No abstract

Unmedicated young CRF patients treated with hemodynamically stable maintenance HD showed preserved capacity of autonomic response (with gradual sympathetic increases) induced by cardiovascular challenges such as orthostatism and HD.

Life-threatening arrhythmias such as ventricular tachycardia and fibrillation often occur during acute myocardial ischemia. During the first few minutes following coronary occlusion, there is a gradual rise in the extracellular concentration of potassium ions ([K(+)](0)) within ischemic tissue. This elevation of [K(+)](0) is one of the main causes of the electrophysiological changes produced by ischemia, and has been implicated in inducing arrhythmias. We investigate an ionic model of a 3 cmx3 cm sheet of normal ventricular myocardium containing an ischemic zone, simulated by elevating [K(+)](0) within a centrally-placed 1 cmx1 cm area of the sheet. As [K(+)](0) is gradually raised within the ischemic zone from the normal value of 5.4 mM, conduction first slows within the ischemic zone and then, at higher [K(+)](0), an arc of block develops within that area. The area distal to the arc of block is activated in a delayed fashion by a retrogradely moving wavefront originating from the distal edge of the ischemic zone. With a further increase in [K(+)](0), the point eventually comes where a very small increase in [K(+)](0) (0.01 mM) results in the abrupt transition from a global period-1 rhythm to a global period-2 rhythm in the sheet. In the peripheral part of the ischemic zone and in the normal area surrounding it, there is an alternation of action potential duration, producing a 2:2 response. Within the core of the ischemic zone, there is an alternation between an action potential and a maintained small-amplitude response ( approximately 30 mV in height). With a further increase of [K(+)](0), the maintained small-amplitude response turns into a decrementing subthreshold response, so that there is 2:1 block in the central part of the ischemic zone. A still further increase of [K(+)](0) leads to a transition in the sheet from a global period-2 to a period-4 rhythm, and then to period-6 and period-8 rhythms, and finally to a complete block of propagation within the ischemic core. When the size of the sheet is increased to 4 cmx4 cm (with a 2 cmx2 cm ischemic area), one observes essentially the same sequence of rhythms, except that the period-6 rhythm is not seen. Very similar sequences of rhythms are seen as [K(+)](0) is increased in the central region (1 or 2 cm long) of a thin strand of tissue (3 or 4 cm long) in which propagation is essentially one-dimensional and in which retrograde propagation does not occur. While reentrant rhythms resembling tachycardia and fibrillation were not encountered in the above simulations, well-known precursors to such rhythms (e.g., delayed activation, arcs of block, two-component upstrokes, retrograde activation, nascent spiral tips, alternans) were seen. We outline how additional modifications to the ischemic model might result in the emergence of reentrant rhythms following alternans. (c) 2000 American Institute of Physics.

Levels of intracellular Ca2+ were monitored using fluorescence from Ca2+-sensitive dyes in chick embryonic heart cells cultured in an annular geometry. There was spontaneous starting and stopping of reentrant waves of activity. The results are modeled using modified FitzHugh-Nagumo equations representing pacemakers embedded in a conducting medium. These results provide a potential mechanism for spontaneous abnormal cardiac rhythms in which there are rapid heart beats (tachycardias) that repetitively start and stop.

The saline oscillator consists of an inner vessel containing salt water partially immersed in an outer vessel of fresh water, with a small orifice in the center of the bottom of the inner vessel. There is a cyclic alternation between salt water flowing downwards out of the inner vessel into the outer vessel through the orifice and fresh water flowing upwards into the inner vessel from the outer vessel through that same orifice. We develop a very stable (i.e., stationary) version of this saline oscillator. We first investigate the response of the oscillator to periodic forcing with a train of stimuli (period=Tp) of large amplitude. Each stimulus is the quick injection of a fixed volume of fresh water into the outer vessel followed immediately by withdrawal of that very same volume. For Tp sufficiently close to the intrinsic period of the oscillator (T0) , there is 1:1 synchronization or phase locking between the stimulus train and the oscillator. As Tp is decreased below T0 , one finds the succession of phase-locking rhythms: 1:1, 2:2, 2:1, 2:2, and 1:1. As Tp is increased beyond T0 , one encounters successively 1:1, 1:2, 2:4, 2:3, 2:4, and 1:2 phase-locking rhythms. We next investigate the phase-resetting response, in which injection of a single stimulus transiently changes the period of the oscillation. By systematically changing the phase of the cycle at which the stimulus is delivered (the old phase), we construct the new-phase--old-phase curve (the phase transition curve), from which we then develop a one-dimensional finite-difference equation ("map") that predicts the response to periodic stimulation. These predicted phase-locking rhythms are close to the experimental findings. In addition, iteration of the map predicts the existence of bistability between two different 1:1 rhythms, which was then searched for and found experimentally. Bistability between 1:1 and 2:2 rhythms is also encountered. Finally, with one exception, numerical modeling with a phenomenologically derived Rayleigh oscillator reproduces all of the experimental behavior.

The aim of this work was to evaluate the short-term fractal index (α ) of heart rate variability (HRV) in chronic renal failure (CRF) patients by identifying the effects of orthostatism and hemodialysis (HD), and by evaluating the correlation between α and the mean RR interval from sinus beats (meanNN). HRV time series were derived from ECG data of 19 CRF patients and 20 age-matched healthy subjects obtained at supine and orthostatic positions (lasting 5 min each). Data from CRF patients were collected before and after HD. α was calculated from each time series and compared by analysis of variance. Pearson's correlations between meanNN and α were calculated using the data from both positions by considering three groups: healthy subjects, CRF before HD and CRF after HD. At supine position, α of CRF patients after HD (1.17 ± 0.30) was larger (P < 0.05) than in healthy subjects (0.89 ± 0.28) but not before HD (1.10 ± 0.34). α increased (P < 0.05) in response to orthostatism in healthy subjects (1.29 ± 0.26) and CRF patients after HD (1.34 ± 0.31), but not before HD (1.25 ± 0.37). Whereas α was correlated (P < 0.05) with the meanNN of healthy subjects (r = -0.562) and CRF patients after HD (r = -0.388), no significance in CRF patients before HD was identified (r = 0.003). Multiple regression analysis confirmed that α was mainly predicted by the orthostatic position (in all groups) and meanNN (healthy subjects and patients after HD), showing no association with the renal disease condition in itself. In conclusion, as in healthy subjects, α of CRF patients correlates with meanNN after HD (indicating a more irregular-like HRV behavior at slower heart rates). This suggests that CRF patients with stable blood pressure preserve a regulatory adaptability despite a shifted setting point of the heart period (i.e., higher heart rate) in comparison with healthy subjects.

No abstract

Theory predicts that a stimulus delivered to an excitation wave circulating on a ring of excitable media will either have no effect, or it will reset or annihilate the excitation depending on the phase and magnitude of the stimulus. We summarize the basis for these theoretical predictions and demonstrate these phenomena in an experimental system consisting of a tissue culture of embryonic chick heart cells cultured in the shape of a ring.