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Objective: To investigate the long-term therapeutic effects and safety of renal denervation (RDN) on hypertensive patients with different cardiovascular risks, as well as its impact on adverse events, cardiovascular death and all-cause mortality. Methods: This was a single-center, single-arm, real-world retrospective study. Patients with refractory hypertension who underwent RDN at Tianjin First Central Hospital from July 6, 2011 to December 23, 2015 were enrolled and divided into either a high or intermediate-low risk group based on baseline cardiovascular risk. The treatment responsiveness of hypertensive patients with different cardiovascular stratification to RDN was assessed by comparing the results of office blood pressure, home blood pressure, and 24-h ambulatory blood pressure monitoring at 1, 5, and 11 years after RDN. Long-term safety of RDN was assessed by creatinine, and estimated glomerular filtration rate (eGFR) at 1 and 11 years after RDN. In addition, the total defined daily dose (DDD) of antihypertensive medications and the incidence of long-term adverse events, cardiovascular deaths, and all-cause deaths after RDN were followed up 11 years after RDN in person or by telephone. Results: A total of 62 patients with refractory hypertension, aged (50.2±15.0) years, of whom 35 (56.5%) were male, were included. There were 35 cases in high-risk group and 27 cases in low and medium risk group. The decrease in clinic systolic blood pressure (high risk vs. low-medium risk: (-38.0±15.1) mmHg vs. (-25.0±16.6) mmHg(1 mmHg=0.133kPa), P =0.002), home self-measured systolic blood pressure ((-28.4±12.7) mmHg vs. (-19.7±13.1) mmHg, P =0.011) and clinic systolic blood pressure 11 years after RDN ((-43.0±18.4) mmHg vs. (-27.8±17.9) mmHg, P =0.003) in the high-risk group was significantly higher than that in the low-medium risk group. The differences in heart rate and the decrease in total DDD number of antihypertensive drugs between the two groups were not statistically significant (all P >0.05). Creatinine and eGFR levels in the two groups at 1 and 11 years after RDN were not statistically significant when compared with the baseline values (all P >0.05). The cumulative cardiovascular mortality rate was 1.6% (1/62) and 8.1% (5/62), and the cumulative all-cause mortality rate was 3.2% (2/62) and 11.3% (7/62) at 5 and 11 years after RDN, respectively. The differences in the incidence rate of adverse events, cardiovascular mortality, and all-cause mortality rate between the two groups were not statistically significant (all P >0.05). Conclusions: RDN has long-term antihypertensive effect and good safety. Hypertensive patients who belong to the high-risk stratification of cardiovascular risk may respond better to RDN treatment.

Objective: to explore the effect of catheter based renal synthetic denervation on renin-angiotensin-aldosterone system (RAAS) and blood pressure reduction in patients with resistant hypertension. and assess the validity and security of the treatment., Methods: Ten patients with resistant hypertension from June 2011 to December 2011 were retrospectively reviewed, and then all of 10 patients screened for eligibility were allocated to renal denervation. Primary endpoints were changes of office blood pressure at 1 week, 1, 3 and 6 months after procedure. We assessed the effectiveness of renal sympathetic denervation with heart rate (HR), renin activity (PRA), angiotensin II (AngII), aldosterone (Ald), and creatinine (Cr) before and 2 weeks after procedure., Results: Office blood pressure after catheter-based renal denervation decreased by 22.8/9.1 mm Hg (1 mm Hg = 0.133 kPa), 34.8/14.7 mm Hg, 42.6/20.7 mm Hg, 43.2/21.6 mm Hg, at 1 week, 1, 3 and 6 months, respectively (P < 0.001). Meanwhile, the level of PRA, AngII, Ald decreased by (1.11 ± 0.89) ng×ml(-1)×h(-1) (P = 0.003), (17.06 ± 13.82) ng/L (P = 0.004), (404.5 ± 285.8) ng/L (P = 0.002), respectively; and heart rate decreased by 5.1 bpm (P = 0.002). However, the Cr level and eGFR did not change significantly (P > 0.05)., Conclusion: Catheter-based renal sympathetic denervation can reduce the level of renin activity, angiotensin II and aldosterone, and causes substantial and sustained blood-pressure reduction.

Objective: Hypertension is the most common risk factor for cardiovascular diseases and stroke. Renal sympathetic hyperactivity is associated with hypertension. The aim of this study was to explore the efficacy of renal denervation for hypertension., Methods: Eighteen mongrel neurogenic hypertensive dogs were divided into intervention [mean arterial pressure: (150.6 ± 18.8) mm Hg (1 mm Hg = 0.133 kPa) plus renal sympathetic denervation by percutaneous catheter-based radiofrequency, n = 10] and control [mean arterial pressure (147.4 ± 13.2) mm Hg, n = 8] group. Mean arterial pressure before and at 2, 4, 6 and 10 weeks after procedure was invasively measured. Renin activity (PRA), angiotensin II (AngII), aldosterone (Ald), and creatinine (Cr) were detected at 2, 6 and 10 weeks after procedure., Results: Mean arterial pressure remained unchanged in control group. In intervention group, mean arterial pressure (MAP) decreased to (130.4 ± 14.1) mm Hg, (136.2 ± 17.1) mm Hg, (128.7 ± 14.7) mm Hg and (126.1 ± 12.7) mm Hg respectively at 2, 4, 6, and 10 weeks after procedure. Meanwhile, the level of PRA, AngII, Ald significantly reduced post procedure compared with pre-procedural level (P < 0.05) and the Cr level remained unchanged post procedure (P > 0.05)., Conclusion: Sympathetic nervous system plays an important role in the progression of hypertension. Catheter-based renal denervation results in substantial and sustained blood-pressure reduction in this model.

Objective: To investigate the relationship between tryptophan hydroxylase (TPH) gene A218C in intron 7 and 5-hydroxytryptamine transporter (5-HTT) gene variable number tandem repeat (VNTR) in intron 2 and gene-linked polymorphic region (LPR) deletion/insertion polymorphism and essential hypertension (EH) in Chinese northern Han population., Methods: A total of 280 EH patients and 200 normotensive controls were genotyped using polymerase chain reaction-restriction fragment length polymorphism technique., Results: There were no significant differences in the frequencies of the genotypes and alleles of TPH gene A218C and 5-HTTVNTR between EH patents and controls (all P > 0.05). The genotype frequencies of SS, LS and LL in the 5-HTTLPR polymorphism was 68%, 29% and 3% in EH patients, 53%, 37% and 10% in the controls respectively (P < 0.01). The frequencies of allele S and L of the 5-HTTLPR were 82% and 18% in EH patients, 72% and 28% in the controls respectively (P < 0.01). Compared with the carriers of L allele (LS + LL), the EH risk was significantly higher in the SS homozygote (OR = 1.90, 95%CI = 1.31 - 2.77, P = 0.001). After adjustment of age, gender, body mass index, blood lipids, fasting blood glucose and blood uric acid level, the binary logistic regression analysis demonstrated that SS genotype in the 5-HTTLPR polymorphism was significantly related to occurrence of EH (OR = 1.47, 95%CI = 1.06 - 2.04, P = 0.021)., Conclusions: The SS genotype of the 5-HTTLPR might be a susceptible gene to EH, while the TPH gene A218C and 5-HTTVNTR polymorphism is not associated with EH in Chinese northern Han population.

Objective: To evaluate the effects of statins on coronary atherosclerotic plaque in patients with stable angina pectoris and type 2 diabetes with mild elevated low density lipoprotein-cholesterol (LDL-C)., Methods: Seventy-eight patients with stable angina pectoris and type 2 diabetes mellitus and mild elevated LDL-C were treated with (n=40) or without (n=38) statins for 12 months. Coronary artery angiography (CAG) and intravascular ultrasound (IVUS) were performed at baseline and after 12 months on lesion and reference segment to compare the plaque volume, lumen volume, vascular volume and remodeling index was calculated as vascular volume index (VVI) at lesion divided by VVI at reference segment One coronary lesion with 50%-70% stenosis was selected as target plaque in each patient., Results: Baseline clinical and angiographic data were comparable between the two groups. After 12 months, LDL-C decreased 31.5% in statin group and remained unchanged in non-statin group. After 12 months, plaque volume was significantly increased [ (76.1 +/- 13.0) mm3 vs. (95.0 +/- 21.9) mm3 , P < 0.05], lumen volume was significantly decreased [(65.0 +/- 10.9) mm3 vs. (45.4 +/- 6.6) mm3, P < 0.05 ] and vascular volume remained unchanged in non-statins group; plaque volume was also significantly increased [(79.5 +/- 15.2) mm3 vs. (87.5 +/- 17.9) mm3 , P < 0.05] while lumen volume and vascular volume remained unchanged in statin group. Remodeling index (RI) remained unchanged in non-statin group but significantly increased in statin group (0.91 +/- 0.08 vs. 0.95 +/- 0.10, P < 0.05) after 12 months., Conclusion: Chronic statin therapy could retard the coronary atherosclerotic progression in patients with stable angina pectoris and type 2 diabetes with mild elevated LDL-C.

Objective: To evaluate the association between poststenting atherosclerotic plaque redistribution/lumen reduction at the stent edge and stent length., Methods: Seventy stents were implanted to 47 patients with stable or unstable angina and 33 stents were < or = 18 mm and 37 stents were > 18 mm. Intravascular ultrasound analysis was performed on proximal stent edge, stent area and distal stent edge. Lumen area (LA) and vascular area (VA) were measured and lumen volume (LV) and vascular volume (VV) were calculated on the three segments. Vascular wall volume (WV) was calculated as VV-LV, volume of plaque redistribution = poststenting WV-prestenting WV., Results: Compared to prestenting, poststenting LV significantly decreased, VV remained unchanged and WV significantly increased at proximal and distal edges of < or = 18 mm group and at proximal edge of > 18 mm group, suggesting reduced lumen due to plaque distribution. At distal edge of > 18 mm group, poststenting LV, VV and WV all equally significantly increased therefore the lumen was not affected by plaque distribution., Conclusion: The poststenting lumen changes due to plaque redistribution were associated with stent length, lumen reduced at proximal and distal edge of short stents and proximal edge of long stents but not at the distal edge of long stents.