Xuejing Yu

Comparison of Carotid‐Femoral and Brachial‐Ankle Pulse‐Wave Velocity in Association With Target Organ Damage in the Community‐Dwelling Elderly Chinese: The Northern Shanghai Study

Background Carotid‐femoral pulse‐wave velocity (cf‐PWV) and brachial‐ankle PWV (ba‐PWV) are the 2 most frequently applied PWV measurements. However, little is known about the comparison of hypertensive target organ damage (TOD) with cf‐PWV and ba‐PWV. Methods and Results A total of 1599 community‐dwelling elderly subjects (age >65 years) in northern Shanghai were recruited from June 2014 to August 2015. Both cf‐PWV and ba‐PWV were measured using SphygmoCor and VP1000 systems, respectively. Within the framework of comprehensive cardiovascular examinations, risk factors were assessed, and asymptomatic TOD, including left ventricular mass index, peak transmitral pulsed Doppler velocity/early diastolic tissue Doppler velocity (E/Ea), carotid intima‐media thickness, arterial plaque, creatinine clearance rate, and urinary albumin‐creatinine ratio were all evaluated. Both PWVs were significantly associated with male sex, age, waist/hip circumference, fasting plasma glucose, and systolic blood pressure, and ba‐PWV was also significantly related to body mass index. Both PWVs were significantly correlated with most TOD. When cf‐PWV and ba‐PWV were both or separately put into the stepwise linear regression model together with cardiovascular risk factors and treatment, only cf‐PWV, but not ba‐PWV, was significantly associated with carotid intima‐media thickness and creatinine clearance rate (P<0.05). When cf‐PWV and ba‐PWV were both or separately put into the same full‐mode model after adjustment for confounders, only cf‐PWV, but not ba‐PWV, showed significant association with carotid intima‐media thickness and creatinine clearance rate (P<0.05). Similar results were observed in logistic regression analysis. Conclusions Taken together, in the community‐dwelling elderly Chinese, cf‐PWV seems to be more closely associated with hypertensive TOD, especially vascular and renal TOD, as compared with ba‐PWV. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT02368938.

Smad Nuclear Interacting Protein 1 Acts as a Protective Regulator of Pressure Overload‐Induced Pathological Cardiac Hypertrophy

Background Smad nuclear interacting protein 1 (SNIP1) plays a critical role in cell proliferation, transformation of embryonic fibroblasts, and immune regulation. However, the role of SNIP1 in cardiac hypertrophy remains unclear. Methods and Results Here we examined the role of SNIP1 in pressure overload–induced cardiac hypertrophy and its mechanisms. Our results demonstrated that SNIP1 expression was downregulated in human dilated cardiomyopathic hearts, aortic banding‐induced mice hearts, and angiotensin II–treated cardiomyocytes. Accordingly, SNIP1 deficiency significantly exacerbated aortic banding–induced cardiac hypertrophy, fibrosis, and contractile dysfunction, whereas cardiac‐specific overexpression of SNIP1 markedly recovered pressure overload–induced cardiac hypertrophy and fibrosis. Besides that, SNIP1 protected neonatal rat cardiomyocytes against angiotensin II–induced hypertrophy in vitro. Moreover, we identified that SNIP1 suppressed nuclear factor‐κB signaling during pathological cardiac hypertrophy, and inhibition of nuclear factor‐κB signaling by a cardiac‐specific conditional inhibitor of κBS 32A/S36A transgene blocked these adverse effects of SNIP1 deficiency on hearts. Conclusions Together, our findings demonstrated that SNIP1 had protective effects in pressure overload–induced pathological cardiac hypertrophy via inhibition of nuclear factor‐κB signaling. Thus, SNIP1 may be a novel approach for the treatment of heart failure.

Hypertensive target organ damage is better associated with central than brachial blood pressure: The Northern Shanghai Study

To compare central and brachial blood pressure (BP) in the association of target organ damage (TOD) in a community‐based elderly population, 1599 (aged 71.4 ± 6.1 years) participants in northern Shanghai were recruited. TOD included left ventricular hypertrophy (n = 1556), left ventricular diastolic dysfunction (n = 1524), carotid plaque (n = 1558), arteriosclerosis (n = 1485), and microalbuminuria (n = 1516). Both central and brachial BP significantly correlated with TOD. In full‐model regression, central BP was significantly associated with all TOD (P ≤ .04), whereas brachial BP was only significantly associated with left ventricular hypertrophy and arteriosclerosis (P ≤ .01). Similarly, in stepwise regression, central BP was significantly associated with left ventricular hypertrophy, left ventricular diastolic dysfunction, arteriosclerosis, and microalbuminuria (P ≤ .04), while brachial BP was not associated with any TOD. Receiver operating characteristic analyses indicated that central BP identified arteriosclerosis and microalbuminuria better than brachial BP (P ≤ .01). In conclusion, central BP showed superiority over brachial BP in the association of hypertensive TOD in a community‐based elderly population.