International Journal of Cardiology 166 (2013) 627–632

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International Journal of Cardiology

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Central hemodynamics and arterial stiffness during the finals of the world cup soccerchampionship 2010

Michael Reppel a,⁎, Klaas Franzen a, Frank Bode a, Joachim Weil a, Volkhard Kurowski a,Susanne Annika Schneider b, Johannes Baulmann a, Tobias von Lukowicz a, Wladimir Mirau a,Eva Mortensen a, Siegfried Wassertheurer c, Heribert Schunkert a, Kai Mortensen a

a Dept. of Cardiology, University of Luebeck, Luebeck, Germanyb Dept. of Neurology, University of Luebeck, Luebeck, Germanyc Health and Environment, Austrian Institute of Technology, Vienna, Austria

⁎ Corresponding author at: Dept. of Cardiology , Medicburger Allee 160, 23538 Lübeck. Tel.: +49 451 5002501

0167-5273/$ – see front matter © 2011 Elsevier Irelanddoi:10.1016/j.ijcard.2011.11.096

a b s t r a c t

a r t i c l e i n f o

Article history:

Received 11 April 2011Received in revised form 19 September 2011Accepted 26 November 2011Available online 21 December 2011

Keywords:Arterial stiffnessCentral hemodynamicsEmotional stressSoccer world cup

Background: Emotional stress is considered a risk factor for cardiovascular events, the underlying pathophys-iology remains unclear.Methods: To evaluate how emotional stress effects hemodynamics, thirteen healthy German soccer fans(mean 37.6 years, 24–56 years) were studied during live TV coverage of the finals with German nationalteam participation (GP) and the respective finals without German participation (noGP). Peripheral bloodpressure, heart rate, central blood pressure, augmentation pressure and index, cardiac output and peripheralresistance were measured.Results: In the 1st hour before the match all parameters were not significantly different between the groups. Inthe GP group peripheral systolic pressure (1st halftime noGP 118±1(s.e.m) versus GP 126±2mmHg, pb0.05,2nd 117±1 vs. 125±2mmHg, pb0.05), mean blood pressure, diastolic blood pressure, heart rate (1st 73±2

vs. 86±3 bpm, pb0.05, 2nd 75±2 vs. 87±2 bpm, pb0.05), cardiac output (1st 4,4±0,1 versus 4,8±0,1 L/min,pb0.05, 2nd 4,6±0,1 versus 4,7±0,11 L/min, p>0.05) and peripheral resistance were significantly increasedcompared to the noGP group during the matches. Systolic central aortic pressure (noGP: 101±2 versus GP107±2 mmHg, pb0.05) and central pulse pressure (noGP: 31.3±1.3 mmHg vs. GP: 38.5±2.7 mmHg,pb0,05) remained elevated during the second hour after the match.Conclusions: We observed persistent changes in central hemodynamics 2 h after emotional stress. Despitenormalization of peripheral values after the end of the finals, we observed prolonged elevation of centralsystolic blood and pulse pressure. Our findings contribute to the understanding of the increased risk of car-diovascular events in emotional stress.

© 2011 Elsevier Ireland Ltd. All rights reserved.

1. Introduction

Emotional stress during World Cup Soccer is associated with anincrease of the risk of an acute cardiovascular event [1]. An interestingprospective study by Wilbert-Lampen and coworkers during the FIFAWorld Cup 2006 in the greater Munich area showed that the riskmore than doubled on days when the German national team played.In more detail, the incidence of cardiovascular emergencies such asacute myocardial infarction and cardiac arrhythmia was two tothree times that of the control period [1]. The highest incidence ofevents was observed during the first two hours after kick-off, butwas still increased during the hours after full time. Interestingly the

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number of deaths due to myocardial infarction in this setting wasnot increased compared to a matched control period [2].

Already during theWorld Cup 1998 in France the risk of admissionfor acute myocardial infarction in a British population was increasedby approximately 25% on the 30th of June 1998, the day Englandlost against Argentina in a penalty shoot-out, and, most importantly,also during the following two days [3]. Likewise, in a Dutch popula-tion cardiovascular mortality in terms of death from all causes andfrommyocardial infarction or stroke was found to be increased by ap-proximately 50% during the quarter final match of the EuropeanChampionship 1996 between Netherlands and France [4]. In linewith these observational data Chida et al. demonstrated in a metaana-lysis that greater responsitivity to acute laboratory mental stress hasan adverse effect on the future cardiovascular risk status [5].

Beside an increase of serum profiles of inflammatory and vasocon-strictive factors that was observed in patients suffering from emo-tional stress-induced acute coronary syndrome during the World

628 M. Reppel et al. / International Journal of Cardiology 166 (2013) 627–632

Cup Soccer matches in the Munich population [6], one might also as-sume profound changes of central hemodynamics due to the relatedemotions as an underlying reason. However, little is known aboutthe effects of real-life emotional stress [7] such as viewing WorldCup Soccer matches and associated emotions on peripheral and espe-cially central hemodynamics.

Recently, central hemodynamic indexes and parameters of arterialstiffness such as central aortic pressures, augmentation index (AIx)and pulse wave velocity were recognized as strong independent pre-dictors of cardiovascular events and all-cause mortality [8–10]. As aconsequence, central hemodynamics and arterial stiffness parametersare increasingly used for risk stratification purposes [11,12]. Althoughthe European Society of Hypertension/ European Society of Cardiolo-gy guidelines for the management of arterial hypertension suggestedthe measurement of arterial stiffness parameters as a tool for assess-ment of subclinical target organ damage [12], the effects of emotionalstress on these surrogate markers have not yet been fully evaluated.The aim of the study was therefore to determine the effects of real-life emotional stress on central and peripheral hemodynamics aswell as on arterial stiffness parameters.

2. Materials and methods

2.1. Study population and measurement setup

Thirteen healthy (no drug intake, no dyslipidemia, no mental disorders or ecg ab-normalities, no diabetic or hypertensive subject, Karnofsky Index was 100% in eachproband) German soccer fans ( 7 women, 6 men, mean age 37.6 years, range 24–56 years, mean height 176.5 cm, range 164–192 cm, mean weight 71.9 kg, range56–97 kg, mean body mass index 23, range 19.3–26.9) were studied during the 2010Soccer World Championships eighthfinal, quarterfinal and semifinal games for effectsof match-induced emotional stress on peripheral and central hemodynamics. The Insti-tutional Ethics Committee gave approval. All participants gave informed consent andwere asked to watch the final games on television in familiar surroundings, and notto drink alcohol and smoke before and during the matches. None of the subjects hadpreviously taken part in any mental stress study. Generally, measurements werestarted 2 h before kick-off, performed every 15 min and were abandoned 2 h afterthe end of the match. The final games with German participation (GP) were matchedwith controls, i.e. corresponding games without German participation (noGP) in thesame study population in order to ensure emotional neutrality. The matches includingresults and the partially different time points during which hemodynamics were stud-ied are listed in Table 1. The study conformed to the Declaration of Helsinki. The au-thors of this manuscript have certified that they comply with the Principles of EthicalPublishing in the International Journal of Cardiology.

2.2. Pulse wave analysis

In all participants the Mobil-O-Graph® (software version HMS CS 4.1, I.E.M. GmbH,Stolberg, Germany), calculating peripheral and central hemodynamics noninvasivelyby pulse wave contour analysis, was used. Validation studies were recently published[13,14]. This novel method determines hemodynamics based on oscillometric bloodpressure measurement with a common cuff at the arteria brachialis [13]. The record-ings were carried out at diastolic pressure level for approximately 10 s using conven-tional blood pressure cuffs for adults and a high fidelity pressure sensor (MPX5050,Freescale Inc., Tempe, AZ, USA). Physiological variations in recording pressure are po-tentially compensated by trend analysis, otherwise the reading is discarded. Beforemeasurements, the cuff size was adapted to the arm circumference and fixed to thenon-dominant arm. The device was set to obtain automatic recordings every 15 min,2 h before, after the game, and of course during the entire matches.

The proportion of the reflected pressure wave is assessed through the augmenta-tion index and it is calculated as the ratio between augmentation pressure and pulsepressure [11].

Table 1Matches during which measurements were performed. noGP (no German participa-tion) versus GP (German participation).

noGP GP

Eightsfinals Argentina:Mexico(3:1, 6/27/2010, 8:30p.m)

Germany:England(4:1, 6/27/2010, 4:00p.m)

Quarterfinals Paraguay:Spain(0:1, 7/3/2010, 8:30p.m)

Argentina:Germany(0:4, 7/3/2010, 4:00p.m)

Semifinals Uruguay:Netherlands(2:3, 7/6/2010, 8:30p.m)

Germany:Spain(0: 1, 7/7/2010, 8:30p.m)

2.3. Peripheral and central hemodynamic parameters

The following parameters were measured/ calculated by the device as reported re-cently [13]: (i) Peripheral systolic-, (ii) mean-, and (iii) diastolic blood pressure, (iv)heart rate, (v) central systolic-, and (vi) diastolic blood pressure, (vii) augmentationpressure, (viii) augmentation index corrected for heart rate (Aix75), (ix) cardiac out-put, and (x) peripheral resistance. Central parameters were estimated by a generalizedtransfer function [13,14]. From (i) and (iii) and from (v) and (vi) peripheral and centralpulse pressure were calculated respectively. Pulse pressure amplification (peripheralpulse pressure/ central pulse pressure), has been shown to be of prognostic value(higher pulse pressure amplification=lower cardiac risk [15]).

2.4. Statistical analysis

For the systolic peripheral blood pressure a total of 239 and 212 measurementscould be obtained successfully and were analysed for noGP and GP matches respective-ly. For the mean blood pressure 235 and 215, for diastolic blood pressure 240 and 215,for heart beat analysis 240 and 215, and for the central systolic blood pressure, centraldiastolic blood pressure, the AIx75, and the measurement of cardiac output, 168 and151 values could be obtained, respectively. Student's t tests using SigmaStat (Chicago,IL, USA) software were performed to compare individual time points of noGP and GPmatches. ANOVA was performed to evaluate statistical differences in-between the dif-ferent time points of measurements. A p-value of b0.05 was considered statisticallysignificant. Our statistics are presented as mean values±s.e.m.

3. Results

3.1. Effects of emotional stress on peripheral hemodynamics

In the GP group soccer-induced emotional stress evoked a signifi-cant increase of peripheral systolic pressures (Fig. 1a). Measurementsstarted 2 h before kick-off. Already at this time point peripheral sys-tolic blood pressure was found to be increased by approximately 6%(116±2 versus 123±1 mmHg, p=0.006) as compared to the noGPgroup. In the noGP group peripheral systolic blood pressure rose inthe last hour before kick-off to almost similar levels as in the GPgroup (121±1 versus 121±2 mmHg, n.s.), followed by a sustaineddecrease throughout and after the matches. During the matches pe-ripheral systolic blood pressure was significantly elevated in the GPgroup by approximately 7% (1st halftime 118±1 versus 126±2mmHg, pb0.001, 2nd halftime 117±1 versus 125±2 mmHg,p=0.007). Also in the GP group a sustained decrease of systolic pres-sures was observed after the matches. See Table 2 for details. Regard-ing ANOVA, the following statistical significances were found for theGP group and noGP group respectively: GP: −2 h, 1st half, and 2ndhalf versus +2 h; noGP: −1 h, 1st half, and +1 h versus +2 h.

Similarly, peripheral mean and diastolic blood pressures were foundto be elevated throughout the matches with a significant decrease afterthe end of the games. See Table 2 for details. Accordingly, ANOVArevealed for both the noGP and the GP group for themean blood pressurevalues significant differences for all time points as compared with +2 h.For diastolic RR values significant differences were found for the follow-ing time points: noGP: −2 h, −1 h, and 1st half versus +2 h, whereasfor the GP group all time points were found to be significantly differentin comparison to the +2 h time point.

The effects on pulse pressure are shown in Fig. 1D. No significantdifferences were found between the noGP and GP group. Also forANOVA no significant differences were found for both groups.

3.2. Effects of emotional stress on heart rate

As for the peripheral blood pressure behaviour similar observa-tions were made for heart rate (Fig. 2). In the GP group heart ratewas significantly elevated in the 2nd hour before kick-off by approx-imately 20% (68±2 versus 81±2 bpm, pb0.001) and throughout thematches (Table 2), but normalized until the 1st hour after the match.In addition, a further decline was observed between the 1st and 2ndhour after the end of the games (Table 2). Accordingly, in the noGPgroup ANOVA revealed significant differences between the followingtime points: −2 h and −1 h versus +2 h and −2 h versus −1 h. For

Fig. 1. Peripheral hemodynamics. A) Peripheral systolic blood pressure, B) mean systolic blood pressure, C) diastolic blood pressure, and D) peripheral pulse pressure shown forfinal matches without German participation (noGP) and matches with German participation (GP).

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the GP group significant differences were found for: −2 h, 1st half,2nd half, and +1 h versus +2 h, and −1 h versus 1st half as well asversus 2nd half.

3.3. Effects of emotional stress on central hemodynamics

Although for both groups a similar behaviour of the central systolicblood pressurewas observed during thematches, one striking differencebecame evident: compared to the noGP group and despite the sustaineddecline of the central blood pressure per se it was still higher in the GPgroup during the 1st and 2nd hour after the matches as compared tothenoGP group (Fig. 3, Table 2). For the noGP groupANOVA revealed sig-nificance for−1 h versus+2 h, whereas in the GP group no significancewas found in-between the different time points.

In contrast to these striking differences, the central diastolic bloodpressure showed the samekinetics as the peripheral pressures. RegardingANOVA we found statistical differences for the following time points inthe noGP group: −2 h, −1 h, 1st half versus +2 h (noGP group). Forthe GP group all time points were significantly different in comparisonto the +2 h value.

Thus, pulse pressure was elevated for at least 2 h after stress in theGP group (Fig. 3C, Table 2). Accordingly, no significant differenceswere found with ANOVA in the noGP group whereas −2 h, −1 h, 1stand 2nd half were all significantly different as compared to the +2 htime point (Fig. 3C).

The augmentation index and augmentation pressure (data notshown) showed no significant changes during the matches (neither

for ANOVA nor for the individual time points in the noGP and GPgroup). However, presumably due to the strong decline of heart rate,augmentation pressure rose in the 2nd hour after the GP groupmatches(5.2±1 versus 9.2±3 mmHg). Nevertheless, and despite this cleartrend, these differences were statistically not significant (p=0.1). Theaugmentation index corrected for heart rate (AIx75) showed a signifi-cant increase (see Fig. 4) during the 1st halftimes in the GP group(14.1±2.1 versus 20.9±2.2, p=0.028). Although this observationwas similar for the second halftimes (13.5±2.1 versus 18.9±2.2), thedifference failed to reach statistical significance (p=0.09). No signifi-cant differences were observed for AIx75 before or after the matches(ANOVA p>0.05). Cardiac output was significantly elevated in the 1sthalftimes of GP group matches (4.4±0.1 versus 4.8±0.1 L/min,p=0.002), whereas at other time points it did not reach statistical sig-nificance. Regarding ANOVAwe found significant differences for cardiacoutput in the noGP group (−1 h and 2nd half versus+2 h) aswell as inthe GP group (1st half and 2nd half versus+2 h). Peripheral resistancewas significantly elevated during the 2nd halftimes in the GP group(1.14±0.03 versus 1.21±0.02×105 dyn×sec×cm−5, pb0.05). SeeTable 2 for the detailed results and statistical analysis. No significant dif-ferences were found with ANOVA.

Data for pulse pressure amplification are shown in Table 2. Statisticalanalysis revealed significant differences between noGP and GP at−2 h.ANOVA did not reveal any significance in the noGP group whereas inthe GP group significant lower pulse pressure amplification valuescould be documented 2 h after the end of the matches (as comparedto the following time points: −2 h, 1st half time, and 2nd half time).

Table 2Statistical analysis for the parameters that were studied. Values are axpressed as mean±s.e.m.. * Indicates statistical significance (pb0.05). See also figures for absolute p-values.

−2 h −1 h 1st half 2nd half +1 h +2 h

Peripheral sysRRnoGP 116.3±1.8 121.0±1.3 118.3±1.4 117.1±1.4 118.1±1.9 110.8±2.0GP 123.1±1.4* 121.0±1.8 126.2±1.8* 125.0±1.7* 121.1±1.7 112.6±1.6

Peripheral mean RRnoGP 96.4±1.8 97.7±1.1 95.0±1.3 93.8±1.3 93.4±1.7 87.4±1.7GP 101.2±1.0* 97.9±1.4 102.0±1.6* 100.3±1.4* 97.0±1.5 88.0±1.5

Peripheral diast RRnoGP 79.3±2.1 78.1±1.3 75.3±1.5 74.0±1.5 72.6±1.8 67.6±1.8GP 82.5±1.3 78.5±1.6 81.4±1.7* 79.3±1.6* 76.6±1.7 67.3±1.9

Peripheral PPnoGP 37.0±1.8 42.9±1.3 43.0±1.2 43.1±1.3 45.5±1.6 43.2±1.8GP 40.6±1.7 42.4±1.7 44.8±1.6 45.7±1.6 44.5±1.7 45.3±1.9

Heart ratenoGP 68.2±2.0 78.4±1.7 72.6±1.9 74.5±1.7 76.1±1.8 69.5±2.0GP 81.2±2.0* 77.0±2.2 85.8±2.6* 86.7±2.3* 80.6±1.9 68.2±2.7

Aortic sys RRnoGP 108.6±2.2 109.8±1.6 107.9±1.6 105.4±1.3 106.2±1.7 100.9±1.8GP 112.1±1.5 110.1±1.9 112.5±1.9 112.7±1.8* 110.4±1.7 106.9±1.8*

Aortic diast RRnoGP 80.7±2.6 80.0±1.5 78.0±1.6 75.8±1.6 75.6±1.9 69.6±2.1GP 84.5±1.4 80.4±1.7 83.1±1.8* 83.2±1.6* 78.7±1.8 68.4±2.0

Aortic PPnoGP 27.9±1.8 29.7±1.3 29.9±1.2 29.6±1.1 30.7±1.2 31.3±1.3GP 27.6±1.5 29.8±1.7 29.4±1.2 29.5±1.3 31.7±1.3 38.5±2.7*

PP amplificationnoGP 1.35±0.05 1.48±0.07 1.49±0.05 1.53±0.05 1.47±0.04 1.38±0.04GP 1.52±0.04* 1.46±0.05 1.60±0.06 1.58±0.05 1.44±0.04 1.24±0.06

Alx@75noGP 12.7±3.6 18.1±2.7 14.1±2.1 13.5±2.1 17.5±2.3 16.1±2.8GP 18.4±2.6 12.2±2.3 20.9±2.2* 18.9±2.2 19.7±2.3 16.2±5.4

cardiac outputnoGP 4.4±0.1 4.6±0.1 4.4±0.1 4.6±0.1 4.5±0.1 4.2±0.1GP 4.6±0.1 4.6±0.1 4.85±0.1* 4.7±0.1 4.6±0.1 4.2±0.2

augm. pressurenoGP 3.4±0.9 3.9±0.7 4.5±0.8 3.5±0.7 4.9±0.9 5.2±1.0GP 4.1±0.8 3.2±1.0 4.0±0.7 4.0±0.8 5.3±0.9 9.2±2.8

periph.resistancenoGP 1.23±0.03 1.19±0.02 1.23±0.02 1.14±0.03 1.17±0.03 1.18±0.04GP 1.27±0.02 1.19±0.03 1.20±0.02 1.21±0.02* 1.19±0.03 1.20±0.06

630 M. Reppel et al. / International Journal of Cardiology 166 (2013) 627–632

4. Discussion

This study shows the acute changes in central blood pressure dur-ing and immediately after long lasting (≥90 min) periods of real lifeemotional stress. In more detail, we observed relevant effects on cen-tral and peripheral hemodynamics, heart rate, cardiac output, periph-eral resistance and heart rate corrected AIx in apparently healthysoccer fans watching the World Cup 2010 finals. Furthermore, wedemonstrated subacute adverse effects, lasting for at least 2 h afterthe final whistle, for central pressures, i.e. elevated central systolicpressure and central pulse pressure. Interestingly, we found a

Fig. 2. Heart rate analysis.

sustained elevation of the central systolic blood pressure togetherwith a faster decline of the diastolic central blood pressure, whichled to a delayed increase in central pulse pressures and worseningpulse pressure amplification 2 h after the matches, thus pointing toendothelial dysfunction [16–18].

Arterial stiffness parameters and central hemodynamics are inde-pendent prognostic predictors of cardiovascular and coronary events,stroke, cardiovascularmorbidity, mortality, and overall mortality in dif-ferent populations [8,9,19–23]. This was recently confirmed in twometa analyses with over five thousand subjects and a mean follow-upof 3.8 years [8] and over fifteen thousand subjects and a mean follow-up of 7.7 years [9]. Beside others, arterial stiffness and wave reflectionshave a causative role in the pathogenesis of systolic hypertension andcoronary artery disease and events [11,24]. Most importantly, centralhemodynamics have been found to be superior to peripheral pressuresin predicting outcome and determining cardiovascular risk [19,25–27].

Only limited data exist for acute effects of different emotionalstress models on arterial stiffness indices, central and peripheral he-modynamics and for their combination [28–30]. These data and astudy evaluating mental stress-induced effects on endothelial dys-function [31] revealed post stress prolonged (up to 90 min) negativeeffects on central hemodynamics, arterial stiffness, and endothelialdysfunction. Nevertheless, most previous studies have focused onchronic negative effects of laboratory stressors on cardiovascular out-comes [32] or on the association of acute laboratory mental stress andmainly peripheral hemodynamics [33]. Interestingly, these studiescould prove that a strong cardiovascular response is associated witha subsequent poor cardiovascular risk status [5].

Fig. 3. Central aortic pressures. A) Central systolic blood pressure, B) Central diastolicblood pressure and C) pulse pressure. noGP: Matches without German participation,GP: Matches with German participation.

Fig. 4. Augmentation index corrected for heart rate (Aix@75).

631M. Reppel et al. / International Journal of Cardiology 166 (2013) 627–632

Our present study is per se in line with existing data of acute men-tal stress and effects on peripheral [5] and central hemodynamics andarterial stiffness [28–30]. We could show for the first time that in ourreal-life observation a continuous, long lasting stressor leads to a per-sistent stress response in terms of enhanced peripheral and centralblood pressures, heart rate, cardiac output, peripheral resistance,and heart rate corrected AIx. Furthermore, we found an instant nor-malization of heart rate and peripheral blood pressures after thematches, whereas central systolic blood pressure and pulse pressureremained elevated. The lower pulse pressure amplification 2 h afterthe matches in the GP group may be indicative for increased cardio-vascular risk [15].

Thus, this suggests that the increased risk of cardiovascular eventsand delayed onset of symptoms observed during and after the FIFAWorld Cup finals 2006 in the greater Munich area [1] may be, atleast in part, explained by these findings and would not have beenexplained by solely studying peripheral blood pressures. Also the25% increase of cardiovascular events in the British population onthe 30th of June 1998 and the following two days -the day Englandlost against Argentina in a penalty shoot-out [3]- may be based onthe prolonged elevation of the central systolic pressure. As it hasbeen recently reported that acute mental stress results in an increaseof catecholamines [34,35], a rise of catecholamine levels during thematches might largely serve as an explanation for the unfavorable ef-fects on peripheral and central hemodynamics. Moreover, one mightassume that the increase of inflammatory and vasoconstrictive factors[6], which was observed during the World Cup Soccer matches in theMunich population, might contribute to endothelial dysfunction andexplain especially the long lasting effects on central hemodynamicsin our study. Consistently, a briefer period of mental stress results inprolonged endothelial dysfunction [31] and an elevation of interleu-kin levels was found for up to 2 h after mental stress [36]. Important-ly, our findings may have an even higher clinical impact on diseasedsubjects such as patients with coronary heart disease [37], diabetes,hypertension and/or heart failure. One could hypothesize that(a) strict stress prevention, (b) nonpharmacological approaches [38]and “Behavioural Cardiology”, a term coined by Rozanski et al. [39],both reducing stress-induced adverse effects on hemodynamics andon the heart, (c) adjustment of medical regimens before, during,and after emotional stress, and/or (d) intensified medical care [37]may reduce cardiovascular events. These issues should be addressedin future prospective trials.

5. Conclusions

We observed persistent changes in central hemodynamics 2 hafter emotional stress. Despite normalization of peripheral valuesafter the end of the finals, we observed prolonged elevation of centralsystolic blood and pulse pressure. Our findings contribute to the un-derstanding of the increased risk of cardiovascular events in emotion-al stress. Future prospective trials addressing this topic are needed.

5.1. Study limitations

Although changes due to acute emotional stress have been de-scribed recently, [28] pulsewave velocity is principally used as amarkerfor chronic and structural deteriorations of arterial stiffness [11,40]. Un-fortunately, we could not determine pulse wave velocity since theMobil-O-Graph® did not offer these measurements at that time. So farthe Mobil-O-Graph® is validated for AIx, central systolic pressure andperipheral blood pressure [13,14,41]. This study consisted of a healthy

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and younger population. Therefore, our resultsmay not be applicable toother populations such as patients suffering from cardiac diseases and/or cardiovascular arteriosclerosis. Despite the limited number of partic-ipants a relatively high number of measurements were achieved. As afurther limitation, it has to be noted that not all matches started at thesame time point (see Table 1). In more detail, in the noGP group allthree kick-offs were at 08:30 p.m., whereas in the GP group only onekick-off was at 08:30 p.m. and the other two at 4:00 p.m. The measure-ments were performed in sitting position whereas most of the evalua-tion studies were performed in lying position. Since a recent study[42] could detect a close agreement between supine and sitting mea-surements, and since the subjects were the same for noGP and GPmatches, we do not assume a major influence on our results. We didnot determine catecholamines during the study which could have pro-vided additional information about the relation between arterial stiff-ness and catecholamine concentrations since taking blood samplesmight have influenced hemodynamics.

Acknowledgement

The authors would especially like to thank the German NationalSoccer Team and their coach Joachim (Jogi) Löw for playing bracing,powerful and successful games during the World Cup Soccer Champi-onship in South Africa. Furthermore, we would like to thank all pro-bands for participating in the study.

The authors of this manuscript have certified that they complywith the Principles of Ethical Publishing in the International Journalof Cardiology.

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