Changes in myocardial metabolism and transcardiac electrolytes during simulated ventricular tachycardia: Effects of β-adrenergic blockade

Peuhkurinen, Keijo; Huikuri, Heikki V.; Linnaluoto, Markku K.; Takkunen, Juha T.

doi:10.1016/0002-8703(94)90015-9

Cited by 4 publications

(1 citation statement)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…27,28,[30][31][32] In contrast, only limited studies have focused on how the rapid ventricular rate itself affects myocardial metabolism. 33 In a study using isolated perfused ferret hearts, electrically induced VF did not markedly alter myocardial energy generation. 32 Also, calcium loading during electrically induced VF did not cause significant differences from loading during strophantidine induced VF.…”

Section: Repetitive Firingmentioning

confidence: 95%

Site of the Arrhythmogenic Focus and Cardiac Vulnerability to Ventricular Fibrillation

Murakawa

Yamashita

Ajiki

et al. 2002

Pacing Clinical Electrophis

View full text Add to dashboard Cite

The aim of this study was to test the hypothesis that a subendocardial arrhythmogenic focus makes the heart more susceptible to VF due to electrical interaction with the Purkinje network. Monofocal ventricular tachycardia (mVT) was created by injecting 5-microg aconitine into the left ventricular subepicardium (EPI-mVT, n = 8) or subendocardium (ENDO-mVT, n = 13) in anesthetized dogs. Despite the similar cycle length of mVT, the incidence of VF was significantly different between EPI-mVT and ENDO-mVT (100 [8/8] vs 46% [6/13], P <0.05). VF was invariably preceded by hemodynamic deterioration. Three-dimensional cardiac mapping (n = 10, 221 +/- 11 recording sites) revealed that VF was triggered solely by focal firing unrelated to the primary arrhythmogenic focus in both mVT models. No interaction between the primary focus and adjacent endocardial tissue was indicated. These results suggest that the proximity of the arrhythmogenic focus to the Purkinje network has little role in cardiac vulnerability to VF, and that progression of mVT to VF is largely caused by sporadic focal firing regardless of the site of the arrhythmogenic focus in the present animal model.

show abstract