There is one clinical trial.
This study tested the hypothesis that response to digoxin is modulated by single Nucleotid Polymorphism (SNP): - Multi Drug Resistance (MDR1) gene haplotypes and Solute carrier organic anion transporter family member 1B3 (SLCO1B3) gene Polymorphism and their role in the response to treatement. - Aldosterone synthase (CYP11B2) gene and sodium channel, voltage-gated, type V alpha subunit gene (SCN5A) correlated with atrial fibrillation and their roles in response to digoxin.
We hypothesized that the T-344C and H558R (His558Arg) SNPs in CYP11B2 and SCN5A gene which are associated with susceptibility to AF could be implicated in the variation of response to Digoxin. --- H558R ---
We hypothesized that the T-344C and H558R (His558Arg) SNPs in CYP11B2 and SCN5A gene which are associated with susceptibility to AF could be implicated in the variation of response to Digoxin. --- H558R --- --- His558Arg ---
Description: In the current study we aimed at outlining the different MDR-1, SLCO1B3, CYP11B12 and SCN5A genotypes in a sample of Tunisian patients, suffering from AF and taking digoxin, to assess the role of SNPs in affecting serum digoxin concentrations, and studying the consequences on patients' clinical outcome. Patients will be monitored for 24 hours in an intensive care unit;Measure: Correlation between the response to digoxin and the genotypes of the patients Time: 24 hours
Description: Rhythm control: rate and delay of return to sinusal rhythm. Rate control: reduction of heart rate : HR <100 bpm or 20% reduction from baselineMeasure: Rhythm and Rate control Time: 24 hours
Description: hypotension during hospitalisation, bradycardia, chest pain, allergic reactionMeasure: Arterial hypotension Bradycardia (HR <45 bpm) Other (chest pain, allergic reaction……) Time: 24 hours