Larger Cell Size in Rabbits With Heart Failure Increases Myocardial Conduction Velocity and QRS Duration

Wiegerinck, Rob F.; Verkerk, Arie O.; Belterman, Charly; Veen, Toon A.B. van; Baartscheer, Antonius; Opthof, Tobias; Wilders, Ronald; Bakker, Jacques M.T. de; Coronel, Ruben

doi:10.1161/circulationaha.105.565804

Cited by 97 publications

(86 citation statements)

References 49 publications

(60 reference statements)

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“…10 At two weeks, heart weight was increased and remained higher in TAC compared with sham, which suggested increased path length. In conjunction, we have established that conduction velocity was slowed after 16 weeks.…”

Section: N T E R U N I V E R S I T Y C a R D I O L O G Y I N S T I mentioning

confidence: 95%

Longitudinal arrhythmogenic remodelling in a mouse model of longstanding pressure overload

Boulaksil¹,

Noorman²,

Engelen³

et al. 2010

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Section: N T E R U N I V E R S I T Y C a R D I O L O G Y I N S T I mentioning

confidence: 95%

Longitudinal arrhythmogenic remodelling in a mouse model of longstanding pressure overload

Boulaksil¹,

Noorman²,

Engelen³

et al. 2010

NHJL

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“…The longitudinal and transversal conduction velocities were calculated from ellipsoid activation patterns as described previously ( Figure 3). 21 Interstitial fibrosis was assessed in histological sections of hearts obtained at postmortem analysis in 6 randomly taken regions of RV and LV each. 22 We studied 3 CTEPH patients who died during surgery (1 underwent electrophysiological study during PEA) and 6 age/sex-matched patients who died of noncardiac causes.…”

Section: Electrophysiological Remodeling: Epicardial Mappingmentioning

confidence: 99%

Right-to-Left Ventricular Diastolic Delay in Chronic Thromboembolic Pulmonary Hypertension Is Associated With Activation Delay and Action Potential Prolongation in Right Ventricle

Hardziyenka

Campian

Bouma

et al. 2009

Circ: Arrhythmia and Electrophysiology

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Background-Delayed left ventricle (LV)-to-right ventricle (RV) peak shortening results in cardiac output reduction in patients with chronic thromboembolic hypertension (CTEPH) and other types of pulmonary arterial hypertension. Why the synchrony between LV and RV is lost is unknown. We hypothesized that RV electrophysiological remodeling, notably, conduction slowing and action potential prolongation, contribute to this loss in synchrony. Methods and Results-We conducted epicardial mapping during pulmonary endarterectomy in 26 patients with CTEPH and compared these findings with clinical, hemodynamic, and echocardiographic variables. We consecutively placed a multielectrode grid on the epicardium of the RV free wall and LV lateral wall. These regions corresponded to RV and LV areas where echocardiographic Doppler sample volumes were placed to measure RV-to-LV diastolic interventricular delay. RV and LV epicardial action potential duration was assessed by measuring activation-recovery interval. Onset of diastolic relaxation of RV free wall with respect to LV lateral wall (diastolic interventricular delay) was delayed by 38Ϯ31 ms in patients with CTEPH versus Ϫ12Ϯ13 ms in control subjects (PϽ0.001), because, in patients with CTEPH, RV completed electric activation later than LV (65Ϯ20 versus 44Ϯ7 ms, PϽ0.001) and epicardial action potential duration, as assessed by activation-recovery interval measurement, was longer in RV free wall than in LV lateral wall (253Ϯ29 versus 240Ϯ22 ms, PϽ0.001). Conclusion-Additive effects of electrophysiological changes in RV, notably, conduction slowing and action potential prolongation, assessed by epicardial activation-recovery interval, contribute to diastolic interventricular delay in patients with CTEPH. (Circ Arrhythmia Electrophysiol. 2009;2:555-561.)

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“…The digital images (128ϫ128 pixels) were gathered from the epicardium of the left ventricle (25ϫ25-mm 2 area), resulting in a spatial resolution of 0.2ϫ0.2 mm 2 per pixel. Because the normal rabbit myocyte averaged 0.1917ϫ0.0327 mm in size, 7 each pixel contained the information from an average of 6.4 epicardial myocytes. In addition, appreciable signal arises from cells 2 mm (61.2 cell layers) below the epicardium.…”

Section: Optical Mappingmentioning

confidence: 99%

Intracellular Calcium and Vulnerability to Fibrillation and Defibrillation in Langendorff-Perfused Rabbit Ventricles

et al. 2006

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Background-The role of intracellular calcium (Ca i ) in defibrillation and vulnerability is unclear. Methods and Results-We simultaneously mapped epicardial membrane potential and Ca i during shock on T-wave episodes (nϭ104) and attempted defibrillation episodes (nϭ173) in 17 Langendorff-perfused rabbit ventricles. Unsuccessful and type B successful defibrillation shocks were followed by heterogeneous distribution of Ca i , including regions of low Ca i surrounded by elevated Ca i ("Ca i sinkholes") 31Ϯ12 ms after shock. The first postshock activation then originated from the Ca i sinkhole 53Ϯ14 ms after the shock. No sinkholes were present in type A successful defibrillation. A Ca i sinkhole also was present 39Ϯ32 ms after a shock on T that induced ventricular fibrillation, followed 22Ϯ15 ms later by propagated wave fronts that arose from the same site. This wave propagated to form a spiral wave and initiated ventricular fibrillation. Thapsigargin and ryanodine significantly decreased the upper limit of vulnerability and defibrillation threshold. We studied an additional 7 rabbits after left ventricular endocardial cryoablation, resulting in a thin layer of surviving epicardium. Ca i sinkholes occurred 31Ϯ12 ms after the shock,

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Larger Cell Size in Rabbits With Heart Failure Increases Myocardial Conduction Velocity and QRS Duration

Cited by 97 publications

References 49 publications

Longitudinal arrhythmogenic remodelling in a mouse model of longstanding pressure overload

Longitudinal arrhythmogenic remodelling in a mouse model of longstanding pressure overload

Right-to-Left Ventricular Diastolic Delay in Chronic Thromboembolic Pulmonary Hypertension Is Associated With Activation Delay and Action Potential Prolongation in Right Ventricle

Intracellular Calcium and Vulnerability to Fibrillation and Defibrillation in Langendorff-Perfused Rabbit Ventricles

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