The impact of apelin and relaxin plasma levels in masked hypertension and white coat hypertension.

Masked hypertension (HTN) and white coat hypertension represent two reverse forms of clinical HTN with questionable prognostic significance. Recent evidence supports that low apelin and relaxin plasma levels contribute to vascular damage accelerating atherogenesis and predisposing to HTN and cardiovascular (CV) events. The aim of this study was to compare apelin and relaxin plasma levels between patients with masked hypertension (MH) and those with white coat HTN (WCH). Overall, 130 patients not receiving antihypertensive therapy were studied. All patients underwent 24-hour ambulatory BP monitoring (ABPM) and office BP measurements. Plasma apelin and relaxin levels were measured by ELISA method. According to BP recordings, 24 subjects had MH (group A) and 32 had WCH (group B). Apelin (200 ± 111 pg/mL vs 305 ± 127 pg/mL, P < 0.01) and relaxin (35.2 ± 6.7 pg/mL vs 46.8 ± 23.6 pg/mL, P < 0.01) plasma levels were significantly lower in patients with MH compared to those with WCH, respectively. In conclusion, our findings showed that patients with MH had significantly lower apelin and relaxin levels compared to those with WCH. This observation implies an additional prognostic role for adipokines supporting the concept that MH is closer to essential HTN whereas WCH is a more benign condition.

Asymmetric dimethylarginine levels are associated with augmentation index across naïve untreated patients with different hypertension phenotypes.

Asymmetric dimethylarginine (ADMA) is a robust marker of endothelial dysfunction in patients with essential hypertension. We investigated ADMA levels and their association with vascular damage in untreated hypertension. We enrolled consecutive patients with untreated, recently diagnosed hypertension and age-matched normotensive individuals. 24-hour blood pressure, central hemodynamics, and arterial stiffness were recorded. A total of 311 individuals were studied: 165 with essential hypertension, 50 with masked hypertension, 25 with white-coat hypertension, and 71 normotensive individuals. ADMA levels significantly correlated with aortic augmentation index (AIx75) (r = .156, P = .006), aortic pulse pressure (r = .153, P = .007) and marginally with carotid-femoral pulse wave velocity (r = .110, P = .051), as well as with diastolic office BP. In the multivariate model, aortic AIx75 and age were the only statistically significant predictors of ADMA. This is the largest study to document an independent association between ADMA and aortic AIx75 but not with other indices of arterial stiffness.

Subclinical Organ Damage in White-Coat Hypertension: The Possible Role of Cystatin C.

The authors investigated the relationship of white-coat hypertension (WCH) with subclinical organ damage and potential relevant mechanisms. A total of 386 untreated patients were enrolled and divided into 204 patients with WCH and 183 with normotension. Flow-mediated dilation (FMD), pulse wave velocity (PWV), intima-media thickness, left ventricular mass index (LVMI), and cystatin C levels were measured. All tests were two-sided, and a P value <.05 was considered statistically significant. The WCH group exhibited higher LVMI and PWV values, decreased E/A ratio and FMD values, and increased prevalence for left ventricular hypertrophy compared with controls (P<.001 for all). Cystatin C was significantly higher in the WCH group compared with controls (P=.035) and was positively associated with LVMI (P<.05 for both). The presence of WCH is associated with more pronounced subclinical organ damage compared with normotension. Cystatin C may play a significant role and therefore warrants further investigation.

The association of circulating miR-30a, miR-29 and miR-133 with white-coat hypertension.

AIM: The aim of the present study was to investigate the association of circulating miRNAs with white-coat hypertension (WCH) and further analyze whether miRNAs could be as potential biomarkers for WCH. METHOD: Quantitative reverse transcriptase PCR (qRT-PCR) was used to evaluate the expression of selected miRNAs. The area under the receiver-operating characteristic curve was used to evaluate diagnostic accuracy. RESULTS: MiR-30a yielded an AUC of 0.984 (95% CI: 0.001-1.00; p < 0.001) and 0.816 (95% CI: 0.718-0.915; p < 0.001); miR-29 yielded an AUC of 0.955 (95% CI: 0.913-0.998; p < 0.001) and 0.799 (95% CI: 0.697-0.902; p < 0.001); miR-133 yielded an AUC of 0.949 (95% CI: 0.900-0.999; p < 0.001) and 0.713 (95% CI: 0.593-0.834; p < 0.001), respectively. CONCLUSION: The study suggested that miR-30a, miR-29 and miR-133 have great potential to be noninvasive screening tools for WCH detection.

Differential expression of hypertension-associated microRNAs in the plasma of patients with white coat hypertension.

White coat hypertension (WCH) is a high cardiovascular risk condition, and a fundamental understanding of the cause and pathophysiology of the disorder is still lacking. Recent studies demonstrated that microRNAs (miRNAs) are involved in hypertension; however, the roles of miRNAs in WCH are not known. The expressions of selected 10 miRNAs were investigated independently in plasma samples from 30 hypertension (HT) patients, 30 WCH patients, and 30 normotensive (NT) subjects. MiR-21, miR-122, miR-637, and let-7e expression levels were significantly upregulated in the HT group compared with the NT groups (P = 0.017, P = 0.022, P = 0.048, and P = 0.013, respectively). MiR-122 and miR-637 expressions were also significantly upregulated in the WCH group compared with the NT group (P = 0.048 and P = 0.039, respectively). MiR-296-5p expression level was significantly downregulated in HT patients and upregulated in the WCH patients compared with the NT group (P = 0.049 and P = 0.039, respectively). Additionally, the ambulatory 24-hour and daytime systolic and diastolic blood pressures were negatively correlated with miR-296-5p. MiR-296 and miR-637 had area under the curve (AUC) values of 0.778 and 0.774, respectively, which demonstrates their sufficiency to distinguish WCH from NT individuals. MiR-296 and miR-637 had AUC values of 0.868 and 0.680, respectively, which shows their potential to distinguish WCH from HT individuals. We report for the first time a plasma miRNA profile for WCH patients and demonstrate a novel link between miRNA and WCH. These findings may reveal crucial insights into the development of WCH.