vitamin-k-semiquinone-radical and Syncope

Adverse drug events (ADE) occur frequently during treatment with vitamin K antagonists (AVK) and contribute to increase hemorrhagic risks.. A retrospective study was conducted over a period of 2 years. Patients treated with AVK and admitted to the emergency room of a tertiary care hospital in Beirut were included. The aim of the study was to identify ADE characterized by a high international normalized ratio (INR) and to determine the predictive factors responsible for these events. Statistical analysis was performed with the SPSS statistical package.. We included 148 patients. Sixty-seven patients (47.3%) with an INR above the therapeutic range were identified as cases. The control group consisted of 81 patients (54.7%) with an INR within the therapeutic range. Hemorrhagic complications were observed in 53.7% of cases versus 6.2% of controls (P < 0.0001). No significant difference was noticed between cases and controls regarding the indication and the dose of AVK. Patients aged over 75 years were more likely to present an INR above the therapeutic range (58.2%, P = 0.049). Recent infection was present in 40.3% of cases versus 6.2% of controls (P < 0.0001) and hypoalbuminemia in 37.3% of cases versus 6.1% of controls (P < 0.0001). Treatment with antibiotics, amiodarone, and anti-inflammatory drugs were also factors of imbalance (P < 0.0001).. Many factors may be associated with ADE related to AVK. Monitoring of INR and its stabilization in the therapeutic range are important for preventing these events.

Topics: Age Factors; Aged; Amiodarone; Anti-Arrhythmia Agents; Anti-Bacterial Agents; Anti-Inflammatory Agents; Anticoagulants; Case-Control Studies; Creatinine; Dizziness; Drug Interactions; Emergency Service, Hospital; Fatigue; Hemoglobins; Hemorrhage; Humans; Hypoalbuminemia; Infections; International Normalized Ratio; Multivariate Analysis; Pallor; Platelet Aggregation Inhibitors; Retrospective Studies; Syncope; Vitamin K

Cardiovascular collapses, syncopes, and sudden deaths have been observed following the rapid administration of intravenous vitamin K. Our objectives were to characterize the effects of vitamin K on cardiac action potentials and to evaluate effects of vitamin K on sodium and potassium currents, namely I(Na), I(Kr), and I(Ks).. Guinea pig hearts (n = 21) were paced at a cycle length of 250 msec and exposed to vitamin K at 1.15-4.6 micromol/L (2.5-10 mg/L). Monophasic action potential duration measured at 90% repolarization (MAPD(90)) was not significantly reduced (-1.6 +/- 0.3 msec; P >.05; N.S.) at 1.15 micromol/L, but increased by 6.5 +/- 0.4 msec (P <.05) at 2.3 micromol/L. MAPD(90) was not measurable at 4.6 micromol/L, as a result of inexcitability. Patch-clamp experiments in ventricular myocytes demonstrated a approximately 50% reduction in I(Na) by 10 micromol/L vitamin K and a concentration-dependent reduction of the K(+) current elicited by short depolarizations (250 msec; I(K250)). Estimated IC(50) for I(K250), mostly representing I(Kr), was 2.3 micromol/L. Vitamin K was less potent to block the K(+) current elicited by long depolarizations (5,000 msec; I(K5000)), mostly representing I(Ks), with an estimated IC(50) over 100 micromol/L.. Therapeutic concentrations ( approximately 1.5 micromol/L) of intravenous vitamin K modulate cardiac action potential by blocking ionic currents involved in cardiac depolarization and repolarization.

Topics: Action Potentials; Animals; Death, Sudden, Cardiac; Dose-Response Relationship, Drug; Guinea Pigs; Heart; Infusions, Intravenous; Potassium Channels; Sodium Channels; Syncope; Vitamin K

Topics: Child; Cholestanes; Humans; Hydrocephalus; Infant; Syncope; Vitamin A; Vitamin D; Vitamin K; Vitamins