Background: Post–cardiac surgery bleeding can have devastating consequences, and it is unknown if warfarin-induced rapid international normalized ratio (INR) rise during the immediate postoperative period increases bleed risk. Objective: To determine the impact of warfarin-induced rapid-rise INR on post–cardiac surgery bleeding. Methods: This was a single-center, retrospective chart review of post–cardiac surgery patients initiated on warfarin at Mayo Clinic Hospital, Rochester. Patients were grouped based on occurrence or absence of rapid-rise INR (increase ≥1.0 within 24 hours). The primary outcome compared bleed events between groups. Secondary outcomes assessed hospital length of stay (LOS) and identified risk factors associated with bleed events and rapid rise in INR. Results: During the study period, 2342 patients were included, and 56 bleed events were evaluated. Bleed events were similar between rapid-rise (n = 752) and non–rapid-rise (n = 1590) groups in both univariate (hazard ratio [HR] = 1.22; P = 0.594) and multivariable models (HR = 1.24; P = 0.561). Those with rapid-rise INR had longer LOS after warfarin administration (discharge HR = 0.84; P = 0.0002). The most common warfarin dose immediately prior to rapid rise was 5 mg. Risk factors for rapid-rise INR were low body mass index, female gender, and cross-clamp time. Conclusion and Relevance: This represents the first report to assess warfarin-related rapid-rise INR in post–cardiac surgery patients and found correlation to hospital LOS but not bleed events. Conservative warfarin dosing may be warranted until further research can be conducted.
Vitamin C for Vasoplegia After Cardiopulmonary Bypass: A Case Series
A&A Practice | July 11, 2018 | Volume: 11 | Issue: 4 | Pages: 96-99
Cardiac vasoplegia remains a significant contributor of morbidity and mortality in cardiac surgery patients after cardiopulmonary bypass. Effective therapeutic options for vasopressor-refractory vasoplegia are limited. We report 3 patients in whom we administered high-dose intravenous ascorbic acid (vitamin C), a cofactor for endogenous catecholamine synthesis, to treat vasoplegia refractory to epinephrine, vasopressin, and norepinephrine after surgery requiring cardiopulmonary bypass. Reductions in vasopressor requirements were observed in all 3 patients, and, in 2 patients, norepinephrine was completely discontinued within 24 hours. Ascorbic acid is a novel potential therapeutic option for cardiac vasoplegia that warrants rigorous prospective studies.
Baseline Thromboelastogram as a Predictor of Left Ventricular Assist Device Thrombosis
Left ventricular assist device (LVAD) pump thrombosis occurs in up to 8.4% of patients within 3-months postimplantation. Thromboelastography (TEG) could be used to signal hypercoagulability at LVAD implantation to predict patients at high risk for thrombosis. We sought to evaluate whether TEG maximum amplitude (MA) hypercoagulability (MA ≥69 mm) at the time of LVAD implantation predicts pump thrombosis. A single center, retrospective, nested case–control study was conducted using patients from January 1, 2005, to March 31, 2015. Each pump thrombosis case was matched to two control subjects based on age ± 5 years, sex, and duration of follow-up. A multivariable logistic regression analysis was performed on the matched sets; the odds ratio with 95% confidence interval (CI) was calculated to estimate the relative risk. Thirty-seven age- and sex-matched case–control sets were included for a total of 111 study participants. TEG-MA hypercoagulability occurred in 10.8% of the case group versus 6.8% of controls. There was no association between TEG-MA hypercoagulability and device thrombosis (odds ratio 1.71, 95% confidence interval 0.42–7.05, p = 0.46). Utilization of baseline TEG-MA hypercoagulability to detect individuals at risk for LVAD thrombosis is a novel concept. This study found no significant association between TEG-MA and LVAD thrombosis.
Therapeutic drug monitoring of mexiletine at a large academic medical center
SAGE Open Medicine | September 21, 2016 | Volume: 4 | Issue: No issue available | Pages: No page available
Introduction: The therapeutic trough range for mexiletine (0.8–2 mcg/mL) was largely established in the setting of arrhythmia prophylaxis following myocardial infarction. Objective: Describe the usage patterns of serum mexiletine concentrations and the impact of these concentrations on mexiletine dosing in modern practice for ventricular arrhythmia treatment. Methods: A single-center, retrospective analysis was conducted using the electronic medical record to identify serum mexiletine concentrations drawn between December 2004 and December 2014. The primary endpoint was the incidence of mexiletine concentrations drawn as troughs. Secondary outcomes included the incidence of mexiletine concentrations that prompted a dose change, association between adverse events and elevated concentrations, and association between baseline characteristics and mexiletine concentrations. Results: A total of 237 individual concentrations were included for analysis with 109 (46.0%) drawn appropriately as trough concentrations. Only 31 (13.1%) of the 237 concentrations drawn prompted a dose change. Mexiletine was primarily used for the treatment of ventricular arrhythmias (96.2%), and 108 (45.6%) concentrations were drawn in an effort to assess efficacy. The median concentration was statistically different between patients with and without an adverse event (0.8 vs 0.7 mcg/mL, respectively; p = 0.017), but may not represent a clinical significance. Patients with hepatic dysfunction had higher median concentrations compared to those without hepatic dysfunction (1.30 vs 1.07 mcg/mL; p = 0.01). Conclusion: Mexiletine concentrations are often drawn at inappropriate times and seldom influence a dose change. This study suggests that routine monitoring of mexiletine concentrations may not be necessary; however, therapeutic drug monitoring may be considered in patients with hepatic dysfunction or to confirm mexiletine absorption in patients where this represents a concern.