Background Evidence from experimental studies showed that Th1, Th2, and Th17 play a pivotal role in hypertension and target organ damage. However, whether changes in the circulating Th1, Th2, and Th17 levels are associated with nondipper hypertension and carotid atherosclerotic plaque in hypertension has yet to be investigated. Methods Th1, Th2, and Th17 levels were detected using a flow cytometric analysis, and their related cytokines were measured by enzyme-linked immunosorbent assay in 45 hypertensive patients and 15 normotensive subjects. Results The frequencies of Th1 and Th17 in hypertensive patients, especially in nondipper patients and patients with carotid atherosclerotic plaque, were markedly higher than those in the control group; this was accompanied by higher IFN-γ and IL-17 levels. In contrast, the Th2 frequencies and IL-4 levels in hypertensive patients, especially in nondipper patients and patients with carotid atherosclerotic plaque, were significantly lower than those in the control group. Conclusions The changes in Th1, Th2, and Th17 activity are associated with the onset of the nondipper type and carotid atherosclerotic plaque in hypertensive patients.

Aim: Omentin-1, as a novel adipocytokine, ameliorates obesity-associated disorders and suppresses the development of atherosclerotic lesions. The present research investigated the correlation between serum omentin-1 and post-infarction myocardial function.Methods: A total of 52 patients with first anterior ST-segment elevation myocardial infarction (STEMI) were recruited into this study. Participants were divided into two subgroups according to median admission omentin-1 concentration. δ1 was defined as (admission omentin-1 level) - (serum omentin-1 at 24 hours after admission) and δ2 was defined as (admission omentin-1 level) - (serum omentin-1 at 72 hours after admission). The change in left ventricular ejection fraction (LVEF) was regarded as (LVEF at 3 months post-STEMI) – (LVEF at 2 days post-STEMI).Results: Admission omentin-1 level was the highest, while omentin-1 decreased over the following 3 days. The high admission omentin-1 group had lower peak muscle brain fraction of creatine kinase (CK–MB). Additionally, the change in LVEF and the global LVEF at 3 months post-STEMI all ameliorated significantly in the high admission omentin-1 group. For the time-dependent change in omentin-1, there were negative associations among δ1, δ2, and peak CK–MB. δ1 and δ2 also correlated positively with LVEF at 3 months post-STEMI. Most importantly, δ1 (r = 0.346, p = 0.012) and δ2 (r = 0.439, p = 0.001) also correlated positively with the change in LVEF. After multivariate linear regression analysis, δ1 (Beta = 0.026, 95% CI 0.011 to 0.041, p = 0.001) and δ2 (Beta = 0.024, 95% CI 0.009 to 0.038, p = 0.003) also remained associated with the change in LVEF.Conclusions: The admission omentin-1 and time-dependent change in omentin-1 level all have a significant correlation with the early improvement of post-infarction myocardial function. While only the time-dependent change in omentin-1 (δ1 and δ2) remained associated with the early improvement of post-infarction myocardial function after multivariate linear regression analysis. The present research indicated that omentin-1 represents a promising adipocytokine to retard negative cardiac remodeling after STEMI.

Background Resistin, a proinflammatory adipocytokine secreted predominately by macrophages in humans, plays an important role in the pathogenesis and development of atherosclerosis. The present research mainly investigated the association between serum resistin level and peak hypersensitive cardiac troponin I (hs-cTnI) in patients with ST-segment elevation myocardial infarction (STEMI).Methods We consecutively enrolled 92 patients with a first STEMI in this cross-sectional and observational study. Resistin concentrations upon admission and 24 h and 72 h after primary percutaneous coronary intervention (PCI) were all measured. The change in resistin (δ Resistin) was defined as (serum resistin concentration at admission)-(serum resistin concentration 24 h after intervention).Results Serum resistin concentration decreased rapidly after primary PCI. Resistin at admission correlated positively with tumour necrosis factor-α (r = 0.522, p<0.001) and macrophage migration inhibitory factor (r = 0.471, p<0.001). Additionally, resistin at admission correlated negatively with the reactive oxygen species scavengers superoxide dismutase (r = -0.261, p = 0.012) and glutathione peroxidase (r = -0.235, p = 0.024). Most importantly, serum resistin concentrations upon admission (r = 0.381, p<0.001) and 24 h (r = 0.372, p<0.001) and 72 h (r = 0.347, p = 0.001) after primary PCI all correlated with peak hs-cTnI, while δ Resistin was not associated with peak hs-cTnI. After multiple linear regression analysis, serum resistin (beta = 13.593, 95% CI 5.951 to 21.235, p < 0.001) at admission and 24 h (beta = 13.972, 95% CI 5.662 to 22.282, p = 0.001) and 72 h (beta = 14.455, 95% CI 5.178 to 23.733, p = 0.003) after intervention remained associated with peak hs-cTnI.Conclusions In our present research, serum resistin concentrations at different time points all correlated positively with peak hs-cTnI, which may suggest that serum resistin concentrations during the acute phase of STEMI are useful for forecasting myocardial infarction size and prognosis in patients after primary PCI. Additionally, our research also indicated that resistin may regulate myocardial IRI partly by promoting the inflammatory process and oxidative stress.