PubMed Health⌕ Search

Biomedical subjects

J J Sims

Publications and source records attributed to J J Sims.

23 records · Page 2Linked to original sources
PubMedDate not supplied

Induction of electrical heterogeneity impairs ventricular defibrillation: an effect specific to regional conduction velocity slowing.

BACKGROUND: This study determined whether dispersion of conduction velocity, refractoriness, or excitability increases biphasic shock defibrillation energy requirements (DERs). METHODS AND RESULTS: Twenty-four swine were instrumented with a mid-LAD perfusion catheter for regional infusion of lidocaine 0.75 mg. kg(-1). h(-1) (n=7), low-dose d-sotalol (0.16 mg. kg(-1). h(-1)) (n=4), high-dose d-sotalol (0.5 mg. kg(-1). h(-1)) (n=6), or saline (n=7). Effective refractory periods (ERPs) were determined at 5 myocardial sites, and regional conduction velocity was determined in LAD-perfused and -nonperfused regions. Regional lidocaine infusion increased DER values by 84% (P=0.008) and slowed conduction velocity by 23% to 35% (P<0.01) but did not affect ERP. Conversely, regional low- and high-dose d-sotalol infusion did not alter DER values or conduction velocity but increased regional ERP by 14% to 17% (P<0.001). Regional lidocaine increased conduction velocity dispersion by 100% to 200% (P=0.01) but did not change ERP dispersion, whereas d-sotalol increased ERP dispersion by 140% (P<0.001) without affecting conduction velocity dispersion. Lidocaine infusion induced ventricular fibrillation (VF) in 6 of 7 animals, whereas regional d-sotalol was not proarrhythmic. Regional infusion of lidocaine and d-sotalol prolonged VF cycle length by 23% to 41% (P<0.05) in the perfused region and increased VF cycle length dispersion by 85% to 240% (P<0.05). Both agents increased pacing threshold (excitability) in the perfused region by 93% to 116% (P<0.05). CONCLUSIONS: Regional conduction velocity slowing increased DER values, which was probably a result of spatial dispersion of conduction velocity. Increasing refractory period dispersion without changing conduction velocity did not alter DFT values. Thus, dispersion of conduction velocity may be a more likely regulator of defibrillation efficacy than dispersion of refractoriness.

Action Potentials↗
PubMedDate not supplied

Lidocaine does not affect myocardial electrical heterogeneity: implications for low proarrhythmic actions.

An area of unidirectional conduction block is one requirement for reentrant arrhythmias to occur. Functional block caused by dispersion of repolarization and refractoriness is the most probable mechanism of drug-induced unidirectional conduction block. We assessed the effects of lidocaine on spatial dispersion of myocardial repolarization and refractoriness in the intact porcine heart. Monophasic action potential duration at 90% repolarization, effective refractory period (ERP), and ventricular fibrillation cycle length (VFCL) were measured at two endocardial and one epicardial sites at baseline and during a treatment phase with D5W (n=11) or lidocaine 10 mg/kg/hour (n=12). Dispersion was calculated as the difference between the maximum and minimum values of the three recording sites. Lidocaine produced significant changes in ERP, VFCL, paced QRS duration, and intraventricular conduction time. It did not change basal levels of dispersion in repolarization and refractoriness. Lidocaine produced changes in myocardial electrophysiology that are uniform across the myocardium and thus did not change myocardial electrical heterogeneity. This may be a mechanism of the agent's lower proarrhythmic effects compared with other sodium channel blockers that increase myocardial electrical heterogeneity.

Action Potentials↗