An appraisal of second degree and paroxysmal atrioventricular block.
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Various opinions have been offered regarding the possibility of extrapolation to man of findings in animals on cardiovascular effects of antidepressants. The present study examines this question by correlating ECG and heart rate effects of antidepressants given to rats to similar effects in clinical studies. For the QRS width and the QT length, correlation were found indicating that at least qualitative extrapolations can be made. For PR length and heart rate, the lack of correlations indicates that effects on variables dependent on more complex regulatory systems are more difficult to predict.
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Tracking spatial and temporal determinants of cardiac arrhythmogenesis at the cellular level presents challenges to the optical mapping techniques employed. In this paper, we describe a compact system combining two nontraditional low-cost solutions for excitation light sources and emission filters in fluorescence measurements of transmembrane potentials, Vm, or intracellular calcium, [Ca2+]i in cardiac cell networks. This is the first reported use of high-power blue and green light emitting diodes (LEDs), to excite cell monolayers stained with Vm - (di-8-ANEPPS) or [Ca2+]i - (Fluo-3) sensitive dyes. In addition, we use simple techniques for fabrication of suitable thin emission filters with uniform properties, no auto-fluorescence, high durability and good flexibility for imaging Vm or [Ca2+]i. The battery-operated LEDs and the fabricated emission filters, integrated with a fiber-optic system for contact fluorescence imaging, were used as tools to characterize conduction velocity restitution at the macro-scale. The versatility of the LEDs for illumination is further emphasized through 1) demonstration of their usage for epi-illumination recordings at the single-cell level, and 2) demonstration of their unique high-frequency light modulation ability. The LEDs showed excellent stability as excitation light sources for fluorescence measurements; acceptable signal-to-noise ratio and negligible cell photodamage and indicator dye photobleaching were observed.
BACKGROUND: Previous clinical reports have suggested that cocaine intoxication may produce severe ventricular arrhythmias due to a direct effect on the heart. However, the effects of high plasma levels of cocaine on the electrophysiology of the heart have not been well characterized and remain poorly understood. METHODS AND RESULTS: The purpose of this study was to characterize the electrophysiological effects of high doses of cocaine on the in situ dog heart. In dogs anesthetized with morphine and alpha-chloralose, cocaine (2-11 micrograms/mL) increased both atrial and ventricular refractory periods and produced rate-dependent increases in atrial, atrioventricular, His-Purkinje, and ventricular conduction intervals. The time constant for the onset of cocaine's conduction slowing effect following a reduction in pacing cycle length from 400 to 260 msec was approximately two beats, and the time constant for diastolic recovery from conduction slowing was approximately 200 msec, which are similar to values reported for several class Ib antiarrhythmic drugs. Cocaine produced a rate-dependent increase in QT interval that was greatest at high heart rates yet produced no change in the ST (QT-QRS) interval. This suggests that high plasma levels of cocaine delay repolarization primarily via slowing of conduction. Cocaine's effects on both atrioventricular and intraventricular conduction were significantly larger in autonomically blocked than in autonomically intact animals. CONCLUSIONS: We conclude that high plasma levels of cocaine, similar to those reported in autopsy reports following fatal cocaine overdose in humans, produce significant rate-dependent conduction slowing effects on atrial, atrioventricular, and ventricular conduction in the in situ heart. These rate-dependent effects are intensified following autonomic blockade.
The influence of the intracardiac reflectory system on the atrioventricular propagation in the experiments on the isolated frog's heart has been investigated. The ability of the intracardiac reflectory cholinergic activation to accelerate or reduce the atrioventricular propagation was confirmed. Both effects remain on the background of the artificially stabilized heart rhythm. The dromotropic effect direction was shown not to be connected with the electrocardiogram (ECG) phase at which the stimulus has been given; the positive or negative dromotropic effect can appear giving the stimulus at the same phase of the ECG. But there is a strong correlation between the moment of the stimulation and the dromotropic effect intensity. The most high degree of the acceleration and inhibition appears when the stimulus is given near the P component of the ECG.
1 The compound Org 6001 (3alpha-amino-2beta-hydroxy-5alpha-androstan-17-one hydrochloride) was found in recent experiments to exhibit anti-arrhythmic activity. Evidence is presented in this paper concerning its mode of action. 2 Org 6001 was 1.8 times more potent than procaine as a local anaesthetic on desheathed frog nerve. 3 Org 6001 had no effect on the resting potential of isolated cardiac muscle of rabbit, but greatly reduced the maximum rate of depolarization tion (MRD). The action potential duration TAPD) WAS MARGINALLY PROLONGED IN ATRIAL AND VENTRICULAR MUSCLE. 4 Org 6001 preferentially shortened APD in that part of the Purkinje system in which APD is normally longer than elsewhere, so that APD
BACKGROUND: Genetically altered mice will provide important insights into a wide variety of processes in cardiovascular physiology underlying myocardial infarction (MI). Comprehensive and accurate analyses of cardiac function in murine models require implementation of the most appropriate techniques and experimental protocols. OBJECTIVE: In this study we present in vivo, whole-animal techniques and experimental protocols for detailed electrophysiological characterization in a mouse model of myocardial ischemia and infarction. METHODS: FVB mice underwent open-chest surgery for ligation of the left anterior descending coronary artery or sham-operation. By means of echocardiographic imaging, electrocardiography, intracardiac electrophysiology study, and conscious telemetric ECG recording for heart rate variability (HRV) analysis, we evaluated ischemic and post-infarct cardiovascular morphology and function in mice. RESULTS: Coronary artery ligation resulted in antero-apical infarction of the left ventricular wall. MI mice showed decreased cardiac function by echocardiography, infarct-typical pattern on ECG, and increased arrhythmia vulnerability during electrophysiological study. Electrophysiological properties were determined comprehensively, but were not altered significantly as a consequence of MI. Autonomic nervous system function, measured by indices of HRV, did not appear altered in mice during ischemia or infarction. CONCLUSIONS: Cardiac conduction, refractoriness, and heart rate variability appear to remain preserved in a murine model of myocardial ischemia and infarction. Myocardial infarction may increase vulnerability to inducible ventricular tachycardia and atrial fibrillation, similarly to EPS findings in humans. These data may be of value as a reference for comparison with mutant murine models necessitating ischemia or scar to elicit an identifiable phenotype. The limitations of directly extrapolating murine cardiac electrophysiology data to conditions in humans need to be considered.
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AIM: To evaluate whether field potential recordings from murine ventricular slice preparations serve as a model to investigate impulse propagation. METHOD: Late-stage embryonic and neonatal murine hearts were sliced by a vibratome. Slices were placed on planar microelectrode arrays (MEAs). Field potentials of spontaneously beating and electrically stimulated contractions were recorded. The maximal negative deflection of the field potentials (dV / dt) was calculated to assess the local activation time, to create activation sequence maps, and to estimate conduction velocity. RESULTS: Mapping of impulse propagation of late-stage embryonic and neonatal murine ventricular slices and estimation of conduction velocities is feasible using the MEA technique showing an impulse propagation reflecting anatomical structures and conduction velocities similar to those obtained with other techniques. CONCLUSION: The combination of viable ventricular slice preparations with the MEA technique offers a versatile and powerful technique to study cardiac impulse propagation.
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This study evaluated whether small shifts in cardiac autonomic balance with standing, as measured by heart rate variability (HRV), were prospectively associated with incident coronary heart disease (CHD) and mortality. Both Black and White men and women aged 45-64 years from the Atherosclerosis Risk in Communities Study (n = 9,267) were followed from 1987 to 1997 for myocardial infarction (n = 296), fatal CHD (n = 63), and non-CHD mortality (n = 533). HRV indices and mean R-R interval length (inverse of heart rate) were measured in the supine and standing positions for 2 minutes each; HRV shift was calculated as the difference between positions. After adjustment for demographic characteristics and medication use, HRV in each position was significantly inversely related to events in Cox proportional hazards models. With the exception of R-R interval length shift and myocardial infarction (hazard ratio = 1.42, 95% confidence interval: 1.02, 1.98 for the smallest vs. the largest quartile), there was no association between HRV shift and the other events. Despite clinical research suggesting that HRV shift with standing is a more sensitive measure of autonomic balance than is HRV in one position, simple measures such as heart rate change and supine and standing HRV were better predictors of events.