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Results for “HEART CONDUCTION SYSTEM”

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PubMed2001

Heart rate variability in patients with congenital long QT syndrome.

BACKGROUND: The congenital long QT syndrome (LQTS) affecting myocardial repolarization is caused by mutations in different cardiac potassium or sodium channel genes. Adrenergic triggers are known to initiate life-threatening torsade de pointes ventricular tachycardias in LQTS patients, and anti-adrenergic therapy has been shown to be effective in many cases. Despite this well-documented adrenergic component, the data about autonomic modulation of the heart rate in LQTS, as described by heart rate variability (HRV) analysis, are very limited. METHODS: Conventional time- and frequency-domain and newer nonlinear measures of HRV were compared in resting conditions among 27 LQTS patients with gene mutations at the LQT1 (n = 8), LQT2 (n = 10) or LQT3 (n = 9) loci and 34 LQTS noncarrier family members. RESULTS: None of the conventional time- or frequency-domain or newer nonlinear measures of HRV differed significantly between the LQTS carriers and LQTS noncarriers or between the LQT1, LQT2, and LQT3 carriers. CONCLUSIONS: These findings suggest that baseline cardiac autonomic modulation of the heart rate measured in resting conditions by traditional or newer nonlinear measures of HRV is not altered in LQTS patients. Furthermore, no differences are observed in HRV parameters between LQTS patients with potassium (KvLQT1, HERG), and sodium (SCN5A) ion channel gene mutations. HRV analysis in resting conditions does not improve phenotypic characterization of LQTS patients.

Adrenergic beta-Antagonists↗
PubMed1976

Direct chronotropic and dromotropic actions of contrast media: ineffectiveness of atropine in the prevention of bradyarrhythmias and conduction disturbances.

Methyl glucamine sodium diatrizoate (Renografin 76) was directly infused into the isolated arteries to the sino-atrial and atrioventricular nodes of anesthetized dogs, causing a dose-related inhibition of sino-atrial nodal automaticity and atrioventricular nodal conductivity; these effects were not attenuated by autonomic blockade or cervical vagotomy. The important negative chronotropic and dramatropic effects of contrast media used for coronary angiography are direct actions and cannot be effectively blocked by premedication with atropine.

Animals↗
PubMed1988

Integration of heart rate and sympathetic neural effects on AV conduction.

Sympathetic activation increases heart rate (HR) and reduces atrioventricular interval (AVI), whereas atrial pacing alone increases AVI. We sought to differentiate the direct effects of sympathetic activation on atrioventricular (AV) conduction time from the indirect changes associated with concurrent alterations in HR. We recorded electrocardiograms, blood pressure (BP), and intracardiac electrograms from chloralose-anesthetized autonomically decentralized dogs. Beat-by-beat HR and AVI data were collected continuously. Sympathetic stimulation (0.25-2.5 Hz; mean 0.81 Hz) resulted in a HR change of +60 beats/min after 60 s. This tachycardia was associated with a mean decrease in AVI of 22 ms. Computer-driven atrial pacing to reproduce the HR associated with control sympathetic stimulation caused a mean AVI increase of 10 ms. Propranolol (200 micrograms) was then administered via the sinoatrial node artery and sympathetic stimulation repeated. Although HR remained constant, AVI decreased by 14.8 ms. The AVIs associated with an identical HR achieved by two different mechanisms (sympathetic stimulation and atrial pacing) were significantly different. Although removal of the contribution of sympathetically induced HR changes on AV conduction might be expected to result in potentiation of neural effects at the AV node, none was evident. Thus sympathetic activity restricted to the AV node is less effective in influencing AV conduction than the response that occurs when HR changes occur concurrently. Therefore, the opposing actions of HR and sympathetic tone on AV conduction may not be predicted by a simple linear relationship.

Animals↗
PubMed1989

A dynamic analysis of cardiovascular regulation using sinusoidal acceleration in dogs.

Control of cardiovascular function during time-dependent pooling of blood in the upper and lower body was studied in intact dogs (n = 5) and in dogs in which hearts had been surgically denervated (n = 5). The animal was positioned horizontally on a platform mounted on the arm of a centrifuge; rotation of the platform at one of nine rates with a period ranging from 3.3 min to 4 s exposed the subject to a sinusoidally varying force (+/- 2 g) that periodically translocated blood from the chest to the lower quarters and back again. The resulting oscillatory changes in arterial blood pressure (BP), cardiac output, stroke volume, heart rate (HR), and peripheral resistance (PR) were analyzed using a fast Fourier transform. Normal dogs were superior to cardiac-denervated dogs in minimizing arterial BP fluctuations, especially in the midfrequency range (i.e., approximately 0.032 Hz); after pharmacological alpha-, beta-, and muscarinic-receptor blockade, the BP oscillations were similar in the two groups. The unblocked denervated dogs regulated BP poorly primarily because of their inability to 1) make appropriately timed changes in HR and 2) minimize inappropriate oscillations in SV. Both groups of dogs in the unblocked state showed large appropriately timed PR fluctuations at the lower frequencies, which minimized BP oscillations; these became less optimally timed as acceleration frequency increased, thereby potentiating the natural disposition for BP to oscillate at the acceleration frequency. Afferent information from cardiac receptors did not appear to be essential for controlling this aspect of vascular function.

Animals↗
PubMed1976

Central nervous system control of cardiac rhythm.

Stimulation of sites in the midbrain reticular formation and in the posterior hypothalamus of the cat resulted in a large to modest rise of arterial pressure and the induction of cardiac dysrhythmias. Most frequently, these arrhythmias developed upon cessation of brain stem stimulation but also occurred during the stimulus period in 5 of 23 cats studied. The arrhythmias disappeared upon cooling and reappeared upon rewarming the vagus nerves. The ventricular dysrhythmias also were abolished by methylscopolamine, by bilateral vagatomy, or by extirpation of the stellate ganglia. Simultaneous stimulation of both distal end of the cut right vagus nerve and the decentralized right stellate ganglion caused arrhythmias similar to those observed after diencephalic stimulation. These data are interpreted to indicate that the cardiac arrhythmias evoked by brain stem stimulation result from the interplay of both sympathetic and parasympathetic influences on the heart. The response patterns of a population of medullary neurons activated by carotid sinus nerve stimulation were modified by condition stimuli to posterior hypothalamic sites. From studies on unit activity of brain stem areas known to participate in cardiovascular adjustment, a schema is proposed of hypothalamic-medulla interaction as a central mechanism that may account for the development of ventricular arrhythmias.

Animals↗
PubMed1991

Cardiovascular neural regulation explored in the frequency domain.

A consistent link appears to exist between predominance of vagal or sympathetic activity and predominance of HF or LF oscillations, respectively: RR variability contains both of these rhythms, and their relative powers appear to subserve a reciprocal relation like that commonly found in sympathovagal balance. In this respect, it is our opinion that rhythms and neural components always interact, just like flexor and extensor tones or excitatory and inhibitory cardiovascular reflexes, and that it is misleading to separately consider vagal and sympathetic modulations of heart rate. In humans and experimental animals, functional states likely to be accompanied by an increased sympathetic activity are characterized by a shift of the LF-HF balance in favor of the LF component; the opposite occurs during presumed increases in vagal activity. In addition, LF oscillation evaluated from SAP variability appears to be a convenient marker of the sympathetic modulation of vasomotor activity. Although based on indirect markers, the exploration in the frequency domain of cardiovascular neural regulation might disclose a unitary vision hard to reach through the assemblage of more specific but fragmented pieces of information.

Animals↗
PubMed1996

Power spectral analysis of heart rate in hyperthyroidism.

The aim of the present study was to evaluate the impact of hyperthyroidism on the cardiovascular system by separately analyzing the sympathetic and parasympathetic influences on heart rate. Heart rate variability was evaluated by autoregressive power spectral analysis. This method allows a reliable quantification of the low frequency (LF) and high frequency (HF) components of the heart rate power spectral density; these are considered to be under mainly sympathetic and pure parasympathetic control, respectively. In 10 newly diagnosed untreated hyperthyroid patients with Graves' disease, we analyzed power spectral density of heart rate cyclic variations at rest, while lying, and while standing. In addition, heart rate variations during deep breathing, lying and standing, and Valsalva's maneuver were analyzed. The results were compared to those obtained from 10 age-, sex-, and body mass index-matched control subjects. In 8 hyperthyroid patients, the same evaluation was repeated after the induction of stable euthyroidism by methimazole. Heart rate power spectral analysis showed a sharp reduction of HF components in hyperthyroid subjects compared to controls [lying, 13.3 +/- 4.1 vs. 32.0 +/- 5.6 normalized units (NU; P < 0.01); standing, 6.0 +/- 2.7 vs. 15.0 +/- 4.0 NU (P < 0.01); mean +/- SEM]. On the other hand components were comparable in the 2 groups (lying, 64.0 +/- 6.9 vs. 62.0 +/- 6.5 NU; standing, 77.0 +/- 6.5 vs. 78.0 +/- 5.4 NU). Hence, the LF/HF ratio, which is considered an index of sympathovagal balance, was increased in hyperthyroid subjects while both lying (11.3 +/- 4.5 vs. 3.5 +/- 1.1; P < 0.05) and standing (54.0 +/- 12.6 vs. 9.8 +/- 2.6; P < 0.02). This parameter was positively correlated with both T3 (r = 0.61; P < 0.05) and free T4 (r = 0.63; P < 0.05) serum levels. Among traditional cardiovascular autonomic tests, the reflex response of heart rate during lying to standing was significantly lower in hyperthyroid patients than in controls (1.12 +/- 0.03 vs. 1.31 +/- 0.04; P < 0.002). No statistically significant difference in reflex responses between the two groups was found in deep breathing or Valsalva's maneuver. In the 8 patients reexamined after methimazole treatment, we observed complete normalization of altered cardiovascular parameters, with slight predominance of the vagal component compared with controls. These results suggest that thyroid hormone excess may determine reduced parasympathetic activity and, thus, a relative hypersympathetic tone.

Adolescent↗
PubMed1976

Both direct and neurally mediated components of the chronotropic actions of aminophylline.

Aminophylline was selectively perfused through either the sinus node or through the AV (atrioventricular) junction of 35 intact canine hearts in situ. The positive chronotropic action observed was equally powerful in accelerating either sinus rhythm (50 +/- 8 percent increment) or AV junctional rhythm (55 +/- 10 percent increment). This positive chronotropic effect has at least three distinct components: a major direct action on autonomic centers, a lesser effect due to local catecholamine release, and a part due to peripheral vagolytic action.

Acetylcholine↗
PubMed1988

Reappraisal of atrioventricular junctional pacemaker automaticity in the sick sinus syndrome. Clinical significance and the role of autonomic chronotropic influences.

Postpacing impulse recovery times of the junctional tissue (junctional automaticity) were determined by atrial or ventricular overdrive pacing in 27 patients with dysfunction of the sinus node. The maximum junctional recovery time (MJRT) could be measured in 22 patients and ranged from 1,630 to 9,730 ms (mean 3,860 +/- 2,077); the maximum corrected junctional recovery time (MJRTc) could be measured in 18 patients and ranged from 140 to 5,986 ms (mean 2,089 +/- 1,529). Autonomic influence on the JRTs was evaluated by intravenous administration of atropine (1.5 mg) alone or in combination with propranolol (5 to 6 mg). Of the seven patients in whom MJRTc and/or MJRT could be measured before and after drug intervention, the JRTs shortened in four and prolonged in three after combination of atropine and propranolol. Atropine alone shortened MJRT in all eight patients studied. Our data reveal that both vagal and catecholamine-dependent factors (especially vagal over-activity) are operative in the escape mechanism of the junctional tissue.

Adult↗
PubMed2002

Autonomic tone as a cardiovascular risk factor: the dangers of chronic fight or flight.

Chronic imbalance of the autonomic nervous system is a prevalent and potent risk factor for adverse cardiovascular events, including mortality. Although not widely recognized by clinicians, this risk factor is easily assessed by measures such as resting and peak exercise heart rate, heart rate recovery after exercise, and heart rate variability. Any factor that leads to inappropriate activation of the sympathetic nervous system can be expected to have an adverse effect on these measures and thus on patient outcomes, while any factor that augments vagal tone tends to improve outcomes. Insulin resistance, sympathomimetic medications, and negative psychosocial factors all have the potential to affect autonomic function adversely and thus cardiovascular prognosis. Congestive heart failure and hypertension also provide important lessons about the adverse effects of sympathetic predominance, as well as illustrate the benefits of beta-blockers and angiotensin-converting enzyme inhibitors, 2 classes of drugs that reduce adrenergic tone. Other interventions, such as exercise, improve cardiovascular outcomes partially by increasing vagal activity and attenuating sympathetic hyperactivity.

Adrenergic beta-Agonists↗