Signal-averaged electrocardiograms (SAEKGs) were performed on 4 dogs with sustained ventricular tachycardia. Quantitative and qualitative analyses of SAEKGs were consistent with the presence of late potentials. Two of the 4 dogs subsequently died suddenly, and ventricular tachycardia and ventricular fibrillation were observed in 1 dog. High-frequency QRS durations (75-90 milliseconds), duration of low amplitude (less than 40 microV) signals during the terminal QRS complex (LAS40) (28-40 milliseconds), root mean square voltages of the terminal 40 milliseconds of the QRS complex (RMS40) (124-6.5 microV), and root mean square voltages of the terminal 30 milliseconds of the QRS complex (RMS30) (13-2.1 microV) differed from results obtained in 68 of 70 control dogs. Echocardiographic data suggested dilated cardiomyopathy in 2 dogs and the cause of the arrhythmia in 2 dogs was not determined. The SAEKG may be a useful adjunct in identifying a subset of dogs with ventricular tachyarrhythmias that are at high risk for sustained ventricular tachycardia and sudden death. The sensitivity, specificity, and predictive accuracies of the technique remain to be determined.

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PubMedDate not supplied

Signal-averaged electrocardiograms in normal Doberman pinschers.

Signal-averaged electrocardiograms (SAECGs) were performed on nonsedated normal dogs in left-lateral recumbency. Following signal averaging, both time-domain and 3-dimensional frequency-domain analyses were performed. For time-domain analysis, the high-frequency QRS (HFQRS) duration, duration of the terminal QRS complex less than 40 microV (LAS40), and root mean square (RMS) voltages (microV) of the terminal 40 milliseconds (RMS40) and 30 milliseconds of the QRS complex were calculated. For frequency-domain analysis, correlation ratios were calculated for 30-, 40-, 50-, and 60-millisecond segment lengths begun 10, 15, or 20 milliseconds before the end of the QRS complex. Spectro-temporal mapping was also performed. All of the parameters of the SAECGs analyzed in the time domain were associated with each other. LAS40 and RMS voltages regressed significantly (P < .0000) on the HFQRS duration. Ninety-five percent of the HFQRSs were 55-75 milliseconds, 95% of the LAS40s were 9-26 milliseconds, and 95% of the RMS40 voltages were 177-444 microV. None of the SAECGs contained evidence of ventricular late potentials. Spectro-temporal maps were similar in each dog when the same segment lengths and starting points were compared. No evidence of ventricular late potentials was observed. Correlation ratios were lower when windowed segments included 15 or 20 milliseconds (versus 10 milliseconds) of the terminal QRS complex. When only 10 milliseconds of the terminal QRS complex were included in windowed segments, the mean correlation ratios for 30- and 40-millisecond segment lengths were > 0.8 and > 0.61 in 67% of all analyses, respectively.

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PubMedDate not supplied

Mathematical model for agonist-induced oscillatory calcium waves in non-excitable mammalian cells.

Many non-excitable cells display cytosolic Ca2+ oscillations resulting from the periodic release of Ca2+ from intracellular stores. Recent observations in hepatocytes and some other cell types have shown that agonist-induced Ca2+ oscillations often display an intracellular spatial organization and do not occur synchronously within the cell. Ca2+ waves evoked by different agonists originate from the same subcellular locus and propagate through the cell with a constant rate of progress and amplitude. This indicates that Ca2+ waves are driven by a self-propagating mechanism and not by diffusion alone. We propose a simplified one-dimensional mathematical model to describe this phenomenon based on the mechanism of calcium-induced calcium release. The numerical solution of the system of two coupled non-linear partial differential equations reproduces many of the main features observed experimentally.

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PubMedDate not supplied

Cytosolic calcium oscillators: critical discussion and stochastic modelling.

In the last few years, an immense amount of experimental data on agonist-induced cytosolic Ca2+ oscillations has emphasized the necessity of theoretical models accounting for these phenomena. In the first part of the paper, a critical analysis of different minimal Ca2+ oscillator models is presented, which reveals that not all of the so far proposed mechanisms are capable to reproduce experimental data adequately. The second part of the paper is devoted to a computational method using a stochastic simulation algorithm which describes the time evolution of Ca2+ oscillations at the molecular level. In contrast to the deterministic formulation of the models presented so far, the stochastic treatment takes account of the inherent fluctuations of cytosolic Ca2+ in cellular subcompartments. In the macroscopic limit, the stochastic models display dynamics analogous to the deterministic ones.

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