Optimal timing of surgery and analysis of prognostic factors for myocardial infarction complicated by ventricular septal rupture

Abstract

Background

The optimal surgical timing for ventricular septal rupture (VSR) complicating acute myocardial infarction (MI) remains controversial, and evidence on safe bridging strategies to delay surgery is limited. This study sought to investigate the optimal timing for surgical treatment and to identify factors influencing postoperative mortality.

Methods

A retrospective analysis was conducted on the clinical data of 138 patients who underwent surgical repair for post-MI VSR at Beijing Anzhen Hospital between January 2008 and June 2025. The study aimed to determine the optimal surgical timing and to identify the factors associated with postoperative mortality using least absolute shrinkage and selection operator (LASSO) regression.

Results

We included 138 patients (87 men; mean age 64.8±9.4 years). Perioperative mortality was 17.3% (24/138). Surgery performed on or after day 8 following VSR was associated with lower perioperative mortality. LASSO and multivariable logistic regression identified opened IRA and VSR-to-surgery ≥8 days as independent protective factors. A LASSO regression analysis of the preoperative variables identified preoperative opened by percutaneous infarct-related artery (IRA) and a VSR-to-surgery interval of ≥8 days as independent factors associated with postoperative mortality. Further analysis revealed that an opened IRA was associated with a significantly increased likelihood of survival to ≥8 days (P=0.046). Regardless of whether opened IRA was performed before or after VSR, most patients survived to undergo surgery beyond day 8 (72.5% vs. 86.5%, P=0.13), and the opened IRA timing (pre- or post-VSR) was not associated with perioperative mortality. With a median follow-up of 6.5 years (range, 0.1–16.5 years), the cumulative survival rates at 2, 5, 8, and 10 years were 83.5%, 78.5%, 70%, and 67.5%, respectively.

Conclusions

A VSR-to-surgery interval of ≥8 days and preoperative opened IRA are critical factors influencing postoperative mortality. Surgery performed on or after day 8 following VSR was associated with lower mortality, and preoperative opened IRA may facilitate patient survival until the optimal surgical window.

Highlight box.

Key findings

• In this single-center retrospective cohort of 138 post-myocardial infarction (MI) ventricular septal rupture (VSR) patients undergoing surgical repair, 24 perioperative deaths occurred. Perioperative mortality was lowest when surgery was performed on or after day 8 following VSR. Multivariable analysis identified opened infarct-related artery (IRA) and a VSR-to-surgery interval ≥8 days as independent factors associated with lower postoperative mortality. Opened IRA also increased the likelihood of surviving to the optimal surgical window; however, the opened IRA timing (pre- vs. post-VSR) did not significantly affect perioperative mortality.

What is known, and what is new?

• The surgical repair of post-MI VSR carries a high risk of mortality, and controversy continues as to the optimal timing of the operation.

• Our findings suggest that preoperative opened IRA may serve as a bridging strategy, increasing the likelihood of survival to a safer operative window rather than functioning solely as a revascularization measure.

What is the implication, and what should change now?

• The study findings support a risk-adapted, heart-team approach for the management of post-MI VSR. When feasible, opened IRA may serve as a bridging strategy to stabilize hemodynamics and enable patients to undergo surgery on or after day 8 following VSR. However, urgent mechanical support and timely repair should remain the priorities in unstable patients.

Introduction

Ventricular septal rupture (VSR) is a rare but often fatal complication following acute myocardial infarction (AMI). Advances in pharmacological therapy, percutaneous interventions, and surgical techniques have improved overall outcomes after myocardial infarction (MI); however, patients with large transmural infarctions or delayed revascularization remain at risk of VSR. Recent studies have reported an incidence of post-MI VSR ranging from 0.17% to 0.44% (1-3), with no significant change in incidence over the past two decades (4).

The mortality rate of VSR following AMI is extremely high. With conservative management, most patients experience unpredictable hemodynamic deterioration within days to weeks of VSR onset, with mortality approaching 100% (2). Given the limited efficacy of medical therapy alone, surgical intervention is considered the definitive treatment for VSR; however, the optimal surgical timing remains highly debated (2-3,5-7). Previous studies have reported an overall 30-day postoperative mortality rate of 42.9%, with rates of 54.1% for surgery performed within 1–7 days of VSR, 30% for surgery performed within 8–21 days, and 10% for surgery performed after 21 days (8). Delayed surgery is associated with reduced operative mortality; however, 24% of patients die within the first week while awaiting surgery, and 80–94% die within one month (9,10). Further, even hemodynamically stable patients may deteriorate abruptly during the waiting period, leading to significantly higher mortality when emergency or salvage surgery is required (11).

Therefore, this study aimed to analyze the optimal surgical timing, identify factors influencing surgical mortality, and explore safe bridging strategies to a more favorable operative window. We present this article in accordance with the STROBE reporting checklist (available at https://cdt.amegroups.com/article/view/10.21037/cdt-2026-1-0080/rc).

Methods

Study population and clinical data

Clinical data were retrospectively collected from 138 patients diagnosed with MI complicated by VSR who underwent surgical repair at Beijing Anzhen Hospital between January 2008 and June 2025.

Inclusion criteria

The inclusion criteria were as follows:

1. A diagnosis of AMI according to established criteria (12), defined as elevated cardiac troponin values above the 99th percentile upper reference limit, with clinical evidence of myocardial ischemia;

2. Echocardiographic evidence of ventricular septal discontinuity, or left ventriculography demonstrating left-to-right shunt; and

3. Receipt of surgical intervention.

Exclusion criteria

The exclusion criteria were as follows:

1. MI complicated by other mechanical complications, such as mitral papillary muscle rupture or free wall rupture;

2. A history of interventional VSR closure; and/or

3. A life expectancy of <1 year.

Study design and methodology

A single-center, observational, retrospective cohort study was conducted. The primary study objectives were to determine the optimal timing of VSR surgery, identify the factors associated with perioperative mortality, and explore strategies to safely bridge patients to a more appropriate surgical window. Perioperative mortality was defined as death within 30 days of surgery.

Data, including baseline characteristics, echocardiographic findings, coronary angiography results, surgical details, and postoperative complications, were collected. Follow-up was conducted via outpatient visits, telephone calls, or WeChat, primarily to assess all-cause mortality. All data were obtained from the electronic database of Beijing Anzhen Hospital, with data entry performed by trained staff. There are no missing data in this study.

This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study protocol was approved by the Institutional Review Board of Beijing Anzhen Hospital (ethics approval No. 2019070X). The requirement for informed consent was waived due to the retrospective and observational nature of this study, which did not require the collection of specific information about patients.

Preoperative management

Upon diagnosis of VSR, hemodynamically stable patients with a previously opened infarct-related artery (IRA) on angiography awaited surgery. If the IRA was unopened, stable patients still awaited surgery, while unstable patients received mechanical circulatory support [e.g., intra-aortic balloon pump (IABP)] before surgery. Patients without prior angiography underwent immediate coronary angiography to identify the IRA. Opened IRA was attempted using thrombus aspiration or balloon angioplasty, avoiding stent implantation to minimize bleeding risks associated with dual antiplatelet therapy. For hemodynamically unstable patients, IABP support was initiated, with escalation to veno-arterial extracorporeal membrane oxygenation (VA-ECMO) or intubation if necessary. The goal of opened IRA was to salvage jeopardized myocardium, prevent VSR expansion, and improve cardiac function.

The definition of “opened IRA” was provided in the Methods section. Opened IRA was defined as the successful restoration of antegrade flow in the IRA to thrombolysis in myocardial infarction (TIMI) grade 3, confirmed by post-procedural angiography. Killip class was assigned at the time of hospital admission based on clinical signs of heart failure and hemodynamic status, according to the standard Killip classification (I–IV).

Surgical technique

Surgery was performed via median sternotomy with standard cardiopulmonary bypass. Left ventriculotomy through an aneurysm was chosen when present; otherwise, a right ventriculotomy near the VSR was performed. To reduce the risk of residual shunt, necrotic tissue around the VSR was debrided. Repair was performed using a double-patch “sandwich” technique, with patches sutured on both sides of the septum and adhesive (medical glue) applied between them (13); alternatively, a small patch was used to close the defect while a larger patch was used to remodel the left ventricle (14), or a small patch was used to close the defect with two larger patches excluding both ventricles (15). Fragile areas were reinforced with interrupted sutures, and the left ventriculotomy was closed with felt pledges. Concomitant coronary artery bypass grafting (CABG) was performed on the IRA and other stenotic coronary arteries as indicated (16).

Statistical analysis

Normally distributed continuous variables are presented as mean ± standard deviation and were compared using the Student’s t-test. Non-normally distributed variables are presented as median [interquartile range (IQR)] and were compared using the Mann-Whitney U test. Categorical variables are expressed as frequencies (percentages) and were compared using the Chi-squared test or Fisher’s exact test. Ordinal data were analyzed using rank-sum tests. Least absolute shrinkage and selection operator (LASSO) regression and binary logistic regression were employed to identify risk factors for postoperative mortality. All tests were two-tailed, with a P value <0.05 considered statistically significant. Analyses were performed using SPSS version 23.0 (IBM Corp.) and R software version 4.0.2.

Results

Patient characteristics and surgical overview

Baseline demographics and clinical profile

During the initial screening, 183 patients diagnosed with post-MI VSR at Beijing Anzhen Hospital between January 2008 and June 2025 were identified. After applying the predefined inclusion and exclusion criteria, 45 patients were excluded for the following reasons: eight had concomitant mechanical complications (mitral papillary muscle rupture or free wall rupture) in addition to VSR; 12 had a history of interventional VSR closure prior to surgical repair; five had a life expectancy of <1 year due to pre-existing malignancies or end-stage organ failure; and 20 refused the surgery. The remaining 138 patients met all the inclusion criteria and were included in the final analysis. A flow diagram detailing patient screening, inclusion, and exclusion is shown in Figure 1.

Figure 1.

Patient screening flowchart. MI, myocardial infarction; VSR, ventricular septal rupture.

The study included 138 patients (87 male, 51 female) with a mean age of 64.8±9.4 years. Forty-five patients (32.6%) had a history of MI, 72 (52.1%) had hypertension, 45 (32.6%) had diabetes, and 66 (47.8%) were smokers. Preoperative coronary angiography identified the left anterior descending artery as the IRA in 124 patients (89.8%). Single-vessel disease was present in 47 patients (34.1%), double-vessel disease in 50 patients (36.2%), and triple-vessel disease in 41 patients (29.7%). Preoperative echocardiography showed a mean left ventricular ejection fraction of 47.8%±9.5%, and 107 patients (77.5%) had a concomitant ventricular aneurysm.

Treatment course and perioperative outcomes

Preoperatively, 52 patients (37.6%) received IABP, five (3.6%) received ECMO, 21 (15.2%) required intubation, and six (4.3%) required continuous renal replacement therapy (CRRT). Thirty-eight patients underwent repair within 7 days of VSR, with 15 perioperative deaths (39.4%); and 100 patients underwent surgery after day 7 following VSR, with 9 perioperative deaths (9.0%). Concomitant procedures included CABG in 111 patients (80.4%), ventricular aneurysm resection in 106 patients (76.8%), mitral valve surgery in 20 patients (14.4%), and tricuspid annuloplasty in 23 patients (16.6%).

Perioperative mortality

Among the 24 patients who died during the perioperative period, the median time from surgery to death was 18 days (IQR, 10–25 days). Among them, two patients (8.3%) died within 48 hours after surgery, five (20.8%) died between the 3rd and 7th day, and 17 (70.8%) died after day 7 but still within the same hospitalization period.

Causes of death

The main causes of perioperative death were as follows: refractory low cardiac output syndrome: eight patients (33.3%); multiple organ failure (including renal failure, liver failure, and respiratory failure): six patients (25.0%); severe septic shock: five patients (20.8%); residual shunt with refractory heart failure: two patients (8.3%); cerebrovascular accident/stroke: one patient (4.2%); and limb ischemic necrosis caused by IABP: two patients (8.3%).

Perioperative data analysis

Basic outcomes and group comparisons

Among the 138 patients, 24 died during the perioperative period, resulting in a perioperative mortality rate of 17.3%. Patients were classified into survival (n=114) and non-survival (n=24) groups based on their perioperative outcomes. An analysis of the relationship between VSR-to-surgery time and mortality indicated the lowest mortality when surgery was performed on or after day 8, with a perioperative mortality rate of 9% beyond day 8 (Figure 2).

Figure 2.

Time from VSR to surgery and corresponding mortality rate. VSR, ventricular septal rupture.

A comparison of the preoperative baseline characteristics revealed significant differences between the two groups in age, Killip class, time from AMI to surgery, time from VSR to surgery, and the proportion of patients with a VSR-to-surgery time ≥8 days (all P<0.05) (Table 1). A comparison of the laboratory indexes also revealed significant differences between the two groups in terms of white blood cell count, albumin, aspartate aminotransferase, and B-type natriuretic peptide (BNP) (all P<0.05), (Table 2).

Table 1. Comparison of preoperative general data between the survival and non-survival groups.

Variables	Survival group (N=114)	Non-survival group (N=24)	P value
Sex (male)	74 (64.91)	13 (54.17)	0.44
Age (years)	64.50 [57.25; 70.00]	71.00 [67.75; 71.75]	0.003
BSA (m2)	1.71 [1.59; 1.83]	1.72 [1.64; 1.78]	0.92
BMI (kg/m2)	24.22 [22.51; 25.95]	24.12 [22.38; 25.58]	0.68
SBP (mmHg)	109.52 [14.99]	107.88 [16.14]	0.65
DBP (mmHg)	70.00 [65.00; 80.00]	64.50 [61.75; 78.50]	0.24
Respiratory rates (breaths/min)	20.00 [19.00; 20.00]	20.00 [18.00; 22.00]	0.82
Heart rate (beats/min)	82.50 [80.00; 98.00]	84.50 [80.00; 104.50]	0.25
Temperature (℃)	36.50 [36.20; 36.60]	36.50 [36.38; 36.50]	0.75
Medical history
Hypertension	62 (54.39)	10 (41.67)	0.36
Diabetes	34 (29.82)	11 (45.83)	0.20
Smoking	56 (49.12)	10 (41.67)	0.66
MI history	37 (32.46)	8 (33.33)	>0.99
PCI history	26 (22.81)	6 (25.00)	>0.99
CVD	20 (17.54)	4 (16.67)	>0.99
COPD	13 (11.40)	2 (8.33)	>0.99
PVD	17 (14.91)	5 (20.83)	0.53
Physical status
Gastrointestinal bleeding	8 (7.02)	3 (12.50)	0.40
Killip class			0.01
I	12 (10.53)	1 (4.17)
II	63 (55.26)	8 (33.33)
III	25 (21.93)	5 (20.83)
IV	14 (12.28)	10 (41.67)
Emergency surgery	16 (14.04)	4 (16.67)	0.75
Acute left heart failure	24 (21.05)	10 (41.67)	0.06
Pulmonary infection	12 (10.53)	3 (12.50)	0.72
Advanced cardiac life support
CRRT	4 (3.51)	2 (8.33)	0.28
IABP	38 (33.33)	14 (58.33)	0.03
ECMO	3 (2.63)	2 (8.33)	0.20
Ventilator supporting	15 (13.16)	6 (25.00)	0.20
Opened IRA	72 (63.16)	5 (20.83)	<0.001
Pre-VSR opened IRA	39 (34.21)	1 (4.17)	0.007
Post-VSR opened IRA	33 (28.95)	4 (16.67)	0.32
Timing of operation
Days from MI to VSR	1.00 [0.00; 3.00]	2.00 [0.75; 4.00]	0.17
Days from MI to surgery	22.50 [11.25; 40.75]	10.00 [7.00; 18.50]	0.002
Days from VSR to surgery	20.00 [9.00; 39.00]	6.50 [5.75; 15.25]	<0.001
VSR-to-surgery interval ≥8 days	91 (79.82)	9 (37.50)	<0.001

Data are expressed as n (%), median [interquartile range], or mean [standard deviation]. BMI, body mass index; BSA, body surface area; COPD, chronic obstructive pulmonary disease; CRRT, continuous renal replacement therapy; CVD, cerebrovascular disease; DBP, diastolic blood pressure; ECMO, extracorporeal membrane oxygenation; IABP, intra-aortic balloon pump; IRA, infarct-related artery; MI, myocardial infarction; PCI, percutaneous coronary intervention; PVD, peripheral vascular disease; SBP, systolic blood pressure; VSR, ventricular septal rupture.

Table 2. Comparison of preoperative examination data between the survival and non-survival groups.

Variables	Survival group (N=114)	Non-survival group (N=24)	P value
Laboratory indexes
White blood cell (109/L)	7.57 [6.55; 10.04]	11.87 [8.33; 14.37]	<0.001
Hemoglobin (g/L)	127.45 [17.68]	122.88 [22.30]	0.35
Platelet (109/L)	207.50 [168.00; 269.00]	183.50 [138.00; 242.00]	0.19
Albumin (g/L)	37.36 [5.22]	33.71 [4.19]	0.001
Aspartate aminotransferase (U/L)	24.00 [18.00; 43.00]	29.50 [21.50; 283.50]	0.047
Alanine aminotransferase (U/L)	23.00 [15.00; 42.75]	27.50 [21.50; 95.25]	0.053
Creatinine (μmol/L)	93.25 [77.40; 117.30]	104.40 [80.52; 149.60]	0.21
Urea (mmol/L)	7.95 [6.35; 10.99]	9.98 [6.81; 18.95]	0.06
Troponin I (ng/mL)	0.91 [0.05; 2.28]	0.57 [0.09; 2.02]	>0.99
BNP (pg/mL)	699.25 [432.00; 1,314.25]	1,201.50 [922.50; 1,631.50]	0.009
pH value	7.44 [7.41; 7.46]	7.44 [7.43; 7.46]	0.35
Lactic acid (mmol/L)	1.70 [1.30; 2.30]	2.50 [1.40; 3.85]	0.08
Echocardiography
Anterior VSR	70 (61.40)	14 (58.33)	0.96
VSR diameter (mm)	11.00 [8.00; 17.00]	10.00 [8.75; 18.00]	0.90
Peak systolic velocity (cm/s)	342.00 [300.00; 405.00]	359.50 [303.00; 407.25]	0.56
Transseptal pressure gradient (mmHg)	45.50 [35.00; 65.50]	47.00 [35.75; 59.75]	0.65
LVA	87 (76.32)	20 (83.33)	0.63
LVA size (mm)	36.00 [29.00; 45.00]	39.00 [30.00; 42.75]	0.64
Thrombus in LVA	11 (9.65)	1 (4.17)	0.69
LVEDD (mm)	53.00 [49.00; 58.75]	51.00 [48.00; 55.25]	0.11
LVESD (mm)	37.00 [33.00; 40.00]	34.00 [32.00; 37.00]	0.09
Ejection fraction (%)	48.50 [40.00; 55.00]	47.00 [39.75; 55.00]	0.66
Mitral regurgitation			0.43
None	37 (32.46)	4 (16.67)
Mild	54 (47.37)	15 (62.50)
Moderate	16 (14.04)	4 (16.67)
Severe	7 (6.14)	1 (4.17)
Tricuspid regurgitation			0.28
None	32 (28.07)	3 (12.50)
Mild	54 (47.37)	12 (50.00)
Moderate	13 (11.40)	5 (20.83)
Severe	15 (13.16)	4 (16.67)
Pericardial effusion			0.63
None	80 (70.18)	15 (62.50)
Mild	32 (28.07)	9 (37.50)
Moderate	2 (1.75)	0
Pleural effusion	33 (28.95)	12 (50.00)	0.07
VSR dissection	11 (9.65)	1 (4.17)	0.69
Multiple VSR	8 (7.02)	1 (4.17)	>0.99
Coronary angiogram
LM	9 (7.89)	1 (4.17)	>0.99
LAD	100 (87.72)	24 (100.00)	0.12
LCX	46 (40.35)	11 (45.83)	0.78
RCA	71 (62.28)	14 (58.33)	0.89
Number of lesions			0.22
1	42 (36.84)	5 (20.83)
2	38 (33.33)	12 (50.00)
3	34 (29.82)	7 (29.17)

Continuous variables are expressed as median [interquartile range], and categorical variables are expressed as number (%). BNP, B-type natriuretic peptide; LAD, left anterior descending; LCX, left circumflex; LM, left main; LVA, left ventricular aneurysm; LVEDD, left ventricular end-diastolic diameter; LVESD, left ventricular end-systolic diameter; RCA, right coronary artery; VSR, ventricular septal rupture.

Intraoperative and postoperative parameters

A comparison of the intraoperative and postoperative data showed that the non-survival group had significantly longer ventilator times [53.00 (25.00; 135.62) vs. 147.25 (73.00; 291.25) h, P=0.002] and intensive care unit (ICU) stays [77.00 (44.08; 159.28) vs. 181.75 (75.15; 323.50) h, P=0.004]. The non-survival group also had higher rates of postoperative CRRT, IABP, and ECMO use (all P<0.05), as well as significantly higher incidences of pulmonary infections, tracheostomy, and reintubation (all P<0.05) (Table 3).

Table 3. Comparison of surgical and postoperative data between the survival and non-survival groups.

Variables	Survival group (N=114)	Non-survival group (N=24)	P value
LVA surgery	86 (75.44)	20 (83.33)	0.57
Mitral surgery	16 (14.04)	4 (16.67)	0.75
Tricuspid surgery	18 (15.79)	5 (20.83)	0.55
CABG	92 (80.70)	19 (79.17)	>0.99
Graft number	1.00 [1.00; 2.00]	1.50 [1.00; 2.00]	0.87
Operation time (h)	5.00 [4.18; 6.00]	6.00 [5.00; 7.00]	0.03
Ventilator time (h)	53.00 [25.00; 135.62]	147.25 [73.00; 291.25]	0.002
Time in ICU (h)	77.00 [44.08; 159.28]	181.75 [75.15; 323.50]	0.004
Cardiac tamponade	5 (4.39)	3 (12.50)	0.14
Residual shunt	14 (12.3)	2 (8.3)	0.84
CRRT	15 (13.16)	16 (66.67)	<0.001
IABP	48 (42.11)	19 (79.17)	0.002
ECMO	4 (3.51)	6 (25.00)	0.002
Pulmonary complications	12 (10.53)	12 (50.00)	<0.001
Tracheotomy	14 (12.28)	10 (41.67)	0.002
Re-tracheostomy	11 (9.65)	7 (29.17)	0.01

Data are expressed as n (%), median [interquartile range], or mean [standard deviation]. CABG, coronary artery bypass grafting; CRRT, continuous renal replacement therapy; ECMO, extracorporeal membrane oxygenation; IABP, intra-aortic balloon pump; ICU, intensive care unit; LVA, left ventricular aneurysm.

Variable selection using LASSO and logistic regression

A total of 40 preoperative candidate variables were entered into the LASSO regression model, including: age, sex, body mass index (BMI), body surface area (BSA), medical history [hypertension, diabetes, smoking, MI history, percutaneous coronary intervention (PCI) history, cerebrovascular disease (CVD), chronic obstructive pulmonary disease (COPD), and peripheral vascular disease (PVD)], gastrointestinal bleeding, Killip class, preoperative laboratory parameters (white blood cell count, hemoglobin, platelet, albumin, aspartate aminotransferase, alanine aminotransferase, creatinine, urea, troponin I, and BNP), echocardiographic parameters [anterior VSR, VSR diameter, peak systolic velocity, transseptal pressure gradient, ejection fraction, left ventricular end diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), mitral regurgitation, and tricuspid regurgitation], coronary angiographic findings (number of diseased vessels), and preoperative interventions (IABP, ECMO, CRRT, ventilator supporting, opened IRA status, and timing of operation).

The LASSO regression analysis of the preoperative baseline data identified opened IRA and a VSR-to-surgery time ≥8 days as independent factors associated with postoperative mortality (Figures 3-5). After the multivariable logistic regression model for a binary outcome, which included variables with P<0.05 in the univariate analysis, VSR-to-surgery time ≥8 days [odds ratio (OR) =0.156, 95% confidence interval (CI): 0.055–0.444, P<0.001], opened IRA (OR =0.214, 95% CI: 0.069–0.665, P=0.008), and age (OR =1.083, 95% CI: 1.012–1.158, P=0.02) remained independent factors associated with postoperative mortality, further validating the protective roles of opened IRA and delayed surgery (≥8 days).

Figure 3.

Distribution map of LASSO coefficients. Vertical dashed lines are drawn at the values selected by 10-fold cross-validation. The optimal λ-SE yields two predictor variables. LASSO, least absolute shrinkage and selection operator; SE, standard error.

Figure 4.

Cross-validation curve of LASSO regression. The dotted line on the left is λ min, and the dotted line on the right is λ-SE. Due to the small sample size in this study, the λ-SE on the right was selected as the final screening criterion. LASSO, least absolute shrinkage and selection operator; SE, standard error.

Figure 5.

Coefficient plots of the two variables affecting postoperative mortality. IRA, infarct-related artery; VSR, ventricular septal rupture.

Relationship between opened IRA, surgical timing, and perioperative mortality

Among patients undergoing surgery ≥8 days after VSR, the proportion with an opened IRA was significantly higher (79.2% vs. 63.9%, P=0.046), indicating that opened IRA was associated with an increased likelihood of survival to the optimal surgical window (Figure 6A). A comparison based on the timing of opened IRA relative to VSR showed that both pre- and post-VSR opened IRA were associated with survival to surgery ≥8 days in most patients (72.5% vs. 86.5%, P=0.13) (Figure 6B). Further, the timing of opened IRA (pre- vs. post-VSR) was not significantly associated with perioperative mortality (2.5% vs. 10.8%, P=0.13) (Figure 6C).

Figure 6.

Relationship between opened IRA, surgical timing, and perioperative mortality. (A) Opened IRA was associated with an increased proportion of patients surviving to surgery ≥8 days. (B) Both pre- and post-VSR opened IRA enabled most patients to survive to surgery ≥8 days. (C) The timing of opened IRA (pre- vs. post-VSR) was not significantly associated with perioperative mortality. IRA, infarct-related artery; VSR, ventricular septal rupture.

Follow-up results

All 114 surviving patients were followed for a median follow-up of 6.5 years (range, 0.1–16.5 years). During follow-up, 34 patients (29.8%) died. Cumulative survival rates at 2, 5, 8, and 10 years were 83.5%, 78.5%, 70%, and 67.5%, respectively (Figure 7).

Figure 7.

Survival curve of the 114 postoperative surviving patients. CI, confidence interval.

Discussion

This study identified surgical timing and preoperative opened IRA as modifiable factors significantly affecting postoperative mortality. Specifically, patients undergoing surgical repair on or after day 8 following VSR diagnosis experienced lower mortality. Preoperative opened IRA facilitated patient survival to this safer surgical window (≥8 days). These findings provide valuable insights into the perioperative management of VSR patients.

The optimal surgical timing for VSR remains contentious (2-3,5-7). Shortly after VSR, myocardial tissue is friable, increasing the risk of suture tear and residual shunt during repair. Conversely, delayed repair allows for fibrosis and scar formation at the rupture margins, providing more robust tissue for patch anchorage, and thereby reducing the risk of perioperative failure and mortality. Our findings support delaying surgery until at least day 8 after VSR. This is consistent with data from the Society of Thoracic Surgeons database, which reported a mortality rate of 54.1% for surgery performed within 7 days of VSR compared to 18.4% for surgery performed after 7 days (8), supporting an 8-day threshold. A literature review similarly reported mortality rates as high as 52% for surgery within 3 days of VSR, compared to 11% for delayed repair (17). Further, a multicenter observational study reported improved outcomes when surgery was performed from day 4 onward compared to within the first 24 hours (18), reinforcing the benefit of avoiding ultra-early surgery in eligible patients. Because this was a retrospective observational study, the independent effects of timing and baseline disease severity cannot be fully separated, and survival bias related surgical timing may be present.

Although delayed surgery reduces operative mortality, 24% of patients die within the first week while awaiting intervention (11,12). Our study demonstrated that preoperative opened IRA may safely bridge patients to the optimal surgical window. Restoration of flow in the IRA improves biventricular function, reduces ischemic burden, and stabilizes hemodynamics, thereby enabling patients to survive until a safer surgical window. For persistent hemodynamic instability, mechanical support with IABP and, if necessary, VA-ECMO, can be used (19). Kusumoto et al. reported that Impella may also be used for VSR (20) to “actively relieve the left ventricular load, reduce the wall stress, and strive for the repair opportunity”, thereby stabilizing patients and facilitating delayed surgical intervention; however, Impella cannot replace surgical radical treatment.

This study found that preoperative opened IRA was associated with more favorable outcomes, suggesting that it may represent a protective factor. This finding is biologically plausible: early restoration of IRA flow may attenuate ongoing ischemia in the peri-infarct border zone, limit infarct expansion, and improve perioperative myocardial perfusion, thereby creating a more favorable substrate for subsequent surgical repair or combined treatment strategies (21,22). Moreover, for patients with single-vessel disease, opening the IRA may obviate the need for simultaneous CABG (23).

The existing literature also supports a more cautious interpretation. Recent reviews emphasize that the timing of mechanical circulatory support, surgical repair, or percutaneous closure should be determined by the cardiac or shock team, rather than setting coronary reperfusion as a mandatory prerequisite (6). Previous surgical experience also suggests that VSR itself is a mechanical complication that requires urgent treatment, and any additional interventional steps may prolong the time window for definitive repair. Once in cardiogenic shock, patient prognosis is extremely poor (24). In addition, reperfusion may theoretically exacerbate myocardial edema, microvascular injury, and intramyocardial hemorrhage. In a necrotic and structurally fragile infarct zone, these changes may further compromise tissue integrity and complicate surgical suturing, particularly when the rupture margins remain friable (25).

Therefore, we suggest that preoperative opened IRA should be considered an individualized treatment option based on the hemodynamic status, coronary artery lesion complexity, and surgical timing, rather than a universally standardized strategy in VSR. Larger multicenter prospective studies are still needed to define the subgroups most likely to benefit and to determine the optimal timing of revascularization, thereby providing a stronger evidence base for the risk-adapted management of VSR.

Additionally, observational data indicate that incomplete revascularization is an independent predictor of 30-day mortality, highlighting the prognostic importance of the revascularization strategy (26). Previous studies have reported poor long-term outcomes in patients with triple-vessel disease after VSR repair (27), while concomitant CABG has been shown to improve prognosis (28). Our study showed favorable long-term survival rates (83.5%, 78.5%, 70%, and 67.5% at 2, 5, 8, and 10 years, respectively), potentially attributable to the high rate of concomitant CABG (80.4%). Therefore, concomitant CABG should be considered whenever feasible to improve long-term outcomes.

Intraoperative and postoperative variables were not included in the multivariable analysis for two primary reasons: first, the study aimed to preoperatively identify prognostic factors to guide surgical decision-making; second, all surgeries followed standardized techniques and protocols, minimizing technical variability and potential confounding bias.

Limitations

This was a single-center retrospective study and thus may be subject to selection bias. The sample size was limited due to the critical nature of post-MI VSR, with some patients dying before surgery could be performed. Future studies will involve continued data collection and further analysis.

Conclusions

Surgical timing and preoperative opened IRA are significant factors associated with postoperative mortality. Mortality decreases significantly when surgery is performed from day 8 after VSR onwards. Preoperative opened IRA may serve as a crucial bridging strategy by stabilizing hemodynamics and enabling patients to reach the optimal surgical window. These findings offer a novel treatment paradigm and may guide the perioperative management of patients with VSR, ultimately improving patient outcomes.

Supplementary

The article’s supplementary files as

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study protocol was approved by the Institutional Review Board of Beijing Anzhen Hospital (ethics approval No. 2019070X). The requirement for informed consent was waived due to the retrospective and observational nature of this study, which did not require the collection of specific information about patients.

Data Sharing Statement

Available at https://cdt.amegroups.com/article/view/10.21037/cdt-2026-1-0080/dss

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DOI: 10.21037/cdt-2026-1-0080