Can diabetes cause pvcs

can diabetes cause pvcs

Forster 2nd Dept. Korsós Æ L. Rudas Dept. Makra Dept. Ábrahám 1st Dept. PVCrelated RR can diabetes cause pvcs fluctuations detected on Holter ECG recordings could be characterized by the heart rate turbulence HRT parameters, including early postextrasystolic acceleration, described by turbulence onset, and late deceleration, described by turbulence slope Can diabetes cause pvcs.

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We have determined the increasing and decreasing spontaneous baroreflex sequence sensitivity up- and down-BRS parameters in supine and in upright position in 12 patients with VVI pacemaker while in sinus rhythm.

Five—five premature ventricular pacemaker extrastmuli were also applied in both body positions and HRT parameters were calculated. The BRS indices decreased significantly upon tilting, which was paralleled by a significant decrease in TS from The relationship is further supported by the similar postural behavior of these parameters.

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Our results suggest that the confounding effect of posture should be considered when analyzing Holter recordings. InSchmidt et al. Heart rate turbulence HRT consists of an early post-extrasystolic acceleration, followed by a late deceleration. Two parameters, turbulence onset TO and turbulence slope TSwere introduced to describe these phases. By now, there is a general agreement regarding the mechanism of HRT.

The PVC results in a 75 temporary arterial pressure drop, which is followed by a gradual, delayed, sympathetically mediated pressure elevation. In turn, the pressure changes are mirrored in RR interval fluctuations via arterial baroreflex mechanism. While traditional BRS tests are performed in laboratory environment with standardized conditions, HRT is usually derived from a Holter segment, without accounting for the factors which could alter the baroreflex responses.

Among the numerous confounders, the role of body posture is abundantly studied and documented [3, 10].

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In the present study, we enrolled patients who underwent permanent ventricular pacemaker implantation; however, their baseline sinus rhythm remained well preserved. We can diabetes cause pvcs their spontaneous BRS indices to their HRT parameters in supine rest conditions; then, in order to assess the effects of upright posture, the tests were repeated following upright tilt. Methods j Patients Participants were recruited can diabetes cause pvcs our pacemaker outpatient clinic.

Subjects with ventricular pacemaker lead and predominant sinus rhythm were selected. All patients gave their written informed consent after a thorough briefing about the study and our local ethical committee approved the protocol.

The patients assumed supine rest position on the tilt table. Their ECG and blood pressure signals were continuously measured with a Marquette bedside monitor and with the Finapres Ohmeda non-invasive blood pressure monitor.

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Following a few minutes of adaptation, uninterrupted ECG and arterial pressure baseline signals were recorded for 5 minutes. After the first captured paced beat, the pace- maker frequency was quickly switched back to the original low backup rate. This maneuver was repeated five times. Each captured paced beat was separated can diabetes cause pvcs at least 60 uninterrupted sinus cycles. After the series of the paced premature contractions had been completed, the patients had a few minutes of rest, then the tilt table was elevated to 70° head-upright position.

In this position another 5-minute ECG and arterial pressure recording was taken. Subsequently the externally paced series of PVC-s was repeated. All recordings were peak can diabetes cause pvcs automatically and checked by the investigators. Arterial pressure, RR interval parameters, and the traditional time domain parameters of heart rate variability parameters were determined from the baseline recordings.

Spontaneous BRS was determined from the supine and upright baseline recordings.

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For BRS calculation we used the spontaneous sequence method [2]. Spontaneous sequences were defined as three or more consecutive cycles of either systolic blood pressure elevation up sequences or fall down sequences coupled with RR interval changes in the same direction. No RR interval limit was set. For all of these sequences, the slope of the line fitted to RRI versus systolic arterial pressure was calculated and averaged separately for up and down sequences up-BRS, down-BRS.

This calculation was performed only if 5—5 or more sequences were identified during the 5-minute recordings. TS was defined as the maximum positive slope can diabetes cause pvcs regression line assessed over any sequence of five subsequent sinus rhythm RR intervals within the first 15 cycles after the paced PVC [22].

The can diabetes cause pvcs of supine and upright TO and TS parameters were calculated separately for each patient. Comparison of supine and upright data was performed using paired t test. Results Discussion Can diabetes cause pvcs male subjects were recruited for the study.

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Their mean age was 61 ± 11 years. Indication for permanent pacemaker implantation was intermittent AV block in 11 cases, and carotid sinus syncope in one. However, the correlation did not reach statistical significance.

Compared to the supine rest position upright tilt resulted in significant RR interval shortening. The systolic arterial pressure remained unchanged and the diastolic pressure showed elevation; however, this did not reach statistical can diabetes cause pvcs.

Similar significant decline was detected in the TS values Table 1. The individual postural changes of baroreflex gains and TS values are shown in Figure 1. In contrast, the TO showed no significant postural decrease Table 1. Supine Upright P ± 37 ± 21 29 ± 20 7. Their capability to predict adverse outcome was first proved by retrospective Holter tape analysis of acute myocardial infarction survivors, who were enrolled in large-scale follow-up studies [22]. The retrospective Holter-tape analysis of the ATRAMI trial population, which included low-risk post-myocardial infarction patients, confirmed the independent value of the new markers in predicting the risk of subsequent cardiac arrest [7].

A recent study extended the previous observations to myocardial infarction survivors who received routine reperfusion therapy [1]. In these studies HRT actually provided better prediction than any of the traditional ECG derived heart rate variability parameters.

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Moore et al. While the HRT analysis gains general acceptance in clinical cardiology, it is important to define the potential limitations of the method.

Cardiovagal baroreflex gain determinations could be influenced by several factors, including circadian variations, sleepwake differences, and the influences of physical activity, emotions, post-prandial state and posture.

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Our present study indicates that TS values are also subject to postural influences. This factor should be considered when assessing TS from Holter tapes; for instance, by performing separate analyses of day and night recordings. The post-extrasystolic RR interval changes are vagally mediated, as it has been shown that atropine administration could abolish these responses [13, 15].

Numerous studies investigated the relationship between baroreflex and HRT phenomenon [5, 7, 9, 13, 14, 24].

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Although the degree of correlation varied with the different baroreflex techniques, all of these studies confirmed the relationship. Thus, HRT could be regarded as a special baroreflex technique, which requires no simultaneous arterial pressure recording. This idea is not entirely unprecedented. Davies et al. The first is related to the time delay between the specific baroreflex test and the Holter recording which supplied material for HRT analysis. Baroreflex 77 Fig.

The time delay between BRS tests and Holter monitoring presumably varied even more widely in certain studies.

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The other factor which deserves comment is related to the methodology of BRS testing. In those studies which utilized vasoactive drug injection, or Valsalva maneuver, the BRS gain calculation was based on relatively large arterial pressure swings, which may extend to the flat portion of the sigmoid arterial pressure-RR interval relationship.

Nevertheless, previous publications confirmed the relationship between HRT parameters and the baroreflex gain determined by bolus phenylephrine injection. Reanalysis of the Holter recordings of the patients included in the study indicated a moderate, but significant correlation between the HRT indices and the phenylephrine baroreflex gain [7]. In another report, Iwasaki et al. The baroreflex gain, calculated from the blood pressure overshoot phase of the Valsalva maneuver, was studied by Lindgren et al.

Unlike the large pressure fluctuations with the above mentioned studies, the post-extrsasystolic blood pressure a cukorbetegség kezelése a klinikában are usually moderate, confined to the vicinity of the resting set point.

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Actually this is also the range of the spontaneous sequences. This assumption was well substantiated by two recent studies, both performed in cardiac electrophysiological laboratories, utilizing paced tilt 0 supine tilt supine tilt PVC-s [13, 21].

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Roach et al. They found that the values were not only closely correlated, but were practically identical. Lin et al. In a recent report, Wichterle et al. This gain showed good correlation not only with the TS, but also with another spontaneous baroreflex index, the transfer function modulus in the low frequency 0.

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