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Item Cardiac Output Monitoring Managing Intravenous Therapy (COMMIT) to Treat Emergency Department Patients with Sepsis(Wolters Kluwer, 2016-08) Hou, Peter C.; Filbin, Michael R.; Napoli, Anthony; Feldman, Joseph; Pang, Peter S.; Sankoff, Jeffrey; Lo, Bruce M.; Dickey-White, Howard; Birkhahn, Robert H.; Shapiro, Nathan I.; Department of Emergency Medicine, IU School of MedicineOBJECTIVE: Fluid responsiveness is proposed as a physiology-based method to titrate fluid therapy based on preload dependence. The objectives of this study were to determine if a fluid responsiveness protocol would decrease progression of organ dysfunction, and a fluid responsiveness protocol would facilitate a more aggressive resuscitation. METHODS: Prospective, 10-center, randomized interventional trial. INCLUSION CRITERIA: suspected sepsis and lactate 2.0 to 4.0 mmol/L. Exclusion criteria (abbreviated): systolic blood pressure more than 90 mmHg, and contraindication to aggressive fluid resuscitation. INTERVENTION: fluid responsiveness protocol using Non-Invasive Cardiac Output Monitor (NICOM) to assess for fluid responsiveness (>10% increase in stroke volume in response to 5 mL/kg fluid bolus) with balance of a liter given in responsive patients. CONTROL: standard clinical care. OUTCOMES: primary-change in Sepsis-related Organ Failure Assessment (SOFA) score at least 1 over 72 h; secondary-fluids administered. Trial was initially powered at 600 patients, but stopped early due to a change in sponsor's funding priorities. RESULTS: Sixty-four patients were enrolled with 32 in the treatment arm. There were no significant differences between arms in age, comorbidities, baseline vital signs, or SOFA scores (P > 0.05 for all). Comparing treatment versus Standard of Care-there was no difference in proportion of increase in SOFA score of at least 1 point (30% vs. 33%) (note bene underpowered, P = 1.0) or mean preprotocol fluids 1,050 mL (95% confidence interval [CI]: 786-1,314) vs. 1,031 mL (95% CI: 741-1,325) (P = 0.93); however, treatment patients received more fluids during the protocol (2,633 mL [95% CI: 2,264-3,001] vs. 1,002 mL [95% CI: 707-1,298]) (P < 0.001). CONCLUSIONS: In this study of a "preshock" population, there was no change in progression of organ dysfunction with a fluid responsiveness protocol. A noninvasive fluid responsiveness protocol did facilitate delivery of an increased volume of fluid. Additional properly powered and enrolled outcomes studies are needed.Item Cardiovascular Magnetic Resonance Imaging in Patients With Ibrutinib-Associated Cardiotoxicity(American Medical Association, 2023) Buck, Benjamin; Chum, Aaron P.; Patel, Mitkumar; Carter, Rebecca; Nawaz, Haseeb; Yildiz, Vedat; Ruz, Patrick; Wiczer, Tracy; Rogers, Kerry A.; Awan, Farrukh T.; Bhat, Seema; Guha, Avirup; Kittai, Adam S.; Simonetti, Orlando P.; Raman, Subha V.; Wallace, Grant; Sanchez, Reynaldo; Bonsu, Janice M.; Gambril, John; Haddad, Devin; Mann, James; Wei, Lai; Kola-Kehinde, Onaopepo; Byrd, John C.; Woyach, Jennifer A.; Addison, Daniel; Medicine, School of MedicineImportance: Ibrutinib has been associated with serious cardiotoxic arrhythmias. In preclinical models, these events are paralleled or proceeded by diffuse myocardial injury (inflammation and fibrosis). Yet whether this is seen in patients or has implications for future cardiotoxic risk is unknown. Objective: To assess the incidence and outcomes of myocardial injury among patients with ibrutinib-related cardiotoxicity. Design, setting, and participants: This cohort study included consecutive patients treated with ibrutinib from 2012 to 2019, phenotyped using cardiovascular magnetic resonance (CMR) from a large US Comprehensive Cancer Center registry. Exposures: Ibrutinib treatment for cancer control. Main outcomes and measures: The primary outcome was the presence of late gadolinium enhancement (LGE) fibrosis. The secondary outcome was the occurrence of major adverse cardiac events (MACE), defined as atrial fibrillation, heart failure, symptomatic ventricular arrhythmias, and sudden death of probable or definite ibrutinib association after CMR. We also assessed parametric-mapping subclinical fibrosis (native-T1, extracellular volume fraction) and inflammation/edema (max-T2) measures. Cardiovascular magnetic resonance measures were compared with those obtained in similar consecutive patients with cancer without ibrutinib treatment (pretreatment controls). Observed measures were also compared with similar-aged broad population rates (general-population controls) and a broader pool of cardiovascular disease (CVD) risk-matched cancer controls. Multivariable regression was used to assess the association between CMR measures and MACE. Results: Overall, 49 patients treated with ibrutinib were identified, including 33 imaged after treatment initiation (mean [SD] age, 65 [10] years, 9 [27%] with hypertension, and 23 [69.7%] with index-arrhythmias); median duration of ibrutinib-use was 14 months. The mean (SD) pretreatment native T1 was 977.0 (73.0) ms, max-T2 56.5 (4.0) ms, and 4 (13.3%) had LGE. Posttreatment initiation, mean (SD) native T1 was 1033.7 (48.2) ms, max-T2 61.5 (4.8) ms, and 17 (54.8%) had LGE (P < .001, P = .01, and P < .001, respectively, pre- vs post-ibrutinib treatment). Native T12SDs was elevated in 9 (28.6%), and max-T22SDs in 21 (63.0%), respectively. Cardiovascular magnetic resonance measures were highest in those with suspected toxic effects (P = .01 and P = .01, respectively). There was no association between traditional CVD-risk or cancer-treatment status and abnormal CMR measures. Among those without traditional CVD, 16 (58.6%) had LGE vs 38 (13.3%) in matched-controls (relative-risk, 4.8; P < .001). Over a median follow-up of 19 months, 13 (39.4%) experienced MACE. In multivariable models inclusive of traditional CVD risk factors, LGE (hazard ratio [HR], 4.9; P = .04), and native-T12SDs (HR, 3.3; P = .05) associated with higher risks of MACE. Conclusions and relevance: In this cohort study, myocardial injury was common in ibrutinib users, and its presence was associated with higher cardiotoxic risk.Item Divergent actions of Myofibroblast and Myocyte β2-Adrenoceptor in Heart Failure and Fibrotic Remodeling(American Heart Association, 2023) Deng, Bingqing; Zhang, Yu; Zhu, Chaoqun; Wang, Ying; Weatherford, Eric; Xu, Bing; Liu, Xuanhui; Conway, Simon J.; Abel, E. Dale; Xiang, Yang K.; Pediatrics, School of Medicine