Journal of electrocardiology
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This study employs a bifurcation analysis approach to elucidate the effect of the key ion channels on cardiac arrhythmias and thereby explain the efficacy of antiarrhythmic drugs in controlling arrhythmias. The model used for the analysis contains the key ion channels involved in the ventricular action potential--fast sodium, slow calcium, and background potassium channels. The cardiac tissue is modeled by a ring structure. ⋯ In the neighborhood of the CRS, the cycle length oscillates with an interesting pattern that depends on ring size and drug type. Although a critical reentrant loop length for stable reentrant excitation has been investigated for a long time, this study is the first demonstration of how the key ion channels in the plasma membrane affect the loop length. Furthermore, the analysis approach provides a theoretical basis for the increased mortality associated with class I drug use in the Cardiac Arrhythmia Suppression Trial Team.
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A mathematic description of the behavior of the Bazett-corrected QTc interval during exercise was developed from the underlying relationship between the unadjusted QT interval and heart rate in 94 normal men. Measurements were made from digitized precordial lead V5 complexes that were averaged by computer over 20-second periods at upright control (mean rate, 78 beats/min), during moderate exercise (mean rate, 125 beats/min), and at peak effort (mean rate, 162 beats/min), using a gently graded treadmill protocol that produces small heart rate increments between 2-minute stages. ⋯ As a consequence of this linearity, the behavior of the QTc interval over a range of heart rates generally found during exercise could be modeled as a function of the slope (m) and intercept (b) of the observed relationship, since the Bazett relationship QTc = QT[ms]/R-R0.5 can, in this context, be rewritten simply as QTc = (481 - 1.32HR)/(60/HR)0.5, which reproduces the observed biphasic QTc interval behavior. Plots of the generalized equation QTc = (b - mHR)/(60/HR)0.5 allow theoretical exploration of QTc interval behavior that might result from varied disorders with different slopes (m) and intercepts (b), and these regression-based descriptors of the QT-heart rate relationship may provide useful, additional definitions of normal and abnormal QT interval behavior during exercise.
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The authors studied power spectral analysis of heart rate variability in the rat, hypothesizing that the quantitative information provided by this analysis reflects the interaction between sympathetic and parasympathetic regulatory activities. For this purpose, an electrocardiogram was recorded from conscious and unrestrained Wistar rats (Nippon, Shizuoka) (12-16 weeks old) by a telemetry system and analyzed by a power spectrum. Because it was thought that the electrocardiogram recorded by the telemetry system could provide more reliable data to assess autonomic nervous activity than the tethering system, the telemetry recording system was used. ⋯ Furthermore, the decrease in the parasympathetic mechanism produced by atropine was reflected by a slight increase in the LF/HF ratio. The LF/HF ratio appeared to follow the reductions of sympathetic activity produced by propranolol. From these results, the LF/HF ratio seemed to be a convenient index of parasympathetic and sympathetic interactions in the rat.(ABSTRACT TRUNCATED AT 250 WORDS)
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Torsade de pointes is a form of polymorphic ventricular tachycardia that is associated with prolongation of the QT interval. Although torsade de pointes is found in many clinical settings, it is mostly drug induced. ⋯ Terfenadine is a widely used antihistamine. The authors report a case of torsade de pointes in a patient with a possible congenital sporadic form of QT interval prolongation who was receiving a therapeutic dose of terfenadine.
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On the assumption that maximum R peak time prolongation in the left-sided leads I, V5, or V6 and its time relationship to the S peak time of the maximum S amplitude in leads V1, V2, or V3 (representing dorsally directed forces of ventricular depolarization) could indicate the extent of left ventricular volume overloading and possibly left ventricular systolic function, these variables and the preoperative findings of angiocardiography were compared between patients with chronic mitral incompetence who, late after corrective valve surgery, had either well-preserved radionuclide left ventricular ejection fraction (group 1, n = 36) or radionuclide left ventricular ejection fraction below 50% (group 2, n = 30). Before surgery, group 2 patients had a highly significant lower mean left ventricular ejection fraction, a highly significant greater mean end-systolic volume index, a significantly greater mean end-diastolic volume index, a significantly greater mean maximum R peak time in leads I, V5, or V6, and a significantly greater prolongation of the maximum R peak time above the S peak time in the right precordial leads, as compared with group 1. R peak times greater than 50 ms or the presence of R peak delay (maximum R peak time greater than the S peak time of the maximum right precordial S amplitude) yields less sensitive but highly reliable results in predicting radionuclide left ventricular ejection fraction below 50% with both specificity and positive predictive values of 100%. Thus, in chronic mitral regurgitation surgery should not be delayed if patients present these signs because they are specific markers of irreversibly impaired chamber function.