Effect of Ibutilide on the Canine Cardiac Conduction System

The objective of the study was to evaluate the effect of ibutilide on canine cardiac sinoatrial and atrioventricular nodes (AVNs). For this purpose, 18 mongrel dogs were injected intravenously with ibutilide and the changes in heart rate, sinus node recovery time, and AVN were measured. Our data show that ibutilide administration caused significant suppression of the sinus atrial node, the peak response time was 20?C30?min, and the heart rate was restored to pre-drug administration level. After receiving ibutilide, 1 animal had a 5?s sinus pause, and after 5?min of ibutilide administration, 1 dog showed 2:1 atrioventricular conduction. Therefore, it was concluded that ibutilide had a suppressive effect on the sinoatrial node and AVN.     

Parasympathetic effects on cardiac electrophysiology during exercise and recovery

Depressed parasympathetic tone is associated with an increased risk of sudden cardiac death. Exercise and the postexercise recovery period, which are associated with parasympathetic withdrawal, are high risk periods for sudden death. However, parasympathetic effects on cardiac electrophysiology during exercise and recovery have not been described. Electrophysiology studies were performed using noninvasive programmed stimulation (NIPS) in nine subjects (age 59 +/- 18 yr) with implanted dual-chamber devices and normal left ventricular function during multiple bicycle exercise sessions. NIPS was performed at rest, during exercise, and in the early recovery period both before and after parasympathetic blockade with atropine. Parasympathetic effect was defined as the value of the parameter of interest in the absence of atropine minus the value of the parameter in the presence of atropine. During exercise, sinus cycle length, atrioventricular (AV) block cycle length, AV interval, and ventricular effective refractory period shortened; in recovery, the values were intermediate between the rest and exercise values (P < 0.0001 by ANOVA). Parasympathetic effects on sinus cycle length, AV block cycle length, AV interval, and ventricular effective refractory period were 247 +/- 140, 58 +/- 20, 76 +/- 20, and 8.6 +/- 7.5 ms at rest, 106 +/- 20, 37 +/- 14, 24 +/- 13, and 2.6 +/- 7.8 ms during exercise, and 209 +/- 114, 50 +/- 23, 35 +/- 21, and 9.5 +/- 11.8 ms during recovery, respectively. There was poor correlation among the parasympathetic effects noted at the sinus node, AV node, and ventricle. Further work evaluating parasympathetic effects on cardiac electrophysiology during exercise and recovery in patients with heart disease is required to elucidate its role in modulating the risk of sudden cardiac death noted at these times.     

Cardiac autonomic function in Blacks with congestive heart failure: vagomimetic action, alteration in sympathovagal balance, and the effect of ACE inhibition on central and peripheral vagal tone.

Cardiac autonomic dysfunction is common in heart disease with or without congestive heart failure, and can cause sudden cardiac death. However, cardiac autonomic abnormalities in non-ischemic (hypertensive) heart failure, which is prevalent in Black Africans is poorly documented. We conducted a cross-sectional study of 32 patients with congestive heart failure, mostly secondary to hypertension (aged 52 +/- 15 years, with ejection fraction of 0.38 +/- 11) and 30 age- and sex-matched healthy volunteers (aged 51 +/- 11 years, 14 males/16 females). Cardiac autonomic function was assessed by the Valsalva's maneuver, respiratory sinus arrhythmia (for cardiac vagal tone) and the pressor and chronotropic changes following forearm isometric handgrip exercise and the assumption of upright posture (tests of sympathetic function). The exercise tolerance of the cardiac patients was assessed by the distance covered during 6 min of walking. The Valsalva ratio was significantly lower in chronic heart failure, 1.10 +/- 0.08 compared to the healthy controls 1.47 +/- 0.20 (p<0.001). Specifically, the phase IV bradycardia in heart failure, was significantly attenuated to 650 +/- 121 msec compared to the value of 935 +/- 101 msec in healthy controls (p<0.001). The phase 11 Valsalva tachycardia did not differ between the patients and controls. The respiratory sinus arrhythmia was also significantly reduced in chronic heart failure (p<0.05) compared to controls. Treatment of the heart failure patients with enalapril-digoxin and diuretics by 4 weeks, resulted in a reversal of the autonomic abnormalities. The phase IV bradycardia increased significantly to 798 +/- 164 msec (p<0.01) and the Valsalva ratio to 1.35 +/- 0.25 (p<0.01) and the respiratory sinus arrhythmia increased toward normal. There was close positive correlation between the Valsalva's ratio and the 6 min self paced distance covered (r = 0.44, p = 0.03 ANOVA), and a weak inverse correlation to cardiac size and cardiothoracic ratio (r = -0.31, p = 0.09). This study demonstrates cardiac autonomic dysfunction (especially reduced vagal tone) in Black Nigerians with mainly non-ischemic congestive heart failure. The parasympathetic dysfunction significantly correlates with severity of heart failure. Current treatment reverses autonomic dysfunction to values seen in healthy age matched controls, mainly through augmentation of cardiac parasympathetic activity.     

Influence of menstrual cycle on baroreflex control of heart rate: comparison with male volunteers

This study was designed to determine baroreflex control of heart rate (HR) to hypotensive and hypertensive stimuli during the early follicular (EF), preovulation (PreOV), and midluteal (ML) phases of the menstrual cycle and to test the hypothesis that cardiovagal reflex responses to hypertensive stimuli would be altered depending on the plasma estradiol levels in healthy women. In addition, these results were compared with those of male volunteers. Fifteen healthy women with regular menstrual cycles and thirteen male volunteers were recruited. Cardiovagal baroreflex sensitivity was defined as the slope of the linear portion relating R-R interval and systolic blood pressure triggered by bolus injections of nitroprusside and phenylephrine, from the overshoot phase of the Valsalva maneuver, and during spontaneous fluctuations. Three measurements were averaged in each test as a representative at each phase, and the order of phases was counterbalanced. Baroreflex sensitivities by the phenylephrine pressor test and Valsalva maneuver during the PreOV phase were significantly greater than those during the EF and ML phases but were similar to those of men. Depressor test sensitivities by nitroprusside and down-sequence spontaneous cardiac baroreflex sensitivity during the EF phase were significantly greater than those of the ML phase and of men. Significant correlations were observed between plasma estradiol concentrations and baroreflex sensitivities assessed by phenylephrine and the Valsalva maneuver. Our results indicate that baroreflex control of HR is altered during the regular menstrual cycle, and estradiol appears to exert cardiovagal modulation in healthy women.     

Teaching cardiac autonomic function dynamics employing the Valsalva (Valsalva-Weber) maneuver

In this report, a brief history of the Valsalva (Valsalva-Weber) maneuver is outlined, followed by an explanation on the use of this approach for the evaluation of cardiac autonomic function based on underlying heart rate changes. The most important methodological and interpretative aspects of the Valsalva-Weber maneuver are critically updated, and some guidelines are established for simple application of the maneuver in a teaching or research laboratory setting. These include the hemodynamic and cardiac autonomic mechanisms involved, technical aspects such as the intensity and duration of the expiratory straining, frequency of maneuver sessions, training and posture of the individuals tested, different time- and grade change-dependent indexes of heart interval variation, and clinical application of the maneuver.     

Middle cerebral artery blood velocity during a valsalva maneuver in the standing position.

Occasionally, lifting of a heavy weight leads to dizziness and even to fainting, suggesting that, especially in the standing position, expiratory straining compromises cerebral perfusion. In 10 subjects, the middle cerebral artery mean blood velocity (V(mean)) was evaluated during a Valsalva maneuver (mouth pressure 40 mmHg for 15 s) both in the supine and in the standing position. During standing, cardiac output decreased by 16 +/- 4 (SE) % (P < 0.05), and at the level of the brain mean arterial pressure (MAP) decreased from 89 +/- 2 to 78 +/- 3 mmHg (P < 0.05), as did V(mean) from 73 +/- 4 to 62 +/- 5 cm/s (P < 0.05). In both postures, the Valsalva maneuver increased central venous pressure by approximately 40 mmHg with a nadir in MAP and cardiac output that was most pronounced during standing (MAP: 65 +/- 6 vs. 87 +/- 3 mmHg; cardiac output: 37 +/- 3 vs. 57 +/- 4% of the resting value; P < 0.05). Also, V(mean) was lowest during the standing Valsalva maneuver (39 +/- 5 vs. 47 +/- 4 cm/s; P < 0.05). In healthy individuals, orthostasis induces an approximately 15% reduction in middle cerebral artery V(mean) that is exaggerated by a Valsalva maneuver performed with 40-mmHg mouth pressure to approximately 50% of supine rest.     

Cardiac electrophysiologic effects of adaprolol maleate, a new beta-blocker, in closed chest dogs.

Adaprolol maleate (adaprolol) is a new beta-adrenergic receptor blocker. The cardiac electrophysiologic characteristics and the duration of action of adaprolol were studied in intact anesthetized dogs. The electrophysiologic parameters were evaluated before drug administration and 10 min after the administration of maintenance infusion of adaprolol (N = 5). The duration of action was measured during constant infusion of isoproterenol, giving the adaprolol as a single i.v. bolus in different concentrations (N = 5). Results of this study showed that adaprolol has marked electrophysiologic effects. Its major action was on sinus node; it prolonged the basic sinus cycle length and had significant effect on intrinsic automaticity as reflected by the prolonged corrected sinus node recovery time and sinuatrial conduction time. There was, also, direct effect on atrial function and AV nodal function. Adaprolol prolonged the effective refractory period of the His-Purkinje system and the ventricle. The onset of action was very rapid (within seconds) and the duration of action was relatively prolonged (3 hrs). The potency of adaprolol's electrophysiologic effects are higher compared to other widely used beta-blockers. Adaprolol appears to be a potent beta-blocker with particularly strong antiarrhythmic effect and it would be very useful in the treatment of both supraventricular and ventricular tachyarrhythmias and ectopic beats.     

Pulse pressure response to the strain of the Valsalva maneuver in humans with preserved systolic function

Arterial pulsepressure response during the strain phase of the Valsalva maneuver hasbeen proposed as a clinical tool for the diagnosis of left heartfailure, whereas responses of subjects with preserved systolic functionhave been poorly documented. We studied the relationship between theaortic pulse amplitude ratio (i.e., minimum/maximum pulse pressure)during the strain phase of the Valsalva maneuver and cardiachemodynamics at baseline in 20 adults (42 ± 14 yr) undergoingroutine right and left heart catheterization. They were normal subjects(n = 5) and patients withvarious forms of cardiac diseases(n = 15), and all had a leftventricular ejection fraction 40%. High-fidelity pressures wererecorded in the right atrium and the left ventricle at baseline and atthe aortic root throughout the Valsalva maneuver. Aortic pulseamplitude ratio 1) did not correlatewith baseline left ventricular end-diastolic pressure, cardiac index(thermodilution), or left ventricular ejection fraction(cineangiography) and 2) waspositively related to total arterial compliance (area method) (r = 0.59) and to basal mean rightatrial pressure (r = 0.57) (eachP < 0.01). Aortic pulse pressureresponses to the strain were not related to heart rate responses duringthe maneuver. In subjects with preserved systolic function, the aorticpulse amplitude ratio during the strain phase of the Valsalva maneuver relates to baseline total arterial compliance and right heart fillingpressures but not to left ventricular function.

     

Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats

Paraplegia may increase susceptibility to ventricular arrhythmias by altering the autonomic control of the heart. Altered cardiac autonomic control has been documented to change the expression of genes that encode cardiac Ca2+ regulatory proteins. Therefore, we tested the hypothesis that paraplegia alters cardiac electrophysiology with concomitant changes in Ca2+ regulatory proteins in a manner that increases the susceptibility to ventricular arrhythmias. To test this hypothesis, intact (n = 10) and paraplegic (n = 6) male Wistar rats were chronically instrumented to measure atrioventricular (AV) interval, sinus cycle length, sinus node recovery time (SNRT), SNRT corrected for spontaneous sinus cycle (cSNRT), Wenckebach cycle length (WCL), and the electrical stimulation threshold to induce ventricular arrhythmias. In addition, relative protein abundance and mRNA expression for sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA), phospholamban, and the Na/Ca exchanger were determined in intact (n = 8) and paraplegic (n = 8) rats. Paraplegia significantly (P < 0.05) reduced AV interval (-25%), sinus cycle length (-24%), SNRT (-28%), cSNRT (-53%), WCL (-19%), and the electrical stimulation threshold to induce ventricular arrhythmia (-48%). Paraplegia significantly increased the relative protein abundances of SERCA (45%) and the Na/Ca exchanger (40%) and decreased phospholamban levels (-28%). In contrast, only the relative mRNA expression of the Na/Ca exchanger was increased (25%) in paraplegic rats. These data demonstrate that paraplegia enhances cardiac electrophysiological properties and alters Ca2+ regulatory proteins in a manner that increases susceptibility to ventricular arrhythmias.     

Finger photoplethysmography during the Valsalva maneuver reflects left ventricular filling pressure

It is often challenging to assess cardiac filling pressure clinically. An improved system for detecting or ruling out elevated cardiac filling pressure may help reduce hospitalizations for heart failure. The blood pressure response to the Valsalva maneuver reflects left heart filling pressure, but its underuse clinically may be due in part to lack of continuous blood pressure recording along with lack of standardization of expiratory effort. In this study, we tested whether Valsalva-induced changes in the pulse amplitude of finger photoplethysmography (PPG), a technology already widely available in medical settings, correlate with invasively measured left ventricular end-diastolic pressure (LVEDP). We tested 33 subjects before clinically scheduled cardiac catheterizations. A finger photoplethysmography waveform was recorded during a Valsalva effort of 20 mmHg expiratory pressure sustained for 10 s, an effort most patients can achieve. Pulse amplitude ratio (PAR) was calculated as the PPG waveform amplitude just before release of expiratory effort divided by the waveform amplitude at baseline. PAR was well correlated with LVEDP (r = 0.68; P < 0.0001). For identifying LVEDP > 15 mmHG, PAR > 0.4 was 85% sensitive [95% confidence interval (95CI): 54-97%] and 80% specific (95CI: 56-93%). In conclusion, finger PPG, a technology already ubiquitous in medical centers, may be useful for assessing clinically meaningful categories of left heart filling pressure, using simple analysis of the waveform after a Valsalva maneuver effort that most patients can achieve.     

The human heart rate response profiles to five vagal maneuvers

Healthy teens and adults performed four vagotonic maneuvers. A large series of strabismus surgery patients had deliberately quantified tension on extraocular rectus muscles during general anesthesia. The mean bradycardia was greatest for diving response (apneic facial exposure to cold) and Valsalva maneuver and least for pressure on the globe and carotid sinus massage. Bradycardia occurred for every subject for the non-surgical maneuvers, however, extraocular muscle tension frequently caused no change in heart rate or even tachycardia. The inter-subject variance in percent heart rate change was greatest for surgical oculocardiac reflex. Of the rectus muscles, the inferior caused the most bradycardia while the lateral caused the least. The percent oculocardiac reflex was not age dependent. Occasional patients demonstrated profound bradycardia with strabismus surgery. Of these maneuvers, diving response has theoretical advantage in treating paroxysmal atrial tachycardia. The human cardiac vagal efferent was stimulated by several carefully controlled maneuvers resulting in wide inter-maneuver differences in bradycardia magnitude. The greatest intra-maneuver variability occurred with surgical oculocardiac reflex.     

Reciprocal splanchnic-thoracic blood volume changes during the Valsalva maneuver

The Valsalva maneuver is frequently used to test autonomic function. Previous work demonstrated that the blood pressure decrease during the Valsalva maneuver relates to thoracic hypovolemia, which may preclude pressure recovery during phase II, even with normal resting peripheral vasoconstriction. We hypothesized that increased regional blood volume, specifically splanchnic hypervolemia, accounts for the degree of thoracic hypovolemia during the Valsalva maneuver. We studied 17 healthy volunteers aged 15-22 yr. All had normal blood volumes by dye dilution. Subjects also had normal vascular resistance while supine as well as normal vasoconstrictor responses during 35 degrees upright tilt. We assessed changes in estimated splanchnic, pelvic-thigh, and lower leg blood volume, along with thoracic blood volume shifts, by impedance plethysmography before and during the Valsalva maneuver performed in the supine position. Early increases in splanchnic blood volume dominated the regional vascular changes during the Valsalva maneuver. The increase in splanchnic blood volume correlated well (r2 = 0.65, P < 0.00001) with the decrease in thoracic blood volume, there was less correlation of the increase in pelvic blood volume (r2 = 0.21, P < 0.03), and there was no correlation of the increase in leg blood volume (r2 = 0.001, P = 0.9). There was no relation of thoracic hypovolemia with blood volume or peripheral resistance in supine or upright positions. Thoracic hypovolemia during the Valsalva maneuver is closely related to splanchnic hyperemia and weakly related to regional changes in blood volume elsewhere. Changes in baseline splanchnic vascular properties may account for variability in thoracic blood volume changes during the Valsalva maneuver.     

降钙素基因相关肽在豚鼠冠脉血流量和心脏传导系统作用的比较

本文目的在于深入研究降钙素基因相关肽（ＣＧＲＰ）对豚鼠冠状血流量以及心脏传导系统各部分的作用。采用Ｌａｎｇｅｎｄｏｒｆｆ法灌流心脏,同步记录心脏表面电图和希氏束电活动。观察应用ＣＧＲＰ前后的冠脉流量、自主心率、在相同心房周期下的房室结（ＡＨ）及希浦系传导时间（ＨＶ）、心脏出现３：２文氏传导及２：１房室传导阻滞所需的最长起搏周期（ＰＣＬ３：２,ＰＣＬ２：１）。ＣＧＲＰ（３－３０ｎｍｏｌ／Ｌ）可显著增     

Rupture of right coronary sinus of Valsalva aneurysm into right ventricle

A sinus of Valsalva aneurysm is a rare cardiac anomaly that may be congenital or acquired; a coexisting cardiac lesion might be present. If the aneurysm ruptures, it causes acute symptoms of dyspnoea. Echocardiography and cardiac magnetic resonance imaging are useful for diagnosis. The treatment of choice is surgery. We present a case of a patient with acute onset of symptoms due to a ruptured sinus of Valsalva aneurysm. (Neth Heart J 2010;18:209-11)     

Functional characterization of a trafficking-defective HCN4 mutation, D553N, associated with cardiac arrhythmia

Hyperpolarization-activated cyclic nucleotide-gated channel 4 gene HCN4 is a pacemaker channel that plays a key role in automaticity of sinus node in the heart, and an HCN4 mutation was reported in a patient with sinus node dysfunction. Expression of HCN4 in the heart is, however, not confined to the sinus node cells but is found in other tissues, including cells of the conduction system. On the other hand, mutations in another cardiac ion channel gene, SCN5A, also cause sinus node dysfunction as well as other cardiac arrhythmias, including long QT syndrome, Brugada syndrome, idiopathic ventricular fibrillation, and progressive cardiac conduction disturbance. These observations imply that HCN4 abnormalities may be involved in the pathogenesis of various arrhythmias, similar to the SCN5A mutations. In this study, we analyzed patients suffering from sinus node dysfunction, progressive cardiac conduction disease, and idiopathic ventricular fibrillation for mutations in HCN4. A missense mutation, D553N, was found in a patient with sinus node dysfunction who showed recurrent syncope, QT prolongation in electrocardiogram, and polymorphic ventricular tachycardia, torsade de pointes. In vitro functional study of the D553N mutation showed a reduced membranous expression associated with decreased If currents because of a trafficking defect of the HCN4 channel in a dominant-negative manner. These data suggest that the loss of function of HCN4 is associated with sinus nodal dysfunction and that a consequence of pacemaker channel abnormality might underlie clinical features of QT prolongation and polymorphic ventricular tachycardia developed under certain conditions.     

Transposition of the pacemaker in the right atrium during stimulation of the vagus nerve in the dog

The heart rate and intraatrial latencies between epicardial electrograms from three sites of the right atrium have been studied during vagal stimulation in open-chest dogs. It has been shown that alterations of latencies started at a certain cardiac cycle length irrespective of pacing frequency. A transitional process of changes from a steady latency value in the control to another steady value during vagal stimulation has been observed. The transitional process has been simulated in experimental procedure in which two sites of the right atrium were paced at close and constant frequencies. To interpret the results obtained one-dimensional model of the sinus node has been constructed. According to the model, pacemaker shift within the sinus node results from a competition between two foci of automaticity with close intrinsic frequencies.     

Sinus rhythm: mechanisms and function

The normal cardiac rhythm originates in a specialized region of the heart, the sinus node that is part of the nodal tissue. The rhythmic, impulse initiation of sinus node pacemaker cells results from a spontaneous diastolic depolarization that is initiated immediately after repolarization of the preceding actions potential. This slow diastolic depolarisation is typical of automatic cells and essential to their function. Several currents are involved in this diastolic depolarisation: a hyperpolarization activated inward current, termed "pacemaker" I(f) current, two Ca2+ currents (a L type and a T type), a delayed K+ current and a Na/Ca exchange current. The frequency of the automatic discharge is the main determinant of heart rate. However the sinus node activity is regulated by adrenergic and cholinergic neurotransmitters. Acetylcholine provokes the hyperpolarization of pacemaker cells and decreases the speed of the spontaneous diastolic depolarisation, thus slowing the sinus rate. Catecholamines lead to sinus tachycardia by increasing the diastolic depolarisation speed. In normal conditions, the observed resting heart rate is lower than the intrinsic frequency of the sinus node due to a "predominance" of the vagal tone. Neural regulation of the heart rate aims at meeting the metabolic needs of the tissues through a varying blood flow. Differences between diurnal and nocturnal mean heart rates are accounted for by neural influences. During the night, the increased vagal tone results in decreased heart rate. The exercise-induced tachycardia results from the sympathetic stimulation. It allows more blood to reach skeletal muscles, and as a consequence an increased supply of oxygen and nutrients. Compared to the variety of clinical arrhythmias, sinus rhythm is the basis for optimal exercise capacity and quality of life.     

Middle cerebral artery blood velocity during intense static exercise is dominated by a Valsalva maneuver.

Lifting of a heavy weight may lead to "blackout" and occasionally also to cerebral hemorrhage, indicating pronounced consequences for the blood flow through the brain. We hypothesized that especially strenuous respiratory straining (a Valsalva-like maneuver) associated with intense static exercise would lead to a precipitous rise in mean arterial and central venous pressures and, in turn, influence the middle cerebral artery blood velocity (MCA V(mean)) as a noninvasive indicator of changes in cerebral blood flow. In 10 healthy subjects, MCA V(mean) was evaluated in response to maximal static two-legged exercise performed either with a concomitantly performed Valsalva maneuver or with continued ventilation and also during a Valsalva maneuver without associated exercise (n = 6). During static two-legged exercise, the largest rise for mean arterial pressure and MCA V(mean) was established at the onset of exercise performed with a Valsalva-like maneuver (by 42 +/- 5 mmHg and 31 +/- 3% vs. 22 +/- 6 mmHg and 25 +/- 6% with continued ventilation; P < 0.05). Profound reductions in MCA V(mean) were observed both after exercise with continued ventilation (-29 +/- 4% together with a reduction in the arterial CO(2) tension by -5 +/- 1 Torr) and during the maintained Valsalva maneuver (-21 +/- 3% together with an elevation in central venous pressure to 40 +/- 7 mmHg). Responses to performance of the Valsalva maneuver with and without exercise were similar, reflecting the deterministic importance of the Valsalva maneuver for the central and cerebral hemodynamic response to intense static exercise. Continued ventilation during intense static exercise may limit the initial rise in arterial pressure and may in turn reduce the risk of hemorrhage. On the other hand, blackout during and after intense static exercise may reflect a reduction in cerebral blood flow due to expiratory straining and/or hyperventilation.     

Evaluation of blood pressure control after bilateral glomectomy: effects of propranolol treatment

The effects of bilateral glomectomy on arterial blood pressure and heart rate and the response to the pressor tests were studied in a women of 37. Arterial pressure and ECG were recorded by the continuous unrestricted Oxford method. Hypotension, increased blood pressure variability and tachycardia rapidly developed 2 days after surgery, indicating sympathetic hyperactivity and/or deactivation of vagal tone. Wide blood pressure fluctuations were present on standing and abnormal blood pressure responses to head up tilting and to the Valsalva maneuver were observed reflecting a less prompt and precise control of blood pressure. Treatment with propranolol reduced tachycardia and blood pressure variability. After 5 and 17 months of this therapy propranolol was withheld for 36 h. Tachycardia was still present and blood pressure fluctuations were recorded on assuming the upright posture. However, the heart rate and pressure response to the Valsalva maneuver were normal after 17 months, indicating an improvement of the reflex control of blood pressure.     

Respiratory sinus arrhythmia in the denervated human heart

We performed this study to test whether the denervated human heart has the ability to manifest respiratory sinus arrhythmia (RSA). With the use of a highly sensitive spectral analysis technique (cross correlation) to define beat-to-beat coupling between respiratory frequency and heart rate period (R-R) and hence RSA, we compared the effects of patterned breathing at defined respiratory frequency and tidal volumes (VT), Valsalva and Mueller maneuvers, single deep breaths, and unpatterned spontaneous breathing on RSA in 12 normal volunteers and 8 cardiac allograft transplant recipients. In normal subjects R-R changes closely followed changes in respiratory frequency (P less than 0.001) but were little affected by changes in VT. On the R-R spectrum, an oscillation peak synchronous with respiration was found in heart transplant patients. However, the average magnitude of the respiration-related oscillations was 1.7-7.9% that seen in normal subjects and was proportionally more influenced by changes in VT. Changes in R-R induced by Valsalva and Mueller maneuvers were 3.8 and 4.9% of those seen in normal subjects, respectively, whereas changes in R-R induced by single deep breaths were 14.3% of those seen in normal subjects. The magnitude of RSA was not related to time since the heart transplantation, neither was it related to patient age or sex. Thus the heart has the intrinsic ability to vary heart rate in synchrony with ventilation, consistent with the hypothesis that changes, or rate of changes, in myocardial wall stretch might alter intrinsic heart rate independent of autonomic tone.