The occurrence of ST elevation myocardial infarction (STEMI) and non-STEMI in patients with post traumatic stress disorder (PTSD) using the large nationwide inpatient sample (NIS).

Am J Cardiovasc Dis 2024;14(3):172-179 www.AJCD.us /ISSN:2160-200X/AJCD0151802 Original Article The occurrence of ST elevation myocardial infarction (STEMI) and non-STEMI in patients with post traumatic stress disorder (PTSD) using the large nationwide inpatient sample (NIS) Abdullah Mohamed Niyas1, Fathima Haseefa1, Mohammad Reza Movahed1,2, Mehrtash Hashemzadeh1, Mehrnoosh Hashemzadeh1 University of Arizona College of Medicine, Phoenix, AZ, USA; 2University of Arizona College of Medicine, Tucson, AZ, USA 1 Received June 17, 2023; Accepted December 27, 2023; Epub June 15, 2024; Published June 30, 2024 Abstract: Background: PTSD leads to increased levels of stress hormones and dysregulation of the autonomic nervous system which may trigger cardiac events. The goal of this study is to evaluate any association between PTSD and the occurrence of STEMI and NSTEMI using a large database. Method: Using the Nationwide Inpatient Sample (NIS) and ICD-9 codes from 2005 to 2014 (n=1,621,382), we performed a univariate chi-square analysis of inhospital occurrence of STEMI and NSTEMI in patients greater than 40 years of age with and without PTSD. We also performed a multivariate analysis adjusting for baseline characteristics including age, gender, diabetes, race, hyperlipidemia, hypertension, and tobacco use. Results: The 2005-2014 dataset contained 401,485 STEMI patients (745, or 0.19%, with PTSD) and 1,219,897 NSTEMI patients (2,441, or 0.15%, with PTSD). In the 2005 dataset, 0.5% of PTSD patients had STEMI compared to 1.0% of non-PTSD patients (OR=0.46, 95% C.I., 0.36-0.59). Similarly, 0.6% of patients with PTSD and 2.2% of patients without PTSD had NSTEMI (OR=0.28, 95% C.I., 0.23-0.35). In the 2014 dataset, 0.3% of PTSD patients had STEMI compared to 0.7% of non-PTSD patients (OR=0.43, 95% C.I., 0.35-0.51). Similarly, 1.4% of patients with PTSD versus 2.9% of patients without PTSD had NSTEMI (OR=0.48, 95% C.I., 0.44-0.52). Similar trends were seen throughout the ten-year period. After adjusting for age, gender, diabetes, race, hyperlipidemia, hypertension, and tobacco use, PTSD was associated with a lower occurrence of STEMI (2005: OR=0.50, 95% C.I., 0.37-0.66; 2014: OR=0.35, 95% C.I., 0.29-0.43) and NSTEMI (2005: OR=0.44, 95% C.I., 0.34-0.57; 2014: OR=0.63, 95% C.I., 0.58-0.69). Conclusion: Using a large inpatient database, we did not find an increased occurrence of STEMI or NSTEMI in patients diagnosed with PTSD, suggesting that PTSD is not an independent risk factor for myocardial infarction. Keywords: STEMI, NSTEMI, myocardial infarction, PTSD, CVD, ischemic heart disease Introduction Posttraumatic stress disorder (PTSD) manifests as persistent maladaptive reactions after experiencing severe emotional or physical distress, including but not limited to, violent assault, military combat, and natural or manmade disasters [1]. According to the latest update to the Diagnostic and Statistical Manual of Mental Disorders, DSM-5, all of the following criteria needs to be met for diagnosis of PTSD: (1) Direct or indirect exposure to death or actual/threatened violence or serious injury; (2) Persistently re-experiencing traumatic events through nightmares, flashbacks, memories; (3) Avoidance of trauma-related stimuli following trauma; (4) Negative thoughts or feelings that began or worsened following trauma; (5) Trauma related arousal and reactivity that began or worsened after trauma; (6) Symptoms must last for longer than one month; (7) Symptoms created distress or functional impairment; (8) Symptoms not explained by medication, substance use, or other illness. Current evidence-based guidelines overwhelmingly lean towards trauma focused psychotherapy as the gold standard for PTSD managehttps://doi.org/10.62347/YTCI7645 STEMI and NSTEMI in PTSD patients ment. The three most established types of therapy with the strongest evidence are eye movement desensitization and reprocessing (EMDR), cognitive processing therapy (CPT), and prolonged exposure (PE). Further therapy modalities are the subject of newer research and will likely be employed in adjunction to the more common types. In patients with more severe or persistent PTSD, pharmacotherapy with selective serotonin reuptake inhibitors (SSRIs) and selective norepinephrine reuptake inhibitors (SNRIs) is shown to be effective alongside psychotherapy. The medications fluoxetine, paroxetine, and venlafaxine have proven to show the most benefit for reducing symptoms [2]. vascular risk factors. Furthermore, a recent literature review by Habbal et al. identified that most research in this area is limited to populations exposed to particular traumatic events and/or from certain geographic areas or demographics [11]. Like most psychiatric disorders, long term prognosis is dependent on multiple factors, including but not limited to degree of trauma, one’s support system, treatment compliance and presence or absence of substance abuse. Thus, studies are highly variable with regards to recovery rates, ranging from unto 30% of PTSD patients usually recover with one or more treatment modalities, with a slightly higher number reporting partial recovery [3]. Data source PTSD has been shown to have an association with a multitude of medical conditions. The link between psychological disorders and cardiovascular disease in particular is a growing area of research, owing mainly to the bidirectional relationship between the two [4]. A majority of these studies show that patients with PTSD are more likely to develop cardiovascular disease (CVD) and eventually die from it [5-9]. There are multiple current hypotheses to explain the underlying mechanism of association between PTSD and CVD. A common theory studied so far is related to persistent autonomic dysregulation in PTSD, which leads to higher catecholamine release and consequently lower resting heart rate. Another concept studied so far implicates the sharp rise of pro inflammatory cytokines in PTSD as a cause of cardiovascular disease. Heightened inflammation can accelerate atherosclerosis and increase risk of plaque rupture [10]. This relationship could develop to become a crucial target for screening and education of patients with PTSD about CVD and vice versa in patients recovering from STEMI or NSTEMI to improve post-MI outcomes. However, it remains unclear whether these associations are causal or confounded by other cardio173 Our study aims to add to the growing literature on PTSD as an independent risk factor for cardiovascular events in the general population. Using a large national inpatient database, we retrospectively analyzed the data to investigate the association between PTSD and STEMI or NSTEMI. Methods This study utilized the Nationwide Inpatient Sample (NIS) database to obtain patient data. The NIS is a component of the Healthcare Cost and Utilization Project (HCUP), which is sponsored by the Agency for Healthcare Research and Quality (AHRQ). The NIS database is the large (...truncated)