Human ventricular repolarization and T wave genesis.
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Biomedical subjects
Publications and source records attributed to M R Franz.
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The Gen-Probe PACE (Probe Assay-Chemiluminescent Enhanced) system for Neisseria gonorrhoeae was compared to Martin-Lewis medium in JEMBEC plates for the direct detection of N. gonorrhoeae in urogenital samples. This 2-hr, nonisotopic chemiluminescent test is based on the use of an acridinium ester-labeled DNA probe that binds with gonococcal target rRNA in a clinical sample. Following the separation of the hybridized probe from the unhybridized probe through the use of magnetic microparticles, the acridinium ester is hydrolyzed from the hybridized probe by the addition of an alkaline hydrogen peroxide solution, resulting in the production of light, which is measured in a luminometer. The amount of light generated is directly proportional to the amount of gonococcal target rRNA present in the sample. A total of 209 urethral and 203 endocervical specimens were collected from a high-risk, clinic population with a gonococcal disease prevalence of 24% during the study period. Statistical analyses of the overall results showed that, compared to culture, the Gen-Probe PACE System had a sensitivity, specificity, and positive and negative predictive values of 90%, 99%, 98%, and 97%, respectively. The comparative results of this study showed that the Gen-Probe PACE System for N. gonorrhoeae is a reasonable, noncultural alternative for detecting gonococci directly in urogenital specimens.
Dispersion of ventricular repolarization is a now widely used term describing nonhomogeneous recovery of excitability or heterogeneity of ventricular repolarization. It is usually expressed as the difference or the range of various repolarization measurements obtained from a heart. Experimentally, an increased dispersion of ventricular repolarization was found to be tightly associated with increased propensity for ventricular arrhythmias, and, therefore, is considered an important arrhythmogenic mechanism. Noninvasively, this arrhythmogenic substrate was approached using multilead body surface potential mapping, but also QT interval dispersion (QTd) and similar electrocardiogram (ECG) variables from the 12-lead surface ECG. Standard QTd from the ECG correlates significantly with dispersion of repolarization measured from the myocardium. A causal relationship is, however, still unclear, and there are 2 main hypotheses to explain the electrophysiological basis of QTd. The local hypothesis explaining QTd with spatial differences in action potential duration mirrored in the various QT intervals competes with the global hypothesis explaining the variation in surface ECG measurements with different projections of a common T-wave vector. Notwithstanding the final explanation for QTd, and particularly for technical reasons, new markers like advanced T-wave loop variables may best reflect the abnormal repolarization substrate on the surface ECG.