Abstract
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: : acute myocardial infarction, cardiovascular disease, depression, mental health, myocardial infarction risk, National Inpatient Database, NSTEMI, retrospective study, STEMI
Plain Language Summary
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.
Plain language summary
Article highlights.
Background
Depression and anxiety significantly impact nearly one-fourth of the USA population, with global prevalence contributing substantially to disability.
These psychiatric conditions are associated with an increased risk of cardiovascular diseases due to various physiological mechanisms.
Methods
An extensive retrospective analysis was conducted using data from the National Inpatient Sample database from 2005 to 2020.
Patients aged over 30 were selected using ICD-9 and ICD-10 codes for ST-segment elevation myocardial infarction, non-ST-segment elevation myocardial infarction and major depression.
Results
The study included 4413,113 ST-segment elevation myocardial infarction patients, 224,430 with depression and 10,421,346 non-ST-segment elevation myocardial infarction patients, 437,058 of whom had depression.
No significant association was found between depression and any type of myocardial infarction (MI).
A consistent trend over the 15-year period showed fewer MI incidents among patients with a diagnosis of depression compared with those without depression.
Conclusion
Our study did not identify an increased risk of MI associated with major depression.
The findings suggest that depression may not independently be a significant risk factor for MI.
Future research should consider prospective cohort studies to establish causality and further explore the impact of depression on cardiovascular health.
Limitations
The study's retrospective design and reliance on ICD-9 and ICD-10 coding within the National Inpatient Sample database may introduce biases.
The duration of depression and a control group without depression were not included, limiting the ability to determine the independent impact of depression on MI.
1. Introduction
Depression and anxiety, often coexisting, exert a significant impact on the well-being of nearly one-fourth of the USA population [1]. Globally, it is estimated that approximately a third of individuals will grapple with an anxiety disorder at some point in their lives, ranking it as the sixth leading contributor to disability [2,3]. Meanwhile, depression stands as one of the foremost causes of disability worldwide and is recognized as the fourth leading cause of the global disease burden [4].
These conditions represent major sources of morbidity and mortality within the USA, significantly compromising the health-related quality of life [5]. Patients afflicted by psychiatric disorders face the harsh reality of a shortened life expectancy, with cardiovascular disease standing as the chief culprit behind premature deaths [6–8].
The scientific literature illustrates a multitude of effects, both direct and indirect, that correlate mental illness with risk factors for cardiovascular disease. The cardiovascular system is regulated by the autonomic nervous system and depression and anxiety have been shown to influence cardiac reactivity by increasing heart rate and blood pressure. Reduced blood flow to the heart, reduced heart rate variability and heightened cortisol are also evident in the literature [9]. Stress-mediated activation of the hypothalamic-pituitary-adrenal axis results in increased circulating catecholamines, with alterations to autonomic systems that contribute to insulin resistance, endothelial dysfunction, inflammation and hypertension (HTN) – all of which are precursors to cardiovascular disease [10–15]. We also observe an increase in norepinephrine associated with anxiety, along with activation of mononuclear cells involved in atherosclerotic lesions and reactive oxygen species [16]. Notably, both depression and anxiety have been linked to higher arterial stiffness among patients with essential HTN [17]. These conditions also exhibit additional effects, such as calcium buildup in the arteries, metabolic disease and consequent heart disease in these patients [18,19].
Hypertension stands as a prominent worldwide contributor to morbidity and mortality. Consequently, effective management of hypertension plays a vital role in reducing the risk of myocardial infarction (MI), congestive heart failure and ultimately, mortality [1]. Patients with depression and/or anxiety are particularly vulnerable because they are at higher risk of developing HTN [1]. The co-occurrence of HTN and psychological disorders is associated with increased rates of cardiovascular disease-related mortality [20,21].
For individuals suffering from depression and anxiety, adhering to medications can be challenging. This is possibly due to fewer effective coping strategies and thus these populations generally show a greater impact of chronic comorbidities overall. The additional responsibility of a behavioral change for their physical health is added to the existing burden of mental health. This burden can be further exacerbated by socioeconomic factors such as unemployment or poverty have a higher prevalence of depression and anxiety. Research indicates an association between current depression, lifetime depression, lifetime anxiety, lifetime cardiovascular disease and adverse health behaviors such as smoking [22]. Nonetheless, substantial studies in this area are lacking.
In 2014, the American Heart Association issued a Scientific Statement proposing that depression be formally recognized as a risk factor for poor prognosis following an acute coronary event. However, they also acknowledged the need for further research due to the heterogeneity of the studies identified [23,24]. The study aims to address this gap in knowledge by evaluating the association between the diagnosis of major depression with MI using a large inpatient database.
2. Methods
2.1. Data collection
This study utilized the Nationwide Inpatient Sample (NIS) to conduct a retrospective review. The NIS is publicly available and is the largest all-payer inpatient care database in the USA from the Healthcare Cost and Utilization Project (HCUP). Its collection of databases is used to analyze national trends in healthcare utilization, quality of healthcare and patient outcomes. The NIS database can be found at www.hcup-us.ahrq.gov.
2.2. Description of data
Inclusion criteria encompassed all adults 30 and over who were discharged from hospitals using the National Inpatient Sample (NIS) database spanning from 2005–2020. Patients were identified using International Classification of Diseases, Clinical Modification (ICD-9-CM and ICD-10-CM) codes with depression (300.4). Additionally, we used the ICD-9-CM codes for acute MI (STEMI and NSTEMI): 410.7, 410.8, 410.9, unstable angina 411.1, ischemic heart disease (410–414 and 401.0–405.9) covering all subgroups including procedures such as coronary artery bypass grafting and percutaneous coronary intervention.
Additionally, we adjusted for age, race, gender and their associations with comorbidities including diabetes mellitus (ICD-9-CM: 250), hypertension (ICD-9-CM: 401.0, 401.1, 401.9), hyperlipidemia (ICD-9-CM: 272.0, 272.1, 272.2, 272.4) and smoking (ICD-9-CM: 305.1, 304.6). The specific ICD-10-CM codes for depression (F32, F33). Acute MI including STEMI (I21.0-I21.3) and non-STEMI (I21.4). Diabetes (E10, E11), hypertension (I10, I11, I12, I13, I15, I16), hyperlipidemia (E78.5, E78.2), tobacco use (Z72.0, F17.2) nicotine dependence (Z87.891) history of tobacco dependence.
Patients under the age of 30 were excluded from the study. Age stratification utilized age 30 as the primary cutoff based on MI incidence rates. MI is very rare under the age of 30. In the Framingham study, MI incidence per 1000 person-years was reported as 12.9, 38.2 and 71.2 for males and 2.2, 5.2 and 13.0 for females in the age groups 30–34, 35–44 and 45–54 years, respectively [25]. This threshold was chosen to focus on adult populations at higher risk for MI.
2.3. Statistical analysis
The Statistical Package for Social Sciences (IBM SPSS Statistics 25.0, USA) software was used on NIS data from 2005 to 2020 to evaluate the correlation of anxiety and depression with cardiac events. Demographic, clinical and hospital features of the patients are presented as averages, accompanied by 95% CIs for continuous variables and proportions with corresponding 95% CIs for categorical variables. The examination of trends over time involved Chi-squared analysis for categorical results and univariate linear regression for continuous variables. Additionally, multivariable logistic regression was employed to determine the odds of binary clinical outcomes in relation to both patient and hospital characteristics, as well as the odds of clinical outcomes evolving over time. All analyses were conducted following the implementation of population discharge weights. A p-value ≤ 0.05 was considered statistically significant.
3. Results
Overall, a total of 4,413,113 patients with STEMI (mean age 67) and 10,421,346 patients with NSTEMI (mean age 69) were evaluated. Of those with STEMI, 224,430 had depression and 437,058 patients had depression in the NSTEMI group. The patients with depression were not found to have an increased association with MI. This trend was seen throughout the 15-year period. Interestingly MI including both STEMI and NSTEMI occurred to a lesser degree in patients with a diagnosis of depression [Figures 1 & 2].
Figure 1.
In patients with depression, STEMI rates were not increased (orange). In fact, rates of STEMI were higher in those without the diagnosis of depression (gray). Y axis showing the percentage rate of STEMI patients.
STEMI: ST-elevation myocardial infarction.
Figure 2.
In patients with depression, NSTEMI rates were not increased (green). In fact, rates of NSTEMI were higher in those without the diagnosis of depression (yellow).
Y axis showing percentage rate of NSTEMI patients.
NSTEMI: Non-ST elevation myocardial infarction.
For example, in 2005 the depression STEMI database: [odds ratio (OR) 0.12, 95% CI: 0.10–15, p < 0.001]. In 2020 the depression STEMI: [OR 0.71, 95% CI, 0.69–0.73, p < 0.001]. This trend was mirrored in the NSTEMI group. The 2005 database for NSTEMI: [OR 0.14, 95% CI, 0.13–0.16, p < 0.001] and 2020: [OR 0.69, 95% CI, 0.68–0.71, p < 0.001]. After multivariate adjustment for baseline characteristics and comorbid condition, acute MI remained lower in patients with diagnosis of major depression.
4. Discussion
There are literature reports of positive associations between depression and acute MI, however, after critical review, many had important limitations and as such, were not convincing [26–33]. This may be in part due to the difficulty of study design, with various confounding variables. Depression and anxiety are often co-occurring and difficult to separate. In studies that claim to show correlation, there is no control for the other variable. The temporal sequence also brings about a challenge in interpreting the results of claimed associations. Many studies on depression and anxiety show potential reverse causation, whereby heart disease precedes depression and anxiety and may have developed in response to symptoms of heart disease.
Issues arose surrounding exclusion criteria as some studies did not exclude those with preexisting ischemic heart disease or adjust for cardiovascular risk factors – thus, not being able to demonstrate depression as an independent risk factor. Furthermore, no intervention study has shown that treatment of depression reduces the occurrence of acute MI [34].
Machado's umbrella review of systematic reviews and meta-analyses on the topic concluded that no meta-analyses provided convincing evidence of a causal association, because the associated were weak or null in studies that had adequately controlled for confounding factors [35]. They demonstrated that many studies lacked structured interviews, had overlapping samples, including other mental disorders and had publication bias. Additionally, the diagnosis of depression was based only on the use of antidepressants in some cases or not using any specific diagnostic criteria.
In support of our findings, a newer paper from the UK conducted as a large prospective study, investigated depression, anxiety, psychotropic drugs and acute MI in men and women with no previous vascular disease [36]. The HUNT study indicated that this correlation was slightly more pronounced in women than in men; however, the analysis did not detect any gender-specific relationship between antidepressant usage and MI [29]. This paper also suggested the use of psychotropic drugs, residual confounding and reverse causation weaken the claims of positive association in the current literature. Their subsequent investigations into various categories of antidepressants revealed that both selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants were linked to a decreased likelihood of MI. SSRIs are the first-line pharmacotherapy for the treatment of major depression. This is generally because of their tolerability and safety profile and are deemed to be safe in the cardiac setting. SSRIs have been shown to have a meaningful effect on major depression [17]. Several studies have suggested that SSRIs may potentially reduce the risk of thrombotic events [27].
The UK study included a gender-specific analysis of 690,335 women with a mean follow-up of 13.9 years. One of its major strengths is that they were able to adjust for many potential confounding variables. These included: deprivation, educational qualifications, smoking status, alcohol consumption, body mass index, frequency of physical activity, use of menopausal hormone therapy, hypertension, diabetes, parental heart disease and self-rated health. There was no significant relationship between depression or anxiety with or without the use of psychotropic drugs and acute MI using their fully adjusted model. The null findings in this large prospective study are consistent with depression not being a risk factor for acute MI independent of behavioral and other cardiovascular risk factors. Note that this study only used women whereas ours includes both sexes and includes more recent data up to the year 2020.
Expanding on these insights, our study builds upon the findings of the UK study by utilizing the NIS database, the largest all-payer inpatient case database in the USA. This allowed for the inclusion of both sexes and provided a comprehensive examination of the association between depression and MI. By analyzing data up to the year 2020, we offer more contemporary insights into this relationship, enhancing the robustness of our findings.
Potential factors contributing to the lower event rates in the depression group compared with the rest of the population may include differences in medical management and lifestyle modifications. Patients diagnosed with depression might receive more intensive medical monitoring and treatment for their cardiovascular health, as their mental health condition necessitates regular healthcare interactions. Additionally, lifestyle changes often recommended for managing depression, such as increased physical activity and healthier diet, may also contribute to improved cardiovascular outcomes. Selection biases could also play a role, as patients with more severe or poorly managed depression may be less likely to be included in the study population, potentially skewing the results. The observed trend of narrowing gap toward the end of the study period might reflect improvements in the overall management of depression and associated cardiovascular risk factors over time.
Our findings raise several important considerations regarding the clinical management of patients at risk of MI with comorbid depression or anxiety. While our study suggests a potential protective effect associated with these mood disorders, the intricacies of this relationship warrant careful assessment. Prospective cohort studies or intervention trials are necessary to elucidate the cause-and-effect relationships between depression, anxiety and cardiac events. Future studies should delve into the specifics of depression treatment, including dosages and types of medications, to provide a clearer picture of how these factors influence MI prevalence. The implications are far-reaching and our findings should serve as a catalyst for a deeper understanding of the complex connections between mental health and heart health.
5. Limitations
Our study has several limitations that should be considered. Firstly, it relies on retrospective analysis using ICD-9 and ICD-10 coding within the NIS database. Such databases may have inherent limitations, including potential coding errors, missing or incomplete data and issues related to the accuracy of diagnoses, which could introduce bias. Secondly, the retrospective nature of this study limits our ability to draw causal inferences; a prospective cohort study would provide a higher level of evidence.
A significant limitation is the inability to ascertain the duration of depression, which plays a crucial role in understanding its impact on MI. The dataset does not provide information on how long patients had been diagnosed with depression or the chronology of the diagnoses of depression and MI. Additionally, this study does not include a control group without depression, making it challenging to isolate the independent impact of depression on MI outcomes.
Future analysis could also include age distribution by decade to provide valuable insights into the relationship between depression and MI across different age groups. Yang et al. highlighted that patients aged <40 years with MI are more likely to use both marijuana and cocaine compared with older patients, whereas those aged 40–50 years are more likely to exhibit traditional risk factors such as hypertension, peripheral vascular disease and higher atherosclerotic cardiovascular disease scores [37]. The distribution of etiological risk factors differs significantly between younger and older MI patients. However, due to current data limitations and resource constraints, we are unable to perform this analysis at this time. We acknowledge the importance of this factor and recommend it as a focus for future research.
6. Conclusion
Our study contributes valuable insights to the growing body of literature on the relationship between depression, anxiety and MI. By leveraging a large-scale database and incorporating contemporary data, we provide compelling evidence that challenges existing assumptions about the role of depression in cardiovascular health. Our results suggest that patients with anxiety or depression have no association with the occurrence of STEMI and NSTEMI. Prospective studied need to be performed to answer the role of depression as a risk factor for coronary artery disease. These findings highlight the importance of addressing mental health concerns in the context of cardiac care and highlight the need for multidisciplinary approaches to improve patient outcomes.
Author contributions
Conceptualization was done by Mehrnoosh Hashemzadeh and Sarah Meskal. Methodology was performed by Mehrnoosh Hashemzadeh and Sarah Meskal, MR Movahed, Mehrtash Hashemzadeh and Manrit Gill. Investigation was performed by Mehrnoosh Hashemzadeh and Sarah Meskal. Formal analysis was performed by Mehrtash Hashemzadeh. Writing (original draft) was done by Sarah Meskal and Mehrnoosh Hashemzadeh. Writing (review and editing) was done by Sarah Meskal, Mehrnoosh Hashemzadeh, MR Movahed and Manrit Gill. Resources by Mehrnoosh Hashemzadeh. Supervision was performed by Mehrnoosh Hashemzadeh
Financial disclosure
The authors have no financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Competing interests disclosure
The authors have no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Writing disclosure
No writing assistance was utilized in the production of this manuscript.
Ethical conduct of research
This study used a publicly available database without any patient identifiers and was exempt from IRB approval.
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