Background: Depression has been suggested to increase the risk of cardiovascular disease, but many studies assessed depression after heart disease onset. This study evaluated the association between depression and myocardial infarction (MI) using a large inpatient database.Methods: We analyzed patients from the National Inpatient Sample hospitals from 2005 to 2020, selecting those aged >30 with ICD-9 and ICD-10 codes for segment elevation (ST) elevation myocardial infarction (STEMI), non-ST elevation myocardial elevation (NSTEMI) and major depression.Results: Our data included 4413,113 STEMI patients (224,430 with depression) and 10,421,346 NSTEMI patients (437,058 with depression). No significant association was found between depression and MI. For STEMI, the 2005 odds ratio was 0.12 (95% CI: 0.10-0.15, p < 0.001) and the 2020 odds ratio was 0.71 (95% CI: 0.69-0.73, p < 0.001). Similar patterns were observed for NSTEMI.Conclusion: Depression may not independently be a significant risk factor for MI.
Keywords: NSTEMI; National Inpatient Database; STEMI; acute myocardial infarction; cardiovascular disease; depression; mental health; myocardial infarction risk; retrospective study.
Depression has been suggested to increase the risk of cardiovascular disease, but many studies assessed depression after heart disease onset. This study evaluated the association between depression and myocardial infarction (MI) using a large inpatient database. We analyzed patients from the National Inpatient Sample hospitals from 2005 to 2020, selecting those aged greater than 30. No significant association was found between depression and MI. Depression may not independently be a significant risk factor for MI. Our results suggest that patients with anxiety or depression have no association with the occurrence of MI.We suspect that the observed results may be related to the effects of selective serotonin reuptake inhibitors on platelets. Selective serotonin reuptake inhibitors primarily increase serotonin levels in the brain by inhibiting its reuptake. However, they can also affect platelet function by inhibiting serotonin reuptake by platelets. This inhibition of serotonin reuptake by platelets can lead to decreased platelet aggregation, which may confer some level of protection against certain conditions involving platelet dysfunction or excessive clotting. This effect is particularly relevant in cardiovascular diseases where abnormal platelet function can contribute to thrombotic events like heart attacks or strokes.