Published online Aug 19, 2026. doi: 10.5498/wjp.v16.i8.117122
Revised: April 20, 2026
Accepted: May 15, 2026
Published online: August 19, 2026
Processing time: 141 Days and 23.3 Hours
Medication compliance in patients with acute myocardial infarction (AMI) is often affected by negative emotions, hindering recovery.
To elucidate the effects of sertraline (STL) combined with psychological inter
A total of 133 patients with AMI + CAD visiting our hospital between December 2021 and December 2024 were enrolled, including 60 patients receiving psychological intervention alone (control group) and 73 receiving STL in addition to the same intervention (research group). Data on cardiac function [cardiac output (CO), stroke volume (SV), left ventricular ejection fraction (LVEF)], adverse mood Hamilton Anxiety/Depression Scale (HAMA/HAMD), resilience Conner-David
Posttreatment, the research group showed significantly higher CO (4.94 ± 1.04 L/minute vs 4.25 ± 1.48 L/minute), SV (53.89 ± 7.89 mL vs 49.32 ± 5.39 mL), LVEF (64.47% ± 6.80% vs 58.30% ± 6.33%), CD-RISC (82.68 ± 6.74 vs 74.75 ± 6.23), and SF-36 scores [physical functioning: 75.74 ± 7.81 vs 70.65 ± 6.47; social functioning: 76.34 ± 7.49 vs 72.35 ± 6.98; role-emotional: 78.53 ± 7.05 vs 72.32 ± 6.92; mental health: 82.00 (76.00, 87.00) vs 77.00 (74.00, 79.00)], and lower HAMA (12.86 ± 3.65 vs 17.87 ± 4.29), HAMD (10.11 ± 2.90 vs 15.63 ± 3.04), and PSQI component scores than the control group.
The results indicate that STL combined with psychological intervention improves cardiac function, resilience, mood, sleep, and quality of life in AMI patients with CAD.
Core Tip: Acute myocardial infarction (AMI) complicated by anxiety and depression adversely affects treatment compliance and smooth recovery. This study evaluated whether adding sertraline (STL) to psychological intervention can further improve heart function, mood, and resilience of such patients. The results indicate that STL combined with psychological intervention was more effective than psychological intervention alone in improving cardiac function, mood, resilience, sleep, and quality of life, supporting its clinical value in managing AMI patients with comorbid anxiety and depression.
- Citation: Chu LJ, Lv JN. Sertraline plus psychological intervention for acute myocardial infarction with anxiety-depression comorbidity: Cardiac function, adverse mood, and resilience impacts. World J Psychiatry 2026; 16(8): 117122
- URL: https://www.wjgnet.com/2220-3206/full/v16/i8/117122.htm
- DOI: https://dx.doi.org/10.5498/wjp.v16.i8.117122
Acute myocardial infarction (AMI), a coronary artery disease characterized by acute myocardial injury and ischemia, accounts for approximately 33.3% of global deaths[1,2]. In China alone, an estimated 500000 cases occur annually, with incidence continuing to rise[3].
Beyond its physical burden, AMI significantly impairs quality of life and life expectancy, often leading to psychological disorders, particularly anxiety and depression[4]. Comorbid anxiety and depression (CAD) not only compromise medi
Although standard treatments, including medication and/or surgery, improve survival, patients often continue to experienced reduced working ability and require lifelong secondary prevention medications[8].
Psychological intervention aims to improve mental health by alleviating negative emotions (e.g., anxiety and depression), enhancing well-being, promoting treatment compliance, and encouraging healthy behaviors[9]. Sertraline (STL), a selective serotonin reuptake inhibitor (SSRI), has demonstrated superior efficacy and safety among SSRIs, particularly in managing poststroke depression[10]. Shapiro et al[11] reported a > 85% tolerability in patients with major depressive disorder (MDD) post-AMI, along with significant improvements in mood and clinical outcomes.
Based on the findings, we hypothesized that STL combined with psychological intervention would provide greater clinical benefits-particularly in cardiac function, emotional status, and resilience-than psychological intervention alone in patients with AMI + CAD. This study was conducted to test this hypothesis and provide reliable evidence to inform clinical management.
This study included 133 patients with post-AMI CAD treated at our hospital between December 2021 and December 2024. Sixty patients received psychological intervention alone (control group), and 73 received additional STL (research group). The selection criteria were as follows.
Inclusion criteria: (1) Confirmed AMI diagnosis via coronary angiography[12]; (2) Age 18-80 years old; (3) New York Heart Association (NYHA) class II-IV[13]; (4) Cardiac troponin elevation > 99th percentile of the upper normal limit; (5) 14-item Hamilton Anxiety Rating Scale (HAMA-14) ≥ 14 and 17-item Hamilton Depression Rating Scale (HAMD-17) ≥ 17[14]; and (6) Normal cognition; and complete clinical data.
Exclusion criteria: (1) History of mental illness or antidepressant use within one month; preexisting anxiety and de
The control group received standard medical therapy, including statins, aspirin, clopidogrel, nitrates, β-blockers, and calcium channel antagonists, along with psychological intervention. Psychological intervention was conducted by trained psychological physicians from the hospital twice weekly (30 minutes/session), with continuous monitoring and timely counseling. Interventions included: (1) Awareness education on AMI pathogenesis, treatment, medical compliance, and proper use of medication to reduce patients’ fear and anxiety; (2) Psychological counseling through active communi
Cardiac function: Cardiac output (CO), stroke volume (SV), and left ventricular ejection fraction (LVEF) were assessed via echocardiography pre and postintervention.
Adverse mood: Patients underwent pre- and postintervention anxiety and depression measurements using HAMA-14 (score range 0-56) and HAMD-17 (score range 0-52), respectively. HAMA-14 is an observer-rated scale with 14 items scored 0-4; 0 indicates symptom free and 4 indicates extremely severe symptoms. HAMD-17 includes 17 items, with 9 scored on a 5-point scale (0-4, with 0 indicating no symptom and 4 indicating extremely severe symptoms) and 8 on a 3-point scale (0-2, with 0 indicating no symptom and 2 indicating severe symptoms). Higher scores indicate greater severity[15].
Resilience: Patients’ resilience levels pre- and postintervention were assessed using the Conner-Davidson Resilience Scale (CD-RISC; total score 0-100), including strength (8 items), tenacity (13 items), and optimism (4 items). Each item is scored from 0 to 4, with higher scores indicating greater resilience[16].
Sleep quality: Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI), comprising seven dimensions-sleep quality, latency, duration, efficiency, and disturbances, as well as hypnotic drug use and daytime dysfunction. Each dimension is scored from 0 to 3, totaling 21 points. Lower scores indicating better sleep quality[17].
Quality of life: Quality of life was assessed using the Short-Form 36 (SF-36). The scale has eight dimensions, with four selected for this study-physical functioning, social functioning, role-emotional, and mental health-with a total score of 0-100/dimension. Higher scores indicate better quality of life[18].
Continuous variables are presented as mean ± SD and were analyzed using independent and paired t-tests for between-group and within-group (pre- vs postintervention) comparisons, respectively. Categorical variables are expressed as n (%) and compared using the χ2 test. Statistical analyses were performed using SPSS 20.0, with P < 0.05 considered statistically significant.
Comparative baseline data analysis (Table 1) showed no significant inter-group differences in sex, age, disease duration, NYHA class, hypertension, diabetes, hyperlipidemia, or education level (P > 0.05).
| Indicators | Control group (n = 60) | Research group (n = 73) | χ2/t | P value |
| Sex | 0.416 | 0.519 | ||
| Male | 32 (53.33) | 43 (58.90) | ||
| Female | 28 (46.67) | 30 (41.10) | ||
| Age (years) | 63.95 ± 6.24 | 64.18 ± 6.37 | 0.209 | 0.835 |
| Disease duration (months) | 6.62 ± 2.55 | 7.05 ± 3.08 | 0.865 | 0.389 |
| NYHA classification | 0.151 | 0.698 | ||
| Grade I | 25 (41.67) | 28 (38.36) | ||
| Grade II | 35 (58.33) | 45 (61.64) | ||
| Hypertension | 24 (40.00) | 21 (28.77) | 1.856 | 0.173 |
| Diabetes | 13 (21.67) | 17 (23.29) | 0.050 | 0.824 |
| Hyperlipidaemia | 16 (26.67) | 18 (24.66) | 0.070 | 0.792 |
| Educational level | 0.376 | 0.540 | ||
| Below junior college | 33 (55.00) | 44 (60.27) | ||
| Junior college or above | 27 (45.00) | 29 (39.73) |
Inter-group comparisons of cardiac function are presented in Figure 1. In the control and research groups, CO was 3.16 ± 0.83 L/minute and 3.00 ± 1.20 L/minute preintervention and 4.25 ± 1.48 L/minute and 4.94 ± 1.04 L/minute post
HAMA and HAMD results are shown in Figure 2. HAMA scores decreased from 30.27 ± 5.49 preintervention to 17.87 ± 4.29 postintervention in the control group and from 30.52 ± 5.54 preintervention to 12.86 ± 3.65 postintervention in the research group. HAMD scores decreased from 24.67 ± 4.33 preintervention to 15.63 ± 3.04 postintervention in the control group and from 25.71 ± 3.90 preintervention to 10.11 ± 2.90 postintervention in the research group. Baseline scores were comparable across groups (P > 0.05). Both groups showed significant reductions postintervention (P < 0.05), with lower posttreatment scores in the research group than in the control group (P < 0.05).
CD-RISC results (Table 2) indicated no significant differences between groups in tenacity, strength, optimism, or total score (P > 0.05). All scores increased significantly postintervention (P < 0.05), with greater improvements in the research group (P < 0.05).
| Indicators | Control group (n = 60) | Research group (n = 73) | Z/t | P value |
| Tenacity (points) | ||||
| Before intervention | 37.00 (33.00, 40.75) | 38.00 (32.00, 43.00) | -0.765 | 0.444 |
| After intervention | 40.00 (38.00, 44.00)a | 45.00 (41.00, 49.00)b | -5.093 | < 0.001 |
| Strength (points) | ||||
| Before intervention | 21.00 (19.00, 25.00) | 24.00 (19.00, 27.00) | -1.646 | 0.100 |
| After intervention | 23.00 (21.25, 26.00)a | 26.00 (23.00, 28.50)b | -3.137 | 0.002 |
| Optimism (points) | ||||
| Before intervention | 7.00 (6.00, 9.00) | 8.00 (6.00, 9.00) | -0.701 | 0.483 |
| After intervention | 10.00 (9.00, 12.00)a | 12.00 (10.00, 13.50)b | -3.056 | 0.002 |
| CD-RISC (points) | ||||
| Before intervention | 65.67 ± 7.46 | 68.23 ± 8.50 | 1.825 | 0.070 |
| After intervention | 74.75 ± 6.23a | 82.68 ± 6.74b | 6.985 | < 0.001 |
PSQI results (Table 3) showed no significant baseline differences across dimensions (sleep quality, latency, duration, efficiency, and disturbances, as well as hypnotic drug use and daytime dysfunction; P > 0.05). All dimensions improved postintervention, with greater reductions in the research group than in the control group (P < 0.05).
| Indicators | Control group (n = 60) | Research group (n = 73) | Z | P value |
| Sleep quality (points) | ||||
| Before intervention | 2.00 (1.00, 2.75) | 1.00 (1.00, 3.00) | -1.013 | 0.311 |
| After intervention | 1.00 (1.00, 2.00)a | 1.00 (0.00, 1.00)b | -5.263 | < 0.001 |
| Sleep latency (points) | ||||
| Before intervention | 2.00 (1.00, 2.75) | 2.00 (1.00, 2.00) | -0.563 | 0.573 |
| After intervention | 1.00 (1.00, 2.00)a | 1.00 (0.00, 1.00)b | -2.835 | 0.005 |
| Sleep duration (points) | ||||
| Before intervention | 2.00 (1.00, 2.00) | 1.00 (1.00, 2.00) | -1.424 | 0.155 |
| After intervention | 1.00 (1.00, 2.00)a | 1.00 (1.00, 1.00)b | -2.494 | 0.013 |
| Sleep efficiency (points) | ||||
| Before intervention | 2.00 (1.00, 2.00) | 2.00 (1.00, 2.00) | -0.245 | 0.807 |
| After intervention | 1.00 (1.00, 2.00)a | 1.00 (1.00, 1.50)b | -2.039 | 0.041 |
| Sleep disturbances (points) | ||||
| Before intervention | 2.00 (1.00, 2.00) | 2.00 (1.00, 3.00) | -0.349 | 0.727 |
| After intervention | 1.00 (1.00, 2.00)a | 1.00 (1.00, 1.50)b | -2.319 | 0.020 |
| Hypnotic drug use (points) | ||||
| Before intervention | 2.00 (1.00, 3.00) | 2.00 (1.00, 2.00) | -0.451 | 0.652 |
| After intervention | 1.00 (1.00, 2.00)a | 1.00 (1.00, 1.50)b | -2.248 | 0.025 |
| Daytime dysfunction (points) | ||||
| Before intervention | 2.00 (1.25, 2.00) | 2.00 (1.00, 2.00) | -1.284 | 0.199 |
| After intervention | 2.00 (1.00, 2.00)a | 1.00 (1.00, 2.00)b | -2.646 | 0.008 |
SF-36 results (Table 4) demonstrated comparable baseline scores across domains (P > 0.05). All domains improved significantly postintervention (P < 0.05), with greater improvements in the research group (P < 0.05).
| Indicators | Control group (n = 60) | Research group (n = 73) | Z/t | P value |
| Physical functioning (points) | ||||
| Before intervention | 64.07 ± 7.68 | 62.36 ± 8.75 | 1.184 | 0.238 |
| After intervention | 70.65 ± 6.47a | 75.74 ± 7.81b | 4.036 | < 0.001 |
| Social functioning (points) | ||||
| Before intervention | 68.55 ± 6.66 | 68.64 ± 6.91 | 0.076 | 0.940 |
| After intervention | 72.35 ± 6.98a | 76.34 ± 7.49b | 3.152 | 0.002 |
| Role-emotional (points) | ||||
| Before intervention | 65.72 ± 6.28 | 66.32 ± 6.81 | 0.524 | 0.602 |
| After intervention | 72.32 ± 6.92a | 78.53 ± 7.05b | 5.097 | < 0.001 |
| Mental health (points) | ||||
| Before intervention | 70.00 (65.00, 74.00) | 71.00 (65.50, 76.00) | -1.162 | 0.245 |
| After intervention | 77.00 (74.00, 79.00)a | 82.00 (76.00, 87.00)b | -4.012 | < 0.001 |
As a major cause of mortality worldwide, AMI risk increases with age and shows a trend toward younger onset[19]. CAD is common in patients with AMI following percutaneous coronary intervention, and depressive symptoms may exacerbate disease progression[20]. However, studies focusing on AMI patients with CAD remain limited; therefore, this study conducted a targeted analysis.
This retrospective study first demonstrated that STL combined with psychological intervention significantly improved cardiac function (CO, SV, and LVEF) in AMI + CAD patients. McFarlane et al[21] reported that STL improved cardiac autonomic function in post-AMI depression, suggesting its ability to accelerate cardiac function recovery through neuroregulatory mechanisms. Finkel et al[22] reported that STL was superior to nortriptyline in efficacy and tolerability in older adults (≥ 70 years) with MDD, consistent with our findings. Moreover, STL is effective and safe for AMI patients with MDD and may reduce adverse cardiac events[23].
STL combined with psychological intervention also more effectively reduced anxiety and depression than psychological intervention alone. This effect may relate to STL-mediated inhibition of presynaptic Na+ channel activity in hippocampal nerve endings[24]. Another study on mice further suggests that STL reduces fear memory retrieval, partially explaining its anxiolytic and antidepressant effects[25]. Additionally, the combined intervention significantly improved resilience and sleep quality than psychological intervention alone. Finally, STL combined with psychological intervention significantly improved overall quality of life in AMI patients with CAD. Lewis et al[26] similarly reported improvements in anxiety, self-assessed mental health, and quality of life with STL in primary care surgeries.
Several previous studies have extensively evaluated STL in clinical applications. Chambergo-Michilot et al[27] reported synergistic effects of STL combined with omega-3 fatty acids in alleviating depressive or anxiety symptoms in adult patients with depression. O'Connor et al[28] found STL to be cost-effective in treating MDD in patients with unstable angina pectoris or recent AMI. Compared with placebo, it validly reduced the rates of psychiatric or cardiovascular hospitalizations without significantly increasing treatment costs. Liu and Qin[29] demonstrated comparable efficacy and cardiac safety between STL and Shugan Jieyu capsules in AMI patients with concurrent depression.
In summary, STL combined with psychological intervention is more effective than psychological intervention alone in patients with post-AMI CAD. It significantly improves patients’ cardiac function, reduces anxiety and depression, strengthens resilience, and improves sleep quality and overall quality of life, supporting its clinical application.
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