[Clinical characteristics and outcomes of patients with acute aortic dissection: impact of hypertension].

OBJECTIVE: To observe the clinical characteristics and outcomes of patients with acute aortic dissection (AAD) and explore the impact of hypertension. METHODS: The present study enrolled 1 087 consecutive patients with AAD who were confirmed by computed tomographic scanning in Fuwai Hospital from January 2008 to December 2010. The major endpoints were in-hospital death and long-term mortality during follow up. RESULTS: A total of 595 (54.7%) patients were Stanford type A and 492 (45.3%) patients were Stanford type B. The median length of follow-up was 24.2 months (interquartile range 10.9, 40.8 months). The prevalence of hypertension was 67.4%(733 cases), and was significantly higher in type B patients than in type A patients (71.3%(351/492) vs. 64.2%(382/595), P=0.01). Regardless of Stanford classification, patients complicating with hypertension were older, had higher comorbidities (coronary heart diseases or diabetes), and less likely to receive surgical treatment compared with those without hypertension (all P<0.05). In Stanford type A AAD group, patients with hypertension had higher levels of admission blood pressure, serum creatinine and inflammatory markers (including WBC count, D-dimer and CRP) than those without hypertension (all P<0.05). In-hospital death (9.9% (38/382)vs. 5.6%(12/213), P=0.07) and long-term mortality (9.0% (31/344) vs. 8.9% (18/201), P=0.98) were similar in hypertensive and normotensive AAD type A patients. In type B AAD group, the in-hospital death rate was significantly higher in patients with hypertension than those without hypertension (5.4%(19/351) vs. 0.7%(1/141), P=0.02), while the long-term mortality was similar (6.9%(23/332) vs. 7.9%(11/140), P=0.71) between patients with and without hypertension. Multiple logistic regression analysis showed that hypertension did not predict the increased risk of in-hospital death of type A or type B AAD patients. The main protective factor of in-hospital mortality was operation in patients with type A AAD. The independent predictors of in-hospital death were age and surgical treatment in patients with type B AAD. CONCLUSIONS: Hypertension is a common co-morbidity in patients with AAD. AAD patients with hypertension are usually elder, have higher comorbidities of cardiovascular diseases, and less likely to receive surgical treatment compared with those without hypertension, but hypertension is not associated with increased risk of in-hospital and long-term mortality in both AAD type A and type B patients.

Effect of soy isoflavones on blood pressure: a meta-analysis of randomized controlled trials.

BACKGROUND AND AIM: The effect of soy isoflavones on blood pressure is controversial. The objective of this study was to evaluate the effect of dietary soy isoflavones on blood pressure. METHODS AND RESULTS: Trials were searched in PubMed, the Cochrane Library, Embase and references cited in related reviews and studies. A total of eleven trials were reviewed. Meta-analysis results showed a mean decrease of 2.5 mm Hg (95% CIs, - 5.35 to 0.34 mm Hg; P = 0.08) for systolic blood pressure and 1.5 mm Hg (95% CIs, - 3.09 to 0.17 mm Hg; P = 0.08) for diastolic blood pressure in the soy isoflavones-treated group compared to placebo. Meta-regression and subgroup analyses indicated that blood pressure status was a significant predictor of heterogeneity for the effect of soy isoflavones on blood pressure. Subgroup analysis of hypertensive subjects revealed that a greater blood pressure reduction was identified in the soy isoflavone-treated group compared to placebo (5 trials; SBP: - 5.94, 95% CIs [- 10.55, - 1.34] mm Hg, P = 0.01; DBP: - 3.35, 95% CIs [- 6.52, - 0.19] mm Hg, P = 0.04). In contrast, treatment with soy isoflavones did not lead to a significant reduction in blood pressure in normotensive subjects (6 trials; SBP: 0.29, 95% CIs [- 2.39, 2.97] mm Hg, P = 0.83; DBP: - 0.43, 95% CIs [- 1.66, 0.81] mm Hg, P = 0.50). CONCLUSION: Soy isoflavones had an effect of lowering blood pressure in hypertensive subjects, but not in normotensive subjects. Larger trials need to be carried out to confirm the present findings.

VIP gene variants related to idiopathic pulmonary arterial hypertension in Chinese population.

A variety of studies has linked vasoactive intestinal peptide (VIP) to idiopathic pulmonary arterial hypertension (IPAH). In this study, we investigated the correlation between VIP gene variants and IPAH in Chinese population. A total of 81 consecutive unrelated patients diagnosed as IPAH from 2006 to 2008 and 250 controls were included in the study. VIP gene variants were screened by direct sequencing, and VIP serum level was determined by enzyme-linked immunosorbent assay. Clinical and hemodynamic data of all patients were also obtained. The variant g.8129T-->C in exon 7 was found to be the only variant in the coding region of VIP gene with a significantly higher frequency in patients (40.7%) than in control samples (15.2%). Moreover, there was marked difference in VIP serum level and hemodynamic data between IPAH patients with and without the variant. The variant g.8129T-->C in exon 7 of VIP gene was correlated with the clinical phenotype of lower VIP serum level, higher mean pulmonary artery pressure and pulmonary vascular resistance in patients with IPAH comparing to those in patients without this variant. The VIP gene variant g.8129T-->C may be one of the risk factors in the pathogenesis of IPAH.

Effect of aldosterone antagonists on blood pressure in patients with resistant hypertension: a meta-analysis.

There is currently limited data on which drug should be used to improve blood pressure (BP) control in patients with resistant hypertension (RH). We performed a systematic review and meta-analysis of published studies evaluating the anti-hypertensive benefit of aldosterone antagonists (AA) as an add-on therapy in patients with RH. A systematic literature search for eligible studies was conducted until June 2014, using literature databases and hand search. Studies were stratified according to controlled vs uncontrolled design and analyzed using random-effect models. We identified 13 eligible studies involving a total of 2640 patients, consisting of 3 randomized controlled trials, and 10 observational studies without a control group. In controlled studies, there was a reduction in mean systolic and diastolic BP of -16.5 (95% confidence interval (CI), -30.0 to -3.0) and -4.1 (95% CI, -7.8 to -0.32) mm Hg, respectively, compared with control. In uncontrolled studies, there was a reduction in mean systolic and diastolic BP of -19.7 (95% CI, -23.2 to -16.2) and -9.1 (95% CI, -10.3 to -7.8) mm Hg, respectively, compared with pre-AA therapy. Subgroup analysis showed that the systolic BP change was more pronounced in patients with baseline systolic BP >150 mm Hg (weighted mean difference (WMD), -23.1 mm Hg) than in patients with ⩽150 mm Hg (WMD, -15.4 mm Hg) (between groups P<0.001), suggesting that the baseline systolic BP was a predictor of the BP response to AA treatment. Furthermore, AA demonstrated a mild increase in serum potassium and creatinine (for both, P<0.001). The findings suggest that AA as an add-on therapy was effective for lowering systolic and diastolic BP in patients with RH.

Prostanoids and aldosterone-induced mild experimental hypertension in rats.

The goal of this study was to determine the role of prostanoids in a new model of mineralocorticoid-dependent hypertension induced by the subcutaneous infusion of aldosterone (1 micrograms/hr) to normal male Sprague-Dawley rats. This regimen caused a mild and gradual increase in systolic pressure over a period of 4 weeks (113 +/- 1 vs. 137 +/- 3 mm Hg) and was associated with an increase in the in vivo formation of prostaglandins I2 and E2 and of thromboxane A2 in the kidney. High sodium intake induced a fall in the urinary levels of prostaglandin E2 and a rise in the arterial pressure of control rats (126 +/- 1 vs. 113 +/- 1 mm Hg) but did not influence aldosterone-induced hypertension. Indomethacin (3.0 mg/kg/day) caused a profound inhibition of the in vivo synthesis of prostaglandin I2 and thromboxane A2 without modifying the renal production of prostaglandin E2. Although indomethacin exerted no effect on aldosterone-induced hypertension in rats fed a normal diet, it caused a further rise in systolic pressure in aldosterone-treated rats fed a high sodium diet (157 +/- 6 vs. 140 +/- 4 mm Hg). The results of this study in a model of aldosterone-induced mild hypertension in the rat indicate that 1) aldosterone exerts a stimulatory effect on the renal synthesis of prostanoid, particularly prostaglandin E2; 2) thromboxane A2 and prostaglandin I2 do not seem to play a role in aldosterone-induced hypertension under conditions of normal dietary salt intake, whereas the role of prostaglandin E2 is unclear; 3) there is enough sodium in a normal diet to allow for the maximal expression of the hypertensive effect of aldosterone; 4) prostaglandin I2 seems to play a significant role in modulating the cardiovascular impact of a high sodium diet in aldosterone-treated rats; and 5) the renal biosynthesis of prostaglandin E2 is particularly resistant to the inhibitory effect of indomethacin in vivo.