Electropharmacological characterization of cardiac repolarization in German shepherd dogs with an inherited syndrome of sudden death: abnormal response to potassium channel blockers

Abstract

These results support the hypothesis of an abnormal cardiac repolarization in affected dogs. The effects of 293B suggest that I(Ks) may be involved in this anomaly.

A case of short‐coupled premature ventricular beat‐induced ventricular fibrillation with early repolarization in the inferolateral leads

“…In this report, the coupling interval of the first initiating PVB of VF was relatively short (297 741 ms), and the PVBs originated from both the left and right ventricles. Several reports described triggered activity, abnormal automaticity, or reentry as possible underlying mechanisms of IVF originating from the Purkinje system [1][2][3][5][6][7][8]. Verapamil is considered effective in preventing such arrhythmic events.…”

ECG of the Month

“…Ventricular arrhythmias can be the result of abnormal electrical impulse generation (eg, abnormal automaticity or triggered activity), abnormal impulse conduction (eg, reentry), or a combination of both. 5 In dogs with GSDIVA, triggered activity (spontaneous early afterdepolarization) in the Purkinje fibers of the left ventricle are thought to be the cause of the VA. [6][7][8] In addition, abnormalities in the autonomic nervous system are thought to have important roles in the development of sudden death in dogs with GSDIVA. 9 The risk of sudden cardiac death is thought to regress as dogs with GSDIVA age and their autonomic nervous system matures.…”

Genetic Analysis of Ventricular Arrhythmia in Young German Shepherd Dogs

“…Causative mutations have primarily been identified in genes encoding specific sodium and potassium channel proteins involved in repolarization 9–19 . In affected GSDs, abnormalities of ion current densities of potassium channels and calcium cycling indicate a global disruption of repolarization reserve 20–30 . Futhermore, heterogeneous sympathetic innervation has been identified 29 .…”

“…[9][10][11][12][13][14][15][16][17][18][19] In affected GSDs, abnormalities of ion current densities of potassium channels and calcium cycling indicate a global disruption of repolarization reserve. [20][21][22][23][24][25][26][27][28][29][30] Futhermore, heterogeneous sympathetic innervation has been identified. 29 Given the failure to identify a singular abnormality, genome-wide analysis of linkage is more likely to be successful in identifying the causative loci for VA in GSDs than a candidate gene approach.…”