A Single-Center, Retrospective Cohort Study Evaluating the Use of Probiotics for the Prevention of Hospital-Onset Clostridioides difficile Infection in Hospitalized Patients Receiving Intravenous Antibiotics.

Background: Exposure to antimicrobials is a known risk factor for Clostridioides difficile infection (CDI). Antimicrobials cause collateral damage by disrupting the natural intestinal microbiota allowing for C. difficile to thrive and production of C. difficile toxins. Probiotics could modulate the onset and course of CDI. However, the data on probiotics for the prevention of CDI is conflicting. Objective: To evaluate the rates of hospital-onset Clostridioides difficile infection (HO-CDI) among patients who received intravenous (IV) antibiotics plus probiotics versus IV antibiotics alone. Design: Retrospective, single-center cohort study. Methods: We included adult patients that received at least 1 dose of IV antibiotics and had a hospital length of stay of at least 3 days between August 2017 and July 2020. Patients were separated into 2 cohorts, either receipt of probiotics or non-receipt of probiotics. Patients with positive C. difficile toxin test prior to antibiotic therapy, or receipt of only C. difficile active treatment were excluded. The primary outcome was incidence of HO-CDI in patients who received IV antibiotics plus probiotics compared to those that received IV antibiotics alone. Logistic regression was performed to account for confounding variables. Results: We identified 17 598 patients that received IV antibiotics alone and 2659 patients received IV antibiotics plus probiotics. HO-CDI occurred in 46 (0.26%) of those that received antibiotics alone compared to 5 (0.19%) of those that received probiotics with IV antibiotics (OR 0.72, 95% CI 0.28-1.81). ICU admission (OR 1.81, 95% CI 1.02-3.19) and history of CDI (OR 3.37, 95% CI 1.07-10.97) in the past 12 months were associated with a higher incidence of HO-CDI. Conclusion: The addition of probiotics did not reduce the incidence of HO-CDI among inpatients receiving IV antibiotics.

Alteplase for the treatment of midline catheter occlusions: a retrospective, single-cohort descriptive study.

BACKGROUND: Despite the increasing popularity of midline catheters, data on the use of alteplase for restoring midline catheter patency is scarce. AIMS: This study aimed to evaluate off-label use of alteplase for midline catheter occlusions. METHOD: Adults who received alteplase into a midline catheter between January 2015 and May 2018 within a multi-hospital health system were included in this study. The primary outcome was restoration of infusion or withdrawal function from at least one lumen of a treated midline catheter. FINDINGS: Following alteplase administration, withdrawal function was restored in 47% (25/53) of occlusion events, infusion function was restored in 65% (11/17) of complete occlusion events, and infusion or withdrawal function was restored in 58% (31/53) of occlusion events. Only 34% (17/50) of catheters were replaced because of malfunction. Local bleeding was documented in 9% (n=5) of occlusion events after alteplase administration. CONCLUSION: Most midline catheter occlusions treated with alteplase demonstrated restoration of infusion or withdrawal function.

Hemodynamic Effects of Dexmedetomidine in Adults With Reduced Ejection Fraction Heart Failure.

BACKGROUND: Dexmedetomidine (DEX) can cause hypotension complicating its use in critically ill patients with labile hemodynamics secondary to an underlying disease state such as heart failure. The aim of this study was to determine the effect of DEX on mean arterial pressure (MAP) in nonsurgical patients with heart failure and reduced ejection fraction (HFrEF). METHODS: This retrospective single-center cohort study evaluated patients who received DEX in the cardiac care and medical intensive care units at a large academic hospital. The primary end point was the change in MAP within 6 hours following DEX initiation. RESULTS: Sixty-five patients with HFrEF diagnosis were compared 1:1 to a control group without HFrEF. Both groups experienced a decrease in MAP over the study period. Patients with HFrEF had a greater absolute percentage reduction in MAP 1 hour following DEX initiation compared to the control group (-9.6% vs -5.2%; P < .01). When accounting for the combined effect of DEX initiation and HFrEF diagnosis on the primary end point, patients with HFrEF did not have a significant difference in MAP compared to the control group over the study period. CONCLUSIONS: Within 6 hours following DEX initiation, both groups experienced a decrease in MAP. The effect of DEX on MAP over the composite time period was not found to be significantly different in the HFrEF group compared to the non-HFrEF group. However, patients with HFrEF experienced a greater reduction in MAP in the first hour following DEX initiation compared to the non-HFrEF group. Prospective studies are needed to evaluate the effect of DEX on patients with acute decompensated HFrEF compared to patients with compensated HFrEF.

Evaluation of the efficacy and safety of apixaban and rivaroxaban in cancer patients receiving concomitant active anti-neoplastic therapy at an outpatient cancer setting.

INTRODUCTION: Venous thromboembolism is a common complication among cancer patients with an estimated risk of 20%. American Society of Clinical Oncology guidelines recommend direct oral anticoagulants for long-term anticoagulation but caution the use of direct oral anticoagulants because of drug-drug interactions with antineoplastic therapies. The clinical impact of these drug-drug interactions is yet to be studied in clinical trials. This study aims to evaluate the effect of the drug-drug interactions on venous thromboembolism recurrence and bleeding. METHODS: This is a retrospective cohort study that included cancer patients with venous thromboembolism receiving apixaban or rivaroxaban with antineoplastic therapy. The impact of the drug-drug interaction was determined by its effect on the rates of venous thromboembolism recurrence and bleeding in patients with a drug-drug interaction compared to patients with no drug-drug interaction. RESULTS: The primary composite endpoint of venous thromboembolism recurrence and bleeding events occurred in 65% versus 62% of patients in drug-drug interaction and non-drug-drug interaction groups accordingly. There was a higher rate of venous thromboembolism recurrence and minor bleeding events with anti-mitotic microtubule inhibitors and a higher rate of minor bleeding events with hormonal therapy and alkylating agents. Among the drug-drug interaction group, there were no major bleeding events reported with mild drug-drug interactions when compared to moderate-to-severe drug-drug interactions. There was no difference in time to venous thromboembolism recurrence between rivaroxaban and apixaban. CONCLUSION: Due to small sample size, our study results could not confirm a higher risk of bleeding or venous thromboembolism recurrence with the drug-drug interactions. Further prospective study is warranted, but clinicians should be aware of these drug-drug interactions and identify them using available literature.

Single-center, retrospective evaluation of safety and efficacy of direct oral anticoagulants versus low-molecular-weight heparin and vitamin K antagonist in patients with cancer.

INTRODUCTION: The safety and efficacy of direct oral anticoagulants in cancer patients is currently unclear. Low-molecular-weight heparin remains the standard of care for cancer patients with venous thromboembolism, with warfarin, a vitamin K antagonist, as an alternative. Clear recommendations do not exist for patients with both active cancer and non-valvular atrial fibrillation. The objectives of this study were to report safety and efficacy outcomes of direct oral anticoagulants, low-molecular-weight heparin, and vitamin K antagonist in cancer patients with venous thromboembolism or non-valvular atrial fibrillation. METHODS: Retrospective chart review of adult cancer patients from 2012 to 2015 who received an antineoplastic agent and an anticoagulant. RESULTS: A total of 258 patients were reviewed: 80 patients in direct oral anticoagulant group, 95 patients in low-molecular-weight heparin group, and 83 patients in vitamin K antagonist group. Sixty-seven percent of patients were on an anticoagulant for acute or chronic venous thromboembolism. Major bleeding events were similar across the groups (15% direct oral anticoagulant vs 17% low-molecular-weight heparin vs 18% vitamin K antagonist). The most common type of major bleeding event was gastrointestinal bleeding. A total of five fatal bleeding events occurred. Venous thromboembolism recurrence rates were higher in both direct oral anticoagulant (18%) and low-molecular-weight heparin (12%) groups while lower in vitamin K antagonist group (10%) compared to previous studies. CONCLUSIONS: Cancer patients receiving direct oral anticoagulants, low-molecular-weight heparin, or vitamin K antagonist had similar rates of major bleeding events, with gastrointestinal bleeding being the most common event. Venous thromboembolism recurrence rates were higher in direct oral anticoagulant and low-molecular-weight heparin groups than prior studies. Randomized trials are warranted to establish clear safety and efficacy in this population.

Comparison of Antifactor Xa and Activated Partial Thromboplastin Time Monitoring for Heparin Dosing in Vascular Surgery Patients: A Single-Center Retrospective Study.

BACKGROUND: Vascular surgery patients often require anticoagulation with intravenous unfractionated heparin monitored through antifactor Xa (anti-Xa) levels or the activated partial thromboplastin time (aPTT). This study compares the 2 monitoring strategies in terms of major bleeding events in the vascular surgery population. METHODS: This was a single-center, retrospective study that included patients treated with a pharmacy-managed heparin protocol monitored by either anti-Xa or aPTT after vascular surgery. The primary outcome was the percentage of patients experiencing major bleeding events after procedure. Secondary outcomes evaluated minor bleeding episodes, postprocedure packed red blood cell transfusions, and the incidence of thrombotic events. In a secondary analysis, simultaneously measured anti-Xa and aPTT values were identified and analyzed for discordance. RESULTS: Major bleeding occurred in 12/72 patients (17%) on the anti-Xa-monitored protocol versus 5/62 patients (8%) on the aPTT-monitored protocol (P = 0.19). Minor bleeding episodes were documented in 10% of the patients in the anti-Xa group versus 6% in the aPTT group (P = 0.54). There were no significant differences between the 2 groups in packed red blood cell transfusions and thrombotic events. Of 109 pairs of simultaneously measured anti-Xa and aPTT values, 39 pairs (36%) showed relatively high aPTT values compared with corresponding anti-Xa levels. Nine patients who had these discordant test results experienced bleeding while their heparin drip was titrated based on lower anti-Xa values. CONCLUSIONS: The use of anti-Xa levels for heparin titration showed higher rates of major bleeding complications in vascular surgery patients compared with aPTT monitoring, but no significant difference was identified in this study. Vascular surgery patients with relatively high aPTT to anti-Xa values may have an increased risk of bleeding complications when heparin is titrated based on anti-Xa levels.

Comparison of anti-Xa and activated partial thromboplastin time monitoring for heparin dosing in patients with cirrhosis.

BACKGROUND: Cirrhosis of the liver results in complex hemostatic changes that place patients at risk for both bleeding and thrombotic events. This study evaluates the adverse effects of anticoagulation with unfractionated heparin among patients with cirrhosis and analyzes the discrepancy between anti-Xa and activated partial thromboplastin time (aPTT) values for heparin monitoring among cirrhotics. METHODS: Patients with cirrhosis receiving unfractionated heparin were matched 2:1 to patients without evidence of cirrhosis anticoagulated with unfractioned heparin. Markers of bleeding events including blood product administration and use of heparin reversal were analyzed between groups. Patients from both groups with aPTT and anti-Xa values obtained at the same time were also analyzed. RESULTS: A higher incidence of blood product administration or use of heparin reversal was observed among patients with cirrhosis [35/105 (33.3%) versus 37/210 (17.6%), P = 0.002]. This finding was consistent among those receiving anticoagulation through an established anti-Xa-based heparin dosing protocol [23/62 (37.1%) versus 25/124 (20.2%), P = 0.013]. A decrease in hemoglobin greater than 2 g/dL or a platelet decrease 50% or greater from baseline was also more frequently identified among cirrhotics when receiving heparin therapy [20/105 (19%) versus 23/210 (11%), P = 0.049 and 21/105 (20%) versus 12/210 (6%), P < 0.001, respectively]. A total of 88 correlated anti-Xa and aPTT values from 35 patients with cirrhosis demonstrated supratherapeutic aPTT values for anti-Xa levels within the therapeutic range (P < 0.001). This discrepancy was not observed among controls. CONCLUSIONS: A greater use of blood products among the cirrhotic population may indicate potential bleeding events on therapy. A discrepancy in correlated anti-Xa and aPTT values among patients with cirrhosis may explain the propensity for adverse effects. Further study is required to identify effective heparin anticoagulation monitoring strategies in liver disease.

Assessment of drug-induced torsade de pointes risk for hospitalized high-risk patients receiving QT-prolonging agents.

BACKGROUND: Although risk factors for torsade de pointes (TdP) are known, identifying hospitalized patients at greatest risk for QTcP who should receive cardiac monitoring is poorly defined. OBJECTIVES: Describe the prevalence of risk for TdP in patients and associations between risk factors and QTc prolongation (QTcP) at a tertiary teaching hospital. METHODS: This retrospective analysis assessed physiological and pharmacological risk factors for TdP of adult patients receiving ≥1 QTc-prolonging medications (QTcMed) during hospitalization. The QTcMeds were stratified by risk for causing TdP (probable, possible, and conditional). Baseline electrocardiograms (ECGs) were assessed for QTcP associated with risk for TdP. RESULTS: During a 6-month period, 12,401 (51%) hospitalizations received ≥1 QTcMed. A baseline ECG was obtained for 2381 (19%) patients. A total of 386 (16%) patients with a baseline ECG were found to have QTcP. Significant associations for QTcP were found with the following physiological risk factors: female (P = .021), left-ventricular ejection fraction <40% (P < .0001), cardiac arrest (P < .0001), and cardioversion (P = .007). Significantly more patients with QTcP (n = 209, 54%) received probable-risk QTcMeds than those without QTcP (n = 542, 27%; P < .0001). Probable-risk QTcMeds administered alone or concomitantly with other QTcMeds were more frequently associated with QTcP. No documented cases of TdP were identified. CONCLUSIONS: Of the population receiving QTcMeds, only a small portion had a baseline ECG, identifying a large population at risk of QTcP without appropriate monitoring. Patients with cardiac disease receiving probable-risk QTcMeds were associated with the highest risk of QTcP and should be monitored closely.

Low molecular weight heparin dosing and monitoring in solid organ transplant recipients.

Anti-Xa monitoring for low molecular weight heparin (LMWH) is currently recommended in obese, renally impaired, and pregnant patients. Substantial evidence indicates that solid organ transplant (SOT) patients are at an increased risk of renal impairment, thus representing a population at risk of LMWH accumulation. The purpose of this study was to review our experience with LMWH dosing and monitoring in a cohort of transplant recipients. This was a retrospective, single-center review of 96 SOT patients receiving enoxaparin treatment and anti-Xa monitoring. The percent of patients with supratherapeutic anti-Xas (>1 IU/mL) was determined, as was the relationship between enoxaparin dosages and anti-Xa levels and bleeding. The cohort had a mean age of 62 yr and creatinine clearance of 59 mL/min and was primarily lung transplant recipients (73%). The mean enoxaparin dose was 0.82 mg/kg, which resulted in a mean anti-Xa level of 0.98 IU/mL. Despite the reduced enoxaparin dose, 44% of patients experienced a supratherapeutic anti-Xa level. Patients with supratherapeutic anti-Xas had higher doses than those within the therapeutic range (0.89 mg/kg vs. 0.77 mg/kg; p = 0.002). No major bleeds occurred. Supratherapeutic anti-Xa levels are common in transplant patients receiving enoxaparin therapy. Empirically reduced dosing of enoxaparin and monitoring may warrant consideration in this population.

Alternative monitoring of argatroban using plasma-diluted thrombin time.

OBJECTIVE: To report a case of heparin-induced thrombocytopenia (HIT) in a patient with concurrent liver dysfunction and a prolonged baseline activated partial thromboplastin time (aPTT) in whom argatroban therapy was monitored with aPTT and a novel plasma-diluted thrombin assay. CASE SUMMARY: An 80-year-old man with HIT and liver dysfunction was treated with argatroban, which was initiated at a dose of 0.5 µg/kg/min and gradually decreased to 0.09 µg/kg/min. The patient had a mildly prolonged aPTT at baseline (37.5 seconds). He was concurrently monitored with aPTT, per institution protocol, and plasma-diluted thrombin time. Plasma-diluted thrombin times were consistently lower than aPTTs, but mirrored the trend of the aPTTs. Eleven hours after argatroban was stopped, the aPTT remained elevated (53.9 seconds), while the plasma-diluted thrombin time returned to normal range (26.4 seconds). The patient's therapy was transitioned to warfarin and he had a hospital course with no thrombotic or bleeding complications. DISCUSSION: Plasma-diluted thrombin time is a novel laboratory test consisting of 1 part patient plasma diluted with 3 parts normal plasma. Plasma-diluted thrombin time has been shown to blunt the sensitivity of the thrombin time and may be more accurate for drug monitoring. A MEDLINE search revealed 2 studies using the plasma-diluted thrombin time assay. The first study compared aPTT and plasma-diluted thrombin times in blood samples mixed with argatroban, bivalirudin, or lepirudin at 3 different concentrations. Blood samples contained lupus inhibitors, vitamin k deficiency, or normal baseline aPTTs. The aPTT overestimated drug concentrations in all samples with lupus anticoagulant and vitamin k deficiency, while the plasma-diluted thrombin time correctly estimated drug concentrations in nearly all samples. The second study looked at monitoring dabigatran with plasma-diluted thrombin time and found a linear relationship between the plasma-diluted thrombin time and the dabigatran dose-response curve. CONCLUSIONS: Plasma-diluted thrombin time may be an alternative for direct thrombin inhibitor monitoring in patients with elevated aPTT values at baseline. Further randomized control trials are needed to determine its applicability in clinical practice.

Evaluating Time to In-Hospital Venous Thromboembolism in Obese Patients.

BACKGROUND: Currently, no consensus approach exists for optimal venous thromboembolism (VTE) prophylaxis in obese (BMI ≥30 kg/m2) patients. Time to development of in-hospital VTE is not well studied. OBJECTIVE: This study evaluates time to in-hospital VTE in obese patients. METHODS: A single-center, retrospective study evaluated obese patients that developed an in-hospital VTE. Patients were categorized into 3 BMI groups: 30 to 34.9 (group 1), 35 to 39.9 (group 2), and ≥40 (group 3) kg/m2. The primary end point compared time to VTE between the groups. RESULTS: A total of 246 patients were included, and time to VTE was similar between the groups, 8 (group 1) versus 8 (group 2) versus 9 days (group 3); P = .38. Secondary outcomes showed time to VTE was shorter in acute care versus ICU patients (7.5 vs 10 days; P = .01), nonsurgical versus surgical patients (6 vs 9 days; P = .004), and no prophylaxis versus mechanical plus pharmacologic prophylaxis (4.5 vs 9 days; P < .001). CONCLUSIONS: BMI category did not significantly impact time to in-hospital VTE. This study provides insight into the timing of in-hospital VTE in obese patients. The differences in prophylactic strategies highlight the importance of optimized prophylaxis.

Cardioprotective medication use after renal transplantation.

Cardiovascular disease is the leading cause of death in renal transplant patients. This study compares the use of cardioprotective medications in adult kidney transplant recipients at a single center with recommendations, which have been validated in the general population. Cardioprotective medication use was retrospectively collected post-renal transplant. Patients were defined as high risk if they had pre-transplant coronary heart disease or equivalent risk. "Optimal" treatment was defined as a patient receiving aspirin, statin, angiotensin-converting enzyme inhibitors/angiotensin receptor blocker, and a beta-blocker according to cardiovascular risk. The percentage of high-risk patients optimally treated at one, three, six, and 12 months was 7.7%, 11.5%, 17.6%, and 18.8%, respectively. Although the use of cardioprotective medications was evident in transplant recipients, opportunities exist to increase the use of optimal cardioprotective regimens after renal transplantation.

Impact of computerized dosing on eptifibatide-associated bleeding and mortality.

OBJECTIVE: The study aimed to determine the impact on eptifibatide-associated bleeding by implementing a computerized dosing algorithm in the cardiac catheterization suite. BACKGROUND: Excessive dosing of eptifibatide is associated with increased bleeding rates and hospital mortality. Although dosing adjustments based on renal function has been recommended, its implementation and clinical impact have not been assessed in daily practice. METHODS: A computerized algorithm was implemented in January 2006 to calculate appropriate eptifibatide infusion dose (1 microg kg(-1) min(-1) for creatinine clearance <50 mL/min or 2 microg kg(-1) min(-1) for creatinine clearance >or=50 mL/min) using the Cockroft-Gault formula. All patients had hemoglobin measured before and the day after the procedure. Bleeding within 24 hours and mortality during hospitalization were compared in consecutive patients before and after implementation of the algorithm. RESULTS: A total of 334 patients qualified for inclusion (pre-algorithm n = 91, post-algorithm n = 243). There was an increase in the proportion of patients receiving recommended doses of eptifibatide dosing (74.7% pre-algorithm vs 97.5% post-algorithm, P

Direct oral anticoagulants versus aspirin for venous thromboembolism prophylaxis after orthopedic surgery.

PURPOSE: The risks of venous thromboembolism (VTE) and bleeding with direct oral anticoagulants (DOACs) and aspirin for thromboprophylaxis after orthopedic surgery were studied. METHODS: A single center, retrospective study was conducted to examine patients who underwent a major orthopedic surgery from 2011 to 2015. The primary endpoint evaluated was the net clinical outcome of bleeding and thrombosis rates between the DOAC and aspirin groups. Secondary endpoints included bleeding rates, thrombosis rates, transfusion rates, and 90-day readmission rates. The primary endpoint was analyzed using adjusted logistic regression model with propensity score added as an independent variable. RESULTS: A total of 420 patients were included in this study. The proportion of patients with composite primary outcome was similar between the groups (12.9% and 13.3%, in the DOAC and aspirin groups, respectively; p > 0.5). VTE events were numerically lower in the DOAC group, but the result was not statistically significant. Readmission due to VTE or bleeding and bleeding events were also similar between the groups. The DOAC group had a higher proportion of blood transfusions of at least 2 units of blood postoperatively compared with the aspirin group (p = 0.04). CONCLUSION: No difference in net clinical outcome was observed in patients who received a DOAC or aspirin for VTE prophylaxis after major orthopedic surgery.

Time to Occurrence Based on Risk Stratification of Hospital-Acquired Venous Thromboembolism: A Retrospective Observational Cohort Study.

BACKGROUND: In-hospital venous thromboembolism (VTE) causes significant morbidity and mortality in hospitalized patients. The objective of our study is to determine the time to in-hospital VTE based on baseline risk stratification. METHODS: All adult patients admitted to a 900-bed academic tertiary referral hospital who developed a VTE during hospital admission from September 1, 2011, to June 30, 2015, were retrospectively analyzed. Patients were excluded if they were younger than 18 years or if the VTE was present on admission. RESULTS: The cohort included 400 patients, 224 (56%) males, median age 66 years. The median time to VTE was 8 days. Significant differences in time to VTE existed between the risk groups. CONCLUSION: Time to VTE in a broad hospitalized patient population differs based on admission risk group. This finding highlights the importance of performing risk assessment upon admission and subsequently with clinical changes to assess increases in risk scores.

Discharge medication complexity and 30-day heart failure readmissions.

BACKGROUND: Limited research exists regarding Medication Regimen Complexity Index (MRCI) and its utility in identifying patients at risk for hospital readmission. OBJECTIVE: This study evaluates the association between discharge MRCI and 30-day rehospitalization in patients with heart failure (HF) after discharge. METHODS: The study involved a retrospective, cohort study at a large tertiary teaching facility from the University HealthSystem Consortium. The consortium database was used to identify HF patients hospitalized from January 2011 to December 2013. A 30-day readmission was defined as being readmitted to the same hospital within 30 days of discharge with a principal discharge diagnosis of HF. Index hospitalizations was defined as the first hospitalization, and readmission was the subsequent hospitalization for HF. A pilot analysis was conducted to compare manual MRCI collection tool and a computerized scoring MRCI system. Multivariable logistic regression was used to examine the association of computerized MRCI (≥15) and 30-day rehospitalization after controlling for other variables. RESULTS: A total of 1,452 patients were included in the study with 81 patients (5.9%) readmitted within 30 days of discharge. The manual and computerized MRCIs were correlated with an R of 0.74 and R2 of 0.55. The multivariate logistic regression analysis found computerized MRCI ≥15 (OR: 1.62; 95% CI: 1.01-2.59) was associated with 30-day rehospitalization after controlling for other factors. Patients prescribed angiotensin-converting-enzyme inhibitors or angiotensin receptor blockers, were less likely (OR: 0.54; CI: 0.33-0.89) to be readmitted 30 days after discharge, and patients with coronary artery disease were more likely (OR: 1.76; CI: 1.03-3.00) to be readmitted 30 days after discharge. CONCLUSIONS: The computerized MRCI score was moderately correlated with manual MRCI score. A significant association was found between computerized MRCI and 30-day HF readmission. Such predictive tools may allow pharmacists to prioritize patient care and optimize patient outcomes through medication therapy management.

Prevalence of in-hospital nonsteroidal antiinflammatory drug exposure in patients with a primary diagnosis of heart failure.

AIM: To determine the prevalence of in-hospital nonsteroidal antiinflammatory drug (NSAID) exposure and associated outcomes in patients admitted with a primary diagnosis of heart failure. METHODS: We performed a propensity-matched cohort analysis of patients admitted to Houston Methodist Hospital System with a primary diagnosis of heart failure according to the International Classification of Diseases-9-Clinical Modification (ICD-9-CM) from January 1, 2011 to December 31, 2014. RESULTS: Of the 9742 patients admitted with a primary diagnosis of heart failure, 384 patients (3.9%) were exposed to NSAID. After applying propensity scores we matched 305 NSAID exposed with 915 unexposed patients. Patients with in-hospital NSAID exposure had a longer length of stay (7.0±8.8 days vs 6.1±8.5; P=.003) and increased prevalence of worsening renal function (34.4% vs 27.9%; P=.030). There were not statically significant differences in in-hospital mortality rate or 30-day all-cause readmission rate. CONCLUSION: Exposure to NSAID in patients admitted with a primary diagnosis of heart failure was low but was associated with adverse outcomes including longer length of stay and higher prevalence or worsening renal function.

In-hospital use of non-steroidal anti-inflammatory drugs in patients with heart failure in academic centers in the United States.

BACKGROUND: Non-steroidal anti-inflammatory drugs are considered potentially harmful for patients with heart failure. OBJECTIVE: To determine the prevalence of in-hospital NSAID use, their type, associated diagnosis and impact in clinical outcomes among patients with a diagnosis of heart failure. METHODS: The University Health System Consortium Database was used to identify all first hospitalizations with an International Classification of Diseases-9 discharge diagnosis code of systolic heart failure as the primary diagnosis between January 1, 2011, and December 31st 2014. RESULTS: Among 65,902 patients admitted for a primary diagnosis of SHF, 2675 (4.1%) were exposed to NSAID. The most frequent NSAID used was ibuprofen (51.63%), followed by ketorolac (29.38%) naproxen (8.07%) celecoxib (5.61%), and others. On multivariable analyses, the length of stay of patients exposed to NSAID was longer compared to non-exposed (OR: 4.67, p < 0.001, 95% CI 4.10-5.25), but differences in mortality were not statistically different (OR: 0.90, p = 0.476, 95% CI 0.69-1.19). CONCLUSION: The use of NSAID in patients admitted with a primary diagnosis of systolic heart failure was low but was associated with longer length of stay. Further studies are needed to understand the impact of NSAID use in this patient population.

Evaluation and Pharmacokinetics of Treatment Dose Enoxaparin in Hospitalized Patients With Morbid Obesity.

BACKGROUND: The pharmacokinetic properties of enoxaparin may lead to supratherapeutic antifactor Xa (anti-Xa) levels and increased bleeding when standard treatment doses are used in patients with morbid obesity. OBJECTIVE: To evaluate the dose of enoxaparin needed to achieve therapeutic anti-Xa levels in a prospective, masked observational cohort of heterogeneous inpatients with morbid obesity and to determine whether patients with morbid obesity treated with 1 mg/kg of enoxaparin are at increased risk of supratherapeutic levels and bleeding events compared to patients receiving lower doses. METHODS: Hospitalized patients with a body mass index ≥40 kg/m(2) or actual body weight ≥140 kg and prescribed treatment doses of enoxaparin >60 mg per day were enrolled and consented to phlebotomy for determination of anti-Xa levels. RESULTS: Forty-one patients were included for data analysis. The dose of enoxaparin that resulted in therapeutic and supratherapeutic anti-Xa levels at steady state was 0.83 mg/kg and 0.98 mg/kg (-0.11; 95% confidence interval [CI] -0.20 to -0.01, P = .02), respectively. Enoxaparin dose as mg/kg of actual body weight was an independent predictor of having a supratherapeutic anti-Xa level. Patients with doses <0.95 mg/kg versus ≥0.95 mg/kg were less likely to have supratherapeutic levels (odds ratio 0.21 [95% CI 0.05-0.84], P = .02) and had similar rates of subtherapeutic levels. Doses <0.95 mg/kg and ≥0.95 mg/kg resulted in similar bleeding rates of 17.9% and 22.2% (P = .71), respectively. CONCLUSION: Patients with morbid obesity required less than the recommended 1 mg/kg enoxaparin dose to achieve therapeutic peak anti-Xa levels; therefore, initiation with lower dosages is prudent and anti-Xa monitoring should guide dosage adjustments.

Case report: Severe hypercalcemia mimicking ST-segment elevation myocardial infarction.

The identification of ST-segment elevation on the electrocardiogram is an integral part of decision making in patients who present with suspected ischemia. Unfortunately, ST-segment elevation is nonspecific and may be caused by noncardiac causes such as electrolyte abnormalities. We present a case of ST-segment elevation secondary to hypercalcemia in a patient with metastatic cancer.