How does stress possibly affect cardiac remodeling?

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The aim of this study was to evaluate the predictive value of adrenocorticotropic hormone (ACTH), cortisol and ACTH receptor polymorphism (ACTHRP) for left ventricular (LV) remodeling. Thirty-six elite male athletes, as chronic stress adaptation models, and twenty sedentary age and sex-mached subjects emabarked on standard and tissue Doppler echocardiography to assess cardiac parameters at rest. They performed maximal cardiopulmonary test, which was used as an acute stress model. ACTH and cortisol were measured at rest (10 min before test), at beginning, at maximal effort, at 3rd min of recovery, using radioimmunometric and radioimmunoassey techniques, respectively. Promoter region of ACTHR gene (18p11.2) was analysed from blood samples using reverse polymerization reaction with the analysis of restriction fragment length polimorphisam by SacI restriction enzyme. Normal genotype was CTC/CTC, heterozygot for ACTHRP CTC/CCC and homozygot CCC/CCC. In all participants, ACTH and cortisol increased during acute stress, whereas in recovery ACTH increased and cortisol remained unchanged. 49/56 examiners manifested CTC/CTC, 7/56 CTC/CCC and 0/56 CCC/CCC. There was no difference in ACTHRP frequency between groups (Symbol, p = 0.67). LV mass (LVM) and LV end-diastolic volume (LVVd) were higher in athletes than in controls (p < 0.01) and lower in CTC/CTC than in CTC/CCC genotype (219.43 ± 46.59(SD)g vs. 276.34 ± 48.86(SD)g, p = 0.004; 141.24 ± 24.46(SD)ml vs. 175.29 ± 37.07(SD)ml, p = 0.002; respectively). In all participants, predictors of LVM and LVVd were ACTH at rest (B = −1.00,−0.44; β = −0.30,−0.31; p = 0.026,0.012, respectively) and ACTHRP (B = 56.63,34; β = 0.37,0.40; p = 0.003,0.001, respectively). These results demonstrate that ACTH and ACTHRP strongly predict cardiac morphology suggesting possible regulatory role of stress system activity and sensitivity in cardiac remodeling.

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