Risultati per: Incontinenza urinaria da stress o mista

Circulation, Volume 146, Issue Suppl_1, Page A11734-A11734, November 8, 2022. Introduction:Chest pain is common in patients with Post-acute Sequelae of SARS-CoV-2 (PASC), also known as long COVID, but the mechanism is unknown.Hypothesis:We hypothesized that PASC patients with chest pain have impaired myocardial perfusion reserve (MPR) measured by stress perfusion cardiovascular magnetic resonance (CMR) imaging.Methods:We retrospectively identified the first 30 consecutive patients who underwent clinically ordered adenosine stress perfusion CMR for chest pain persisting >4 weeks after SARS-CoV-2 infection (PASC). Patients with a history of coronary artery disease (CAD) or left ventricular ejection fraction (LVEF) 2 SD below mean MPR for controls.Results:In 30 PASC (67% female, age 43±13) and 13 controls (54% female, age 50±12), with LVEF (61±6% vs 59±8%), native T1 (1001±49 vs 992±57 ms), T2 (49.5±3.7 vs 48.0±3.3 ms), and ECV (24.6±2.9 vs 24.6±2.6%) were similar (p >0.2 for all). Prior pericarditis (n=2) or prior myocarditis (n=3) were infrequent, with no acute disease by CMR. PASC patients had significantly lower global MPR than controls (1.54±0.25 vs. 2.20±0.36, p

Circulation, Volume 146, Issue Suppl_1, Page A15067-A15067, November 8, 2022. Introduction:Ischemia with non-obstructive coronary arteries (INOCA) is a relatively new condition, often observed in patients with angina. However, the exact pathophysiology of INOCA is not fully understood, and its management remains very debated.Hypothesis:We hypothesized that admission hyperglycemia in INOCA patients could be associated with the risk of being re-hospitalized for chest pain.Methods:We evaluated INOCA patients referred to our Institution between 2016 and 2021 for percutaneous coronary intervention (PCI). We divided our population in quintiles according to the values of the stress hyperglycemia ratio (SHR), calculated as the ratio of admission blood glucose (expressed as mmol/L) and HB1Ac (%). We calculated Kaplan-Meier product limits for cumulative ratio of reaching the endpoint and we applied the log-rank test. To further confirm our results, we performed a multivariable analysis in order to adjust for potential confounders.Results:2874 INOCA patients were enrolled in our study. At 1-year follow-up, the risk of hospitalization for chest pain was progressively higher in patients with higher SHR values (p

Circulation, Volume 146, Issue Suppl_1, Page A13156-A13156, November 8, 2022. Introduction:The presence of multiple high-risk prognostic features enhances risk-stratification of plaques prone to destabilization and major adverse cardiac events (MACE). Spatial superimposition of high-risk features (concordance) likely amplifies local risk. Local endothelial shear stress (ESS) and plaque structural stress (PSS) metrics predict MACE, but their spatial concordance and their location relative to the minimal lumen area (MLA) is unknown. If the highest-risk plaque area is distant from the MLA, then PCI of the MLA alone will leave high-risk plaque areas untreated.Purpose:To identify the site of high-risk features of low ESS and high PSS heterogeneity (HI) along the course of a plaque in patients who develop MACE, and the site of their spatial concordance relative to the MLA.Methods:We examined ESS, PSS, and PSS HI in 22 non-culprit lesions (NCL) leading to MACE, and 64 randomly selected control NCLs without MACE from the PROSPECT study. ESS was calculated by computational fluid dynamics and PSS by finite element analysis on co-registered lesions. We examined high-risk plaques with empirically-derived (ROC curve) ESS < 1.3 Pa and PSS HI > 0.29 in 16 lesions leading to future MACE, and 11 control lesions without MACE.Results:MACE outcomes were significantly more frequent in plaques with combined low ESS+high PSS HI vs plaques with low ESS alone (72.7% vs 27.3%, p

Circulation, Volume 146, Issue Suppl_1, Page A12919-A12919, November 8, 2022. Introduction:The SARS-CoV-2 virus has potential to cause acute and long-term cardiac effects. The vaccines were developed to prevent severe illness, but there are concerns about vaccine related side effects. Specific to the heart there have been case reports of mRNA vaccine related cardiomyopathies, particularly myocarditis. We present a case of a patient with presumptive stress induced cardiomyopathy in the setting of recent Covid-19 mRNA vaccination.Case Presentation:A 93-year-old female with a past medical history of hypertension presented with worsening shortness of breath and bilateral lower extremity edema. She received her second dose of the Covid-19 mRNA vaccine five days prior to presentation. She had no history of heart disease, was a nonsmoker, and denied alcohol or drug use. In the ED she was noted to be fluid-overloaded, and her CT chest showed minimal coronary calcification and bilateral pleural effusions. She was admitted for heart failure exacerbation and started on IV furosemide. Her transthoracic echocardiogram showed an ejection fraction of 40-45%. The pattern of left ventricular dysfunction was consistent with stress induced cardiomyopathy with apical akinesis and basal sparing of the left ventricular wall segments. Cardiology was consulted and recommended management with diuretics and beta blocker. She had a diuresis of 5 liters during her hospitalization. At clinic follow-up, dyspnea had improved, and her peripheral edema had resolved. Repeat echocardiogram showed recovery of left ventricular ejection fraction to 61% by Simpsons biplane technique with no regional wall motion abnormalities. Further cardiac assessment to evaluate for obstructive coronary artery disease and myocarditis was discussed and offered to the patient but was declined due to her positive response to conservative management.Discussion:The precise etiology of stress induced cardiomyopathy is unknown, but it is thought to be secondary to the sudden release of stress hormones. There are isolated reports of stress induced cardiomyopathy associated with Covid-19 vaccination, but the potential mechanism is unclear. An improved understanding of the potential effects of mRNA vaccines may help guide decisions regarding future booster vaccinations.

Circulation, Volume 146, Issue Suppl_1, Page A12929-A12929, November 8, 2022. Introduction:Posttraumatic stress disorder (PTSD) has been associated with ischemic heart disease in women veterans. To date, the evidence for the potential association of PTSD with other cardiovascular disorders remains limited. Furthermore, the overwhelming majority of the research in this area has been conducted predominately in men. The goal of this investigation was to evaluate the association of PTSD with incident stroke in a large cohort of women veterans.Methods:Veterans Affairs (VA) electronic health records were used to identify women veterans aged ≥18 years who visited any VAs nationwide from 1/1/2000-12/31/2017. Diagnosis of each risk factor and disorder was based on administrative billing codes (International Classification of Disease versions 9 and 10). The final study cohorts included 1:2 matched group of patients with and without PTSD respectively. The cohorts were matched for age, traditional risk factors such as diabetes, hypertension, hyperlipidemia and smoking, as well as obesity, chronic kidney disease, psychiatric disorders (depression, anxiety), female specific risk factors (e.g., pre-eclampsia), drug and alcohol dependence, neuroendocrine disorders (e.g., hypo or hyperthyroidism), and number of visits. Cox regression was used to model incident stroke as a function of PTSD.Results:The study population included 398,769 patients, including 132,293 with PTSD and 265,846 matched patients without PTSD. The cox regression analysis revealed that PTSD was significantly associated with greater rates of incident stroke (hazard ratio [HR]=1.64, 95% confidence interval: 1.43-1.86, p

Circulation, Volume 146, Issue Suppl_1, Page A11736-A11736, November 8, 2022. Background:Parents of infants born with congenital heart disease (CHD) are at increased risk for mental health problems, including anxiety, depression, and post-traumatic stress (PTS). Few studies have examined to what extent the hospital experience influences these mental health symptoms over time. The purpose of this pilot study was to determine hospital factors predicting parent anxiety, depression, and PTS at 3 months post-discharge.Methods:A convenience sample of 28 biological mother-father dyads was enrolled consecutively from August 2018 to October 2019 from one children’s hospital in the Northeast, US. Parents were instructed to complete questionnaires, including valid and reliable instruments for mental health symptoms, within one week of their infant’s surgery and 3 months post discharge. Associations between hospital factors and each mental health symptom at 3 months post discharge were assessed using linear mixed effects models, accounting for the anticipated correlation between parents of the same infant using an unstructured covariance matrix. Separate linear mixed effects models were constructed for each mental health symptom using backward selection method.Results:For each one unit increase in parental role alteration, anxiety symptoms were estimated to be increased by 5.98 (SE+1.60; p=0.002). Parents with at least a college education were estimated to have greater anxiety symptoms compared to parents with high school/technical school or less (10.89+3.75; p=0.009). For each one unit increase in role alteration, depressive symptoms were estimated to be increased (4.41+1.72; p=0.02). PTS was also significantly predicted by role alteration (5.06+1.91; p=0.02) along with timing of CHD diagnosis, with postnatal diagnosis estimated to increase PTS symptoms by 21.80 (SE+10.07; p=0.04) units compared to prenatal diagnosis.Conclusion:Role alteration experienced by parents during their infant’s hospitalization significantly predicts anxiety, depression, and PTS symptoms 3-months after discharge. Additional factors were identified that can inform mental health screening in this population. Future interventions to enhance the role of parents during infant hospitalization may support parent mental health post discharge.

Circulation, Volume 146, Issue Suppl_1, Page A10270-A10270, November 8, 2022. Introduction:Computational modeling studies indicated that pathological high shear stress (HSS) of 100 dynes/cm2is generated in pulmonary arteries (PA) (100-500μM) in patients with a ventricular septal defect or idiopathic pulmonary arterial hypertension (PAH) and occlusive vascular remodeling. Endothelial-to-mesenchymal transition (EndMT) is a feature of PAH.Hypothesis:Pathological HSS induces EndMT, which contributes to the initiation and progression of PAH.Methods:We applythe Ibidi perfusion system to human PA endothelial cells (EC), to determine whether HSS (100 dynes/cm2) induces EndMT, when compared to normal laminar shear stress (LSS) (15 dynes/cm2). We assessed the mechanism and targeted it to prevent PAH in a mouse with HSS resulting from an aortocaval (AV) shunt.Results:HSS induced EndMT, as assessed by an increase in transcription factors, SNAI1 and SNAI2, reduced BMPR2 (previously shown to inhibit EndMT), decreased EC markers PECAM1 and CDH5, and increased mesenchymal markers, ACTA2 and FSP-1. While the flow-induced transcription factors, KLF2 and KLF4 were similar in LSS and HSS, the co-transcription factor ERG was reduced with HSS. IndeedERGsiRNA under LSS caused EndMT whereas under HSS, transfection ofERGprevented EndMT. To address the significance of our observations in an animal model we created an AV shunt in mice and compared PAH in those sham operated vs transfected with an adeno-associated viral (AAV2- ESGHGYF) vector selectively targeting PAEC with aluciferase(control) or anERGexpressing construct (N=10 per group). Eight weeks after AV shunt, right ventricular systolic pressures was 21.9 ±0.6 mmHg in sham, 37.2±1.0 mmHg in AV shunt with luciferase vector (p

Circulation, Volume 146, Issue Suppl_1, Page A13379-A13379, November 8, 2022. Background:Cardiovascular disease (CVD) is highly prevalent among older persons with HIV (OPWH) occurring on average a decade earlier than non-infected individuals largely due to chronic inflammation, vascular pathology, and psychosocial stressors. Effective cardiovascular risk reduction strategies such as exercise have been shown to lower both physiological and psychosocial stressors but have not been widely reported in the HIV population.Objective:To evaluate the effect of a one-year, moderate intensity aerobic exercise intervention on perceived stress among OPWH with ≥ 2 CVD risk factors.Methods:A secondary analysis was performed utilizing data from Project FiTBRAiN, a 2-arm RCT that included Let’s Move (moderate intensity aerobic exercise intervention) or Let’s Flex (flexibility/stretching attention control) groups. The 14-item Perceived Stress Scale (PSS) was utilized to measure participants’ perceived stress. Data analysis included an analysis of variance with pairwise and between-group differences reported.Results:Participants (n=115) reported a mean age of 55±5.2, and the majority were African American (n=100, 87.0%) and male (n=66, 57.4%). The most common cardiovascular comorbidities were elevated: total cholesterol (n=114, 99.1%), systolic blood pressure (n=108, 93.9%), diastolic blood pressure (n=98, 85.2%), and participants had a mean BMI of 28.29. Baseline 14-item PSS scores for the Let’s Move Program and Let’s Flex Program were 19.49 (SD=7.94) and 21.13 (SD=8.64), respectively, indicating moderate stress levels. Over all time points, the control group (Let’s Flex) had higher perceived stress than the intervention group (Let’s Move), but were not significant.Conclusions:Our findings suggest that moderate levels of psychological stress were present in this population and may be a risk factor for CVD among OPWH. The consistent finding that perceived stress remained lower over time indicates that aerobic exercise may be beneficial for stress reduction. Additional research is needed to determine the optimal dose and mode of exercise that is most beneficial for stress reduction in this population.

Circulation, Volume 146, Issue Suppl_1, Page A14699-A14699, November 8, 2022. Introduction and Hypothesis:Endothelial shear stress (ESS) is the tangential force produced by luminal blood flow on arterial endothelium. Both high ESS and low ESS are known to have atherogenic effects, however, it remains poorly understood how these different forces influence coronary atherosclerosis. We evaluated the impact of ESS changes on biochemical and phenotypic difference of coronary atheroma, as assessed by a novel dual-modal optical coherence tomography-fluorescence lifetime imaging (OCT-FLIm)in vivoin beating human coronary arteries.Methods and Results:We constructed a fully-integrated OCT and multispectral FLIm system based on a low-profile dual-modal imaging catheter. High-speed OCT-FLIm could be performed safely in patients undergoing coronary revascularization (Pullback speed: 10-20mm/sec). 3D artery model for computational fluid dynamics was reconstructed by fusion of OCT and angiography. We analyzed spatial associations between ESS and multispectral FLIm information: ch.3(542nm) = fibroatheroma with inflammation; ch.1 (390nm) = loose fibrous tissue (healed plaque). OCT-FLIm visualized coronary microstructure clearly and offered correctly-coregistered biochemical readouts of coronary atherosclerotic plaquein vivoin a label-free manner. Fibroatheromas with increased inflammation activity, as assessed by ch.3 FLIm, were found in low ESS area. On the other hands, high ESS area colocalized with regions with increased ch.1 lifetime, a FLIm signature of loose fibrous tissue (healed plaque). Based on a coregistered ESS-FLIm data, we found a statistically significant negative correlation between ESS and ch.3 lifetime (p >0.001) and a positive correlation between ESS and ch.1 lifetime (p >0.001).Conclusions:Low ESS was associated with lipid and macrophage infiltration whereas high ESS was associated with presence of loose fibrous tissue, a histologic marker of recent plaque disruption leading to rapid plaque progression. Our novel imaging strategy enabling comprehensive evaluation of complex interaction between ESS and biochemical phenotype of plaques is expected to enhance understanding of coronary atherosclerosis biology.

Circulation, Volume 146, Issue Suppl_1, Page A10014-A10014, November 8, 2022. Background:Work-related stress is a psychosocial risk factor linked to a higher risk of adverse health outcomes, especially cardiovascular disease (CVD). However, the association between work-related stress and ideal cardiovascular health (CVH) is not well established. We examined whether work-related stress was negatively associated with favorable CVH in a multi-ethnic population of adults free of CVD at baseline.Methods:We analyzed cross-sectional data of 6,486 men and women aged 45-84 years. Work-related stress was assessed by the presence or absence of ongoing job difficulty and ongoing job difficulty for >6 months. CVH was measured by a scoring system that assigned points to 7 metrics (smoking, physical activity, body mass index, diet, total cholesterol, blood pressure and blood glucose). Each metric had 3 categories: poor (0 points), intermediate (1 point) and ideal (2 points). The total score attainable was 14 points, categorized as inadequate (0-8 points), average (9-10 points) and optimal (11-14 points). We used polytomous logistic regression to examine the association of work-related stress with the CVH score and number of ideal metrics, adjusted for sociodemographic factors.Results:The mean age (SD) was 62 (10) years and 53% were women. Ongoing job difficulty was reported by 14% of participants while 13% reported ongoing job difficulty for >6 months. Participants who reported ongoing job difficulty had 21% and 24% lower odds of having average and optimal CVH scores, respectively(Table).Additionally, the presence of ongoing job difficulty for >6 months was associated with 23% and 24% lower odds of having average and optimal CVH scores, respectively. A similar trend was observed for the association of work-related stress with the number of ideal metrics.Conclusion:Work-related stress was negatively associated with favorable CVH. Stress reduction and CVH promotion programs in the workplace may decrease the incidence of CVD.

Circulation, Volume 146, Issue Suppl_1, Page A12063-A12063, November 8, 2022. Introduction:Antidepressants, namely selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs), are efficacious in reducing posttraumatic stress disorder (PTSD) symptoms, but their implications for cardiovascular health are unclear. Although SSRI/SNRI treatment could improve PTSD—thus decreasing cardiovascular risk, antidepressant use has also predicted cardiovascular events. This study examined if antidepressant use was associated with developing ischemic heart disease (IHD) in women veterans with PTSD.Methods:The Veterans Affairs (VA) electronic health record (EHR) database was used to identify women veterans with PTSD who engaged with VA healthcare from 2000-2019. Antidepressant use (documented in the EHR) was categorized as SSRIs, SNRIs, both SSRIs/SNRIs, other, or none (ref). We used Cox regression with time-varying exposure and covariates to estimate effects of antidepressants on risk of incident IHD (angina, MI, CAD). Once a woman was exposed to antidepressants, she was considered exposed until IHD onset or censoring. Age, race, ethnicity, and a range of time-varying risk factors [traditional risk factors (e.g., hypertension), other medical risk factors (e.g., obesity), women-specific risk factors (e.g., preeclampsia), psychiatric risk factors (e.g., depression)], were covariates.Results:The analytic sample comprised 143,324 women without IHD at start of follow-up; mean age was 36.1 years (SD=11.0). Over a median follow-up of 8.6 years, there were 6,633 incident IHD cases. When adjusting for demographics and traditional IHD risk factors, exposure to SNRIs was associated with a 33% greater rate of IHD (95% CI: 1.24-1.43), SSRIs with a 27% greater rate (95% CI: 1.20-1.34), both SSRIs/SNRIs with a 59% greater rate (95% CI: 1.01-2.49), and other antidepressants with a 24% greater rate (95% CI: 1.17-1.31). Associations with SNRIs (HR=1.21, 95% CI: 1.12-1.30), SSRIs (HR=1.15, 95% CI: 1.09-1.22), and other antidepressants (HR=1.19, 95% CI: 1.13-1.26) remained significant in fully adjusted models.Conclusions:Antidepressant use in women veterans with PTSD may exacerbate risk of IHD. Mechanism-focused research and further work in women veterans without PTSD is also needed.

Circulation, Volume 146, Issue Suppl_1, Page A15056-A15056, November 8, 2022. Ischemic heart disease (IHD), a major cause of heart failure, is characterized by metabolic dysfunction and myocardial cell death. Cellular hypoxia activates hypoxia inducible factor 1α (HIF1α) to initiate metabolic, angiogenic, and growth-factor related responses. Under normoxia, HIF1α is degraded by prolyl hydroxylase (PHD) domain-containing proteins via the proteasome. Due to the short half-life of HIF1α (

Circulation, Volume 146, Issue Suppl_1, Page A10038-A10038, November 8, 2022. Introduction:Low endothelial shear stress (ESS) is a pro-atherogenic stimulus associated with coronary plaque development, while high plaque structural stress (PSS) and its heterogeneity is associated with plaque destabilization. Previous studies showed that combining ESS and PSS additively predicts plaque progression, but no studies have determined their ability to predict major adverse cardiovascular events (MACE). We examined whether combining ESS and PSS improves MACE prediction in patients with acute coronary syndrome.Methods:We examined baseline ESS, ESS gradient, PSS, and PSS heterogeneity index (HI) in 22 non-culprit lesions (NCL) leading to future MACE, and 64 randomly selected control NCLs without MACE from the PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree) study. ESS was calculated by computational fluid dynamics and PSS by finite element analysis on co-registered lesions.Results:86 lesions (55 thin-cap and 31 thick-cap fibroatheromas) were analyzed from 67 patients. Lesions that caused future MACE showed baseline higher PSS HI (0.32 vs. 0.24, p

Circulation, Volume 146, Issue Suppl_1, Page A11502-A11502, November 8, 2022. Background -Mitral valve prolapse (MVP) is a common valvular abnormality found in approximately 2.4% of the population. Whereas the majority of cases are benign, an increasingly recognized sequela of MVP is sudden cardiac death (SCD), but triggers and risk factors for SCD are not well-defined. It is theorized that increased stretch on the papillary muscles due to MVP leads to papillary muscle fibrosis and cellular changes of local conduction properties, increasing the risk of ventricular arrhythmias and SCD.Hypothesis- We hypothesized that patients with MVP and SCD would have increased ventricular arrhythmias and ECG changes compared to MVP controls during exercise stress testing.Methods -The study population was generated from the Duke Epic. Patients were included if they had guideline-based diagnosis of MVP on echocardiogram or cardiac magnetic resonance imaging. Increase in ventricular arrhythmias during exercise was defined as >/= 10 PVCs per minute, multifocal PVCs, or >/= 2 PVCs in a row.Results-A total 2,513 patients with MVP were screened. 18 patients with SCD. Patients with SCD were younger [(47.22 +/- 12.2 ) vs. (58.0 +/- 18.7), p=0.02], more likely to be female (89.9% vs 64%, p=0.04) and had increased rate of bileaflet prolapse (72% vs. 40%, p=0.01) compared to controls. Patients with sudden cardiac death had either dynamic T wave changes or increased ventricular arrhythmias with stress testing versus controls [12/18 (66.7%) vs 17/75 (22.6%), p

Circulation, Volume 146, Issue Suppl_1, Page A11202-A11202, November 8, 2022. Introduction:Caregivers of patients with heart failure (HF) are at high risk of low quality of life due to stress-related to caregiving. Self-reported measures are commonly used to assess relatively long-term stress related to caregiving. Still, biological markers of stress, a short-term stress measure, are rarely used. There is limited knowledge on whether both can predict the quality of life in caregivers of patients with HF.Hypothesis:The stress biomarker (serum cortisol) and subjective distress related to caregiving (Caregiver Burden Inventory) predict the quality of life in caregivers of patients with HF.Methods:In this cross-sectional study, Taiwanese caregivers of patients with HF completed surveys including stress-related caregiving and quality of life measured by the Caregiving Burden Inventory and the Short Form-36, respectively. A blood sample for serum cortisol was collected between 9 and 12 AM. Independent t-test and multivariable linear regression analysis were conducted adjusting for age, gender, education, marital status, relationship with care-recipient and depressive symptoms (Patient Health Questionnaire).Results:Of the 113 caregivers (mean age 54.5 years, 70.8% female, 78% married/cohabitated), 59% cared for patients with NYHA class III/V. Single caregivers had higher serum cortisol levels than married caregivers (11.4 vs. 8.5, p =.002). Males had a significantly higher serum cortisol level than females (10.7 vs. 8.5, p =.010), but males reported a lower caregiver burden than females (1.3 vs. 1.6, p =.049). Both serum cortisol (β =-.36, P=.012) and caregiver burden (β = -.29, P= .018) were significant predictors of physical well-being. Serum cortisol (β= -.28, p=.026) and caregiver burden (β =-.25, p =.027) also significantly predicted mental well-being.Conclusions:Although stress levels are different by caregivers’ characteristics, both cortisol level and self-report caregiver burden have similar predictability of quality of life in caregivers of patients with HF. Reducing stress and caregiver burden is necessary to improve the quality of life in this population.

Circulation, Volume 146, Issue Suppl_1, Page A14139-A14139, November 8, 2022. Introduction:AHA guidelines recommend non-invasive cardiac testing (NIT) within 72 hours after an emergency department (ED) evaluation for suspected acute coronary syndrome (ACS), after acute myocardial infarction (AMI) has been excluded. However, the effectiveness of this strategy to reduce the risk of future AMI or death, in low-risk patients is contested.Hypothesis:We hypothesized that in patients with low risk based on history, electrocardiogram, age, risk factors and troponin (HEART) based scoring, early NIT may not be beneficial compared to higher risk.Methods:We compared the effectiveness of early NIT vs. no early testing, in a retrospective cohort of adult (age ≥18) members of the Kaiser Permanente Southern California health system from 05/2016-12/2020. We included all adults presenting at EDs with suspected ACS and who had data to compute HEART score. We stratified the cohort into low risk (score 0-3); intermediate risk (score 4-6) and high-risk (score ≥7) based on HEART score. Within each group, confounder adjusted instrumental variables models were used to evaluate the marginal effect of early NIT, and the number needed to treat (NNT) was calculated as the inverse of the absolute composite risk reduction in death/AMI within 30 days of ED discharge.Results:The cohort included 174,936 patients [61% Low risk (mean age 53; female 58%; early NIT 5%), 36% intermediate risk (mean age 71; female 72%; early NIT 18%), and 3% high risk (mean age 74, female 45%; early NIT 23%)]. The risk reduction in 30-day death/AMI due to early NIT increased progressively through the intermediate-risk (NNT = 59) and high-risk groups (NNT = 24) (Table 1). Risk reduction in the low-risk group was not statistically significant.Conclusions:HEART score based high risk patients may benefit the most from early NIT. However, the majority of the suspected ACS cohort was classified as low risk and the benefit of early NIT on 30-day death/AMI was uncertain in this low-risk group.