LA reservoir, conduit and pump function in the mild MR group. Cameli et al. [28] reported a compensatory increase of LA strain was observed for patients with mild MR and a progressive impairment in those with moderate or severe MR. This controversial result may be caused by different aetiology of MR since the previous study included only organic MR, which was excluded in this study. As well-known, the association between MR and LA remodeling was common in moderate to severe MR, while the study suggested a substantial LA maladaptive process also in the early stage of functional MR.
CABG surgery is an effective common revascularization treatment for severe coronary artery disease to reduce the risk of sudden cardiac death and improve myocardial function [12]. Functional MR is commonly observed after MI and an independent predictor of mortality and cardiovascular morbidity [13]. CABG companied with mitral valve surgery may improve left ventricular performance, reverse left ventricular remodeling and then provide a more durable correction of moderate IMR [14]. However, mild MR is often overlooked and the dynamic changes of MR are relatively scarce in patients undergoing CABG surgery over time. In this study, patients with mild MR at baseline showed different trends on follow-up, about half regressed from mild MR and the rest remained in mild MR. LV remodeling increases annular tethering force and LV dysfunction decreases closing force, together leading to incomplete closure of the mitral valve [29]. MR regression indicates that effective revascularization promotes reverse remodeling, suggesting reversible ischemia rather than nonviable scar formation in MI region, while preoperative left main coronary artery occlusion may impede the process. We also found that one in eight individuals without MR at baseline progressed to mild MR on follow-up. Older age and lower LVEF were associated with this development. Further observations in our present analysis, LA volume could predict alterations in MR and larger LAVi was associated with progression to mild MR. Generally, LA is believed to play a role as cushion between the mitral valve or left ventricle and the pulmonary circulation and LV remodeling after MI directly impacts LA function and structure [26]. Maria et al. [30] reported patients with mild or moderate MR displayed greater LA myopathy, evidenced by worse LA remodeling and dysfunction, which tended to be associated with adverse outcomes. Tourneau et al. [10] found that greater LAVi incur excess mortality and frequent cardiac events, which is a strong and independent predictor of mitral valve surgery results of patients with chronic organic MR. Our results are in line with previous study, showing significant remodeling and impaired contractile function in patients with progressed MR after isolated CABG. This is the first time to provide new insights by evaluating the relationship between LA remodeling and dysfunction and functional MR following isolated CABG and the current data indicate that greater LA volume is associated with the presence of mild MR on 1-year follow-up. Thus, larger proportion of individuals and longer period of follow-up are required to observe such a transition and subsequent dynamic changes in MR.
Several limitations should be mentioned. First, it was performed with a relatively small sample size and restricted duration of follow-up time. Second, the study was a single-center study, which may influence the generalizability of its results. Third, this study excluded patients with poor quality images, which might cause selection bias. Thus, a multicenter study, in larger sample size and longer follow-up period, will be needed.
Patients with mild SMR after MI had LV and LA dysfunction, and about half regressed on follow-up following isolated CABG, while preoperative left main coronary artery occlusion may impede the improvement. One in eight individuals without MR at baseline progressed to mild MR on follow-up and LA volume has the potential for predicting this process.
HanW, HaoW—Conceptualization; HanW, BZ, HaoW—Methodology; HanW, ZHZ—Data acquisition, analysis, and interpretation; HanW—Writing original draft preparation; HanW, WCW—Writing, review and editing; HanW, HaoW—Supervision.
All participants provided their informed consent for inclusion before they participated in the study. The study was conducted in accordance with the Declaration of Helsinki, and the protocol was approved by the Ethics Committee of Fuwai hospital (2021-HG06).
We gratefully acknowledge all individuals who participated in this study. We thank all members who contributed to the study and all the peer reviewers for their opinions and suggestions.
This research received no external funding.
The authors declare no conflict of interest.
See Table 6.
Variable | Interobserver | Intraobserver | ||
ICC | p | ICC | p | |
LVGLS | 0.952 | 0.982 | ||
LASr | 0.946 | 0.973 | ||
LAScd | 0.931 | 0.961 | ||
LASct | 0.933 | 0.934 | ||
RVGLS | 0.899 | 0.921 | ||
RVFWS | 0.896 | 0.908 | ||
ICC, intraclass correlation coefficient; LVGLS, left ventricular global longitudinal strain; LASr, left atrial reservoir strain; LAScd, left atrial conduit strain; LASct, left atrial contraction strain; RVGLS, right ventricular global longitudinal strain; RVFWS, right ventricular free wall strain. |