IndraLab

Statements


9 | 8

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"Flecainide blocks the Nav1.5 channel in its inactivated state [ 8 ], therefore reducing the inward flow of sodium in the cell and slowing the physiological recovery of the Nav1.5 from the inactivated [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"The drug flecainide prevents arrhythmia in humans and mouse models of CPVT by blocking NaV1.5 and RYR2 channels."

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"Disease processes such as atrial fibrillation and left-sided versus right-sided heart failure affect cardiac cells within specific regions, although current pharmacotherapies for these may not specifically target the affected region-specific cell types, resulting in adverse outcomes (for example, the SCN5A blocker flecainide is used to treat atrial fibrillation but can induce ventricular arrhythmias )."

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"Flecainide blocks flow of the cardiac NaV1.5 sodium channel, slowing the upstroke and prolonging the cardiac action potential with minimal effect on repolarization."

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"Due to their distinct properties, several classes of well-known reference pharmacological agents, including hERG blockers such as cisapride ( Rampe, Roy, Dennis, & Brown, 1997 ) and dofetilide ( Kiehn[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"This conclusion is supported by the frequency dependence of wave inhibition by flecainide (Supplementary Figure S1); previous studies have demonstrated that flecainide inhibition of Nav1.5 is use/frequency dependent (Mestre et al., 2000)."

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"Flecainide further reduced theta ' max in the Scn5a +/- RV epicardium (from 0.05 (0.01) to 0.03 (0.028) ms -1; U = 18.0, P = 0.026, r = 0.54)."

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"Flecainide reduced the BCD ' in the Scn5a +/- RV epicardium (from 3.42 (0.77) to 2.66 (0.82); U = 20.0, P = 0.030, r = 0.48)."

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No evidence text available