Effects of aging and cardiac denervation on heart rate variability during sleep.
(65/896)
BACKGROUND: Cardiac vagal predominance increases the RR interval and RR high-frequency (HF) variability during non-rapid eye movement (non-REM) sleep (stages I through IV) in young subjects. Aging suppresses deep sleep, but effects of age-related changes in sleep architecture on RR are unknown. Whether mechanical effects of changes in the breathing pattern on the sinus node during sleep affect RR variability is unclear. METHODS AND RESULTS: Polygraphic sleep recordings and RR and RR spectral profiles were determined in 8 young (22.5+/-3.3 years) and 8 older (55.0+/-7.3 years) healthy volunteers. HF oscillations in RR of 8 cardiac-denervated heart transplant recipients determined mechanical effects of respiration on the sinoatrial node during sleep. Transition from wakefulness to non-REM sleep increased the RR interval in young and older subjects and increased the HF variability of RR in the young (P:<0.05) but not in the older subjects. Older subjects disclosed a faster RR (P:<0.01) and a lower HF variability (P:<0.05) during non-REM sleep than the young subjects. Aging did not affect light and REM sleep but decreased deep sleep (stage IV) from 39+/-23 to 6+/-6 minutes (P:<0.001). Reduction in sleep stage IV with aging blunted the increase in RR and in RR HF variability during non-REM sleep (r>0.55, P:<0.05). Transition from wakefulness to non-REM sleep doubled the markedly reduced HF variability of RR in the heart transplant recipients (P:<0.05). CONCLUSIONS: Disappearance of deep sleep with aging impairs nocturnal increase in cardiac vagal activity. Mechanical effects of changes in breathing pattern during sleep favor increases in HF oscillations of the RR interval during non-REM sleep. (+info)
Cardiac memory in canine atrium : identification and implications.
(66/896)
BACKGROUND: Memory is a diverse biological phenomenon whose importance in the ventricle has been demonstrated. We hypothesized its occurrence in the atrium, contributing to the modulation of cardiac rhythm. METHODS AND RESULTS: We analyzed P and Ta waves in conscious chronically instrumented dogs with complete heart block. Animals were atrioventricularly sequentially paced at 5% greater than the sinus rate from the lateral right atrium (RA) during control, followed by 2 periods of 1-hour test pacing at 50% greater than the sinus rate, or by equivalent test pacing from the left atrial appendage (LAA) at 5% or 50% greater than the sinus rate. Recovery RA pacing periods of 20- and 30-minute duration, respectively, succeeded each test pacing period. RA test pacing at either rate did not affect the variables measured, but changing the pacing site from RA to LAA altered the P and Ta waves. Displacement of the spatial atrial gradient vector occurred during recovery from LAA pacing, was more marked at rapid pacing rates, and manifested accumulation and resolution consistent with cardiac memory. Concurrently, the right effective refractory period decreased. CONCLUSIONS: Memory is demonstrable in canine atrium, showing rapid onset, accumulation during successive pacing periods, and resolution on cessation of pacing. Given its association with a reduced effective refractory period, it may contribute to the substrate for atrial arrhythmias. (+info)
Gradient model versus mosaic model of the sinoatrial node.
(67/896)
BACKGROUND: A radical reinterpretation (mosaic model) of the makeup of the sinoatrial (SA) node has been proposed to explain the characteristic regional differences in electrical activity between the periphery and center of the SA node. According to the mosaic model, the differences result from a change in the mix of atrial cells and uniform SA node cells from periphery to center, whereas according to the alternative gradient model, there are no atrial cells within the functional SA node, and the differences result from a change in the intrinsic properties of SA node cells from periphery to center. METHODS AND RESULTS: A mosaic model of peripheral and central tissue has been constructed computationally by use of a coupled ordinary differential equation network (CODE) in a 2D lattice (20x20), with each node of the lattice designated randomly as an atrial cell or SA node cell (in correct proportions for periphery and center). The mosaic model fails to predict the characteristic differences in action potential rate and shape between the periphery and center, whereas the existing gradient model can do so. CONCLUSIONS: The mosaic model of the SA node is untenable, and the SA node is adequately described by the gradient model. (+info)
Molecular characterization of the ventricular conduction system in the developing mouse heart: topographical correlation in normal and congenitally malformed hearts.
(68/896)
OBJECTIVES: Within the adult heart, it is convention to distinguish the conduction system and working (atrial and ventricular) myocardium. The adult conduction system (CS) comprises the sinoatrial (SAN), and atrioventricular (AVN) nodes, the atrioventricular bundle (AVB), the bundle branches and the peripheral Purkinje fibers, each of which display distinct functional properties and distinct profile of gene expression. Characterization of the mouse cardiac conduction system during development is rudimentary at present, even though genetically-modified mice are an increasing source of information regarding cardiac function and embryonic heart development. METHODS: We have performed a detailed study of the pattern of expression of myosin heavy chain (MHC), myosin light chain (MLC), troponin I (TnI) isoforms, connexin 43 (Cx43), desmin and alpha-smooth muscle actin (alpha-SMA), in the ventricular conduction system of normal and congenitally malformed mouse hearts (iv background) from embryonic day 14.5 to 19.5. RESULTS: The AVN is characterized by co-expression of MHC and MLC isoforms and no detectable expression of Cx43, desmin or alpha-SMA. The AVB expresses betaMHC and MLC2v, but no alphaMHC, MLC2a, Cx43, desmin or alpha-SMA. The right and left bundle branches display enhanced expression of desmin and alpha-SMA but no Cx43. The normal expression profile is maintained in congenitally malformed hearts such as double-outlet right ventricle and common atrioventricular canal. Three-dimensional reconstruction of the conduction system shows normal arrangement of the bundle branches in congenitally malformed hearts, but abnormal location and/or extension of the AVN. CONCLUSIONS: Molecular characterization allows to follow the development of the CS in both, normal and malformed mouse hearts. Normal phenotypic expression of the CS is independent of heart situs but shows minor modifications in the presence of heart malformations. It is concluded that the AVN derives from the atrioventricular canal myocardium, the bundle of His from the ventricular myocardium, and the bundle branches from the ventricular trabeculations. Our results do not provide evidence to support an extra-cardiac origin of the ventricular CS. (+info)
Comparison of spontaneous vs. metronome-guided breathing on assessment of vagal modulation using RR variability.
(69/896)
R-R interval variability (RR variability) is increasingly being used as an index of autonomic activity. High-frequency (HF) power reflects vagal modulation of the sinus node. Since vagal modulation occurs at the respiratory frequency, some investigators have suggested that HF power cannot be interpreted unless the breathing rate is controlled. We hypothesized that HF power during spontaneous breathing would not differ significantly from HF power during metronome-guided breathing. We measured HF power during spontaneous breathing in 20 healthy subjects and 19 patients with heart disease. Each subject's spontaneous breathing rate was determined, and the calculation of HF power was repeated with a metronome set to his or her average spontaneous breathing rate. There was no significant difference between the logarithm of HF power measured during spontaneous and metronome-guided breathing [4.88 +/- 0.29 vs. 5.29 +/- 0.30 ln(ms(2)), P = 0.32] in the group as a whole and when patients and healthy subjects were examined separately. We did observe a small (9.9%) decrease in HF power with increasing metronome-guided breathing rates (from 9 to 20 breaths/min). These data indicate that HF power during spontaneous and metronome-guided breathing differs at most by very small amounts. This variability is several logarithmic units less than the wide discrepancies observed between healthy subjects and cardiac patients with a heterogeneous group of cardiovascular disorders. In addition, HF power is relatively constant across the range of typical breathing rates. These data indicate that there is no need to control breathing rate to interpret HF power when RR variability (and specifically HF power) is used to identify high-risk cardiac patients. (+info)
Morphological and membrane characteristics of spider and spindle cells isolated from rabbit sinus node.
(70/896)
This study reports the comparative quantitative, morphological, and electrophysiological properties of two pacemaker cell types, spider and spindle-shaped cells, isolated from the rabbit sinoatrial node. Isolated nodal cells were studied with perforated and ruptured patch whole cell recording techniques. The basic spontaneous cycle length of the spider cells was 381 +/- 12 ms, and the basic spontaneous cycle length of the spindle cells was 456 +/- 17 ms (n = 12, P < 0.05). The spider cells had a more positive maximum diastolic potential (-54 +/- 1 mV) compared with the spindle cells (-68 +/- 1mV, P < 0.05). The overshoot and action potential amplitudes were also smaller in the spider cells. The hyperpolarization-activated inward (I(f)) current density, measured from their tail currents, was 15 +/- 1.3 pA/pF for the spider cells and 9 +/- 0.7 pA/pF for the spindle cells (P < 0.01). I(f) current activation voltage was more positive in the spider cells than the spindle cells. Isoproterenol (1 microM) decreased the spontaneous cycle length of the spider cells by 28 +/- 3% and the spindle cells by 20 +/- 1.5% (P < 0.05). Acetylcholine (0.5 microM) hyperpolarized the membrane potential of the spider cells to -86 +/- 0.7 mV and the spindle cells to -76 +/- 0.8 mV (P < 0.05). In summary, there are at least two distinct pacemaker cell types in the sinus node with different electrophysiological characteristics. (+info)
Modulation by muscarinic receptor antagonists on negative chronotropic effects of tetrandrine.
(71/896)
AIM: To investigate the influence of selective antagonist for muscarinic (M) receptor subtype on tetrandrine (Tet) reducing heart rate, inhibiting sinoatrial node (SAN) function, and its ionic mechanism. METHODS: Effects of reducing heart rate of Tet were maintained in isolated right atrium and pithed rats. Modification on action potentials (AP) of SAN cells and L-type calcium current (ICa-L) by Tet were recorded by means of standard microelectrode and patch-clamp whole cell recording techniques. RESULTS: Tet inhibited spontaneous beating rate of isolated right atrium (EC50, 23.7 mumol.L-1) and reduced heart rates in pithed rats in a concentration-dependent manner (EC50, 18.6 mg.kg-1). Automaticity of SAN was inhibited by Tet. AP upstroke velocity (Vmax), spontaneous depolarization rates in phase 4 (SP4) were decreased and sinus cycle length (SCL) was prolonged when treated with Tet. Tet (30 mumol.L-1) caused a reduction in peak value of ICa-L from (1275 +/- 190) pA to (498 +/- 94) pA in isolated single cardiomyocyte. Atropine and AF-DX 116 (M2 subtype selective antagonist) could attenuate such effects of Tet in a competitive mode. CONCLUSION: Negative chronotropic effects of Tet are due to its inhibition of ICa-L. Modification on ICa-L is the major mechanism of M receptor modulating Tet effects. (+info)
Ventricular preexcitation in children and young adults: atrial myocarditis as a possible trigger of sudden death.
(72/896)
BACKGROUND: Sudden death (SD) in ventricular preexcitation (VP) syndrome is believed to be the result of atrial fibrillation with rapid ventricular response over the accessory pathway. Previous reports are anecdotal and often lack autopsy validation. METHODS AND RESULTS: Prevalence and clinicopathological features of VP were investigated in a series of 273 SDs in children and young adults (aged +info)