Introduction: Cardiac device extraction procedures are associated with increased risk of in-hospital mortality. The objective of this study was to determine risk factors for in-hospital mortality of patients undergoing cardiac device extraction. Methods: We studied patients undergoing cardiac device removal between January 2016 and December 2019 at a single tertiary care center. Baseline patient characteristics, comorbidities, and preoperative laboratory data were obtained by database query (Table 1) . The outcome of interest was in-hospital death following cardiac device extraction. Odds ratios (OR) and confidence intervals (CI) were used to measure relationships between exposures and the main outcome. Results: Our cohort consisted of 333 patients who underwent cardiac device extraction procedures. Cardiac device infection was the indication for procedure in 48% of patients (n=161). In-hospital mortality occurred in 9% of patients (n=29). Patients that died inpatient post-operatively were more likely to be male gender (OR 3.59, 95% CI [1.2, 10.6], p = 0.02), have acute kidney failure (OR 3.17, 95% CI [1.42, 7.05], p = 0.005), have anemia (OR 3.22, 95% CI [1.49, 6.99], p = 0.003), or have a diagnosis of severe malnutrition (OR 2.88, 95% CI [1.26, 6.58], p = 0.01). In a subgroup analysis, patients with diabetes undergoing extraction for infectious reasons had an increased risk of in-hospital mortality (OR 4.36, 95% CI [1.54, 12.34], p = 0.005). Conclusion: Patients undergoing cardiac device extraction are high risk for in-hospital mortality. Patients experiencing in-hospital mortality were more likely to be male, have acute renal failure, anemia and severe malnutrition. Careful analysis of preoperative risk factors, laboratory data, and nutritional status can help stratify risk for patients and providers.

Background There are poorer outcomes following ST elevation myocardial infarction in blacks compared to white patients despite comparable door‐to‐reperfusion time. We hypothesized that delays to hospital presentation may be contributory. Methods and Results We conducted a retrospective analysis of the 1144 patients admitted for STEMI in our institution from 2008 to 2013. The door‐to‐balloon time (D2 BT ) and symptom‐onset‐to‐door time ( SODT ) were compared by race. Bivariate analysis was done comparing the median D2 BT and SODT . Stratified analyses were done to evaluate the effect of race on D2 BT and SODT , accounting for insurance status, age, sex and comorbidities. The mean age was 59±13 years; 56% of this population was black and 41% was white. Males accounted for 66% of this population. The median D2 BT was 60 minutes (interquartile range [ IQR ] 42–82), and median SODT was 120 minutes ( IQR 60–720). There was no significant difference in D2 BT by race ( P =0.86). Black patients presented to the emergency room ( ER ) later than whites ( SODT =180 [ IQR 60–1400] vs 120 [ IQR 60–560] minutes, P <0.01) and were more likely to be uninsured ( P <0.01). After controlling for comorbidities, insurance, and socioeconomic status, blacks were 60% more likely to present late after a STEMI ( OR 1.6, P <0.01). A subset analysis excluding transferred patients showed similar results. Conclusions Black patients present later to the ER after STEMI with no difference in D2 BT compared to whites. This difference in time to presentation may be one of the factors accounting for poor outcomes in this population.

ST-elevation myocardial infarction (STEMI) requires emergent diagnostic catheterization and therapeutic percutaneous coronary intervention. These therapies may cause acute kidney injury (AKI), a serious procedural complication that contributes to morbidity and mortality in STEMI patients. Identifying patients at risk for renal complications may save lives and reduce healthcare costs, but there is no validated tool for predicting AKI in STEMI patients. Methods: The UT-Methodist STEMI program is a racially diverse series of 1144 consecutive patients. We derived and validated the UT-AKI score to predict the risk of AKI in patients referred for STEMI (and not currently on dialysis). AKI was categorized by the modified AKI Network and RIFLE indices. The UT-AKI score was derived from logistic regression analysis performed on a randomly selected derivation dataset using variables with significant univariate relationships to AKI and markers of renal function. Receiver operator characteristic (ROC) curves for the UT-AKI were assessed in the derivation and validation datasets. Statistical significance was measured by appropriate parametric and non-parametric tests; a p<0.05 was considered significant. Results: The incidence of AKI was similar in patients undergoing diagnostic catheterization with or without PCI (12% vs. 14%, p=0.34). ROC curve analysis of the validation data set showed that the UT-AKI score (AUC 0.76 (95% CI 0.70-0.82)) was significantly better at classifying patients at risk for AKI than the ACEF (AUC 0.65 (95% CI: 0.58-0.73)), AGEF (AUC 0.65 (95% CI: 0.58-0.72)), or Mehran (AUC 0.67 (95% CI: 0.59-0.75)). The classification accuracy for the UT-AKI index was comparable for milder and severe forms of AKI. Conclusions: In the largest analysis of STEMI patients to date, we found no significant difference in the risk of AKI from PCI vs. diagnostic catheterization. The validation study indicates that the UT-AKI index was significantly better than other scores at classifying which patients will develop AKI. Accurate prediction of AKI may help physicians to personalize therapies and develop novel strategies to reduce kidney injury in patients with STEMI.

Diabetes mellitus (DM) is a pro-thrombotic state with enhanced thrombin generation and platelet reactivity. For most patients undergoing percutaneous coronary intervention (PCI), bivalirudin demonstrates efficacy comparable with that of heparin and glycoprotein IIb/IIIa inhibitors (GPIs). Yet, because of their pro-thrombotic condition, we hypothesized that patients with DM may benefit from more aggressive dual antithrombin and antiplatelet therapy. The aim of this paper was to provide a systematic review comparing outcomes of PCI with bivalirudin versus heparin plus GPI in patients with DM using meta-analytical techniques. Eligible studies needed to have reported a subgroup analysis of outcomes among diabetic patients. Six trials comprising 5924 diabetic patients were eligible. At 30 days, bivalirudin was associated with a reduction in net adverse cardiac events [relative risk (RR) 0.81, 95 % confidence interval (CI) 0.70–0.93, p = 0.002] and major bleeds (RR 0.68, 95 % CI 0.49–0.95; p = 0.02), with no difference in composite ischemia (RR 0.92, 95 % CI 0.74–1.14; p = 0.43) or mortality (RR 0.71, 95 % CI 0.45–1.13; p = 0.15). At 1 year, bivalirudin was associated with a significant reduction in all-cause mortality (RR 0.73, 95 % CI 0.54–1.00, p = 0.05) despite similar composite ischemia (RR 1.02, 95 % CI 0.56–1.21, p = 0.811). In conclusion, thrombin inhibition with bivalirudin alone was associated with reduced 30-day major bleeding and 1-year all-cause mortality compared with heparin plus GPI in diabetic patients undergoing PCI.

Introduction: Time to reperfusion has been shown to be a major predictor of mortality after an ST elevation myocardial infarction (STEMI). Reducing delays to ER presentation should significantly improve time to reperfusion. This study sought to explore the factors that predict late presentation to ER after STEMI. Methods: A retrospective analysis was conducted using data from our tertiary institution 2008-2013. All patients admitted for STEMI during this period were identified. The “Symptom onset to door time (SODT)” was computed and a binary outcome variable (late presentation) was defined as a SODT >180 minutes. The role of patient demographics, insurance status, socioeconomic factors, mode of transportation, and comorbidities were controlled for in the multivariable regression analysis to identify the predictors of late presentation. A subset analysis was conducted excluding patients transferred from outlying facilities. Results: During this period, 1144 patients were admitted for acute STEMI, with 348 of these patients having been transferred from outlying facilities. Mean age was 59 (+12.8) years, males accounted for 67% of this population, 28% had private insurance, 50% had public insurance and 22% were uninsured; 56% of this population was Black. 47.5% of patients presented after 180 minutes. On bivariate analysis, blacks, older age, insurance status, female gender and a family history of coronary artery disease were predictors of late presentation after STEMI. On controlling for confounders in our model, the only significant predictors for late presentation were race and insurance status. A subset analysis excluding transferred patients showed qualitatively similar results. Conclusion: Minority patients, publically insured and uninsured patients are more likely to present late after a STEMI, this difference in time to presentation may be a surrogate for health literacy in these populations and may be ameliorated by better health education.

Tumor cell metastasis, a process which increases the morbidity and mortality of cancer patients, is highly dependent upon matrix metalloproteinase (MMP) production. Small molecule inhibitors of MMPs have proven unsuccessful at reducing tumor cell invasion in vivo. Therefore, finding an alternative approach to regulate MMP is an important endeavor. Tetraspanins, a family of cell surface organizers, play a major role in cell signaling events and have been implicated in regulating metastasis in numerous cancer cell lines. We stably expressed tetraspanin CD9 in an invasive and metastatic human fibrosarcoma cell line (CD9-HT1080) to investigate its role in regulating tumor cell invasiveness. CD9-HT1080 cells displayed a highly invasive phenotype as demonstrated by matrigel invasion assays. Statistically significant increases in MMP-9 production and activity were attributed to CD9 expression and were not due to any changes in other key tetraspanin complex members or MMP regulators. Increased invasion of CD9-HT1080 cells was reversed upon silencing of MMP-9 using a MMP-9 specific siRNA. Furthermore, we determined that the second extracellular loop of CD9 was responsible for the upregulation of MMP-9 production and subsequent cell invasion. We demonstrated for the first time that tetraspanin CD9 controls HT1080 cell invasion via upregulation of an integral member of the MMP family, MMP-9. Collectively, our studies provide mounting evidence that altered expression of CD9 may be a novel approach to regulate tumor cell progression.