Shady Abohashem

Harvard Medical School | HMS
42.83 · Doctor of Medicine
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Introduction
Leveraging advanced multi-imaging modalities to understand mechanistic link between environmental stressors, polygenic risk, lifestyle and CVD.
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Harvard Medical School | HMS
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Instructor
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Purdue University Northwest
University of Ferrara
Massachusetts General Hospital
Tabriz University of Medical Sciences
T.C. Süleyman Demirel Üniversitesi
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Harvard University
Semmelweis University
Saint Vincent Hospital
Massachusetts General Hospital
Massachusetts General Hospital
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Projects (10)
Air Pollution and Cardiovascular diseases
LAAC and Atrial Fibrillation
Systemic review and meta-analysis
Liver fat content and arterial inflammation
mechanistic insights: liver fat content and MACE
Research
Research Items (98)
Aims: Chronic noise exposure associates with increased cardiovascular disease (CVD) risk; however, the role of confounders and the underlying mechanism remain incompletely defined. The amygdala, a limbic centre involved in stress perception, participates in the response to noise. Higher amygdalar metabolic activity (AmygA) associates with increased CVD risk through a mechanism involving heightened arterial inflammation (ArtI). Accordingly, in this retrospective study, we tested whether greater noise exposure associates with higher: (i) AmygA, (ii) ArtI, and (iii) risk for major adverse cardiovascular disease events (MACE). Methods and results: Adults (N = 498) without CVD or active cancer underwent clinical 18F-fluorodeoxyglucose positron emission tomography/computed tomography imaging. Amygdalar metabolic activity and ArtI were measured, and MACE within 5 years was adjudicated. Average 24-h transportation noise and potential confounders were estimated at each individual's home address. Over a median 4.06 years, 40 individuals experienced MACE. Higher noise exposure (per 5 dBA increase) predicted MACE [hazard ratio (95% confidence interval, CI) 1.341 (1.147-1.567), P < 0.001] and remained robust to multivariable adjustments. Higher noise exposure associated with increased AmygA [standardized β (95% CI) 0.112 (0.051-0.174), P < 0.001] and ArtI [0.045 (0.001-0.090), P = 0.047]. Mediation analysis suggested that higher noise exposure associates with MACE via a serial mechanism involving heightened AmygA and ArtI that accounts for 12-26% of this relationship. Conclusion: Our findings suggest that noise exposure associates with MACE via a mechanism that begins with increased stress-associated limbic (amygdalar) activity and includes heightened arterial inflammation. This potential neurobiological mechanism linking noise to CVD merits further evaluation in a prospective population.
BACKGROUND: Chronic exposure to socioeconomic or environmental stressors associates with greater stress-related neurobiological activity (ie, higher amygdalar activity [AmygA]) and higher risk of major adverse cardiovascular events (MACE). However, among individuals exposed to such stressors, it is unknown whether neurobiological resilience (NBResilience, defined as lower AmygA despite stress exposure) lowers MACE risk. We tested the hypotheses that NBResilience protects against MACE, and that it does so through decreased bone marrow activity and arterial inflammation. METHODS: Individuals underwent 18F-fluorodeoxyglucose positron emission tomography/computed tomography; AmygA, bone marrow activity, and arterial inflammation were quantified. Chronic socioeconomic and environmental stressors known to associate with AmygA and MACE (ie, transportation noise exposure, neighborhood median household income, and crime rate) were quantified. Heightened stress exposure was defined as exposure to at least one chronic stressor (ie, the highest tertile of noise exposure or crime or lowest tertile of income). MACE within 5 years of imaging was adjudicated. Relationships were evaluated using linear and Cox regression, Kaplan-Meier survival, and mediation analyses. RESULTS: Of 254 individuals studied (median age [interquartile range]: 57 years [46–67], 36.7% male), 166 were exposed to at least one chronic stressor. Among stress-exposed individuals, 12 experienced MACE over a median follow-up of 3.75 years. Among this group, higher AmygA (ie, lower resilience) associated with higher bone marrow activity (standardized β [95% CI]: 0.192 [0.030–0.353], P=0.020), arterial inflammation (0.203 [0.055–0.351], P=0.007), and MACE risk (standardized hazard ratio [95% CI]: 1.927 [1.370–2.711], P=0.001). The effect of NBResilience on MACE risk was significantly mediated by lower arterial inflammation (P<0.05). CONCLUSIONS: Among individuals who are chronically exposed to socioeconomic or environmental stressors, NBResilience (AmygA <1 SD above the mean) associates with a >50% reduction in MACE risk, potentially via reduced arterial inflammation. These data raise the possibility that enhancing NBResilience may decrease the burden of cardiovascular disease.
Aims Air pollution [i.e. particulate matter with diameter <2.5 μm (PM2.5)] is a risk factor for major adverse cardiovascular events (MACE). While PM2.5 promotes leucopoiesis and atherosclerotic inflammation in experimental models, it is unknown whether this occurs in humans. We tested in humans (a) whether PM2.5 associates with higher leucopoietic tissue activity and arterial inflammation (ArtI), (ii) whether these associations persist after accounting for the effects of potential confounders including socioeconomics, traffic noise, and risk factors, and (iii) whether these tissue effects mediate the association between air pollution and MACE. Methods and results Individuals (N = 503) without cardiovascular disease (CVD) or active malignancy underwent 18 F-fluorodeoxyglucose positron emission tomography/computed tomography. Major adverse cardiovascular event was adjudicated over 5 years of follow-up. Leucopoietic tissue activity (in bone marrow and spleen) as well as ArtI were measured. Annual PM2.5 levels were assessed at each individual’s home address. At baseline, higher PM2.5 associated with increased leucopoietic activity [standardized (95% CI): 0.129 (0.042, 0.215), P = 0.004] as well as ArtI [0.088 (0.006, 0.171), P = 0.036] after adjusting for CVD risk factors. Over a median 4.1 years, 40 individuals experienced MACE. PM2.5 exposure associated with MACE [Cox HR (95% CI): 1.404 (1.135, 1.737), P = 0.002], remaining significant after adjustment for CVD risk factors and other potential confounders. Mediation analysis demonstrated that increased leucopoietic activity and ArtI serially mediate the link between PM2.5 exposure and MACE. Conclusions Higher air pollution exposure associates with heightened leucopoietic activity and ArtI and independently predicts MACE through a biological pathway that includes higher leucopoietic activity and ArtI in series.
Aims Activity in the amygdala, a brain centre involved in the perception of and response to stressors, associates with: (i) heightened sympathetic nervous system and inflammatory output and (ii) risk of cardiovascular disease. We hypothesized that the amygdalar activity (AmygA) ratio is heightened among individuals who develop Takotsubo syndrome (TTS), a heart failure syndrome often triggered by acute stress. We tested the hypotheses that (i) heightened AmygA precedes development of TTS and (ii) those with the highest AmygA develop the syndrome earliest. Methods and results Individuals (N=104, median age 67.5 years, 72% female, 86% with malignancy) who underwent clinical 18 F-FDG-PET/CT imaging were retrospectively identified: 41 who subsequently developed TTS and 63 matched controls (median follow-up 2.5 years after imaging). AmygA was measured using validated methods. Individuals with (vs. without) subsequent TTS had higher baseline AmygA (P=0.038) after adjusting for TTS risk factors. Further, AmygA associated with the risk for subsequent TTS after adjustment for risk factors [standardized hazard ratio (95% confidence interval): 1.643 (1.189, 2.270), P=0.003]. Among the subset of individuals who developed TTS, those with the highest AmygA (>mean + 1 SD) developed TTS ∼2 years earlier after imaging vs. those with lower AmygA (P=0.028). Conclusion Higher AmygA associates with an increased risk for TTS among a retrospective population with a high rate of malignancy. This heightened neurobiological activity is present years before the onset of TTS and may impact the timing of the syndrome. Accordingly, heightened stress-associated neural activity may represent a therapeutic target to reduce stress-related diseases, including TTS.
Background Chronic transportation noise exposure associates with cardiovascular events through a link involving heightened stress-associated neurobiological activity (as amygdalar metabolic activity, AmygA) on ¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography (¹⁸F-FDG-PET/CT). Increased AmygA also associates with greater visceral adipose tissue (VAT) and type 2 diabetes mellitus (DM). While relationships between noise exposure and VAT and DM have been reported, the underlying mechanisms remain incompletely understood. We tested whether: 1) transportation noise exposure associates with greater a) baseline and gains in VAT and b) DM risk, and 2) heightened AmygA partially mediates the link between noise exposure and these metabolic diseases. Methods VAT was measured in a retrospective cohort (N=403) who underwent clinical ¹⁸F-FDG-PET/CT. AmygA was measured in those with brain imaging (N=238). Follow-up VAT was remeasured on available imaging (N=67). Among individuals (N=224) without baseline DM, incident DM was adjudicated over two years from clinical records. Noise (24-hour average) was modeled at each individual’s home address. Linear regression, survival, and mediation analyses were employed. Results Higher noise exposure (upper tertile vs. others) associated with greater: baseline VAT (standardized β [95% confidence interval (CI)]=0.230 [0.021, 0.438], p=0.031), gains in VAT (0.686 [0.185, 1.187], p=0.008 adjusted for baseline VAT), and DM (hazard ratio [95% CI]=2.429 [1.031, 5.719], p=0.042). The paths of: ↑noise exposure→↑AmygA→↑baseline VAT and ↑noise exposure→↑AmygA→↑subsequent DM were significant (p<0.05). Conclusions Increased transportation noise exposure associates with greater VAT and DM. This relationship is partially mediated by stress-associated neurobiological activity. These findings suggest altered neurobiology contributes to noise exposure’s link to metabolic diseases.
Background: Air pollution and noise exposures individually associate with major adverse cardiovascular events (MACE) via a mechanism involving arterial inflammation (ArtI); however, their combined impact on ArtI and MACE remains unknown. We tested whether dual (vs. one or neither) exposure associates with greater ArtI and MACE risk and whether MACE risk is mediated via ArtI. Methods: Individuals (N = 474) without active cancer or known cardiovascular disease with clinical 18F-FDG-PET/CT imaging were followed for 5 years for MACE. ArtI was measured. Average air pollution (particulate matter ≤ 2.5 μm, PM2.5) and transportation noise exposure were determined at individual residences. Higher exposures were defined as noise > 55 dBA (World Health Organization cutoff) and PM2.5 ≥ sample median. Results: At baseline, 46%, 46%, and 8% were exposed to high levels of neither, one, or both pollutants; 39 experienced MACE over a median 4.1 years. Exposure to an increasing number of pollutants associated with higher ArtI (standardized β [95% CI: .195 [.052, .339], P = .008) and MACE (HR [95% CI]: 2.897 [1.818-4.615], P < .001). In path analysis, ArtI partially mediated the relationship between pollutant exposures and MACE (P < .05). Conclusion: Air pollution and transportation noise exposures contribute incrementally to ArtI and MACE. The mechanism linking dual exposure to MACE involves ArtI.
Funding Acknowledgements Type of funding sources: None. Background Physical inactivity and sedentary behavior are among the leading modifiable risk factors worldwide for cardiovascular (CV) disease and mortality. However, data about disparities of CV mortality related to physical inactivity, has been limited and/or inconsistent. Purpose We sought to evaluate county-level associations between physical inactivity and cardiovascular mortality (CVM) in overall population and among different age, gender, and racial/ethnic subgroups. Methods Age-adjusted CV mortality rates (ACVM) between 2011 to 2019, were obtained using Wide-ranging Online Data for Epidemiologic Research tool of Center for Disease Control (CDC). Behavioral Risk Factors Surveillance System, CDC Diabetes Interactive Atlas, Census population estimates, environmental public health network and drinking water information system, were utilized to acquire county physical inactivity levels (percentage of adults reporting no physical activity in past month), demographics, rates of obesity, diabetes, smoking and environmental factors. Poisson generalized linear mixed models were employed to assess incidence rate ratios (IRR) of ACVM associated with physical inactivity while adjusting for other potential confounders. The burden of additional yearly deaths (AYD) per 100,000 individuals was calculated by multiplying the baseline CV death rates by the percentage increase attributable to physical inactivity in each subgroup. Results Among 303,857,140 residents (49.5% men, 11.9% non-Hispanic blacks, 23.8% [45-64 age group]) lived at 2900 US counties in 2011, total 7,226,447 (2.4%) CV deaths occurred between 2011-2019. In fully adjusted model*, physical inactivity significantly associated with high ACVM (IRR: 1.02; 95% CI: 1.01 to 1.02), that translated to 4.4 AYD per 100,000 individuals. Notably, physical inactivity associated with a relatively higher ACVM among middle aged adults [45 to 64] (IRR: 1.04; 95% CI: 1.03 to 1.04) versus elderly [≥65] (IRR: 1.02; 95% CI: 1.01 to 1.02), and in males (IRR: 1.03; 95% CI: 1.02 to 1.03) versus females (IRR: 1.01; 95% CI: 1.01 to 1.02). Interestingly, middle aged adults were relatively most impacted by physical inactivity as compared to elderly, among each of gender and racial/ethnic subgroups, (Figure). Additionally, physical inactivity seemed to have similar impact on both non-Hispanic whites (IRR: 1.02), and non-Hispanic blacks (IRR: 1.02), with a slightly larger impact among Hispanics (IRR: 1.03), (Figure). Conclusion Physical inactivity is robustly associated with age-adjusted CVM independent of other well-established determinants of CV death, including CV risk factors, socioeconomic, environmental and health care access factors. Physical inactivity appears to confer greater negative impact among middle-aged adults, males, and Hispanic individuals. Therefore, public health policies directed towards greater efforts at preventing sedentary behavior and promoting adequate physical activity, are desperately needed.
Funding Acknowledgements Type of funding sources: None. Background Food insecurity is a global public health challenge, that is defined as a social condition of limited or uncertain access to adequate food. Food insecurity is significantly linked to a myriad of negative health outcomes including high risk of cardiovascular (CV) morbidities and mortality. However, data on disparities of CV mortality attributable to food insecurity, is limited. Purpose We sought to investigate the independent association between food insecurity and cardiovascular mortality among age, gender, and race/ethnicity subgroups. Methods Age-adjusted CV mortality rates (ACVM) between 2014 to 2019, were obtained using Wide-ranging Online Data for Epidemiologic Research tool of Center for Disease Control (CDC). Food insecurity levels were obtained using the Core Food Insecurity Model. Census population estimates, CDC Diabetes Interactive Atlas, and the Behavioral Risk Factors Surveillance System, were utilized to acquire county-level demographics, rates of obesity, diabetes, and smoking data. Poisson generalized linear mixed models were employed to assess incidence rate ratios (IRR) of CV mortality associated with food insecurity while adjusting for other potential confounders. The burden of additional yearly deaths (AYD) per 100,000 individuals was calculated by multiplying the baseline CV death rates by the percentage increase attributable to food insecurity in each subgroup. Results Of 317,203,618 residents (49.6% men, 12.1% black) lived at 2878 US counties in 2014, total 4,933,002 (1.6%) CV deaths occurred between 2014-2019. In fully adjusted model*, food insecurity significantly associated with high levels of ACVM (IRR: 1.03; 95% CI: 1.02 to 1.04), that translated to 6.9 AYD per 100,000 individuals. Notably, food insecurity associated with a relatively higher ACVM among middle aged adults [45 to 64] (IRR: 1.04) as compared to elderly [≥65] (IRR: 1.02), and in non-Hispanic blacks (IRR: 1.05) versus non-Hispanic whites (IRR: 1.03). Interestingly, food insecurity had a relatively larger impact on middle aged adults among non-Hispanic whites (IRR: 1.07; 10.6 AYD), while among non-Hispanic blacks, elderly group were most impacted (IRR: 1.05; 76.5 AYD). Additionally, ACVM associated with food insecurity, was significantly similar among males (IRR: 1.03), and females (IRR: 1.03), with a greater impact among middle aged subgroup of each gender (IRR: 1.06; IRR: 1,04, respectively), (Figure). Conclusion Food insecurity is strongly associated with county-level age-adjusted CV mortality, independent of other well-established determinants of CV death, including CV risk factors, socioeconomic, environmental and health care access factors. Food insecurity has the greatest impact among those most vulnerable and disadvantaged, namely middle-aged adults and non-Hispanic black individuals. Accordingly, reducing levels of food insecurity, and addressing disparities in associated CV mortality rates, are an emergent public health priority.
Introduction: A significant rise in the rates of Diabetes Mellitus (DM) amongst U.S. adults has been observed in recent decades. Although associations between DM and cardiovascular mortality (CVM) are well-known, disparities in related CVM are unclear. Hypothesis: We sought to study the independent impact of DM on CVM among age, sex, and race/ethnic subgroups. Methods: County-level age adjusted CVM rates (ACVM) were obtained from the CDC WONDER database. DM prevalence, demographics, socioeconomic, environmental, and other cardiovascular risk factors obtained from the County Health Rankings project database. Multivariate generalized linear mixed models were used to investigate the independent association between ACVM and DM amongst different subgroups using incidence rate ratios (IRRs) to evaluate the relative impact and additional yearly deaths (AYD) to evaluate the absolute impact of DM. Results: Among 309,886,995 residents (50% women, 11.7% non-Hispanic blacks, 23.8% [45-64 age group]) lived at 2900 US counties in 2011, total 7,381,448 (2.4%) CV deaths occurred between 2011-2019. In fully adjusted model*, DM significantly associated with ACVM (IRR: 1.013; 95% CI: 1.006 to 1.020; AYD: 3). This association remained robust amongst those aged 45 to 64 (IRR: 1.023; 95% CI: 1.013 to 1.033; AYD: 3.4), those aged ≥65 (IRR: 1.010; 95% CI: 1.003 to 1.017; AYD: 14.5), males (IRR: 1.023; 95% CI: 1.014 to 1.031; AYD: 6.2), females (IRR: 1.010; 95% CI: 1.001 to 1.018; AYD: 1.8), non-Hispanic Whites (IRR: 1.011; 95% CI: 1.003 to 1.018; AYD: 2.5); and 45-64 age group of non-Hispanic blacks (IRR: 1.033; 95% CI: 1.001 to 1.066; AYD: 9.2); Figure. Conclusion: Increased DM prevalence is independently associated with high ACVM among different age, sex, and race/ethnic groups, and this impact is most pronounced in the middle-aged group of males, non-Hispanic whites, and non-Hispanic blacks. Population-level interventions are imperative to effectively combat this ongoing epidemic.
Background The extent to which health care systems have adapted to the COVID-19 pandemic to provide necessary cardiac diagnostic services is unknown. Objectives The aim of this study was to determine the impact of the pandemic on cardiac testing practices, volumes and types of diagnostic services, and perceived psychological stress to health care providers worldwide. Methods The International Atomic Energy Agency conducted a worldwide survey assessing alterations from baseline in cardiovascular diagnostic care at the pandemic’s onset and 1 year later. Multivariable regression was used to determine factors associated with procedure volume recovery. Results Surveys were submitted from 669 centers in 107 countries. Worldwide reduction in cardiac procedure volumes of 64% from March 2019 to April 2020 recovered by April 2021 in high- and upper middle-income countries (recovery rates of 108% and 99%) but remained depressed in lower middle- and low-income countries (46% and 30% recovery). Although stress testing was used 12% less frequently in 2021 than in 2019, coronary computed tomographic angiography was used 14% more, a trend also seen for other advanced cardiac imaging modalities (positron emission tomography and magnetic resonance; 22%-25% increases). Pandemic-related psychological stress was estimated to have affected nearly 40% of staff, impacting patient care at 78% of sites. In multivariable regression, only lower-income status and physicians’ psychological stress were significant in predicting recovery of cardiac testing. Conclusions Cardiac diagnostic testing has yet to recover to prepandemic levels in lower-income countries. Worldwide, the decrease in standard stress testing is offset by greater use of advanced cardiac imaging modalities. Pandemic-related psychological stress among providers is widespread and associated with poor recovery of cardiac testing.
Importance: Long-term disability after stroke is associated with socioeconomic status (SES). However, the reasons for such disparities in outcomes remain unclear. Objective: To assess whether lower SES is associated with larger admission infarct volume and whether initial infarct volume accounts for the association between SES and long-term disability. Design, setting, and participants: This cohort study was conducted in a prospective, consecutive population (n = 1256) presenting with acute ischemic stroke who underwent magnetic resonance imaging (MRI) within 24 hours of admission. Patients were recruited in Massachusetts General Hospital, Boston, from May 31, 2009, to December 31, 2011. Data were analyzed from May 1, 2019, until June 30, 2020. Main outcomes and measures: Initial stroke severity (within 24 hours of presentation) was determined using clinical (National Institutes of Health Stroke Scale [NIHSS]) and imaging (infarct volume by diffusion-weighted MRI) measures. Stroke etiologic subtypes were determined using the Causative Classification of Ischemic Stroke algorithm. Long-term stroke disability was measured using the modified Rankin Scale. Socioeconomic status was estimated using zip code-derived median household income and census block group-derived area deprivation index (ADI). Regression and mediation analyses were performed. Results: A total of 1098 patients had imaging and SES data available (mean [SD] age, 68.1 [15.7] years; 607 men [55.3%]). Income was inversely associated with initial infarct volume (standardized β, -0.074 [95% CI, -0.127 to -0.020]; P = .007), initial NIHSS (standardized β, -0.113 [95% CI, -0.171 to -0.054]; P < .001), and long-term disability (standardized β, -0.092 [95% CI, -0.149 to -0.035]; P = .001), which remained significant after multivariable adjustments. Initial stroke severity accounted for 64% of the association between SES and long-term disability (standardized β, -0.063 [95% CI, -0.095 to -0.029]; P < .05). Findings were similar when SES was alternatively assessed using ADI. Conclusions and relevance: The findings of this cohort study suggest that lower SES is associated with larger infarct volumes on presentation. These SES-associated differences in initial stroke severity accounted for most of the subsequent disparities in long-term disability in this study. These findings shift the culpability for SES-associated disparities in poststroke disability from poststroke factors to those that precede presentation.
Background: The literature on the mortality and 30-day readmissions for acute heart failure and for acute myocardial infarction among renal-transplant recipients is limited. Objective: To study the in-hospital mortality, cardiovascular complications, and 30-day readmissions among renal transplant recipients (RTRs). Methods: Data from the national readmissions database sample, which constitutes 49.1% of all hospitals in the United States and represents more than 95% of the stratified national population, was analyzed for the years 2012-2018 using billing codes. Results: A total of 588,668 hospitalizations in renal transplant recipients (mean age 57.7 ± 14.2 years; 44.5% female) were recorded in the study years. A total of 15,788 (2.7%) patients had a diagnosis of acute heart failure; 11,320 (71.7%) had acute heart failure with preserved ejection fraction and 4468 (28.3%) had acute heart failure with reduced ejection fraction; 17,256 (3%) patients had myocardial infarction, 3496 (20%) had ST-Elevation myocardial infarction while 13,969 (80%) had non-ST-elevation myocardial infarction. Overall, 11,675 (2%) renal-transplant patients died, of whom 757 (6.5%) had acute heart failure, 330 (2.8%) had acute reduced and 427 (3.7%) had acute preserved ejection fraction failure. Among 1652 (14.1%) patient deaths with myocardial infarction, 465 (4%) were ST-elevation- and 1187 (10.1%) were non-ST-Elevation-related. The absolute yearly mortality rate due to acute heart failure increased over the years 2012-2018 (p-trend 0.0002, 0.001, 0.002, 0.05, respectively), while the mortality rate due to myocardial infarction with ST-elevation decreased (p-trend 0.002). Conclusion: Cardiovascular complications are significantly associated with hospitalizations among RTRs. The absolute yearly mortality, and rate of heart failure (with reduced or preserved ejection fraction) increased over the study years, suggesting that more research is needed to improve the management of these patients.
Objective To study coronary interventions and mortality among patients with ST-elevated myocardial infarction (STEMI) who were admitted with septic shock. Methods Data from the national emergency department sample (NEDS) that constitutes 20% sample of hospital-owned emergency departments in the United States was analyzed for the septic shock related visits from 2016 to 2018. Septic shock was defined by the ICD codes. Results Out of 1 375 507 adult septic shock patients, 521 300 had a primary diagnosis of septic shock (mean age 67.41±15.67 years, 51.1% females) in the national emergency database for the years 2016 to 2018. Of these patients, 2768 (0.53%) had STEMI recorded during the hospitalization. Mortality rates for STEMI patients were higher than patients without STEMI (52.3% vs 23.5%). Mortality rates improved with PCI among STEMI patients (43.8% vs 56.2%). Coronary angiography was performed among 16% of patients of which percutaneous coronary intervention (PCI) rates were 7.7% among patients with STEMI septic shock. PCI numerically improved mortality, however, had no significant difference than patients without PCI on multivariate logistic regression and univariate logistic regression post coarsened exact matching of baseline characteristics among STEMI patients. Among the predictors, STEMI was a significant predictor of mortality in septic shock patients (OR 2.87, 95% CI 2.37-3.49; P<.001). Age, peripheral vascular disease, were predominant predictors of mortality in STEMI with septic shock subgroup ( P <.001). Pneumonia was the predominant underlying infection among STEMI (36.4%) and without STEMI group (29.5%). Conclusion STEMI complicating septic shock worsens mortality. PCI and coronary angiography numerically improved mortality, however, had no significant difference from patients without PCI. More research will be needed to improve mortality in such a critically ill subgroup of patients.
Introduction: Air pollution (particulate matter of diameter <2.5 μm, PM2.5) and genetic risk for coronary artery disease (CAD) each associate with cardiovascular disease (CVD). It is unknown whether genetic risk for CAD enhances CVD risk associated with air pollution exposure. Hypothesis: We tested the hypothesis that high genetic risk for CAD accentuates the adverse impact of air pollution on CVD, (as coronary artery calcium [CAC]) and major adverse cardiovascular events [MACE]). Methods: Participants (N=9340, median age 66 yrs, 49% male) in the Mass General Brigham Biobank with genetic and air pollution data were studied. Genome wide polygenic risk score for CAD (PRSCAD) and principal components of ancestry (PCI) were determined. Average PM2.5 exposure one year before each person’s enrollment was derived using home addresses and Environmental Protection Agency data. CAC was assessed on those with available CT images (N=548). MACE and CVD risk factors were evaluated via International Classification of Diseases codes. Socioeconomic status (SES) was assessed as residential zip code level income using US Census data. The presence of an interaction between high PM2.5 and PRSCAD vs. MACE was tested. Results: The Combination of high PRSCAD and PM2.5 (both ≥ median vs. others) associated with greater CAC [standardized β (95% CI): 0.13 (0.06, 0.19), p=0.0002, Fig.1A] after adjusting for age, sex, and PCI and with further adjustment for CVD risk factors (p=0.007). Over 5 years median follow up, 1139 subjects experienced first time MACE. Combined high PRSCAD and PM2.5 also associated with higher MACE risk [OR (95% CI): 1.20 (1.15, 1.25), p<0.001, p (interaction) <0.001, Fig.1B] after adjusting for age, sex, and PCI and with further adjustment for CVD risk factors (p<0.001) and SES (p<0.001). Conclusions: Among individuals exposed to air pollution, genetic risk for CAD accentuates CAC and MACE risk in a graded manner. Genetic context may impact the health effects of air pollution.
Introduction: Implantable continuous-flow left ventricular assist devices (LVADs) are used in patients with end-stage heart failure as a bridge to transplant or as a destination therapy. In order to prevent pump malfunction as well as strokes, long term warfarin therapy is prescribed which puts them at risk of bleeding at the same time. Small retrospective studies have suggested the relationship between bloodstream infections and increased risk for intracranial hemorrhages (ICH).
IIntroduction: Higher stress-related neural activity (SNA) associates with subsequent risk of cardiovascular disease. We investigated whether heightened SNA predicts subsequent heart failure (HF). Methods: Individuals (N=2,112; median age 69 years; 48% female) enrolled in the Mass General Brigham Biobank without baseline HF who underwent clinically indicated 18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT) imaging were retrospectively identified. SNA was measured using validated methods, as amygdalar metabolic activity corrected for regulatory brain (i.e., medial prefrontal cortical) activity. Subsequent development of HF was determined via medical record review using International Classification of Diseases 10 (ICD-10) codes. Survival analyses using Cox and Kaplan-Meier models were performed. Results: Over a median follow-up period of 3.9 years after imaging, 210 individuals developed HF (57 systolic, 93 diastolic). Individuals with subsequent HF (versus no HF) had higher baseline SNA (mean Z-score 0.19 ± 1.07 versus -0.08 ± 0.99; p=0.005, adjusted for age and sex). SNA associated with subsequent HF when divided into tertiles (Figure) and as a continuous measure (standardized HR [95% CI]: 1.38 [1.11-1.70], p=0.003, adjusted for age, sex, hypertension, hyperlipidemia, diabetes and smoking). The association between SNA and HF subtype was stronger for diastolic HF (1.37 [1.00-1.88], p=0.047) than for systolic HF (1.14 [0.87-1.49], p=0.348) in models additionally adjusting for history of myocardial infarction. Conclusion: In this retrospective study of individuals with clinical FDG-PET/CT imaging, higher SNA predicted subsequent HF with a somewhat stronger association for diastolic HF. Understanding the link between heightened stress-associated neural activity and subsequent HF may provide important insights into better HF prevention and management strategies.
Introduction: Exercise associates with dose-dependent decreases in stress-associated neural activity (SNA) which, in part, mediate exercise's beneficial impact on major adverse cardiovascular event (MACE) risk. SNA can be assessed as a ratio of the resting metabolic activity of the brain's fear centers (i.e., the amygdala [Amyg]), to that of regulatory centers (i.e., the medial prefrontal cortex [PFC]). However, it is unknown whether exercise reduces SNA by impacting the activity of Amyg, mPFC, or both.
Background: Depression and anxiety disorders are linked with a greater risk of major adverse cardiac events (MACE) via unclear mechanisms. Since heightened stress-related neural activity (SNA) associates with a greater risk of MACE, we hypothesized that the link between depression/anxiety disorders and MACE is in part mediated by increased SNA.
Introduction: High-risk conduction (HRC) disorders are frequently encountered post transcatheter aortic valve replacement (TAVR). There is a robust expert consensus statement about the management of such patients (e.g.performance of an electrophysiology (EP) study). Yet, it is unclear what the real-world practices are and how they might be influencing outcomes.
Background Anxiety disorders and depression associate with an increased risk of deep venous thrombosis (DVT). However, it is unclear if this association persists after robust adjustment for confounders. Further, the mechanism mediating this potential link remains unknown. Prior studies show that anxiety and depression associate with heightened stress-associated neural activity (notably in the amygdala: AmygA), which in turn promotes chronic inflammation, a driver of thrombosis syndromes. Purpose To evaluate whether the association between anxiety/depression and DVT risk: A) persists after robustly accounting for potential confounders, and B) is mediated by upregulated stress-associated neural activity (namely AmygA). Methods Data were obtained from the Mass General Brigham Biobank, which included detailed health information on 118 871 adult participants. A subset of 1520 study subjects underwent clinical 18F-fluorodeoxyglucose positron emission tomography imaging during the follow up period, from which AmygA was measured as the ratio of amygdalar to regulatory (ventromedial pre-frontal cortex) activity. International Classification of Disease (ICD) codes in the medical record were used to define anxiety disorders, depression, and lower extremity DVT. Individuals on anticoagulant therapies for atrial fibrillation prior to enrolment and/or imaging were excluded. Cox analysis were performed wherein patients who developed DVT prior to Biobank enrolment (2599 subjects) were excluded. Mediation analysis was used to examine the role of AmygA in mediating the link between anxiety/depression and DVT. Results The median age of the study population was 57 years [interquartile range (IQR) 28] and 58.4% were female. DVT occurred in 1231 participants (1.2%) over a median follow up period of 3.3 years (IQR 3.0). Cox regression analysis showed that anxiety disorders and depression were independent predictors of incident DVT after controlling for confounders (Table 1; p<0.0001 for all analyses). In the subset of 1383 participants who underwent brain imaging, anxiety disorders and depression associated with increased AmygA activity after controlling for risk factors including age, sex, Charlson index, hormone use and cancer history (standardized β [95% CI]: 0.124 [0.017–0.232], p=0.023 and 0.151 [0.041–0.260], p=0.007 respectively). Further, AmygA associated with DVT (odds ratio (OR) [95% CI]: 1.248 [1.064–1.465], p=0.007). Path analysis demonstrated that increased AmgyA mediated the effect of both anxiety and depression on DVT (log OR [95% CI]: 0.0256 (0.0009–0.0592), p<0.05 and 0.0314 (0.0033 to 0.0718), p<0.05 respectively, Figure 1). Conclusion Anxiety disorders and depression associate with an increased risk of DVT via a mechanism that includes heightened stress-related neurobiological activity. Future studies should evaluate whether modulating this neural pathway could reduce the incidence of DVT.
Background Prior studies suggest that moderate alcohol intake may associate with a lower incidence of deep venous thrombosis (DVT). However, it is unclear if this association persists after robust adjustment for confounders. Moreover, the mechanisms mediating this potential benefit are unclear. Prior studies show that chronic stress promotes stress-related neural activity (amygdalar activity: AmygA), which in turn triggers inflammation and elevates thrombosis risk. Since moderate alcohol intake decreases AmygA, we hypothesize that this neural effect of alcohol may partially mediate its beneficial impact on DVT risk. Purpose To evaluate whether the association between moderate alcohol intake and decreased DVT risk: A) persists after robustly accounting for potential confounders and B) is mediated by reductions in stress-related neural activity. Methods Data were obtained from the Mass General Brigham Biobank, which included detailed health, lifestyle, and follow-up outcomes information on 53 059 adult participants. Alcohol intake was classified as low (<1 drink/week), moderate (1–14 drinks/week), or high (>14 drinks/week). A subset of 656 study subjects underwent clinical 18F-fluorodeoxyglucose positron emission tomography imaging from which AmygA was measured as the ratio of amygdalar to regulatory (ventromedial pre-frontal cortex) activity. Individuals on anticoagulant therapies for atrial fibrillation prior to enrolment and/or imaging were excluded. Cox analysis were performed wherein patients who developed DVT prior to Biobank enrolment (1064 subjects) were excluded. Mediation analysis was used to examine the role of AmygA in mediating the link between alcohol intake and DVT. Results The median age of the study population was 59 years [interquartile range (IQR) 26] and 51.9% were female. DVT occurred in 573 participants (1.2%) over a median follow up period of 3.4 years (IQR 2.9). Cox regression analysis showed that moderate alcohol intake was associated with lower incident DVT rates after controlling for confounders (hazard ratio [95% confidence intervals (CI)] 0.773 [0.644,0.929], p=0.006, Table 1). In the subset of participants who underwent brain imaging, moderate alcohol intake associated with decreased AmygA activity (standardized β [95% CI]: −0.218 [−0.370, −0.065], p=0.005). Further, AmygA associated with DVT (odds ratio (OR) [95% CI]: 1.374 [1.089, 1.734], p=0.007). Path analysis demonstrated that decreased AmgyA mediated the salutary effect of moderate alcohol on DVT (log OR [95% CI]: −0.0635 [−0.1383, −0.0078], p<0.05, Figure 1). Conclusion Moderate alcohol intake is associated with a decreased risk of DVT via a mechanism that may involve a reduction in stress-related neurobiological activity. Alternative therapies targeting this neural pathway should be identified with the goal of reducing the burden of DVT.
Michael uebel Thank for the response, but i am a bit confused about the differenc between the sum of individual effects or the product effects? What is the difference?
Michael uebel Thank for the response, but i am a bit confused about the differenc between the sum of individual effects or the product effects? What is the difference?
Thank you for the answer. I did try that, but for some reason if i do that for binomial variables ( coded 0 or 1) it gives me a variable coded only as 1, i had to do it out side in excel then merge it back. But my concern was if that's statistically valid to do it with linear regression rather than logistic one where inside spss, it allows you to create the intetaction term rightaway in the lg model.
Thank you for the answer. I did try that, but for some reason if i do that for binomial variables ( coded 0 or 1) it gives me a variable coded only as 1, i had to do it out side in excel then merge it back. But my concern was if that's statistically valid to do it with linear regression rather than logistic one where inside spss, it allows you to create the intetaction term rightaway in the lg model.
Thank you for the answer. I did try that, but for some reason if i do that for binomial variables ( coded 0 or 1) it gives me a variable coded only as 1, i had to do it out side in excel then merge it back. But my concern was if that's statistically valid to do it with linear regression rather than logistic one where inside spss, it allows you to create the intetaction term rightaway in the lg model.
Thank you for the answer. I did try that, but for some reason if i do that for binomial variables ( coded 0 or 1) it gives me a variable coded only as 1, i had to do it out side in excel then merge it back. But my concern was if that's statistically valid to do it with linear regression rather than logistic one where inside spss, it allows you to create the intetaction term rightaway in the lg model.
Thank you for the answer. I did try that, but for some reason if i do that for binomial variables ( coded 0 or 1) it gives me a variable coded only as 1, i had to do it out side in excel then merge it back. But my concern was if that's statistically valid to do it with linear regression rather than logistic one where inside spss, it allows you to create the intetaction term rightaway in the lg model.
Thank you for the answer. I did try that, but for some reason if i do that for binomial variables ( coded 0 or 1) it gives me a variable coded only as 1, i had to do it out side in excel then merge it back. But my concern was if that's statistically valid to do it with linear regression rather than logistic one where inside spss, it allows you to create the intetaction term rightaway in the lg model.
Thank you for the answer. I did try that, but for some reason if i do that for binomial variables ( coded 0 or 1) it gives me a variable coded only as 1, i had to do it out side in excel then merge it back. But my concern was if that's statistically valid to do it with linear regression rather than logistic one where inside spss, it allows you to create the intetaction term rightaway in the lg model.
Thank you for the answer. I did try that, but for some reason if i do that for binomial variables ( coded 0 or 1) it gives me a variable coded only as 1, i had to do it out side in excel then merge it back. But my concern was if that's statistically valid to do it with linear regression rather than logistic one where inside spss, it allows you to create the intetaction term rightaway in the lg model.
Thank you for the answer. I did try that, but for some reason if i do that for binomial variables ( coded 0 or 1) it gives me a variable coded only as 1, i had to do it out side in excel then merge it back. But my concern was if that's statistically valid to do it with linear regression rather than logistic one where inside spss, it allows you to create the intetaction term rightaway in the lg model.
.In SPSS, you can create your interaction term either in logistic regression model or cox model, when you have contious variable as an outcome, LR will be used, in that case, is it valid to create my interaction term manually? Or there any other statistical models are meant to be used?
can LR be used to test interaction given that it's not exponential test, using SPSS? If yes, how?
how both types of interaction could be interpreted differently
I am looking for a validated survey that assess the mental wellbeing of physicians.
Any open sources for cardiovascular morbidity and mortality caused by air pollution during COViD?
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
Studies showed that low-middle income countries at highest risk
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