Preventive Effects of Nicorandil Against Contrast-Induced Nephropathy in Patients With Moderate Renal Insufficiency Undergoing Percutaneous Coronary Intervention.

We investigated the preventive effect of nicorandil on contrast-induced nephropathy (CIN) in patients with moderate renal insufficiency undergoing percutaneous coronary intervention (PCI). A total of 250 patients with a creatinine clearance (crCl) ≤60 mL/min undergoing PCI were randomly assigned to either a nicorandil group (nicorandil 10 mg 3 times/d and hydration; n = 125) or a control group (hydration only; n = 125). The first end point was the incidence of CIN defined as an increase in serum creatinine (Scr) levels by ≥0.5 mg/dL or ≥25% within 72 hours after exposure to the contrast medium. The secondary end points were (1) changes in Scr, blood urea nitrogen, and crCl and (2) the incidence of major adverse events during hospitalization. The incidence of CIN was 1.6% (2/125) in the nicorandil group and 9.6% (12/125) in the control group (P = .011). There was no obvious difference in the incidence of major adverse events during hospitalization between the nicorandil and the control group (4.0% vs 4.8%, P = 1.000). Multivariate logistic regression analysis showed that nicorandil was a protective factor for CIN (odds ratios = 0.126, 95% confidence interval: -19.996 to -0.932, P = .012). Prophylactic administration of nicorandil may prevent against CIN in patients with moderate renal insufficiency undergoing PCI.

Preventive Effects of Alprostadil Against Contrast-Induced Nephropathy Inpatients With Renal Insufficiency Undergoing Percutaneous Coronary Intervention.

We investigated the preventive effect of alprostadil on contrast-induced nephropathy (CIN) in patients with renal insufficiency undergoing percutaneous coronary intervention (PCI). A total of 300 patients with creatinine clearance (crCl) ≤60 mL/min undergoing PCI were randomly assigned to alprostadil or a control group. The primary end point was the incidence of CIN defined as an increase in serum creatinine (Scr) levels by ≥0.5 mg/dL or≥ 25% after administration of the contrast media within 72 hours. The secondary end points were (1) changes in Scr and crCl within 72 hours and (2) the incidence of major adverse events during hospitalization. The incidence of CIN was 2.7% (4/150) in the alprostadil group, and 8.7% (13/150) in the control group (χ2 = 5.05, P = .043).There was no difference regarding the incidence of major adverse events during hospitalization between the alprostadil group and control groups (2.7% vs 4.0%, P = .750). Multivariate logistic regression analysis showed that alprostadil was an independent protective factor for CIN (odds ratio = 0.136, 95% confidence interval: 0.020-0.944, P = .044). Prophylactic administration of alprostadil may prevent CIN in patients with renal insufficiency undergoing PCI.

Predictive Value of Cumulative Blood Pressure for All-Cause Mortality and Cardiovascular Events.

The predictive value of cumulative blood pressure (BP) on all-cause mortality and cardiovascular and cerebrovascular events (CCE) has hardly been studied. In this prospective cohort study including 52,385 participants from the Kailuan Group who attended three medical examinations and without CCE, the impact of cumulative systolic BP (cumSBP) and cumulative diastolic BP (cumDBP) on all-cause mortality and CCEs was investigated. For the study population, the mean (standard deviation) age was 48.82 (11.77) years of which 40,141 (76.6%) were male. The follow-up for all-cause mortality and CCEs was 3.96 (0.48) and 2.98 (0.41) years, respectively. Multivariate Cox proportional hazards regression analysis showed that for every 10 mm Hg·year increase in cumSBP and 5 mm Hg·year increase in cumDBP, the hazard ratio for all-cause mortality were 1.013 (1.006, 1.021) and 1.012 (1.006, 1.018); for CCEs, 1.018 (1.010, 1.027) and 1.017 (1.010, 1.024); for stroke, 1.021 (1.011, 1.031) and 1.018 (1.010, 1.026); and for MI, 1.013 (0.996, 1.030) and 1.015 (1.000, 1.029). Using natural spline function analysis, cumSBP and cumDBP showed a J-curve relationship with CCEs; and a U-curve relationship with stroke (ischemic stroke and hemorrhagic stroke). Therefore, increases in cumSBP and cumDBP were predictive for all-cause mortality, CCEs, and stroke.

Ideal cardiovascular health and incident hypertension: The longitudinal community-based Kailuan study.

Ideal cardiovascular health (CVH) has been defined by the American Heart Association as the absence of disease and presence of 7 key health factors. Since it is unknown whether cumulative exposure to CVH reduces the risk of developing arterial hypertension, we prospectively examined the potential association between cumulative CVH (cumCVH) score (except for blood pressure metrics) and incident hypertension.Of the 101,510 participants with an age range of 18 to 98 years in this longitudinal community-based Kailuan study, our cohort included those 15,014 participants without hypertension at baseline and who had follow-up examinations 2, 4, and 6 years later. CumCVH was calculated as the summed CVH score for each examination multiplied by the time between the 2 examinations (points × year). Based on the cumCVH score, the study population was stratified into groups of <44 points, 44 to 48 points, 49 to 54 points, 55 to 59 points, and ≥60 points.Incidence of hypertension ranged from 16.76% in the lowest cumCVH category to 11.52% in the highest cumCVH category. After adjusting for age, sex, education level, income level, high-sensitivity C-reactive protein concentration, uric acid concentration, resting heart rate, parental history of hypertension at baseline, and medication usage before the third follow-up examination, participants in the highest cumCVH category had a significantly reduced risk of incident hypertension compared with those in the lowest cumCVH category (adjusted odds ratio 0.60, 95% confidence interval 0.50-0.71). For every increase in category based on the cumCVH score, the risk of hypertension decreased by approximately 2% (odds ratio 0.98, 95% confidence interval 0.97-0.98). The effect was consistent across sex and age groups.A higher cumCVH score is associated with a lower risk of incident hypertension.

Pattern of instent neointimal formation compared to native atherosclerosis in the coronary bifurcation lesions: volumetric intravascular ultrasound analysis.

BACKGROUND: No clinical study has systematically analyzed and compared circumferential neointimal and plaque distribution of stent neointimal proliferation and in native atherosclerotic plaques. This study aimed to investigate and compare the pattern of instent neointimal formation and native atherosclerosis in the coronary bifurcation lesions by volumetric analysis using systematic intravascular ultrasound (IVUS). METHODS: We examined bifurcation lesions in native coronary artery (plaque group, n = 102) and stented bifurcations at 9-month follow-up (neointima group, n = 51) using volumetric IVUS analysis of both the main vessel (MV) and side branch (SB). Three 5-mm segments were analyzed; the proximal MV (MVp), distal MV (MVd) and SB ostium (SBo). For each segment, volumetric analysis was performed in each of four quadrants (divided according to the branch takeoff and the geometric center of the lumen); carinal, epicardial, abcarinal, and myocardial. The eccentricity index was defined as the ratio of the abcarinal plaque (or neointimal) volume to the carinal plaque (or neointimal) volume. RESULTS: The plaque distribution differed significantly between the four quadrants, with the largest in the abcarinal quadrant, followed by the myocardial, epicardial, and carinal quadrants. The distribution of neointima was similar in the MV, but the four quadrants in the SB did not differ significantly. The eccentricity indices of both the MVd (P < 0.001) and SBo (P = 0.001) were significantly higher for the plaque group than the neointima group. CONCLUSIONS: The distribution of neointimal proliferation seems to have a similar pattern to that of atherosclerotic plaque in native coronary arteries, particularly in the main vessel, but the trend is less prominent.

[The effect of catheter based renal synthetic denervation on renin-angiotensin-aldosterone system in patients with resistant hypertension].

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.

[Efficacy of catheter-based renal denervation in mongrel neurogenic hypertensive dogs].

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.

[Association of tryptophan hydroxylase gene A218C and serotonin transporter gene polymorphism with essential hypertension in Chinese northern Han population].

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.

[Effects of statins on coronary atherosclerotic plaque in patients with coronary heart disease and type 2 diabetes with mild elevated LDL-C].

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.

[Relationships between PON1 L55M polymorphism and coronary heart diseases complicated with fasting hyperglycemia in Han populations in Guangdong].

OBJECTIVE: To investigate the relationships between Paraoxonase1 (PON1) gene L55M polymorphism and coronary heart diseases (CHD) complicated with fasting hyperglycemia (FHG) or type 2 diabetes mellitus (T2DM). METHODS: Two hundreds and eighty four patients were recruited in this study, which comprised 86 patients with CHD, 62 with CHD and FHG, 46 with CHD and T2DM, and 90 patients without the above conditions. The sequences of the PON1 gene L55M polymorphism were analysed by the SNPs methods. RESULTS: The frequency of allele L was 0.86. No significant differences in the frequencies of the three genotypes (LL, LM, and MM) were found among the four groups of patients. The L allele of PON1 L55M was not associated with the number and range of coronary arterial lesions (chi2 = 0.56, P = 0.76; chi2 = 0.11, P = 0.74, respectively). CONCLUSION: PON1 gene L55M polymorphism exists in Han populations in Guangdong, with LL as the main genotype. PON1 L55M gene polymorphism and allelic genes are not associated with the level of fasting blood glucose or diabetes mellitus. There is no evidence to support the relationship between PON1 L55M gene polymorphism and coronary artery lesions.

[Effect of puerarin injection on the mRNA expressions of AT1 and ACE2 in spontaneous hypertension rats].

OBJECTIVE: To study the effect of puerarin on angiotensin II type 1 receptor (AT1) and angiotensin-converting enzyme 2 (ACE2) in spontaneous hypertension rat (SHR). METHODS: SHRs, 12 weeks old, were randomly divided into four groups: the model control group (A), the Verapamil group (B), and the two puerarin groups (C and D) treated by low dose and high dose of puerarin respectively. After being treated for 3 weeks, total RNA from tissues of heart, aorta and kidney in rats were extracted and mRNA expression levels of AT1 and ACE2 were determined by RT-PCR. RESULTS: As compared with Group A, the mRNA expressions of AT1 and ACE2 in heart tissue were lower in Group C, and those in kidney tissue were higher in Group D (all P < 0.05); ACE2 mRNA expression was higher in Group D than in Group C (P < 0.05); no significant differences of the two indexes in aorta were shown among various groups. Besides, mRNA expressions of AT1 and ACE2 in heart and kidney tissue were proved to be positively linearly correlated. CONCLUSION: High dose puerarin could increase the mRNA expressions of AT1 and ACE2 in kidney, while low dose puerarin could decrease them in heart; there might be a feed back correlation between AT1 and ACE2.

[Intravascular ultrasonic evaluation of poststenting atherosclerotic plaque redistribution and lumen reduction at the stent edge: does stent length matter?].

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.