scholarly journals Abnormal Action Potential Duration Restitution in the Right Ventricular Outflow Tract and Inducibility of Ventricular Fibrillation in Brugada Syndrome

2008 ◽  
Vol 67 (5) ◽  
pp. 293-298
Author(s):  
Sonoko Ashino ◽  
Ichiro Watanabe ◽  
Masayoshi Kofune ◽  
Yasuo Okumura ◽  
Kimie Ohkubo ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Right Ventricular ◽  
Brugada Syndrome ◽  
Action Potential Duration ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Outflow Tract ◽  
The Right ◽  
Action Potential Duration Restitution

scholarly journals Endocardial Electrograms From the Right Ventricular Outflow Tract After Induced Ventricular Fibrillation in Patients With Brugada Syndrome

2007 ◽  
Vol 71 (8) ◽  
pp. 1258-1262 ◽  
Author(s):  
Kimie Ohkubo ◽  
Ichiro Watanabe ◽  
Yasuhiro Takagi ◽  
Yasuo Okumura ◽  
Sonoko Ashino ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Right Ventricular ◽  
Brugada Syndrome ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Outflow Tract ◽  
The Right

Action Potential Alternans in the Right Ventricular Outflow Tract in a Patient With Asymptomatic Brugada Syndrome

2009 ◽  
Vol 73 (3) ◽  
pp. 580-583 ◽  
Author(s):  
Masayoshi Kofune ◽  
Ichiro Watanabe ◽  
Sonoko Ashino ◽  
Kimie Ohkubo ◽  
Yasuo Okumura ◽  
...  
Keyword(s):  
Action Potential ◽  
Right Ventricular ◽  
Brugada Syndrome ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Outflow Tract ◽  
The Right

Dormant conduction in the right ventricular outflow tract unmasked by adenosine in a patient with Brugada syndrome

2021 ◽  
Vol 32 (4) ◽  
pp. 1182-1186
Author(s):  
Tsukasa Kamakura ◽  
Josselin Duchateau ◽  
Frédéric Sacher ◽  
Pierre Jais ◽  
Michel Haïssaguerre ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Brugada Syndrome ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Outflow Tract ◽  
Dormant Conduction ◽  
The Right

scholarly journals Blockade of CaMKII depresses conduction preferentially in the right ventricular outflow tract and promotes ischemic ventricular fibrillation in the rabbit heart

2017 ◽  
Vol 312 (4) ◽  
pp. H752-H767 ◽  
Author(s):  
Mark Warren ◽  
Katie J. Sciuto ◽  
Tyson G. Taylor ◽  
Vivek Garg ◽  
Natalia S. Torres ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Ventricular Fibrillation ◽  
Right Ventricular ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Outflow Tract ◽  
Dependent Protein Kinase ◽  
Calcium Calmodulin Dependent ◽  
Dependent Protein ◽  
The Right

Calcium/calmodulin-dependent protein kinase II (CaMKII) regulates the principle ion channels mediating cardiac excitability and conduction, but how this regulation translates to the normal and ischemic heart remains unknown. Diverging results on CaMKII regulation of Na+ channels further prevent predicting how CaMKII activity regulates excitability and conduction in the intact heart. To address this deficiency, we tested the effects of the CaMKII blocker KN93 (1 and 2.75 μM) and its inactive analog KN92 (2.75 μM) on conduction and excitability in the left (LV) and right (RV) ventricles of rabbit hearts during normal perfusion and global ischemia. We used optical mapping to determine local conduction delays and the optical action potential (OAP) upstroke velocity (d V/d tmax). At baseline, local conduction delays were similar between RV and LV, whereas the OAP d V/d tmax was lower in RV than in LV. At 2.75 μM, KN93 heterogeneously slowed conduction and reduced d V/d tmax, with the largest effect in the RV outflow tract (RVOT). This effect was further exacerbated by ischemia, leading to recurrent conduction block in the RVOT and early ventricular fibrillation (at 6.7 ± 0.9 vs. 18.2 ± 0.8 min of ischemia in control, P < 0.0001). Neither KN92 nor 1 μM KN93 depressed OAP d V/d tmax or conduction. Rabbit cardiomyocytes isolated from RVOT exhibited a significantly lower d V/d tmax than those isolated from the LV. KN93 (2.75 μM) significantly reduced d V/d tmax in cells from both locations. This led to frequency-dependent intermittent activation failure occurring predominantly in RVOT cells. Thus CaMKII blockade exacerbates intrinsically lower excitability in the RVOT, which is proarrhythmic during ischemia. NEW & NOTEWORTHY We show that calcium/calmodulin-dependent protein kinase II (CaMKII) blockade exacerbates intrinsically lower excitability in the right ventricular outflow tract, which causes highly nonuniform chamber-specific slowing of conduction and facilitates ventricular fibrillation during ischemia. Constitutive CaMKII activity is necessary for uniform and safe ventricular conduction, and CaMKII block is potentially proarrhythmic.

scholarly journals Longer Repolarization in the Epicardium at the Right Ventricular Outflow Tract Causes Type 1 Electrocardiogram in Patients With Brugada Syndrome

2008 ◽  
Vol 51 (12) ◽  
pp. 1154-1161 ◽  
Author(s):  
Satoshi Nagase ◽  
Kengo Fukushima Kusano ◽  
Hiroshi Morita ◽  
Nobuhiro Nishii ◽  
Kimikazu Banba ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Brugada Syndrome ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Outflow Tract ◽  
The Right
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