Next Article in Journal
The Power of Discourse: Associations between Trainers’ Speech and the Responses of Socialized Wolves and Dogs to Training
Next Article in Special Issue
Cardiac Changes after Lactate-Guided Conditioning in Young Purebred Arabian Horses
Previous Article in Journal
Effects of Dietary Vegetable Oil Mixtures including Soybean Oil on Intestinal Oxidative Stress in Gilthead Sea Bream (Sparus aurata)
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
Animals
Volume 13
Issue 6
10.3390/ani13061070
animals-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles thumb_up
...
Endorse textsms
...
Comment
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Article

Assessment of P Wave Indices in Healthy Standardbred Horses

by
Rebecca White
,
Laura Nath
,
Michelle Hebart
and
Samantha Franklin
*
School of Animal and Veterinary Sciences, The University of Adelaide, Roseworthy Campus, Roseworthy, SA 5371, Australia
*
Author to whom correspondence should be addressed.
Animals 2023, 13(6), 1070; https://doi.org/10.3390/ani13061070
Submission received: 16 February 2023 / Revised: 11 March 2023 / Accepted: 11 March 2023 / Published: 16 March 2023
(This article belongs to the Special Issue Recent Progress in Large Animal Cardiology and Electrocardiography)
Browse Figures
Review Reports Versions Notes

Abstract

:

Simple Summary

Electrical activity of the heart is recorded using an electrocardiogram and represented as a series of waveforms. Measurements of the P wave component are used as non-invasive markers of remodelling and susceptibility to heart disease in humans. However, their usefulness has not been fully investigated in animals. The aim of this study was to measure P wave indices in healthy standardbred horses and investigate variables that might influence them. We found significant associations with exercise status as well as a positive correlation with exercise duration (number of years raced). These findings are similar to those reported in human athletes versus sedentary individuals. These changes are likely to be associated with the remodelling of the heart chambers that occurs with exercise training and may explain why these athletes are at increased risk of heart rhythm disturbances.

Abstract

P wave indices are used as non-invasive electrocardiographic markers of atrial remodelling in humans. Few studies have investigated their use in animals. The aim of this study was to measure P wave duration and P wave dispersion (Pd) in healthy standardbred horses and investigate variables that might influence these measurements. A 12-lead electrocardiogram was recorded at rest and P wave indices were calculated in 53 horses. A general linear model was used to investigate the main effects: age, bodyweight, sex, resting heart rate, presence of a murmur, exercise status and the number of years raced. There were significant associations with exercise status for both the maximum P wave duration and Pd, with both values being increased in strenuously exercising versus non-active horses. Furthermore, a significant moderate positive correlation was identified between the duration of exercise (number of years raced) and both Pmax and Pd. No other significant associations were identified. These findings are similar to those reported in elite human athletes versus sedentary individuals. The increases in these P wave indices most likely occur due to prolongation and heterogeneity in atrial conduction time, which are associated with structural and electrical remodelling, and may explain the increased risk of atrial fibrillation in athletic horses.

1. Introduction

P wave duration and P wave dispersion (Pd) reflect the activation of atrial muscle and are used as non-invasive electrocardiographic markers of atrial remodelling in human medicine [1,2,3,4,5,6]. P wave dispersion is defined as the difference between the maximum (Pmax) and minimum (Pmin) P wave duration on a standard 12-lead surface electrocardiogram (ECG) [6]. Increased P wave duration reflects a prolongation in atrial conduction time, whereas increased Pd is a marker of heterogeneity in atrial conduction time [7]. These indices have been suggested to be sensitive predictors for the development of atrial arrhythmias, especially atrial fibrillation (AF) in human patients [3,4,5,6,7,8,9,10,11,12].
P wave duration and dispersion have also been shown to be increased in elite human athletes [13,14,15], and Pd is positively correlated with training duration [14,15,16]. These findings may explain the increased risk for the development of AF in this population. Numerous studies have identified an increased risk of AF in athletes compared with non-athletes, especially in those performing endurance exercise [17,18,19,20]. The mechanism for this increased risk is most likely related to the electrical and structural cardiac remodelling that occurs in response to athletic training [20,21,22,23,24].
Athletic horses, like human athletes, have been shown to experience cardiac remodelling in response to training [25,26,27,28]. Furthermore, similar to human athletes, AF is the most common arrhythmia affecting athletic performance in horses, especially racehorses, with a reported prevalence of 0.1–4.9% [29,30,31,32]. Atrial fibrillation may occur as a paroxysmal (PAF) or persistent event, with progression from PAF to persistent AF likely to occur over time in both humans [33,34] and horses [32,35]. The recurrence of AF is common both in horses with PAF [32] and horses with persistent AF that have undergone cardioversion [32,36]. This is a particular issue for racehorses that may be prevented from competing if they experience multiple episodes of post-race arrhythmia. A non-invasive measure to predict horses at an increased risk of developing AF would be extremely valuable.
Few studies have reported the use of P wave indices in veterinary medicine [37,38,39,40,41,42]. In dogs, Pd has been shown to be significantly increased in those with chronic valvular disease and disturbances of supraventricular conduction [38,42] and was also found to be a useful predictor of arrhythmia recurrence following electrical cardioversion of AF [39]. In horses, only one study has been performed to determine the values of Pd in healthy Silesian and Polish primitive horses [40].
The aim of this study was to measure P wave duration and dispersion in healthy standardbred (SB) horses and to investigate variables that might influence these measurements.

2. Materials and Methods

2.1. Study Population

This study was performed on 60 healthy SB horses with no history of cardiac arrhythmia, including 30 retired or unraced horses from the University of Adelaide’s teaching herd and 30 client-owned horses in race training.

2.2. Clinical Examination

Examinations were performed in the field (in small yards), both for horses from the teaching herd and client-owned racehorses. All horses underwent a brief clinical examination that included heart rate (HR), respiratory rate (RR), rectal temperature and thoracic auscultation. For teaching horses, bodyweight was recorded using electronic weigh scales, while those examined at racing yards had bodyweight estimated according to the following equation: girth2 × length [43]. Echocardiography was not performed.

2.3. ECG Recording and Analysis

Following the clinical examination, all horses underwent an ECG recording at rest using a wireless 12-lead Holter recorder (NR-1207-3; Norav Medical; www.noravmedical.com; accessed on 15 February 2023) attached to a surcingle. Horses were restrained by a handler, with a headcollar and lead rope, during the ECG collection to ensure that they stood quietly. Electrode placement was performed according to the modified method described by Hesselkilde et al. [44]:
  • LA = on top of the left scapula;
  • RA = on top of the right scapula;
  • LL = left of midline, caudal to xiphoid process;
  • RL = on top of right scapula next to RA;
  • V1 = between superficial pectoral muscles;
  • V2 = left ventral triceps;
  • V3 = left thorax in 6th intercostal space, at level of the shoulder joint;
  • V4 = left thorax in 6th intercostal space, at the level of the elbow joint;
  • V5 = right thorax in 6th intercostal space, at the level of the elbow joint;
  • V6 = right ventral triceps.
Continuous digital ECG recordings were obtained over a 5 min period. Subsequent analysis of ECG traces was performed using proprietary software (Norav Rest ECG; Norav Medical; www.noravmedical.com; accessed on 15 February 2023) using a paper speed of 100 mm/s and amplitude of 40 mm/mV. Manual measurement of P wave duration was performed across all 12 leads for five cardiac cycles at a time when the HR was lowest, without 2nd-degree atrioventricular block, and when there was minimal interference in the baseline. Each P wave was measured separately on each lead, using digital callipers, with a precision of ±2 ms. P wave duration was measured as the distance between the onset (positive or negative deflection from the isoelectric line) and the offset (return of the isoelectric line) [7,45]. The minimum (Pmin) and maximum (Pmax) P wave duration were identified for each complex from the 12 leads, and Pd was calculated as the difference between Pmax and Pmin. The mean Pmin, Pmax and Pd were then calculated for each horse.

2.4. Statistical Analysis

Statistical analysis was performed using SPSS Statistics Version 25, and graphs were created in Prism version 9. All data were tested for normality with histogram and predicted scatter plots, and data are presented as mean ± standard deviation (SD) unless otherwise specified. Pearson’s correlations were used to investigate associations between Pmin, Pmax and Pd. Variables that might be associated with a change in Pmin, Pmax and Pd were examined, for all horses, using a general linear model (GLM). The main effects considered in the analysis were age, bodyweight, sex, resting HR, presence of a murmur, exercise status and the number of years raced. Exercise status was categorized as “non-active” (retired or unraced horses), “low intensity” (horses in pre-training or early in their training preparation and not exercising maximally) and “high intensity” (horses that were race-fit/racing). All one-way and two-way interactions were tested. Only terms where p < 0.05 remained in the multivariable models and stepwise backward elimination was utilized. The sex distribution, age, bodyweight, and resting HR were compared between non-active (retired/unraced) horses and client-owned horses in race training using a chi-squared test (sex) or independent sample T-test (age, bodyweight, HR). The potential effect of prior race training on P wave indices was investigated in non-active horses by comparing values for Pmin, Pmax and Pd between those that had previously raced and those that had never raced, using independent sample T-tests. Finally, the effect of exercise duration (number of years raced) on P wave indices was further investigated by performing Pearson’s correlations using a subset of horses (n = 38) that excluded horses from the non-active group that had raced previously. Statistical significance was set at p < 0.05.

3. Results

3.1. Animals

The final analysis included 53 horses, with 7 horses excluded due to incomplete ECG data across all leads because of an artefact that made accurate measurement of P wave duration difficult in some leads. The included horses consisted of 32 females and 21 geldings, with a mean (SD) age of 8.5 (4.7) years (range: 2–18 years) and mean (SD) bodyweight of 476 (57) kg. Twenty-four horses were non-active (of which nine were unraced and fifteen had raced previously; the mean (SD) time out of racing was 6.8 (2.1) years), fourteen were classified as “low intensity” exercise and fifteen were classified as “high intensity” exercise. On clinical examination, the mean (SD) resting HR for all horses was 36 (4) bpm. Six horses (five in training and one non-active) had low-grade (≤grade 3/6) right-sided systolic murmurs, typical of tricuspid regurgitation, identified on cardiac auscultation. There were differences in the sex distribution, age, bodyweight, and resting HR for the non-active horses compared with horses that were in race training (Table 1).

3.2. P Wave Duration and Dispersion

Clear P waves were not identified in Lead I and were not included in the calculations. P wave indices were therefore calculated from the remaining 11 leads. The mean (SD) values of the entire population for Pmin, Pmax and Pd were 118.7 (15.5) ms, 162.3 (17.2) ms and 43.6 (9.4) ms, respectively.
There was a strong positive correlation between Pmax and Pmin (r = 0.842; p < 0.001). A similar but weaker correlation was found between Pmax and Pd (r = 0.449; p < 0.001). However, there was no correlation between Pmin and Pd (r = −0.104; p = 0.46).

3.2.1. Variables Associated with P Wave Duration and Dispersion

The results of the univariable analysis from all 53 horses are presented in Table 2. There were no significant associations between Pmin and any of the measured variables. There was a significant association with exercise status for both Pmax and Pd, with both values being increased in strenuously exercising versus non-active horses (Figure 1a–c). In addition, the presence of a murmur and the number of years raced were associated with increased Pd. However, in the multivariable model for Pd, only exercise status remained significant.

3.2.2. Effects of Prior Racing and Exercise Duration on P Wave Indices

There were no significant differences between non-active horses that had previously raced compared with those that had never raced for Pmin (115.6 (23.9) ms versus 114.8 (14.5) ms; p = 0.93), Pmax (155.2 (22.5) ms vs. 154.7 (18.7) ms; p = 0.95) or Pd (39.6 (7.1) ms versus 39.9 (7.0) ms; p = 0.93).
In a subset of 38 horses that excluded the 15 retired horses that had previously raced, significant positive correlations with exercise duration (number of years raced) were identified for both Pmax (r = 0.39; p = 0.02) and Pd (r = 0.41; p = 0.01) but not Pmin (Figure 2a,b).

4. Discussion

This study reports on P wave indices in healthy SB horses and investigates potential variables that might influence these measurements. The P wave durations recorded in this study were similar to those reported in SB horses in a previous study using the same 12-lead configuration [44]. In that study, mean (SD) values for P wave duration varied between 131 (14) ms and 158 (19) ms in each of the 12 leads, although Pmin and Pmax were not reported per se. P wave dispersion has not previously been described in SB horses but was reported in one study that examined Polish and Silesian horses [40]. The mean (SD) Pd reported in that study was slightly lower (30.2 (4.3) ms) compared with this study (43.6 (9.4) ms). These differences may be related to differences between breeds, exercise status or differences in the methodology used. In this study, P wave durations were measured over 11 leads, whilst in the study by Michlik et al., only 9 leads were used [40]. Previous studies in animals have used either six or nine leads to calculate the P wave indices [37,38,39]. However, it has been reported that the use of adjacent leads with shared vectorial orientation may provide greater sensitivity for distinguishing inhomogeneity of atrial activation [46], and it has been suggested that ECGs with ≤nine leads should be excluded from the analysis [9,45,46]. Nevertheless, no studies to date have correlated P wave indices measured in different leads or reported which leads are most useful to derive the calculated P wave indices. The positioning of the electrodes in this study was based on a previously published configuration, whereby the precordial electrodes were positioned ventral to the heart (except for V3) [44]. Placement of the electrodes in a more dorsal position (to be better optimized for the atria) may have increased the amplitude of the recorded P waves and led to improved accuracy in the measurement of P wave duration and dispersion.
The only variable that we found to have a significant association with P wave duration and dispersion, in this study, was exercise status. We found that non-active horses had significantly lower Pmax and Pd in comparison with horses that were racing. Another study, which recorded ECG parameters in a single lead (Lead II), has also identified a significant increase in P wave duration in trained versus untrained SB horses [47]. Contradictory results have been reported in the few studies investigating P wave indices in human athletes. Several have reported Pmax and Pd to be increased in elite human athletes compared with sedentary controls [13,14,15]. Furthermore, a positive correlation between training duration and Pd has been identified in humans, and these changes have been suggested to be associated with the cardiac remodelling that occurs in association with exercise training [14,15,16]. However, another study found no differences in P wave duration and dispersion between trained college athletes and control subjects [48]. Furthermore, Elliott et al. found no difference in P wave duration using a three-lead ECG, between recreational endurance athletes grouped according to lifetime training hours, although no control group was included [21]. We identified an association between the number of years a horse had spent racing and Pd using the univariable analysis. However, this did not remain significant in the final multivariable model. Over half of the non-active horses in our study had raced previously, and this may have influenced the results since the cardiac remodelling associated with exercise training may be reversible. Previously, it has been reported that deconditioning resulted in a reduction in cardiac dimensions and indices of cardiac function over a 12-week period in a group of 3–4-year-old SB horses [49]. We found no differences in P wave indices of non-active horses that had previously raced compared with those that had never raced, suggesting that reverse remodelling may have occurred in those horses that previously raced. When non-active horses that had previously raced were removed from the analysis, we found significant moderate positive correlations between exercise duration (in years) and both Pd and Pmax.
Exercise training induces structural, functional and electrical adaptations within the heart including atrial dilation, myocardial fibrosis and modulation of autonomic tone associated with heightened vagal activity [21,22,23,50]. These changes in the “athletic heart” are believed to contribute to the increased risk of arrhythmogenesis and development of AF [23,51,52]. Atrial fibrillation is the most common performance-limiting arrhythmia of horses [29,30,31,32] and human endurance athletes [18,19,53]. In human athletes, the risk of AF is associated with the cumulative volume of exercise training [50,54,55], and this has also been suggested in SB racehorses [31]. P wave duration quantifies the time required for atrial depolarisation and depends on the mass of atrial tissue to be activated; thus, when prolonged, it might be considered a useful indicator of atrial enlargement [1,41,56]. Atrial size is an important factor for the perpetuation of AF since it facilitates the development of re-entry circuits by increasing the conduction time [35,50,57]. However, whilst a prolongation in P wave duration is commonly associated with AF [4,5,12,46,58], only a few studies have related the increase in P wave duration to atrial enlargement per se [59,60]. In athletes, lifetime training hours were associated with the prolongation in P wave duration and an increase in left atrial volume in one study [16]. However, a recent multicentre study found that although left atrial enlargement was common in competitive human athletes, it was not associated with a significant modification in electrocardiographic indices including the P wave duration [61]. Furthermore, although an association was found between P wave duration and the left atrial to aortic ratio (LA/Ao) in dogs with cardiovascular disease, this was not considered to be a reliable indicator of left atrial enlargement [41]. Prolonged P wave duration that occurs independent of an increase in atrial dimensions may reflect abnormal intra- and inter-atrial conduction due to atrial remodelling. Recently, increased P wave duration has been shown to be independently associated with left atrial fibrosis and mechanical dysynchrony [62]. In addition to P wave duration, it is well accepted that changes in P wave morphology and dispersion also have the potential to provide information regarding the anatomical substrate predisposing to AF [1,4,63]. Increased Pd is a marker of heterogeneity in the atrial conduction time [7]. It is considered a sensitive marker for atrial remodelling and a predictor of PAF [2]. Increased Pd has been found to be an independent predictor of PAF in patients with normal left atrial size and is proposed to occur due to changes within the atrial microarchitecture that increase the heterogeneity in sinus impulse conduction, which may occur before changes in LA dimensions [64]. Associations between left atrial size and Pd have been identified in patients with normal sinus rhythm [65] and PAF [64]. However, other studies on athletes have found no such association with atrial size [13,14]. Echocardiographic measurements of atrial size and function were not performed in this study. Measurement and calculation of left atrial fractional area, left atrial fractional shortening and tissue doppler measurements are well described in horses and have been shown to be useful in the assessment of atrial remodelling and reverse remodelling in cases with induced and naturally occurring AF [66,67,68]. Further studies incorporating echocardiographic measurements of cardiac dimensions and atrial function should be performed to investigate the potential associations between atrial size, atrial structural remodelling, and P wave duration and dispersion in horses.
Exercise training is associated with changes in autonomic tone and a reduction in the resting heart rate in human athletes [16,21]. P wave duration is also influenced by the autonomic nervous system, with β-adrenergic stimulation shortening and β-blockade lengthening P wave duration, whilst parasympathetic blockade shortens P wave duration [69]. Metin et al. [13] identified a negative correlation between resting heart rate and Pd in elite female basketball players. However, Puerta et al. [14] found a positive relationship between resting HR and Pd in the elite athletes they studied. Resting HR in the horses in this study ranged from 32 to 40 bpm during the ECG data collection period and no associations were identified with P wave duration or dispersion. Recently, Nissen et al. reported that trained SB horses had lower resting heart rates and increased frequency of 2nd-degree AV block compared with untrained horses [47]. In contrast, we found a slightly lower HR in non-active horses compared with those in race training, although HR in both groups was higher than those reported by Nissen et al. In that study, ECG was monitored for 2 h whilst horses stood quietly in their stable. In our study, horses were handled for the brief 5 min ECG recording, which may have promoted sympathetic stimulation and hence, the measurements of HR may not reflect the true resting rate.
Studies in humans have also identified associations between P wave indices and age, sex and bodyweight. P wave duration increases with age [8,70]. Males have been found to have increased Pd compared with females [71], and there is also a positive correlation with bodyweight [13,71]. The associations with sex and bodyweight in human patients have been suggested to be related to atrial size since increased bodyweight is one of the most important determinants of atrial size [72] and males tend to be heavier than females. In dogs, increased Pd has also been associated with greater bodyweight but not sex differences [42]. We found no significant association between age, sex or bodyweight and P wave duration or dispersion in this study. Michlik et al. also found no association between Pd and age, sex or bodyweight in the horses that they studied [40]. Changes in cardiac size are expected to occur in foals and young growing horses. Both Young et al. and Buhl et al. reported increases in cardiac dimensions over time in young (2- and 3-year-old) racehorses undergoing athletic training [25,26]. However, no untrained age-matched controls were included, making it difficult to differentiate between training-related changes and those associated with growth and development. Further changes in cardiac size do not appear to be associated with age in mature animals [73,74]. Several studies have investigated potential associations between body size and echocardiographic dimensions in adult horses. Long et al. examined Thoroughbred racehorses with a wide range of body weights (342–648 kg) and found no correlation between bodyweight and any cardiac dimensions [75]. Similarly, Bakos et al. found little or no linear correlation between cardiac dimensions and bodyweight in a group of SB horses weighing between 350 and 490 kg [76]. Zucca et al. did find a weak but statistically significant association between bodyweight and some cardiac dimensions including left ventricular and aortic size but not left atrial size [73]. In contrast, Buhl et al. observed a strong positive correlation between left ventricular size and body weight in their study and also reported that male horses had significantly larger ventricles than female horses [26]. However, no measurements of atrial size were reported.
There were a number of limitations to this study. The 12-lead electrode configuration used may not have been optimized for an assessment of the atria. However, we wanted to use a method that had previously been validated in horses. P wave measurements were performed manually and by a single observer and hence, could be subject to error and/or bias. However, manual measurement of P wave indices using digital callipers is commonly accepted and reported in other studies [45,46]. Reliability of P wave indices measurements requires accurate determination of the P wave onset and offset. This may be challenging if there is interference in the baseline, for example, if the animal moves during data collection. It has been suggested that leads should be excluded from the analysis if the baseline noise exceeds 10 mV and/or the peak to isoelectric line P wave amplitude is less than 15 mV [45], and in this study, seven horses were excluded due to excessive baseline interference. There were significant differences in the age, bodyweight and sex distributions between the non-active and exercising horses included in our study, and these could potentially influence the results. The non-active horses were older and heavier, and there was a higher proportion of females. Whilst we found no associations between these parameters and the measured P wave indices, it is possible that there might be some differences due to changes in atrial size in association with these parameters, as discussed above. Nevertheless, despite the increased age and bodyweight of non-active horses, we found that they had lower Pmax and Pd in comparison with exercising horses, suggesting that exercise training was the most important factor influencing these P wave indices. The lack of echocardiographic measurements is a further limitation of this study and would be useful to incorporate in future studies to determine the effect of atrial size and remodelling on P wave indices. Finally, whilst horses used in this study were assumed to be healthy and had no known history of arrhythmia, it is possible that some horses may have experienced episodes of PAF that were not identified.

5. Conclusions

This study reports on values for Pmin, Pmax and Pd in apparently healthy SB horses. We identified significant associations between exercise status and duration of time in racing and Pmax and Pd. Further studies are required to investigate potential associations between these P wave indices and left atrial size and function and to determine whether they might be useful as non-invasive predictors of AF.

Author Contributions

Conceptualization, S.F. and L.N.; methodology, R.W. and S.F.; formal analysis, R.W., M.H. and S.F.; data curation, R.W.; writing—original draft preparation, R.W.; writing—review and editing, L.N., M.H. and S.F.; supervision, L.N., M.H. and S.F.; project administration, S.F.; funding acquisition, S.F. All authors have read and agreed to the published version of the manuscript.

Funding

This research was partially funded by Racing Victoria Research Program (Ref: 0006001877) who funded the purchase of the 12-lead ECG, and The University of Adelaide who provided internal funding for Rebecca White’s honours project.

Institutional Review Board Statement

This study was approved by the University of Adelaide Animal Ethics Committee (AEC Approval No. 32159 (v1)).

Informed Consent Statement

Informed consent was obtained for all client-owned horses.

Data Availability Statement

Not applicable.

Acknowledgments

The authors would like to acknowledge the staff of the Teaching Support Unit at the University of Adelaide, for the care of the school horses and to owners and trainers who allowed us to use their horses for this project.

Conflicts of Interest

The authors declare no conflict of interest.

References

  1. Platonov, P.G. P-wave morphology: Underlying mechanisms and clinical implications. Ann. Noninvasive Electrocardiol. 2012, 17, 161–169. [Google Scholar] [CrossRef]
  2. Pérez-Riera, A.R.; de Abreu, L.C.; Barbosa-Barros, R.; Grindler, J.; Fernandes-Cardoso, A.; Baranchuk, A. P-wave dispersion: An update. Indian Pacing Electrophysiol. J. 2016, 16, 126–133. [Google Scholar] [CrossRef]
  3. Okutucu, S.; Aytemir, K.; Oto, A. P-wave dispersion: What we know till now? JRSM Cardiovasc. Dis. 2016, 5, 2048004016639443. [Google Scholar] [CrossRef] [Green Version]
  4. Centurión, O.A.; García, L.B.; Marecos, A.; Torales, J.; Scavenius, K.; Miño, L.; Sequeira, O. P-wave morphology, amplitude, duration and dispersion in atrial arrhythmias. J. Cardiol. Ther. 2018, 6, 1–6. [Google Scholar] [CrossRef]
  5. Hari, K.J.; Nguyen, T.P.; Soliman, E.Z. Relationship between P-wave duration and the risk of atrial fibrillation. Expert Rev. Cardiovasc. Ther. 2018, 16, 837–843. [Google Scholar] [CrossRef] [PubMed]
  6. Dilaveris, P.E.; Stefanadis, C.I. P wave dispersion: A valuable non-invasive marker of vulnerability to atrial arrhythmias. Hosp. Chron. 2006, 1, 130–137. [Google Scholar]
  7. Gialafos, J.E.; Dilaveris, P.E.; Gialafos, E.J.; Andrikopoulos, G.K.; Richter, D.J.; Triposkiadis, F.; Kyriakidis, M.K. P wave dispersion: A valuable electrocardiographic marker for the prediction of paroxysmal lone atrial fibrillation. Ann. Noninvasive Electrocardiol. 1999, 4, 39–45. [Google Scholar] [CrossRef]
  8. Aytemir, K.; Özer, N.; Atalar, E.; Sade, E.; Aksöyek, S.; Övünç, K.; Oto, A.; Özmen, F.; Kes, S. P wave dispersion on 12-lead electrocardiography in patients with paroxysmal atrial fibrillation. Pacing Clin. Electrophysiol. 2000, 23, 1109–1112. [Google Scholar] [CrossRef]
  9. Dilaveris, P.E.; Gialafos, J.E. P-wave dispersion: A novel predictor of paroxysmal atrial fibrillation. Ann. Noninvasive Electrocardiol. 2001, 6, 159–165. [Google Scholar] [CrossRef]
  10. Perzanowski, C.; Ho, A.T.; Jacobson, A.K. Increased P-wave dispersion predicts recurrent atrial fibrillation after cardioversion. J. Electrocardiol. 2005, 38, 43–46. [Google Scholar] [CrossRef]
  11. Yıldız, B.Ş.; Şahin, A.; Yıldız, M. P wave dispersion detected from the surface electrocardiography and atrial fibrillation. Koşuyolu Heart J. 2014, 17, 128–130. [Google Scholar] [CrossRef] [Green Version]
  12. Nielsen, J.B.; Kühl, J.T.; Pietersen, A.; Graff, C.; Lind, B.; Struijk, J.J.; Olesen, M.S.; Sinner, M.F.; Bachmann, T.N.; Haunsø, S. P-wave duration and the risk of atrial fibrillation: Results from the Copenhagen ECG Study. Heart Rhythm 2015, 12, 1887–1895. [Google Scholar] [CrossRef]
  13. Metin, G.; Yildiz, M.; Bayraktar, B.; Yucesir, I.; Kasap, H.; Cakar, L. Assessment of the p wave dispersion and duration in elite women basketball players. Indian Pacing Electrophysiol. J. 2010, 10, 10. [Google Scholar]
  14. Puerta, R.C.; Aliz, E.L.; Lopez-Calleja, M.A.R.; Ramirez, R.R.; Pena, G.P. Increased P wave dispersion in elite athletes. Indian Pacing Electrophysiol. J. 2011, 11, 73. [Google Scholar]
  15. Puerta, R.C.; Martín, R.R.; López-Calleja, M.A.R.; León, J.M.; González, L.P.; Torres, Y.C.; González, E.C. Increased P wave dispersion in high performance soccer players and its relationship with sport practice time. CorSalud (Rev. Enferm. Cardiovasc.) 2014, 5, 155–160. [Google Scholar]
  16. Wilhelm, M.; Roten, L.; Tanner, H.; Wilhelm, I.; Schmid, J.-P.; Saner, H. Atrial remodeling, autonomic tone, and lifetime training hours in nonelite athletes. Am. J. Cardiol. 2011, 108, 580–585. [Google Scholar] [CrossRef]
  17. Abdulla, J.; Nielsen, J.R. Is the risk of atrial fibrillation higher in athletes than in the general population? A systematic review and meta-analysis. Europace 2009, 11, 1156–1159. [Google Scholar] [CrossRef]
  18. Elliott, A.D.; Mahajan, R.; Lau, D.H.; Sanders, P. Atrial fibrillation in endurance athletes: From mechanism to management. Cardiol. Clin. 2016, 34, 567–578. [Google Scholar] [CrossRef] [PubMed]
  19. Flannery, M.D.; Kalman, J.M.; Sanders, P.; La Gerche, A. State of the art review: Atrial fibrillation in athletes. Heart Lung Circ. 2017, 26, 983–989. [Google Scholar] [CrossRef] [PubMed]
  20. Sanchis-Gomar, F.; Perez-Quilis, C.; Lippi, G.; Cervellin, G.; Leischik, R.; Löllgen, H.; Serrano-Ostáriz, E.; Lucia, A. Atrial fibrillation in highly trained endurance athletes—Description of a syndrome. Int. J. Cardiol. 2017, 226, 11–20. [Google Scholar] [CrossRef] [PubMed]
  21. Elliott, A.D.; Mahajan, R.; Linz, D.; Stokes, M.; Verdicchio, C.V.; Middeldorp, M.E.; La Gerche, A.; Lau, D.H.; Sanders, P. Atrial remodeling and ectopic burden in recreational athletes: Implications for risk of atrial fibrillation. Clin. Cardiol. 2018, 41, 843–848. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  22. Trivedi, S.J.; Claessen, G.; Stefani, L.; Flannery, M.D.; Brown, P.; Janssens, K.; Elliott, A.; Sanders, P.; Kalman, J.; Heidbuchel, H. Differing mechanisms of atrial fibrillation in athletes and non-athletes: Alterations in atrial structure and function. Eur. Heart J. Cardiovasc. Imaging 2020, 21, 1374–1383. [Google Scholar] [CrossRef]
  23. Peritz, D.C.; Catino, A.B.; Csecs, I.; Kaur, G.; Kheirkhahan, M.; Loveless, B.; Wasmund, S.; Kholmovski, E.; Morris, A.; Marrouche, N.F. High-intensity endurance training is associated with left atrial fibrosis. Am. Heart J. 2020, 226, 206–213. [Google Scholar] [CrossRef] [PubMed]
  24. La Gerche, A. The potential cardiotoxic effects of exercise. Can. J. Cardiol. 2016, 32, 421–428. [Google Scholar] [CrossRef] [PubMed]
  25. YOUNG, L.E. Cardiac responses to training in 2-year-old Thoroughbreds: An echocardiographic study. Equine Vet. J. 1999, 31, 195–198. [Google Scholar] [CrossRef]
  26. Buhl, R.; Ersbøll, A.K.; Eriksen, L.; Koch, J. Changes over time in echocardiographic measurements in young Standardbred racehorses undergoing training and racing and association with racing performance. J. Am. Vet. Med. Assoc. 2005, 226, 1881–1887. [Google Scholar] [CrossRef]
  27. Buhl, R.; Ersbøll, A.K. Echocardiographic evaluation of changes in left ventricular size and valvular regurgitation associated with physical training during and after maturity in Standardbred trotters. J. Am. Vet. Med. Assoc. 2012, 240, 205–212. [Google Scholar] [CrossRef]
  28. Shave, R.; Howatson, G.; Dickson, D.; Young, L. Exercise-induced cardiac remodeling: Lessons from humans, horses, and dogs. Vet. Sci. 2017, 4, 9. [Google Scholar] [CrossRef] [Green Version]
  29. Holmes, J. Cardiac arrhythmias on the racecourse. Equine Exerc. Physiol. 1987, 2, 781–785. [Google Scholar]
  30. Ohmura, H.; Hiraga, A.; Takahashi, T.; Kai, M.; Jones, J.H. Risk factors for atrial fibrillation during racing in slow-finishing horses. J. Am. Vet. Med. Assoc. 2003, 223, 84–88. [Google Scholar] [CrossRef] [PubMed]
  31. Slack, J.; Boston, R.; Soma, L.; Reef, V. Occurrence of cardiac arrhythmias in S tandardbred racehorses. Equine Vet. J. 2015, 47, 398–404. [Google Scholar] [CrossRef]
  32. Nath, L.C.; Elliott, A.D.; Weir, J.; Curl, P.; Rosanowski, S.M.; Franklin, S. Incidence, recurrence, and outcome of postrace atrial fibrillation in Thoroughbred horses. J. Vet. Intern. Med. 2021, 35, 1111–1120. [Google Scholar] [CrossRef] [PubMed]
  33. Hoogsteen, J.; Schep, G.; Van Hemel, N.M.; Van Der Wall, E.E. Paroxysmal atrial fibrillation in male endurance athletes. A 9-year follow up. EP Eur. 2004, 6, 222–228. [Google Scholar] [CrossRef] [PubMed]
  34. Simantirakis, E.N.; Papakonstantinou, P.E.; Kanoupakis, E.; Chlouverakis, G.I.; Tzeis, S.; Vardas, P.E. Recurrence rate of atrial fibrillation after the first clinical episode: A prospective evaluation using continuous cardiac rhythm monitoring. Clin. Cardiol. 2018, 41, 594–600. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  35. Decloedt, A.; Van Steenkiste, G.; Vera, L.; Buhl, R.; van Loon, G. Atrial fibrillation in horses part 1: Pathophysiology. Vet. J. 2020, 263, 105521. [Google Scholar] [CrossRef]
  36. Decloedt, A.; Schwarzwald, C.C.; De Clercq, D.; Van Der Vekens, N.; Pardon, B.; Reef, V.B.; van Loon, G. Risk factors for recurrence of atrial fibrillation in horses after cardioversion to sinus rhythm. J. Vet. Intern. Med. 2015, 29, 946–953. [Google Scholar] [CrossRef] [Green Version]
  37. Noszczyk-Nowak, A.; Pasławska, U.; Szałas, A.; Nicpoń, J. P-wave dispersion in healthy dogs. A preliminary study. Bull. Vet. Inst. Pulawy 2008, 52, 683–688. [Google Scholar]
  38. Noszczyk-Nowak, A.; Szałas, A.; Pasławska, U.; Nicpoń, J. Comparison of P-wave dispersion in healthy dogs, dogs with chronic valvular disease and dogs with disturbances of supraventricular conduction. Acta Vet. Scand. 2011, 53, 18. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  39. Noszczyk-Nowak, A. P-wave dispersion in prediction of maintenance of sinus rhythm after an electrical cardioversion of atrial fibrillation in dogs. J. Vet. Res. 2012, 56, 99–102. [Google Scholar] [CrossRef] [Green Version]
  40. Michlik, K.; Noszczyk-Nowak, A.; Pasławska, U.; Janus, I.; Nicpoń, J. Physiological values of P-wave dispersion in Silesian breed horses and Polish Primitive horses. J. Vet. Res. 2013, 57, 85–89. [Google Scholar] [CrossRef] [Green Version]
  41. Savarino, P.; Borgarelli, M.; Tarducci, A.; Crosara, S.; Bello, N.M.; Margiocco, M. Diagnostic performance of P wave duration in the identification of left atrial enlargement in dogs. J. Small Anim. Pract. 2012, 53, 267–272. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  42. Dittrich, G.; Campos, G.M.V.d.B.; Sousa, M.G.; Oliveira, S.T. P wave dispersion in obese dogs with and without mitral valve disease. Ciência Rural 2018, 48. [Google Scholar] [CrossRef]
  43. Carroll, C.; Huntington, P. Body condition scoring and weight estimation of horses. Equine Vet. J. 1988, 20, 41–45. [Google Scholar] [CrossRef] [PubMed]
  44. Hesselkilde, E.M.; Isaksen, J.L.; Petersen, B.V.; Carstensen, H.; Jespersen, T.; Pehrson, S.; Kanters, J.K.; Buhl, R. A novel approach for obtaining 12-lead electrocardiograms in horses. J. Vet. Intern. Med. 2021, 35, 521–531. [Google Scholar] [CrossRef] [PubMed]
  45. Dilaveris, P.; Batchvarov, V.; Gialafos, J.; Malik, M. Comparison of different methods for manual P wave duration measurement in 12-lead electrocardiograms. Pacing Clin. Electrophysiol. 1999, 22, 1532–1538. [Google Scholar] [CrossRef]
  46. Magnani, J.W.; Williamson, M.A.; Ellinor, P.T.; Monahan, K.M.; Benjamin, E.J. P wave indices: Current status and future directions in epidemiology, clinical, and research applications. Circ. Arrhythmia Electrophysiol. 2009, 2, 72–79. [Google Scholar] [CrossRef] [Green Version]
  47. Nissen, S.D.; Weis, R.; Krag-Andersen, E.K.; Hesselkilde, E.M.; Isaksen, J.L.; Carstensen, H.; Kanters, J.K.; Linz, D.; Sanders, P.; Hopster-Iversen, C. Electrocardiographic characteristics of trained and untrained standardbred racehorses. J. Vet. Intern. Med. 2022, 36, 1119–1130. [Google Scholar] [CrossRef]
  48. Karakaya, O.; Saglam, M.; Barutcu, I.; Esen, A.M.; Ocak, Y.; Melek, M.; Kaya, D.; Turkmen, M.; Onrat, E.; Ozdemir, N. Comparison of the predictors for atrial rhythm disturbances between trained athletes and control subjects. Tohoku J. Exp. Med. 2005, 207, 165–170. [Google Scholar] [CrossRef] [Green Version]
  49. Kriz, N.G.; Hodgson, D.R.; Rose, R.J. Changes in cardiac dimensions and indices of cardiac function during deconditioning in horses. Am. J. Vet. Res. 2000, 61, 1553–1560. [Google Scholar] [CrossRef]
  50. Elliott, A.D.; Linz, D.; Verdicchio, C.V.; Sanders, P. Exercise and atrial fibrillation: Prevention or causation? Heart Lung Circ. 2018, 27, 1078–1085. [Google Scholar] [CrossRef]
  51. Guasch, E.; Benito, B.; Qi, X.; Cifelli, C.; Naud, P.; Shi, Y.; Mighiu, A.; Tardif, J.-C.; Tadevosyan, A.; Chen, Y. Atrial fibrillation promotion by endurance exercise: Demonstration and mechanistic exploration in an animal model. J. Am. Coll. Cardiol. 2013, 62, 68–77. [Google Scholar] [CrossRef] [Green Version]
  52. Benito, B.; Gay-Jordi, G.; Serrano-Mollar, A.; Guasch, E.; Shi, Y.; Tardif, J.-C.; Brugada, J.; Nattel, S.; Mont, L. Cardiac arrhythmogenic remodeling in a rat model of long-term intensive exercise training. Circulation 2011, 123, 13–22. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  53. Newman, W.; Parry-Williams, G.; Wiles, J.; Edwards, J.; Hulbert, S.; Kipourou, K.; Papadakis, M.; Sharma, R.; O’Driscoll, J. Risk of atrial fibrillation in athletes: A systematic review and meta-analysis. Br. J. Sport. Med. 2021, 55, 1233–1238. [Google Scholar] [CrossRef] [PubMed]
  54. Mascia, G.; Perrotta, L.; Galanti, G.; Padeletti, L. Atrial fibrillation in athletes. Int. J. Sport. Med. 2013, 34, 379–384. [Google Scholar] [CrossRef] [PubMed]
  55. La Gerche, A.; Heidbuchel, H. Can intensive exercise harm the heart? You can get too much of a good thing. Circulation 2014, 130, 992–1002. [Google Scholar] [CrossRef] [Green Version]
  56. Lombard, C.W.; Spencer, C.P. Correlation of radiographic, echocardiographic, and electrocardiographic signs of left heart enlargement in dogs with mitral regurgitation. Vet. Radiol. 1985, 26, 89–97. [Google Scholar] [CrossRef]
  57. Mont, L.; Tamborero, D.; Elosua, R.; Molina, I.; Coll-Vinent, B.; Sitges, M.; Vidal, B.; Scalise, A.; Tejeira, A.; Berruezo, A. Physical activity, height, and left atrial size are independent risk factors for lone atrial fibrillation in middle-aged healthy individuals. Europace 2008, 10, 15–20. [Google Scholar] [CrossRef]
  58. Centurión, O.; Aquino, N.; Torales, J.; Scavenius, K.; Miño, L.; Sequeira, O. P Wave Duration and Dispersion as a Useful Conventional Electrocardiographic Marker for Atrial Fibrillation Prediction. J. Cardiol. Curr. Res. 2017, 8, 00285. [Google Scholar]
  59. Ariyarajah, V.; Mercado, K.; Apiyasawat, S.; Puri, P.; Spodick, D.H. Correlation of left atrial size with p-wave duration in interatrial block. Chest 2005, 128, 2615–2618. [Google Scholar] [CrossRef] [Green Version]
  60. Puerta, R.C.; Martínez, E.L.; López-Calleja, M.A.R.; Peña, G.P.; Torres, Y.C.; Elizundia, J.M.C.; González, F.R.; Vázquez, L.Á.G.; González, E.C. New Parameter of the Second Half of the P-Wave, P-Wave Duration, and Atrial Conduction Times Predict Atrial Fibrillation during Electrophysiological Studies. Med. Princ. Pract. 2021, 30, 462–469. [Google Scholar] [CrossRef]
  61. Herrera, C.; Bruña, V.; Comella, A.; de la Rosa, A.; Díaz-González, L.; Ruiz-Ortiz, M.; Lacalzada-Almeida, J.; Lucía, A.; Boraita, A.; Bayés-de-Luna, A. Left atrial enlargement in competitive athletes and atrial electrophysiology. Rev. Española Cardiol. (Engl. Ed.) 2022, 75, 421–428. [Google Scholar] [CrossRef]
  62. Ciuffo, L.; Bruña, V.; Martínez-Sellés, M.; de Vasconcellos, H.D.; Tao, S.; Zghaib, T.; Nazarian, S.; Spragg, D.D.; Marine, J.; Berger, R.D. Association between interatrial block, left atrial fibrosis, and mechanical dyssynchrony: Electrocardiography-magnetic resonance imaging correlation. J. Cardiovasc. Electrophysiol. 2020, 31, 1719–1725. [Google Scholar] [CrossRef]
  63. Aizawa, Y.; Watanabe, H.; Okumura, K. Electrocardiogram (ECG) for the prediction of incident atrial fibrillation: An overview. J. Atr. Fibrillation 2017, 10, 1724. [Google Scholar] [CrossRef] [PubMed]
  64. Tüukek, T.; Akkaya, V.; Atilgan, D.; Demirel, Ş.; ÖZCAN, M.; Güuven, Ö.; Korkut, F. Effect of left atrial size and function on P-wave dispersion: A study in patients with paroxysmal atrial fibrillation. Clin. Cardiol. 2001, 24, 676–680. [Google Scholar] [CrossRef] [PubMed]
  65. Ozyigit, T.; Kocas, O.; Karadag, B.; Ozben, B. Three dimensional left atrial volume index is correlated with P wave dispersion in elderly patients with sinus rhythm. Wien. Klin. Wochenschr. 2016, 128, 182–186. [Google Scholar] [CrossRef] [PubMed]
  66. De Clercq, D.; Van Loon, G.; Tavernier, R.; Duchateau, L.; Deprez, P. Atrial and ventricular electrical and contractile remodeling and reverse remodeling owing to short-term pacing-induced atrial fibrillation in horses. J. Vet. Intern. Med. 2008, 22, 1353–1359. [Google Scholar] [CrossRef]
  67. Decloedt, A.; Verheyen, T.; Van Der Vekens, N.; Sys, S.; De Clercq, D.; van Loon, G. Long-term follow-up of atrial function after cardioversion of atrial fibrillation in horses. Vet. J. 2013, 197, 583–588. [Google Scholar] [CrossRef]
  68. Hesselkilde, E.Z.; Carstensen, H.; Flethøj, M.; Fenner, M.; Kruse, D.D.; Sattler, S.M.; Tfelt-Hansen, J.; Pehrson, S.; Braunstein, T.H.; Carlson, J. Longitudinal study of electrical, functional and structural remodelling in an equine model of atrial fibrillation. BMC Cardiovasc. Disord. 2019, 19, 228. [Google Scholar] [CrossRef] [Green Version]
  69. Cheema, A.N.; Ahmed, M.W.; Kadish, A.H.; Goldberger, J.J. Effects of autonomic stimulation and blockade on signal-averaged P wave duration. J. Am. Coll. Cardiol. 1995, 26, 497–502. [Google Scholar] [CrossRef]
  70. Kose, S.; Kiliç, A.; İyisoy, A.; Kursaklioglu, H.; Lenk, M.K. P wave duration and P dispersion in healthy children. Turk. J. Pediatr. 2003, 45, 133–135. [Google Scholar]
  71. Yildiz, M.; Aygin, D.; Pazarli, P.; Sayan, A.; Semiz, O.; Kahyaoglu, O.; Yildiz, B.S.; Hasdemir, H.; Akin, I.; Keser, N. Assessment of resting electrocardiogram, P wave dispersion and duration in different genders applying for registration to the School of Physical Education and Sports–results of a single centre Turkish Trial with 2093 healthy subjects. Cardiol. Young 2011, 21, 545–550. [Google Scholar] [CrossRef] [PubMed]
  72. Pritchett, A.M.; Jacobsen, S.J.; Mahoney, D.W.; Rodeheffer, R.J.; Bailey, K.R.; Redfield, M.M. Left atrial volume as an index ofleft atrial size: A population-based study. J. Am. Coll. Cardiol. 2003, 41, 1036–1043. [Google Scholar] [CrossRef] [Green Version]
  73. Zucca, E.; Ferrucci, F.; Croci, C.; Di Fabio, V.; Zaninelli, M.; Ferro, E. Echocardiographic measurements of cardiac dimensions in normal Standardbred racehorses. J. Vet. Cardiol. 2008, 10, 45–51. [Google Scholar] [CrossRef]
  74. Young, L.; Rogers, K.; Wood, J. Left ventricular size and systolic function in Thoroughbred racehorses and their relationships to race performance. J. Appl. Physiol. 2005, 99, 1278–1285. [Google Scholar] [CrossRef] [PubMed]
  75. LONG, K.J.; Bonagura, J.; Darke, P. Standardised imaging technique for guided M-mode and Doppler echocardiography in the horse. Equine Vet. J. 1992, 24, 226–235. [Google Scholar] [CrossRef]
  76. Bakos, Z.; Vörös, K.; Järvinen, T. Two-dimensional and M-mode echocardiographic measurements of cardiac dimensions in healthy standardbred trotters. Acta Vet. Hung. 2002, 50, 273–282. [Google Scholar] [CrossRef] [PubMed]
Animals 13 01070 g001 550
Figure 1. Mean ± SD values for: (a) Pmin, (b) Pmax and (c) Pd for horses according to exercise status (** p < 0.005); *** p < 0.001; ns not significant).
Figure 1. Mean ± SD values for: (a) Pmin, (b) Pmax and (c) Pd for horses according to exercise status (** p < 0.005); *** p < 0.001; ns not significant).
Animals 13 01070 g001
Animals 13 01070 g002 550
Figure 2. Relationship between exercise duration (number of years raced) and (a) Pmax and (b) Pd.
Figure 2. Relationship between exercise duration (number of years raced) and (a) Pmax and (b) Pd.
Animals 13 01070 g002
Table
Table 1. Baseline details for non-active horses compared with those in race training.
Table 1. Baseline details for non-active horses compared with those in race training.
ParameterNon-Active (n = 24)Exercised (n = 29)p Value
Sex:
Male (gelding)6 (25%)15 (52%)0.048
Female18 (75%)14 (48%)
Age (years): Mean (SD)12.4 (2.9)5.4 (3.3)<0.001
Bodyweight (kg): Mean (SD)509 (41)449 (54)<0.001
Resting HR (bpm): Mean (SD)35 (4)37 (4)0.03
Table
Table 2. Univariable linear regression of the relationship between each variable and Pmin, Pmax and Pd. Means (standard deviations) for fixed effects, Sex, Exercise Status and Murmur, regression coefficients β (standard error) for covariates (Age, Bodyweight, Resting HR and Years raced),
Table 2. Univariable linear regression of the relationship between each variable and Pmin, Pmax and Pd. Means (standard deviations) for fixed effects, Sex, Exercise Status and Murmur, regression coefficients β (standard error) for covariates (Age, Bodyweight, Resting HR and Years raced),
Variable (n)PminPmaxPd
Mean (SD)p ValueMean (SD)p ValueMean (SD)p Value
Sex:
Female (32)120.0 (15.2)0.463161.6 (17.0)0.71741.6 (8.0)0.056
Gelding (21)117.7 (16.1)163.4 (18.0)46.0 (10.6)
Exercise Status:
Non-active (24)115.3 (20.5)0.355155.0 (20.8)0.01239.7 (6.9)0.003
Low intensity (14)122.1 (8.7)165.7 (8.9)43.6 (9.8)
High intensity (15)120.9 (9.5)170.7 (12.0)49.8 (9.5)
Murmur:
No (43)118.1 (16.1)0.445160.6 (17.5)0.05142.6 (9.0)0.020
Yes (6)123.3 (9.5)175.1 (7.5)51.9 (8.5)
β (SE)p Valueβ (SE)p Valueβ (SE)p Value
Age:−0.424 (0.473)0.358−0.575 (0.507)0.263−0.151 (0.278)0.591
Bodyweight:0.023 (0.039)0.5470.019 (0.042)0.650−0.004 (0.468)0.873
Resting HR:0.437 (0.477)0.1750.986 (0.564)0.0920.264 (0.313)0.402
Years raced:−0.118 (0.835)0.8861.038 (0.902)0.2551.156 (0.468)0.017
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

White, R.; Nath, L.; Hebart, M.; Franklin, S. Assessment of P Wave Indices in Healthy Standardbred Horses. Animals 2023, 13, 1070. https://doi.org/10.3390/ani13061070

AMA Style

White R, Nath L, Hebart M, Franklin S. Assessment of P Wave Indices in Healthy Standardbred Horses. Animals. 2023; 13(6):1070. https://doi.org/10.3390/ani13061070

Chicago/Turabian Style

White, Rebecca, Laura Nath, Michelle Hebart, and Samantha Franklin. 2023. "Assessment of P Wave Indices in Healthy Standardbred Horses" Animals 13, no. 6: 1070. https://doi.org/10.3390/ani13061070

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop