Concerns about sources of electromagnetic interference in patients with pacemakers.
(33/1706)
Electromagnetic noise is rapidly increasing in our environment so electromagnetic interference (EMI) with pacemakers (PM) may become a more important problem despite technological improvements in PM. The aim of this study was to evaluate the kinds of EMI which affect the quality of life of PM patients. The participants (1,942 Japanese Association for Pacemaker Patients: Pacemaker-Tomonokai) were asked to respond to a questionnaire about their major EMI troubles, and 1,567 patients (80.7%) responded by mail. The main concerns were from mobile telephones (MT) (39%), magnetic resonance imaging (MRI) (17%), electronic kitchen appliances, automobile engines and high voltage power lines. If possible, PM implantation sites should be carefully selected not only according to the physician's convenience but also considering information on each patient's habits and physical limitations. (+info)
Regulation of ET: pulmonary release of ET contributes to increased plasma ET levels and vasoconstriction in CHF.
(34/1706)
Endothelin (ET) contributes to the increased systemic vascular resistance and elevated cardiac filling pressures seen in congestive heart failure (CHF). We investigated to what extent ET-mediated vasoconstriction in CHF occurs through an endocrine action of elevated plasma ET or by an autocrine/paracrine mechanism related to induction of vascular ET gene expression. Three weeks of pacing (225 beats/min) induced a marked release of ET-1 from the pulmonary circulation with a sixfold elevation of arterial plasma ET in CHF pigs compared with sham-operated pigs. Arterial plasma ET was the strongest and only independent predictor of systemic vascular resistance. In contrast, vascular preproET-1 and ET-receptor mRNA expression were unaltered or decreased in CHF pigs and did not correlate with indexes of vascular tone. However, myocardial preproET-1 mRNA expression increased twofold in CHF pigs. PreproET-2 and preproET-3 mRNAs were not detectable in cardiovascular tissues. In conclusion, plasma ET was markedly increased because of an augmented release from the pulmonary circulation during CHF, and arterial plasma ET correlated with systemic vascular resistance. The absence of ET induction in the peripheral vasculature suggests that ET increases vascular tone during CHF by an endocrine, not an autocrine/paracrine, mechanism. (+info)
Short-term effects of rapid pacing on mRNA level of voltage-dependent K(+) channels in rat atrium: electrical remodeling in paroxysmal atrial tachycardia.
(35/1706)
BACKGROUND: Atrial fibrillation causes electrophysiological changes of the atrium, thereby facilitating its maintenance. Although the expression of ion channels is modulated in chronic atrial fibrillation, it is yet unknown whether paroxysmal atrial fibrillation can also lead to electrical remodeling by affecting gene expression. METHODS AND RESULTS: To examine the short-term effects of rapid pacing on the mRNA level of voltage-dependent K(+) channels, high-rate atrial pacing was performed in Sprague-Dawley rat hearts. Total RNA was prepared from the atrial appendages from 0 to 8 hours after the onset of pacing, and mRNA levels of Kv1.2, Kv1. 4, Kv1.5, Kv2.1, Kv4.2, Kv4.3, erg, KvLQT1, and minK were determined by RNase protection assay. Among these 9 genes, the mRNA level of the Kv1.5 channel immediately and transiently increased, with bimodal peaks at 0.5 and 2 hours after the onset of pacing. Conversely, the pacing gradually and progressively decreased the mRNA levels of the Kv4.2 and Kv4.3 channels. The increase of Kv1.5 and the decrease of Kv4.2 and Kv4.3 mRNA levels were both rate dependent. In correspondence with the changes in the mRNA level, Kv1. 5 channel protein transiently increased in the membrane fraction of the atrium during a 2- to 8-hour pacing period. Electrophysiological findings that the shortening of the action potential produced by 4-hour pacing was almost abolished by a low concentration of 4-aminopyridine implied that the increased Kv1.5 protein was functioning. CONCLUSIONS: Even short-term high-rate atrial excitation could differentially alter the mRNA levels of Kv1.5, Kv4.2, and Kv4.3 in a rate-dependent manner. In particular, increased Kv1.5 gene expression, having a transient nature, implied the possible biochemical electrical remodeling unique to paroxysmal tachycardia. (+info)
Effects of physiologic pacing versus ventricular pacing on the risk of stroke and death due to cardiovascular causes. Canadian Trial of Physiologic Pacing Investigators.
(36/1706)
BACKGROUND: Evidence suggests that physiologic pacing (dual-chamber or atrial) may be superior to single-chamber (ventricular) pacing because it is associated with lower risks of atrial fibrillation, stroke, and death. These benefits have not been evaluated in a large, randomized, controlled trial. METHODS: At 32 Canadian centers, patients without chronic atrial fibrillation who were scheduled for a first implantation of a pacemaker to treat symptomatic bradycardia were eligible for enrollment. We randomly assigned patients to receive either a ventricular pacemaker or a physiologic pacemaker and followed them for an average of three years. The primary outcome was stroke or death due to cardiovascular causes. Secondary outcomes were death from any cause, atrial fibrillation, and hospitalization for heart failure. RESULTS: A total of 1474 patients were randomly assigned to receive a ventricular pacemaker and 1094 to receive a physiologic pacemaker. The annual rate of stroke or death due to cardiovascular causes was 5.5 percent with ventricular pacing, as compared with 4.9 percent with physiologic pacing (reduction in relative risk, 9.4 percent; 95 percent confidence interval, -10.5 to 25.7 percent [the negative value indicates an increase in risk]; P=0.33). The annual rate of atrial fibrillation was significantly lower among the patients in the physiologic-pacing group (5.3 percent) than among those in the ventricular-pacing group (6.6 percent), for a reduction in relative risk of 18.0 percent (95 percent confidence interval, 0.3 to 32.6 percent; P=0.05). The effect on the rate of atrial fibrillation was not apparent until two years after implantation. The observed annual rates of death from all causes and of hospitalization for heart failure were lower among the patients with a physiologic pacemaker than among those with a ventricular pacemaker, but not significantly so (annual rates of death, 6.6 percent with ventricular pacing and 6.3 percent with physiologic pacing; annual rates of hospitalization for heart failure, 3.5 percent and 3.1 percent, respectively). There were significantly more perioperative complications with physiologic pacing than with ventricular pacing (9.0 percent vs. 3.8 percent, P<0.001). CONCLUSIONS: Physiologic pacing provides little benefit over ventricular pacing for the prevention of stroke or death due to cardiovascular causes. (+info)
Regional myocardial blood flow in patients with sick sinus syndrome randomized to long-term single chamber atrial or dual chamber pacing--effect of pacing mode and rate.
(37/1706)
OBJECTIVES: This study aimed to evaluate regional myocardial blood flow (MBF) and global left ventricular ejection fraction (LVEF) during chronic pacing in patients with sick sinus syndrome (SSS) randomized to either single chamber atrial (AAI) or dual chamber (DDD) pacing. BACKGROUND: Experimental studies indicate that chronic pacing in the right ventricular apex changes regional MBF, thereby compromising left ventricular function. METHODS: Thirty patients (age 74 +/- 10 years) were randomized to AAI (n = 15) or DDD (n = 15) pacemakers. After 22 +/- 7 months of pacing, MBF was quantified with 13N-labeled ammonia positron emission tomography scanning at 60 beats per min and 90 beats per min. Patients in the DDD group furthermore underwent MBF measurement at temporary AAI pacing, 60 beats per min. Myocardial blood flow was assessed in the anterior, lateral, inferior and septal regions, and the global mean MBF was calculated. Left ventricular ejection fraction was determined by echocardiography at pacemaker implantation and at the time of MBF measurements. RESULTS: Myocardial blood flow at rates 60 and 90 beats per min did not differ between the AAI and DDD groups. During temporary AAI pacing in the DDD group, MBF was significantly higher than during DDD pacing in both the inferior (p = 0.001) and septal (p = 0.004) regions and also globally (0.61 +/- 0.15 vs. 0.53 +/- 0.13 mL x g(-1) x min(-1), p = 0.005). In the DDD group, LVEF decreased from pacemaker implantation to time of MBF measurements (0.61 +/- 0.09 vs. 0.56 +/- 0.07, p = 0.013). Left ventricular ejection fraction during temporary AAI pacing at time of MBF measurements was not different from LVEF at pacemaker implantation. CONCLUSIONS: In patients with SSS, chronic DDD pacing reduced inferior, septal and global mean MBF as well as LVEF, as compared with temporary AAI pacing. The LVEF reversed to baseline level during temporary AAI pacing despite 22 months of permanent ventricular pacing preceding it. Augmenting pace rate to 90 beats per min increased MBF equally in the two treatment groups. (+info)
Modulation of the sympathovagal balance in drug refractory dilated cardiomyopathy, treated with permanent atrioventricular sequential pacing.
(38/1706)
The aim of this study was to assess the long term efficacy of DDD pacing mode in selected patients with idiopathic dilated cardiomyopathy (IDCM) and drug refractory heart failure. The patients were evaluated according to the long term alteration of the sympathovagal balance (SVB). Patients with IDCM were considered eligible for DDD pacing if during temporary VDD pacing a 15% or more increase in the resting cardiac output was demonstrated. From the 29 patients studied, finally 20 patients (15M, 5F, 69 +/- 10 years) fulfilled the aforementioned criterion and therefore were considered candidates for permanent DDD pacing (NYHA class: 3.5 +/- 0.3, Ejection fraction: 27 +/- 7%, Resting cardiac index (CI) 2.6 +/- 0.4 l/min). The ECG of the patients demonstrated LBBB in 13, RBBB in 4 and RBBB + LAH in 3, with a PR interval of 232 +/- 28 ms and QRS duration of 138 +/- 15 ms. The pacemaker was programmed at 40-150 bpm, and AV delay of 105 +/- 20 ms. The lower heart rate programmed, in conjunction with the heart failure state of these patients, was responsible for essentially continuous atrial tracking, ventricular pacing. We evaluated the SVB in the pre- and post-implant periods (3rd and 6th month), using the hourly power spectral analysis (PSA) of heart rate variability during 24 hour Holter monitoring. As SVB we considered the ratio: low (0.04-0.15 Hz) to high frequency (0.15-0.40 Hz). We compared the SVB (LF/HF) during the day and night time for the pre- and post-implant periods. Post-pacing, the NYHA class was significantly improved (2.9 +/- 0.2 and 2.7 +/- 0.3 the 3rd and 6th month respectively). The mean heart rate was 78 +/- 8 bpm in the 3rd and 80 +/- 7 bpm in the 6th month postoperatively, which was lower than the 84 +/- 9 bpm preoperatively, but this difference did not reach statistical significance. During the night time the LF/HF decreased from 1.45 +/- 0.2 (LF: 7.19 +/- 0.43, HF: 4.95 +/- 0.54) in the pre-implant period to 0.9 +/- 0.09 (p < 0.001) (LF: 6.96 +/- 0.63, HF: 7.73 +/- 0.48) in the 3rd month. No further changes were observed in the 6th month (0.82 +/- 0.05, p = NS) (LF: 6.83 +/- 0.51, HF: 8.53 +/- 0.86) compared to the 3rd month. During the day time the LF/HF decreased from 1.5 +/- 0.5 (LF: 7.87 +/- 0.67, HF: 5.24 +/- 0.32) to 1.43 +/- 0.6 (p = NS) (LF: 7.34 +/- 0.71, HF: 5.24 +/- 0.42) in the 3rd month and to 1.41 +/- 0.09 in the 6th month (p = NS) (LF: 7.51 +/- 0.74, HF: 5.36 +/- 0.63). Comparing the LF/HF of day and the night time period, while in the pre-implant period there was no significant difference (1.5 +/- 0.5 vs 1.45 +/- 0.2, p = NS), the difference became significant in the 3rd (1.43 +/- 0.6 vs 0.9 +/- 0.09, p < 0.001) and 6th month (1.41 +/- 0.09 vs 0.82 +/- 0.05, p < 0.001). In conclusion, DDD pacing with individualized AV delay as an adjunct therapy could be a valuable method in selected patients with IDCM and drug refractory heart failure. DDD pacing improves the SVB over the long term. This improvement is attributed to sympathetic activity withdrawal and is more pronounced during night and less during day time. (+info)
The influence of heart rate on augmentation index and central arterial pressure in humans.
(39/1706)
Arterial stiffness is an important determinant of cardiovascular risk. Augmentation index (AIx) is a measure of systemic arterial stiffness derived from the ascending aortic pressure waveform. The aim of the present study was to assess the effect of heart rate on AIx. We elected to use cardiac pacing rather than chronotropic drugs to minimize confounding effects on the systemic circulation and myocardial contractility. Twenty-two subjects (13 male) with a mean age of 63 years and permanent cardiac pacemakers in situ were studied. Pulse wave analysis was used to determine central arterial pressure waveforms, non-invasively, during incremental pacing (from 60 to 110 beats min-1), from which AIx and central blood pressure were calculated. Peripheral blood pressure was recorded non-invasively from the brachial artery. There was a significant, inverse, linear relationship between AIx and heart rate (r = -0.76; P < 0.001). For a 10 beats min-1 increment, AIx fell by around 4 %. Ejection duration and heart rate were also inversely related (r = -0. 51; P < 0.001). Peripheral systolic, diastolic and mean arterial pressure increased significantly during incremental pacing. Although central diastolic pressure increased significantly with pacing, central systolic pressure did not. There was a significant increase in the ratio of peripheral to central pulse pressure (P < 0.001), which was accounted for by the observed change in central pressure augmentation. These results demonstrate an inverse, linear relationship between AIx and heart rate. This is likely to be due to alterations in the timing of the reflected pressure wave, produced by changes in the absolute duration of systole. Consideration of wave reflection and aortic pressure augmentation may explain the lack of rise in central systolic pressure during incremental pacing despite an increase in peripheral pressure. (+info)
Successful removal of an infected pacemaker electrode by open heart surgery under extracorporeal circulation.
(40/1706)
A 33-year-old male with sick sinus syndrome, who had received a pacemaker implant 18 years earlier, was complicated with a generator infection. Although the infected generator was removed, he was suffered from the recurrent local infection associated with a retained pacemaker lead. After a new pacemaker system implantation from the other side of the subclavian vein, we attempted to remove the lead utilizing a pacemaker removal kit. However, this intervention procedure was unsuccessful, because fibrous adhesions had developed around the lead, accompanied by calcification along its course. As a last resort, we opened the heart under extracorporeal circulation and removed the lead under direct vision. The post-operative course was uneventful. In order to remove a long-term implanted pacemaker lead, the direct surgical procedure with extracorporeal circulation is a favorable mean alternative to conventional intervention techniques. (+info)