Background and objective <p>Patients with coronary heart disease (CHD) often have comorbid depression and anxiety, which worsen prognosis. Escitalopram, a selective serotonin reuptake inhibitor, is used for these symptoms, but evidence on its psychological and cardiovascular effects in CHD is limited. This systematic review and meta-analysis evaluated its effects on psychological symptoms and cardiovascular outcomes in CHD.</p> Methods <p>We systematically searched five databases for randomized controlled trials (RCTs) of escitalopram vs. control in adults with CHD. Data were extracted to avoid double counting; extended follow-up data were analyzed separately. Outcomes included depression/anxiety scale changes, major adverse cardiovascular events (MACE), all-cause mortality, myocardial infarction, and revascularization. Random-effects models and sensitivity analyses were used.</p> Results <p>Five RCTs were included. Overall depression score change was not significant (SMD = -0.70, 95% CI -1.57 to 0.18), but medium-term (12–24&#xa0;weeks) follow-up showed improvement (SMD = -0.39, 95% CI -0.58 to -0.20). Anxiety scores significantly decreased with escitalopram (SMD = -0.64, 95% CI -1.12 to -0.17). Pooled data from two studies were compatible with reductions in MACE (RR = 0.74, 95% CI 0.59 to 0.94) and myocardial infarction (RR = 0.53, 95% CI 0.29 to 0.96), however, approximately 90% of the pooled weight came from the post-treatment follow-up of a single trial, so these findings are hypothesis-generating. No statistically significant between-group differences were observed for all-cause mortality or revascularization.</p> Conclusion <p>Escitalopram appears effective for selected psychological symptoms in CHD without evidence of major cardiovascular harm; current evidence is insufficient to establish a cardiovascular benefit, and the observed MACE and myocardial infarction reductions are hypothesis-generating. Treatment should aim primarily to improve psychological well-being and quality of life.</p>

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Escitalopram for psychological symptoms and cardiovascular outcomes in patients with coronary heart disease: a systematic review and meta-analysis of randomized controlled trials

  • Xu Wang,
  • Yijing Tan,
  • Shiruo Hu,
  • Bengang Pan,
  • Weifen Qiu,
  • Chun’e Wang,
  • Guozhong Zhou,
  • Qingyi Luo,
  • Jun Qian

摘要

Background and objective

Patients with coronary heart disease (CHD) often have comorbid depression and anxiety, which worsen prognosis. Escitalopram, a selective serotonin reuptake inhibitor, is used for these symptoms, but evidence on its psychological and cardiovascular effects in CHD is limited. This systematic review and meta-analysis evaluated its effects on psychological symptoms and cardiovascular outcomes in CHD.

Methods

We systematically searched five databases for randomized controlled trials (RCTs) of escitalopram vs. control in adults with CHD. Data were extracted to avoid double counting; extended follow-up data were analyzed separately. Outcomes included depression/anxiety scale changes, major adverse cardiovascular events (MACE), all-cause mortality, myocardial infarction, and revascularization. Random-effects models and sensitivity analyses were used.

Results

Five RCTs were included. Overall depression score change was not significant (SMD = -0.70, 95% CI -1.57 to 0.18), but medium-term (12–24 weeks) follow-up showed improvement (SMD = -0.39, 95% CI -0.58 to -0.20). Anxiety scores significantly decreased with escitalopram (SMD = -0.64, 95% CI -1.12 to -0.17). Pooled data from two studies were compatible with reductions in MACE (RR = 0.74, 95% CI 0.59 to 0.94) and myocardial infarction (RR = 0.53, 95% CI 0.29 to 0.96), however, approximately 90% of the pooled weight came from the post-treatment follow-up of a single trial, so these findings are hypothesis-generating. No statistically significant between-group differences were observed for all-cause mortality or revascularization.

Conclusion

Escitalopram appears effective for selected psychological symptoms in CHD without evidence of major cardiovascular harm; current evidence is insufficient to establish a cardiovascular benefit, and the observed MACE and myocardial infarction reductions are hypothesis-generating. Treatment should aim primarily to improve psychological well-being and quality of life.