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J E Val-Mejias

Publications and source records attributed to J E Val-Mejias.

5 recordsLinked to original sources

ICD waveform optimization: a randomized, prospective, pair-sampled multicenter study.

The theoretical tissue model-based estimates of phase 1 and phase 2 duration of biphasic waveforms are considerably shorter than the pulse widths currently used in ICDs with standard tilt. This study used a tissue resistance/capacitance (RC) model to identify optimal biphasic pulse widths. By paired step-down defibrillation threshold (DFT) testing, the efficacy of standard versus "tuned" biphasic waveforms was evaluated in 91 patients. Standard waveforms consisted of a phase 1 set to 65% tilt and phase 2 = phase 1. The tuned waveform was based on an RC model of membrane characteristics with a time constant of 3.5 ms. The optimal phase 1 truncation point is at the peak of membrane response. The optimal phase 2 duration ends with a membrane response near or just below 0. In paired analysis, no significant differences were found in DFT or impedance between standard and tuned waveforms. In patients with DFTs > 400 V, the tuned waveform lowered the DFT by an average of 38 V (P < 0.05). Multivariate analyses showed a significant inverse relationship between DFT and impedance (P < 0.001). As impedance increased, the tuned waveform was associated with DFTs comparable to the standard waveform with shorter pulse duration and lower delivered energy. No single tilt value allowing an easy calculation of delivered energy was related to ICD waveform efficacy. The use of ICDs with tuned optimal pulse durations offer a greater flexibility of choice for patients with high DFTs.

Aged↗

Evaluation of a rat model for assessing interventions to salvage ischaemic myocardium: effects of ibuprofen and verapamil.

Coronary ligated rats were administered intraperitoneal injections of 6.24, 12.52, and 25.00 mg . kg-1 ibuprofen and 5.00 and 10.00 mg . kg-1 verapamil 1 h before ligation, 1 h after ligation, and then every 8 h for 48 h. Ibuprofen at 50.00 mg . kg-1 was administered 1 h before ligation, 1 h after ligation and 5 h after ligation. Infarct size was determined either by weighing the stained excised infarcted area or by measuring the creatine kinase activity from the excised left ventricle. Ibuprofen and verapamil treatment resulted in less myocardial damage after 48 h than placebo treatment but the differences were generally not statistically significant. The reduction in infarct size was greater in the ibuprofen treated animals compared with verapamil treated rats. In addition, there was a lower mortality with ibuprofen treatment than for either verapamil or placebo. This rat model was useful as a screening tool for the initial evolution of therapeutic interventions to reduce myocardial infarct size. It required substantially less time than large animal models and can be used to examine a variety of treatment doses. These experiments also demonstrated the importance of randomisation to treatment and control groups because of the possibility of disproportionate mortality affecting infarct size.

Animals↗