| dc.description.abstract | Coping met emosionele stres kan óf effektief wees vir die neutralisering van stres óf dit kan negatiewe kardiovaskulêre uitkomste fasiliteer. Verdedigende-coping (DefS) en sosiale ondersteunings-coping is op effektiewe stresbestuur gemik, terwyl vermydings-coping gewoonlik fisiologiese verlies-van-beheer behels. In die Suid-Afrikaanse swart bevolking van die Sympathetic activity and Ambulatory Blood Pressure in Africans- (SABPA) studie, is DefS as synde oneffektief bewys. DefS het tot simpatiese hiperaktiwiteit, vaskulêre hiperresponsiwiteit, miokardiale skade en linkerventrikulêre wand-stres bygedra. Die swart bevolking het ook in die algemeen hoër kardiale stres reaktiwiteit tydens akute mentale stres getoon, in vergelyking met die wit bevolking. Verhoogde kardiale wand-stres gaan gewoonlik gepaard met die vrylating van biomerkers van kardiale stres, bv. kardiale troponien T (cTnT); N-terminale pro-brein natriuretiese peptied (NT-proBNP). Die stresrespons ontlok ook hipotalamiese-pituïtêre-adrenale (HPA) aksis-aktiwiteit en kopeptien/vasopressien vrystelling as ʼn akute kompenserende meganisme wanneer ʼn ontwrigting in volume-belading homeostase voorkom. Dit word ondersteun deur bevindings van verhoogde kopeptien-vlakke na kardiale stres en bewyse van kopeptien en kardiale stresmerkers [(cTnT); NT-proBNP)] wat klinies diagnostiese waarde inhou vir miokardiale infarksie, hartversaking en ventrikulêre hermodellering. Óf dit geld wanneer DefS toegepas word, is nie duidelik nie. Die wyse waarop DefS die HPA aksis-aktiwiteit, sowel as verbande tussen kopeptien, hemodinamiese reaktiwiteit en kardiale stresmerkers in rasgroepe sal beïnvloed, moet nog nagevors word.
Doelwitte
Die oorhoofse doelstelling van ons studie was om kennis uit te brei rakende coping, asook akute mentale stresresponse van kopeptien, slag-tot-slag bloeddruk (BD), cTnT en NT-proBNP. Die hoofdoelwitte was dus om vas te stel of akute mentale stresresponse van kopeptien, vaskulêre responsiwiteit, cTnT en NT-proBNP positief met mekaar geassosieer sal word in rasgroepe wanneer DefS toegepas word.
Metodes
Hierdie studie maak deel uit van die dwarsdeursnit, teikenpopulasie SABPA-studie (n=409), wat swart- sowel as wit verstedelike-onderwysers van beide geslagte (tussen 20 en 65 jaar oud) ingesluit het. Vir hierdie sub-studie is deelnemers met timpanum temperature bo 37.5°C, atriale fibrillasie, ʼn geskiedenis van miokardiale infarksie en/of beroerte, die teenwoordigheid van elektrokardiogram linkerventrikulêre hipertrofie, asook α- of ß-blokker gebruikers, en ‘n cTnT uitskieter (237.5 ng/L, selfmoord gepleeg) bykomend uitgesluit. Die finale studiesteekproef het bestaan uit 378 deelnemers.
Coping-strategieë is aan die hand van die Coping Strategie Indikator-vraelys bepaal. Akute mentale stresreaktiwiteit is bepaal deur die Stroop-Kleur-Woord-Konflik toets (Stroop-CWT) 1-minuut lank toe te pas. Slag-tot-slag BD, slagvolume (SV), kardiale omset (KO), arteriële meegewendheid en totale perifere weerstand (TPW) van die klein en groot arteries is deurlopend gemeet voor en tydens strestoetsing. Vastende bloedmonsters is ook voor en 10-minute post-strestoetsing geneem en vir kopeptien, cTnT en NT-proBNP geanaliseer. Interaksieterme vir hoofeffekte (ras x geslag x DefS) is vir risiko-merkers bereken. T-toetse vir onafhanklike groepe is gebruik om basislyn kenmerke van die twee rasse te bepaal. Chi-kwadraattoetse het proporsies en voorkoms bepaal. Twee-rigting ANCOVA’s het basislyn en akute mentale stresreaktiwiteit-response vergelyk deur oorweging te skenk aan a priori veranderlikes (ouderdom, middellyfomtrek, fisiese aktiwiteit, kotinien, gamma-glutamiel-transferase en oestradiol). Parsiële en meervoudige regressie-analises is uitgevoer om akute mentale stres risikomerker-assosiasies in verskeie modelle te bepaal terwyl oorweging geskenk is aan ‘n coping-strategie. Logistieke regressie-analises is bereken om die waarskynlikheid te bepaal van NT-proBNP persentasieverandering (%), copeptin% en TPR% om ʼn voorafbepaalde stresverwante cTnT afsnypunt van 4.2 ng/L in DefS-groepe te voorspel.
Resultate
Interaksie-effekte (p≤0.05) vir kopeptien% tydens die Stroop-CWT het die verdeling van deelnemers in ras- en DefS- (≥26, bo-mediaan-telling) groepe bepaal. In die DefS swart bevolking, het Stroop-CWT-blootstelling toenames in cTnT%, NT-proBNP%, diastoliese-BD% en TPW% teweeggebring. Geen rasverskille was vir kopeptien sigbaar nie. Weereens, by hierdie individue, met meervoudige regressie-analises, was positiewe assosiasies sigbaar tussen kopeptien% en TPW%; met inverse assosiasies tussen kopeptien% en cTnT% (p ≤ 0.05). Geeneen van hierdie assosiasies is by die DefS wit bevolking gevind nie. Voorts het TPW% die stresverwante cTnT afsnypunt van 4.2 ng/L slegs by die DefS swart bevolking voorspel.
Gevolgtrekking
Akute mentale stres by die DefS swart bevolking het kardiale wand-stres laat toeneem deur simpatiese hiperaktiwiteit en die kopeptien/vasopressien-stelsel (HPA-aksis aktiwiteit), wat koronêre hipoperfusie en kardiale skade potensieel teweegbring. Vermoedelike hipo-responsiewe HPA-aksis aktiwiteit tydens stresblootstelling kon egter nie koronêre perfusie tekorte via kopeptien/vasopressien-vrystelling teenwerk nie. Die teenwoordigheid van verdedigende-coping kan kliniese implikasies vir voorkomende kardiologie inhou.
Coping with emotional stress can either be effective for stress neutralisation or it may facilitate negative cardiovascular outcomes. Defensive coping (DefS) and social support coping are aimed at effective stress management, while avoidance coping usually involves physiological loss-of-control. In South African Blacks from the Sympathetic activity and Ambulatory Blood Pressure in Africans (SABPA) study, DefS proved to be ineffective. DefS contributed to sympathetic hyperactivity, vascular hyper-responsiveness, myocardial injury and left ventricular wall stress. The Blacks also presented with overall higher cardiac stress reactivity during acute mental stress testing, compared to Whites. Elevated cardiac wall stress is usually accompanied by the release of biomarkers of cardiac stress e.g. cardiac troponin T (cTnT); N-terminal pro-brain natriuretic peptide (NT-proBNP). The stress response also elicits hypothalamic-pituitary-adrenal (HPA) axis activity and copeptin/vasopressin release as an acute compensatory mechanism when there is a disruption in volume-loading homeostasis. This is supported by findings of increased copeptin levels following cardiac stress and evidence of copeptin and cardiac stress markers [(cTnT); NT-proBNP)] having clinical diagnostic value in myocardial infarction, heart failure and ventricular remodelling. Whether this holds true when DefS is utilised, is not clear. The manner in which DefS will influence HPA axis activity and associations between copeptin, hemodynamic reactivity and cardiac stress markers in race groups, needs to be investigated.
Objectives
The main aim of our study was to expand knowledge on coping, as well as acute mental stress responses of copeptin, beat-to-beat BP, cTnT and NT-proBNP. Therefore, the main objectives were to determine whether acute mental stress responses of copeptin, vascular responsiveness, cTnT and NT-proBNP will differ between racial groups when utilising DefS. Furthermore, we also aimed at establishing whether acute mental stress responses of copeptin, vascular responsiveness, cTnT and NT-proBNP will be positively associated with one another in racial groups when utilising DefS.
Methods
This study forms part of the cross-sectional, target population SABPA study (n=409), which included both black- and white urban-dwelling teachers of both sexes (aged 20-65 years). For this sub-study, participants with tympanum temperatures above 37.5°C, atrial fibrillation, a history of myocardial infarction and/or stroke, the presence of electrocardiographic left ventricular hypertrophy, as well as α- or ß-blocker users, and a cTnT outlier (237.5 ng/L, committed suicide) were additionally excluded. The final study sample comprised 378 participants.
Coping strategies were determined by applying the Coping Strategy Indicator questionnaire. Acute mental stress reactivity was determined by utilising the Stroop-Colour-Word-Conflict test (Stroop-CWT) for 1-minute. Beat-to-beat BP, stroke volume (SV), cardiac output (CO), arterial compliance and total peripheral resistance (TPR) of the small and large arteries were continuously measured prior to and throughout stress testing. Fasting blood samples were also taken prior to and 10-minutes post-stress testing and analysed for copeptin, cTnT and NT-proBNP. Interaction terms on main effects (race х sex х DefS) for risk markers were computed. T-tests for independent groups were used to determine baseline characteristics of the two races. Chi-square tests determined proportions and prevalence. Two-way ANCOVAs compared baseline and acute mental stress reactivity responses considering a priori covariates (age, waist circumference, physical activity, cotinine, gamma-glutamyl transferase and oestradiol). Partial and multiple regression analyses were used to determine acute mental stress risk marker associations in various models considering coping style. Logistic regression analyses were computed to determine the probability of NT-proBNP percentage change (%), copeptin% and TPR% to predict a previously derived stress-related cTnT cut-point of 4.2 ng/L in DefS groups.
Results
Interaction effects (p≤0.05) for copeptin% during the Stroop-CWT determined stratification of participants into race and DefS (≥26, above-median score) groups. In DefS Blacks, Stroop-CWT exposure elicited increases in cTnT%, NT-proBNP%, diastolic-BP% and TPR%. No race differences were apparent for copeptin. Again, in these individuals, in multiple regression analyses, positive associations were evident between copeptin% and TPR%; with inverse associations between copeptin% and cTnT% (p≤0.05). None of these associations were found in DefS Whites. Furthermore, TPR% predicted the stress-related cTnT cut-point of 4.2 ng/L in DefS Blacks only.
Conclusions
Acute mental stress in DefS Blacks increased cardiac wall stress through sympathetic hyperactivity and the copeptin/vasopressin system (HPA axis activity), potentially inducing coronary hypo-perfusion and cardiac injury. However, presumably hypo-responsive HPA axis activity during stress exposure could not counteract coronary perfusion deficits via copeptin/vasopressin release. The presence of defensiveness may have clinical implications in preventive cardiology. | en_US |
