Fixed Rate Ventricular Pacing Research Articles

Takotsubo syndrome presenting as syncope in a patient with permanent pacemaker

Takotsubo syndrome is an acute reversible heart failure syndrome triggered by physical or emotional stress, especially in postmenopausal women. Herein, we describe a case of a 31-year-old pacemaker dependent lady who presented with syncope after she was bereaved of her father. Electrocardiogram at admission revealed ventricular paced rhythm at 60/min, prolonged QT interval and frequent runs of torsades de pointes. Transthoracic echocardiogram and left ventriculogram revealed findings typical of Takotsubo syndrome. QT prolongation and torsade de pointes in the context of fixed-rate ventricular pacing imply direct catecholamine toxicity on the ventricular myocardium independent of heart rate.

Vagal stimulation suppresses ischemia-induced myocardial interstitial myoglobin release

Aims To evaluate vagal stimulation-mediated myocardial protection against ischemia and reperfusion in in vivo ischemic myocardium. Main methods We measured myocardial interstitial myoglobin levels in the ischemic region using a cardiac microdialysis technique in anesthetized and vagotomized cats. We occluded the left anterior descending coronary artery (LAD) for 60 min and reperfused it for 60 min (VX group, n = 6). The effects of bilateral vagal stimulation (10 V, 5 Hz, 1-ms pulse duration), initiated immediately after LAD occlusion, were examined (VS group, n = 6). To examine the involvement of phosphatidylinositol 3-kinase (PI3K), vagal stimulation was performed after pretreatment with a PI3K inhibitor wortmannin (0.6 mg/kg, i.v.) (VS-W group, n = 6). To examine the contribution of bradycardia, vagal stimulation was performed with fixed-rate ventricular pacing (VS-P group, n = 6). Key findings The average myoglobin level during the ischemic period was 1170 ± 141 in VX (in ng/ml, mean ± SE), which was significantly attenuated in VS (466 ± 87, P < 0.05) and VS-W (613 ± 124, P < 0.05) but not in VS-P (953 ± 203). Reperfusion increased the myoglobin level to 2500 ± 544 in VX, whereas it was suppressed in VS (824 ± 213, P < 0.05) and VS-W (948 ± 315, P < 0.05) but not in VS-P (1710 ± 253). Significance Vagal stimulation, initiated immediately after LAD occlusion, attenuated the myocardial injury. Moreover, bradycardia, independent of PI3K pathway, plays a significant role in vagally induced cardioprotection during acute myocardial ischemia.

UKPACE: to die, or not to die ... Is that the question?

Publication of the United Kingdom Pacing and Cardiovascular Events (UKPACE) trial in 20051 brings to three the number of important randomized clinical trials that call into question what formerly had seemed to be a bullet-proof principle of modern cardiac pacemaker therapy, namely the apparent desirability of maintaining a normal atrioventricular (AV) timing relationship. Indeed, as a group, UKPACE and two earlier North American trials [the Canadian Trial of Physiological Pacing (CTOPP) and the Mode Selection Trial (MOST) in sinus node dysfunction (SND)]2,3 may influence physicians and health insurers to advocate, based on a mortality cost-effectiveness basis, for a return to the predominance of single-chamber ventricular pacing. However, before turning back the clock, the messages delivered by these studies warrant careful examination. CTOPP and MOST compared outcomes during dual-chamber and single-chamber ventricular pacing in over 4500 patients with AV block and/or SND and reported no overall difference in mortality or stroke. However, more than two-thirds of the patients enrolled in these two trials were paced for treatment of SND, a condition in which the frequency of pacing may vary widely from patient to patient, and death is a less relevant endpoint than is preventing syncope, reducing thromboembolic risk or improving exercise tolerance. UKPACE, the most recently published of the three major clinical trials noted earlier, randomized cardiac pacemaker treatment candidates ≥70 years of age with AV block between dual- ( n =1012) and single-chamber devices ( n =1009), and further subdivided the single-chamber population into two groups: fixed-rate ventricular pacing ( n =504), and rate-modulated single-chamber pacing ( n =505). The resulting three subgroups proved to be reasonably comparable in terms of age, gender, New York Heart Association (NYHA) functional class, AV conduction disease, symptoms, co-morbidities, and medications. Further, a high pacing ‘burden’ was anticipated in all patients by virtue of …

Vagal stimulation suppresses ischemia-induced myocardial interstitial norepinephrine release

Although electrical vagal stimulation exerts beneficial effects on the ischemic heart such as an antiarrhythmic effect, whether it modulates norepinephrine (NE) and acetylcholine (ACh) releases in the ischemic myocardium remains unknown. To clarify the neural modulation in the ischemic region during vagal stimulation, we examined ischemia-induced NE and ACh releases in anesthetized and vagotomized cats. In a control group (VX, n = 8), occlusion of the left anterior descending coronary artery increased myocardial interstitial NE level from 0.46 ± 0.09 to 83.2 ± 17.6 nM at 30–45 min of ischemia (mean ± SE). Vagal stimulation at 5 Hz (VS, n = 8) decreased heart rate by approximately 80 beats/min during the ischemic period and suppressed the NE release to 24.4 ± 10.6 nM ( P < 0.05 from the VX group). Fixed-rate ventricular pacing (VSP, n = 8) abolished this vagally mediated suppression of ischemia-induced NE release. The vagal stimulation augmented ischemia-induced ACh release at 0–15 min of ischemia (VX: 11.1 ± 2.1 vs. VS: 20.7 ± 3.9 nM, P < 0.05). In the VSP group, the ACh release was not augmented. In conclusion, vagal stimulation suppressed the ischemia-induced NE release and augmented the initial increase in the ACh level. These modulations of NE and ACh levels in the ischemic myocardium may contribute to the beneficial effects of vagal stimulation on the heart during acute myocardial ischemia.

Developmental sequelae of fixed-rate ventricular pacing in the immature canine heart: An electrophysiologic, hemodynamic, and histopathologic evaluation

Permanent, fixed-rate ventricular pacing (VVI) is associated with hemodynamic deterioration in the adult with compromised myocardial function. The effects of this pacing mode on the intact, immature heart, however, are largely unknown. Twelve beagle puppies (age 3 to 4 months) were equally divided into paced and age-matched control groups. All underwent identical hemodynamic and electrophysiologic evaluations. Transepicardial atrioventricular block and pacemaker insertion were additionally carried out in the paced group. After 4 months of observation, repeat hemodynamic and electrophysiologic measurements followed by histopathologic examinations were done in all puppies. The paced group exhibited significant (p less than 0.05) elevations of right atrial and pulmonary artery pressures, alterations in sinus node function, and prolongation of ventricular refractory periods compared with the control group. Initiation of dysrhythmias by programmed electrical stimulation was observed only among the paced group of puppies. Histologic examination demonstrated myofibrillar cellular disarray, dystrophic calcifications, prominent subendocardial Purkinje cells, and an increase in variable-sized, disorganized mitochondria only in the paced specimens. These findings indicate that permanent, apically-initiated VVI pacing ultimately predisposes to adverse cellular changes associated with hemodynamic and electrophysiologic deterioration in the intact, developing immature canine heart.

The Reliability of Rate‐Pressure Product as an Index of Myocardial Oxygen Consumption in Atrial Synchronized Versus Fixed Rate Ventricular Pacing

The product of heart rate and blood pressure was tested as an index of myocardial oxygen consumption (MVO2) and compared with directly determined MVO2 during ventricular demand (VVI) fixed rate pacing and atrial synchronized (VAT) pacing at rest and during exercise. Systolic brachial artery pressure, pulmonary wedge pressure and MVO2 were similar in the two pacing modes and showed similar response to exercise. The correlation between rate-pressure product and MVO2 was closer with VAT than with VVI pacing (r = 0.74 and r = 0.64, respectively), and the latter value was not improved by using the product of atrial rate and systolic pressure (r = 0.61). The rate-pressure product was significantly higher during VAT pacing compared to VVI during exercise, although MVO2 was similar. The similarity of MVO2 during exercise indicated some other contributory factor than heart rate in VVI pacing, probably increase of contractility and/or volume. Because such factors are not included in currently used indices of MVO2 assessments must be interpreted cautiously, particularly in cases of complete heart block with VVI pacing.

Single-chamber Cardiac Pacing with Two Forms of Respiration-controlled Rate-responsive Pacemaker

Ventilatory changes correlate with the heart rate response during exercise, and such changes have been used to determine an appropriate chronotropic response in the Biorate (RDP3 and MB-1) and Meta pacemakers, both of which use a thoracic impedance measurement principle. Ten patients with the Biorate and 11 patients with the Meta were studied. In both groups, significant rate response and improvement in exercise duration compared with fixed rate ventricular pacing were achieved during symptom-limited treadmill exercise tests, with good correlations between the pacing rate and estimated oxygen consumption. Motion artefacts affected the measured impedance of both pacemakers, with rate response occurring during arm movements in the absence of respiratory activity. This observation suggested that both pacemakers have the potential of activity sensing. The earlier version of the Biorate (RDP3) was limited by myopotential interference, and erosion of the auxiliary lead can be problematic in some patients.

Long‐Term Follow‐Up of Patients with the QT Rate Adaptive Pacemaker

We report a 5-year follow-up of eight patients implanted with the QT sensing rate adaptive pacemaker, the Vitatron TX. Careful programming was undertaken shortly after implantation utilizing repeated exercise testing to ensure optimal settings. Further exercise testing was not carried out during follow-up as the patients remained symptomatically well. Of six patients assessed with repeat exercise testing at 5 years, four demonstrated a satisfactory rate adaptive response with improved exercise performance compared to fixed rate ventricular pacing, one patient had an abrupt onset of increased pacing rate with exercise associated with improved exercise ability, and another developed an increased pacing rate after exercise but an appropriate rate adaptive response after reprogramming. One patient developed an inappropriately high pacing rate associated with congestive heart failure several months after a large myocardial infarction. One patient died from carcinoma. The QT sensing rate adaptive pacemaker appears to be reliable in lon-term clinical use when carefully programmed using exercise testing after implantation.

Rate‐Responsive Pacing by Means of Activity Sensing Versus Single Rate Ventricular Pacing: A Double‐Blind Cross‐Over Study

The clinical applicability of rate-responsive pacing (RRP) by means of activity sensing has been tested in 15 patients. The patients (ages 24-85) had sinus node dysfunction (2), atrial fibrillation (7), or sinus rhythm (6) combined with complete atrioventricular block. Exercise capacity was investigated on a bicycle ergometer and on a treadmill in a double-blind cross-over study design following one week each of fixed rate ventricular pacing (70 bpm) and rate-responsive pacing (60/125-150 bpm). The patients answered a questionnaire concerning subjective symptoms. A Holter ECG was recorded during 24 hours of all day activity on rate-responsive pacing. During exercise in the rate-responsive mode, heart rate increased more on the treadmill than on the bicycle. A majority of the patients (13 of 15) preferred rate-responsive pacing mainly due to less dyspnea and tiredness. Exercise capacity improved significantly both on bicycle (+7%; p less than 0.01) and on treadmill (+19%; p less than 0.01) during rate-responsive pacing. There were no complications during the follow-up period. In conclusion, the activity-sensing pacemaker is a valuable supplement to existing types of pacemakers. It should be used in patients in whom an atrial electrogram cannot be used for rate triggering.

The haemodynamic importance of atrioventricular synchrony and rate increase at rest and during exercise.

To compare the added haemodynamic importance of atrioventricular synchrony to rate increase, we studied 10 patients, healthy except for atrioventricular block, treated with atrioventricular synchronous pacemakers. Haemodynamic data were obtained by brachial and pulmonary arterial catheterisation. Recordings were made at rest and during upright bicycle ergometry at two submaximal work loads (50% and 80% of maximal aerobic exercise tolerance). The investigation was first performed in the atrioventricular synchronous mode of pacing (VDD) and later repeated during fixed-rate ventricular pacing (VVI) at ventricular rates adjusted to the levels achieved during atrioventricular synchronous pacing. At rest (mean rate 74 bpm), preserved atrioventricular synchrony increased cardiac output (5.0 +/- 0.7 l min-1; mean +/- SD) compared with asynchrony (4.5 +/- 1.0; P less than 0.05), owing to a higher stroke volume (70 +/- 19 versus 64 +/- 22 ml; P less than 0.05), illustrating the importance of the atrial contribution to ventricular filling. During exercise at 50% (mean rate 122 bpm) and 80% (mean rate 146 bpm) of maximal aerobic tolerance, there were no significant differences in cardiac output (50%: VVI 10.1 +/- 2.5, VDD 10.5 +/- 1.6 NS; 80%: VVI 12.8 +/- 4.1, VDD 12.3 +/- 3.5, NS) or in stroke volume (50%: VVI 83 +/- 23, VDD 88 +/- 17, NS; 80%: VVI 89 +/- 32, VDD 85 +/- 27, NS). We conclude that the capacity for rate increase is of major importance while preserved atrioventricular synchrony seems to be much less important for the ability of the individual to increase cardiac output during exercise, at least in patients without myocardial disease.

Systolic Time Intervals, Relation to Atrial Contraction and Leg Elevation in Patients with Transvenous Pacemakers and Fixed Rate Pacing

Systolic time intervals were measured in 15 patients with complete heart block and fixed rate ventricular pacing during supine position and 60° leg elevation. Twelve patients had independent atrial activity appearing at variable relationship to ventricular beats. Three patients were in atrial fibrillation. Systolic time interval ratio PEP/LVET, ejection fraction and derived stroke volume measured from ventricular beats preceded by atrial activity at various PR interval between 0.10 to 0.50 sec were compared to those without atrial activity in the same patient and those in atrial fibrillation.