Affective temperaments (anxious, depressive, cyclothymic, irritable and hyperthymic) measure subclinical manifestations of major mood disorders. Furthermore, cumulating evidence suggests their involvement in somatic disorders as well. We aimed to assess associations between affective temperament scores and blood pressure and arterial stiffness parameters in hypertensive patients. In this cross-sectional study, 173 patients with well-controlled or grade 1 chronic hypertension, with no history of depression, completed the TEMPS-A, Beck Depression Inventory (BDI) and Hamilton Anxiety Scale (HAM-A) questionnaires in three GP practices. Arterial stiffness was measured with tonometry (PulsePen). According to multiple linear regression analysis, cyclothymic temperament score was positively associated with brachial systolic blood pressure independently of age, sex, total cholesterol, brachial diastolic blood pressure, BDI, HAM-A and the use of alprazolam (β = 0.529, p = 0.042), while hyperthymic temperament score was negatively related to augmentation index independent of age, sex, smoking, heart rate, BDI, HAM-A and the use of alprazolam (β = -0.612, p = 0.013). A significant interaction was found between cyclothymic temperament score and sex in predicting brachial systolic blood pressure (p = 0.025), between irritable and anxious temperament scores and sex in predicting pulse wave velocity (p = 0.021, p = 0.023, respectively) and an interaction with borderline significance between hyperthymic temperament score and sex in predicting augmentation index (p = 0.052). The present findings highlight elevated blood pressure among subjects with high cyclothymic temperament as well as an increased level of arterial stiffening in subjects with low hyperthymic scores suggesting that affective temperaments may play a role in the development of hypertension and arterial stiffening and may thus represent markers of cardiovascular risk. Sex differences were also present in these associations.

Brain-derived neurotrophic factor (BDNF) has neuroprotective, proangiogenic and myogenic effects and, therefore, possibly acts as a psychosomatic mediator. Here, we measured serum BDNF (seBDNF) level in hypertensive patients (HT) and healthy controls (CONT) and its relation to affective temperaments, depression and anxiety scales, and arterial stiffness parameters. In this cross-sectional study, affective temperaments, anxiety, and depression were studied with questionnaires (TEMPS-A, HAM-A, and BDI, respectively). SeBDNF level and routine laboratory parameters were measured as well. Arterial stiffness was evaluated with a tonometric method. Allover, 151 HT, and 32 CONT subjects were involved in the study. SeBDNF level was significantly higher in HT compared to CONT (24880 ± 8279 vs 21202.6 ± 6045.5 pg/mL, p < 0.05). In the final model of regression analysis, hyperthymic temperament score (Beta = 405.8, p = 0.004) and the presence of hypertension (Beta = 6121.2, p = 0.001) were independent determinants of seBDNF. In interaction analysis, it was found that in HT, a unit increase in hyperthymic score was associated with a 533.3 (95 %CI 241.3–825.3) pg/mL higher seBDNF. This interaction was missing in CONT. Our results suggest a complex psychosomatic involvement of BDNF in the pathophysiology of hypertension, where hyperthymic affective temperament may have a protective role. BDNF is not likely to have an effect on large arteries.

Background: Hypertension is a major risk factor of cardiovascular mortality. Mood disorders represent a growing public health problem worldwide. A complex relationship is present between mood disorders and cardiovascular diseases. However, less data is available about the level of depression and anxiety in different hypertension phenotypes. The aim of our study was to evaluate psychometric parameters in healthy controls (Cont), in patients with white-coat hypertension (WhHT), with chronic, non-resistant hypertension (non-ResHT), and with chronic, treatment-resistant hypertension (ResHT). Methods: In a cross-sectional study setup 363 patients were included with the following distribution: 82 Cont, 44 WhHT, 200 non-ResHT and 37 ResHT. The patients completed the Beck Depression Inventory (BDI) and the Hamilton Anxiety Scale (HAM-A). Results: BDI points were higher in WhHT (7 (3–11)) and ResHT (6 (3–11.5)) compared with Cont (3 (1–6), p < 0.05). Similarly, HAM-A points were higher in WhHT (8 (5–15)) and ResHT (10.5 (5.25–18.75)) compared with Cont (4 (1–7), p < 0.05) and also compared with non-ResHT (5 (2–10), p < 0.05). ResHT was independently associated with HAM-A scale equal or above 3 points (Beta = 3.804, 95%CI 1.204–12.015). WhHT was independently associated with HAM-A scale equal or above 2 points (Beta = 7.701, 95%CI 1.165–18.973) and BDI scale equal or above 5 points (Beta = 2.888, 95%CI 1.170–7.126). Conclusions: Our results suggest psychopathological similarities between white-coat hypertension and resistant hypertension. As recently it was demonstrated that white-coat hypertension is not a benign condition, our findings can have relevance for future interventional purposes to improve the outcome of these patients.

Background/objectives: Calculation of vascular age can help patients to understand the importance of adherence to a healthy lifestyle and medications. There are different methods of calculating vascular age, but different methods can provide different vascular age results. Our aim was to evaluate vascular age based on the Systematic Coronary Risk Evaluation (SCORE), Systematic Coronary Risk Evaluation 2 (SCORE 2) and Framingham Risk Score (FRS) methods. Methods: Subjects between the ages of 40–65 were involved. Vascular ages were defined based on SCORE, SCORE2 and FRS methods according to data from the literature. Results: In total, 141 patients were involved in the study; among them 94 had hypertension (HT) and 23 had white-coat hypertension. In the total population, SCORE2 and FRS vascular ages were higher compared to chronological age. SCORE2 and FRS vascular ages were higher than SCORE vascular age, and FRS vascular age was higher compared to SCORE2 as well. These tendencies were the same in the case of hypertensive patients and in patients with white-coat hypertension. In healthy patients, there were no differences between chronological age and vascular age. Conclusions: The differences found between the calculated vascular ages and the proportion of subjects with elevated vascular age warrant further comparison of different vascular age calculation methods.