Association of Parenteral Anticoagulation Therapy With Outcomes in Non-ST-Segment Elevation Acute Coronary Syndrome Patients Without Invasive Therapy: Findings from the Improving Care for Cardiovascular Disease in China (CCC) project.

Our previous study showed that parenteral anticoagulation therapy (PACT) in the context of aggressive antiplatelet therapy failed to improve clinical outcomes in patients undergoing percutaneous coronary intervention for non-ST-segment elevation acute coronary syndrome (NSTE-ACS). However, the role of PACT in patients managed medically remains unknown. This observational cohort study enrolled patients with NSTE-ACS receiving medical therapy from November 2014 to June 2017 in the Improving Care for Cardiovascular Disease in China-Acute Coronary Syndrome project. Eligible patients were included in the PACT group and non-PACT group. The primary outcomes were in-hospital all-cause mortality and major bleeding. The secondary outcome included minor bleeding. Among 23,726 patients, 8,845 eligible patients who received medical therapy were enrolled. After adjusting the potential confounders, PACT was not associated with a lower risk of in-hospital all-cause mortality (adjusted odds ratio (OR), 1.25; 95% confidence interval (CI), 0.92-1.71; P = 0.151). Additionally, PACT did not increase the incidence of major bleeding or minor bleeding (major bleeding: adjusted OR, 1.04; 95% CI, 0.80-1.35; P = 0.763; minor bleeding: adjusted OR, 1.27; 95% CI, 0.91-1.75; P = 0.156). The propensity score analysis confirmed the primary analyses. In patients with NSTE-ACS receiving antiplatelet therapy, PACT was not associated with a lower risk of in-hospital all-cause mortality or a higher bleeding risk in patients with NSTE-ACS receiving non-invasive therapies and concurrent antiplatelet strategies. Randomized clinical trials are warranted to reevaluate the safety and efficacy of PACT in all patients with NSTE-ACS who receive noninvasive therapies and current antithrombotic strategies.

Circular RNA circRNA_000203 aggravates cardiac hypertrophy via suppressing miR-26b-5p and miR-140-3p binding to Gata4.

AIMS: Circular RNAs (circRNAs) are involved in gene regulation in a variety of physiological and pathological processes. The present study aimed to investigate the effect of circRNA_000203 on cardiac hypertrophy and the potential mechanisms involved. METHODS AND RESULTS: CircRNA_000203 was found to be up-regulated in the myocardium of Ang-II-infused mice and in the cytoplasma of Ang-II-treated neonatal mouse ventricular cardiomyocytes (NMVCs). Enforced expression of circRNA_000203 enhances cell size and expression of atrial natriuretic peptide and ß-myosin heavy chain in NMVCs. In vivo, heart function was impaired and cardiac hypertrophy was aggravated in Ang-II-infused myocardium-specific circRNA_000203 transgenic mice (Tg-circ203). Mechanistically, we found that circRNA_000203 could specifically sponge miR-26b-5p, -140-3p in NMVCs. Further, dual-luciferase reporter assay showed that miR-26b-5p, -140-3p could interact with 3'-UTRs of Gata4 gene, and circRNA_000203 could block the above interactions. In addition, Gata4 expression is transcriptionally inhibited by miR-26b-5p, -140-3p mimic in NMVCs but enhanced by over-expression of circRNA_000203 in vitro and in vivo. Functionally, miR-26b-5p, -140-3p, and Gata4 siRNA, could reverse the hypertrophic growth in Ang-II-induced NMVCs, as well as eliminate the pro-hypertrophic effect of circRNA_000203 in NMVCs. Furthermore, we demonstrated that NF-κB signalling mediates the up-regulation of circRNA_000203 in NMVCs exposed to Ang-II treatment. CONCLUSIONS: Our data demonstrated that circRNA_000203 exacerbates cardiac hypertrophy via suppressing miR-26b-5p and miR-140-3p leading to enhanced Gata4 levels.

Utility of age, creatinine, and ejection fraction score in patients with type B aortic dissection undergoing thoracic endovascular aortic repair.

BACKGROUND: Older age, renal and cardiac dysfunction are predictors of poor outcome in aortic dissection. The aim of this study was to evaluate the association of the age, creatinine and ejection fraction (ACEF) score with adverse events in patients with type B aortic dissection (TBAD) undergoing thoracic endovascular aortic repair (TEVAR). METHODS: The study enrolled 605 patients from January 2010 to July 2015, who were classified into three groups according to the tertiles of ACEF score: Tertile 1 (≤0.77, n = 204), Tertile 2 (0.77-0.96, n = 205) and Tertile 3 (>0.96, n = 196). The association between ACEF, AGEF (age, glomerular filtration rate and ejection fraction) and the updated version of the ACEF (ACEF II) score with adverse events was analyzed. RESULTS: After a median 3.4 years follow-up, 63 (10.4%) patients died. Multivariable analysis revealed that ACEF score was independently associated with long-term mortality (adjusted hazard ratio = 3.54; 95% confidence interval, 2.09-6.01; p < 0.001). ACEF, AGEF and ACEF II score had similar predictive ability for both in-hospital and long-term death. The in-hospital mortality (1.5% vs. 1.0% vs. 6.6%, p = 0.001) were significantly higher in Tertile 3. In addition, cumulative long-term mortality in Tertile 3 was significantly higher than that in Tertile 1 and 2 (Log-Rank = 23.74; p < 0.001). CONCLUSION: ACEF score could be served as an useful and relatively simple tool for pre-TEVAR risk stratification in TBAD patients.

The Smad3-miR-29b/miR-29c axis mediates the protective effect of macrophage migration inhibitory factor against cardiac fibrosis.

Although macrophage migration inhibitory factor (MIF) is known to have antioxidant property, the role of MIF in cardiac fibrosis has not been well understood. We found that MIF was markedly increased in angiotension II (Ang-II)-infused mouse myocardium. Myocardial function was impaired and cardiac fibrosis was aggravated in Mif-knockout (Mif-KO) mice. Functionally, overexpression of MIF and MIF protein could inhibit the expression of fibrosis-associated collagen (Col) 1a1, COL3A1 and α-SMA, and Smad3 activation in mouse cardiac fibroblasts (CFs). Consistently, MIF deficiency could exacerbate the expression of COL1A1, COL3A1 and α-SMA, and Smad3 activation in Ang-II-treated CFs. Interestingly, microRNA-29b-3p (miR-29b-3p) and microRNA-29c-3p (miR-29c-3p) were down-regulated in the myocardium of Ang-II-infused Mif-KO mice but upregulated in CFs with MIF overexpression or by treatment with MIF protein. MiR-29b-3p and miR-29c-3p could suppress the expression of COL1A1, COL3A1 and α-SMA in CFs through targeting the pro-fibrosis genes of transforming growth factor beta-2 (Tgfb2) and matrix metallopeptidase 2 (Mmp2). We further demonstrated that Mif inhibited reactive oxygen species (ROS) generation and Smad3 activation, and rescued the decrease of miR-29b-3p and miR-29c-3p in Ang-II-treated CFs. Smad3 inhibitors, SIS3 and Naringenin, and Smad3 siRNA could reverse the decrease of miR-29b-3p and miR-29c-3p in Ang-II-treated CFs. Taken together, our data demonstrated that the Smad3-miR-29b/miR-29c axis mediates the inhibitory effect of macrophage migration inhibitory factor on cardiac fibrosis.

Association of Parenteral Anticoagulation Therapy With Outcomes in Chinese Patients Undergoing Percutaneous Coronary Intervention for Non-ST-Segment Elevation Acute Coronary Syndrome.

Importance: The association of parenteral anticoagulation therapy with improved outcomes in patients with non-ST-segment elevation acute coronary syndrome was previously established. This benefit has not been evaluated in the era of dual antiplatelet therapy and percutaneous coronary intervention. Objective: To evaluate the association between parenteral anticoagulation therapy and clinical outcomes in patients with non-ST-segment elevation acute coronary syndrome undergoing percutaneous coronary intervention. Design, Setting, and Participants: This cohort study included 8197 adults who underwent percutaneous coronary intervention for non-ST-segment elevation acute coronary syndrome from January 1, 2010, to December 31, 2014, at 5 medical centers in China. Patients receiving parenteral anticoagulation therapy only after percutaneous coronary intervention were excluded. Exposures: Parenteral anticoagulation therapy. Main Outcomes and Measures: The primary outcome was in-hospital all-cause death and in-hospital major bleeding as defined by the Bleeding Academic Research Consortium definition (grades 3-5). Results: Of 6804 patients who met the final criteria, 5104 (75.0%) were male, with a mean (SD) age of 64.2 (10.4) years. The incidence of in-hospital death was not significantly different between the patients who received and did not receive parenteral anticoagulation therapy (0.3% vs 0.1%; P = .13) (adjusted odds ratio, 1.27; 95% CI, 0.38-4.27; P = .70). A similar result was found for myocardial infarction (0.3% vs 0.3%; P = .82) (adjusted odds ratio, 0.77; 95% CI, 0.29-2.07; P = .61). In-hospital major bleeding was more frequent in the parenteral anticoagulation group (2.5% vs 1.0%; P < .001) (adjusted odds ratio, 1.94; 95% CI, 1.24-3.03; P = .004). At a median (interquartile range) follow-up of 2.96 years (1.93-4.46 years), all-cause death was not significantly different between the 2 groups (adjusted hazards ratio, 0.87; 95% CI, 0.71-1.07; P = .19), but the incidence of major bleeding was higher in the parenteral anticoagulation group (adjusted hazards ratio, 1.43; 95% CI, 1.01-2.02; P = .04). The propensity score analysis confirmed these primary analyses. Conclusions and Relevance: In the patients undergoing percutaneous coronary intervention for non-ST-segment elevation acute coronary syndrome, parenteral anticoagulation therapy was not associated with a lower risk of all-cause death or myocardial infarction but was significantly associated with a higher risk of major bleeding. These findings raise important safety questions about the current practice of routine parenteral anticoagulation therapy while we await randomized trials of this practice.

Targeting myocyte-specific enhancer factor 2D contributes to the suppression of cardiac hypertrophic growth by miR-92b-3p in mice.

The role of microRNA-92b-3p (miR-92b-3p) in cardiac hypertrophy was not well illustrated. The present study aimed to investigate the expression and potential target of miR-92b-3p in angiotensin II (Ang-II)-induced mouse cardiac hypertrophy. MiR-92b-3p was markedly decreased in the myocardium of Ang-II-infused mice and of patients with cardiac hypertrophy. However, miR-92b-3p expression was revealed increased in Ang-II-induced neonatal mouse cardiomyocytes. Cardiac hypertrophy was shown attenuated in Ang-II-infused mice received tail vein injection of miR-92b-3p mimic. Moreover, miR-92b-3p inhibited the expression of atrial natriuretic peptide (ANP), skeletal muscle α-actin (ACTA1) and ß-myosin heavy chain (MHC) in Ang-II-induced mouse cardiomyocytes in vitro. Myocyte-specific enhancer factor 2D (MEF2D), which was increased in Ang-II-induced mouse hypertrophic myocardium and cardiomyocytes, was identified as a target gene of miR-92b-3p. Functionally, miR-92b-3p mimic, consistent with MEF2D siRNA, inhibited cell size increase and protein expression of ANP, ACTA1 and ß-MHC in Ang-II-treated mouse cardiomyocytes. Taken together, we demonstrated that MEF2D is a novel target of miR-92b-3p, and attenuation of miR-92b-3p expression may contribute to the increase of MEF2D in cardiac hypertrophy.

Concomitant coronary and renal revascularization improves left ventricular hypertrophy more than coronary stenting alone in patients with ischemic heart and renal disease.

Percutaneous transluminal renal artery stenting (PTRAS) has been proved to have no more benefit than medication alone in treating atherosclerotic renal artery stenosis (ARAS). Whether PTRAS could improve left ventricular hypertrophy (LVH) and reduce adverse events when based on percutaneous coronary intervention (PCI) for patients with coronary artery disease (CAD) and ARAS is still unclear. A retrospective study was conducted, which explored the effect of concomitant PCI and PTRAS versus PCI alone for patients with CAD and ARAS complicated by heart failure with preserved ejection fraction (HFpEF). A total of 228 patients meeting inclusion criteria were divided into two groups: (1) the HFpEF-I group, with PCI and PTRAS; (2) the HFpEF-II group, with PCI alone. Both groups had a two-year follow-up. The left ventricular mass index (LVMI) and other clinical characteristics were compared between groups. During the follow-up period, a substantial decrease in systolic blood pressure (SBP) was observed in the HFpEF-I group, but not in the HFpEF-II group. There was marked decrease in LVMI in both groups, but the HFpEF-I group showed a greater decrease than the HFpEF-II group. Regression analysis demonstrated that PTRAS was significantly associated with LVMI reduction and fewer adverse events after adjusting for other factors. In HFpEF patients with both CAD and ARAS, concomitant PCI and PTRAS can improve LVH and decrease the incidence of adverse events more than PCI alone. This study highlights the beneficial effect of ARAS revascularization, as a new and more aggressive revascularization strategy for such high-risk patients.

Safe limits of contrast vary with hydration volume for prevention of contrast-induced nephropathy after coronary angiography among patients with a relatively low risk of contrast-induced nephropathy.

BACKGROUND: Few studies have investigated the safe limits of contrast to prevent contrast-induced nephropathy (CIN) based on hydration data. We aimed to investigate the relative safe maximum contrast volume adjusted for hydration volume in a population with a relatively low risk of CIN. METHODS AND RESULTS: The ratios of contrast volume-to-creatinine clearance (V/CrCl) and hydration volume to body weight (HV/W) were determined in patients undergoing cardiac catheterization. Receiver-operator characteristic curve analysis based on the maximum Youden index was used to identify the optimal cutoff for V/CrCl in all patients and in HV/W subgroups. Eighty-six of 3273 (2.6%) patients with mean CrCl 71.89±27.02 mL/min developed CIN. Receiver-operator characteristic curve analysis indicated that a V/CrCl ratio of 2.44 was a fair discriminator for CIN in all patients (sensitivity, 73.3%; specificity, 70.4%). After adjustment for other confounders, V/CrCl >2.44 continued to be significantly associated with CIN (adjusted odds ratio, 4.12; P<0.001) and the risk of death (adjusted hazard ratio, 2.62; P<0.001). The mean HV/W was 12.18±7.40. We divided the patients into 2 groups (HV/W ≤12 and >12 mL/kg). The best cutoff value for V/CrCl was 1.87 (sensitivity, 67.9%; specificity, 64.4%; adjusted odds ratio, 3.24; P=0.011) in the insufficient hydration subgroup (HV/W, ≤12 mL/kg; CIN, 1.32%) and 2.93 (sensitivity, 69.0%; specificity, 65.0%; adjusted odds ratio, 3.04; P=0.004) in the sufficient hydration subgroup (HV/W, >12 mL/kg; CIN, 5.00%). CONCLUSIONS: The V/CrCl ratio adjusted for HV/W may be a more reliable predictor of CIN and even long-term outcomes after cardiac catheterization. We also found a higher best cutoff value for V/CrCl to predict CIN in patients with a relatively sufficient hydration status, which may be beneficial during decision-making about contrast dose limits in relatively low-risk patients with different hydration statuses.

Contrast-induced nephropathy following chronic total occlusion percutaneous coronary intervention in patients with chronic kidney disease.

OBJECTIVES: Contrast-induced nephropathy (CIN) has not been systematically studied in high-risk patients with chronic kidney disease (CKD) undergoing percutaneous coronary intervention (PCI) for chronic total occlusion (CTO). METHODS: We prospectively observed 515 consecutive patients with CKD undergoing PCI. Patients were divided into three groups: patients who underwent attempted PCI for CTO (group A, n = 85), patients who did not receive PCI for CTO (group B, n = 45) and patients without CTO (group C, n = 385). RESULTS: CIN developed in 55 patients (10.68 %). Group A patients received a larger CM dose than group B or group C (p = 0.024). The intravenous hydration volume, age and CIN Mehran score were not significantly different between the three groups. The incidence of CIN was 9.4 % for group A, 6.7 % for group B and 11.4 % for group C (p = 0.344). In-hospital mortality and required renal replacement therapy (p = 0.325) were not significantly different between the groups. Multivariate analysis showed that after adjusting for potential confounding factors, the odds ratio for CIN was 1.03 (p = 0.944) for group A and 0.64 for group B (p = 0.489) compared to group C. CONCLUSIONS: Attempts to achieve recanalization of CTO in patients with CKD might not increase the risk of CIN if appropriate preventative measures are taken. KEY POINTS: • Contrast-induced nephropathy can increase morbidity and mortality • Chronic kidney disease patients are at the greatest risk of CIN • Patients with CKD undergoing CTO-PCI are common • Incidence of CIN has not been reported in CKD patients • CTO-PCI in CKD patients might not increase the risk of CIN.

[Prophylactic antibiotics: a necessity in totally percutaneous thoracic endovascular aortic repair?].

OBJECTIVE: To study the benefit of prophylactic antibiotics (PA) in totally percutaneous aortic endovascular repair (PEVAR) in the catheterization laboratory for reducing stent-graft infection and postimplantation syndrome (PIS). METHODS: The clinical data were analyzed of patients undergoing thoracic endovascular aortic repairs. The patients were divided into non-PA group and PA group according to the use of prophylactic antibiotics before PEVAR. The diagnosis of infection was made by two senior physicians with reference to Hospital Acquired Infection Diagnostic Criteria Assessment released by the Ministry of Health of China. RESULTS: The 95 enrolled patients included 35 with PA and 60 without PA group, who were comparable for baseline characteristics. Infection-related deaths occurred in 1 case in non-PA group and retrograde Stanford type A dissection and death occurred in 1 case in PA group (1.67% vs 2.85%, P=1.00). The PA and non-PA groups showed no significant difference in the incidence of postoperative infection (5% vs 2.86%, P=1.000), hospital stay (9.30±7.21 vs 10.06±5.69, P=0.094), infection-related mortality (1.67% vs 0%, P=1.00), or postoperative fever (70.90% vs 91.43%, P=0.20). The body temperature showed significant variations at different time points after procedure (F=19.831, P<0.001) irrelevant to the use of prophylactic antibiotics (F=0.978, P=0.326). CONCLUSION: The current data do not support the benefit of PA in reducing postoperative infection and PIS in patients undergoing PEVAR, but the patients without PA may have worse clinical outcomes in the event of postoperative infections.

Decrease of glomerular filtration rate may be attributed to the microcirculation damage in renal artery stenosis.

BACKGROUND: The decrease of glomerular filtration rate has been theoretically supposed to be the result of low perfusion in renal artery stenosis (RAS). But the gap between artery stenosis and the glomerular filtration ability is still unclear. METHODS: Patients with selective renal artery angiogram were divided by the degree of renal artery narrowing, level of estimated glomerular filtration rate (eGFR), respectively. The different levels of eGFR, renal microcirculation markers, and RAS severity were compared with each other, to determine the relationships among them. RESULTS: A total of 215 consecutive patients were enrolled in the prospective cohort study. Concentrations of microcirculation markers had no significant difference between RAS group (RAS ≥ 50%) and no RAS group (RAS < 50%) or did not change correspondingly to RAS severity. The value of eGFR in RAS group was lower than that in the no RAS group, but it did not decline parallel to the progressive severity of RAS. The microcirculation markers presented integral difference if grouped by different eGFR level with negative tendency, especially that plasma cystatin C (cysC) and urinary microalbumin to creatinine ratio (mACR) increased with the deterioration of eGFR, with strong (r = -0.713, P < 0.001) and moderate (r = -0.580, P < 0.001) correlations. In the subgroup analysis of severe RAS (RAS ≥ 80%), the levels of plasma cysC and urinary mACR demonstrated stronger negative associations with eGFR, (r = -0.827, P < 0.001) and (r = -0.672, P < 0.001) correlations, respectively. CONCLUSIONS: Severity of RAS could not accurately predict the value of eGFR, whereas microcirculation impairment may substantially contribute to the glomerular filtration loss in patients with RAS.

LDL cholesterol as a novel risk factor for contrast-induced acute kidney injury in patients undergoing percutaneous coronary intervention.

BACKGROUND: Low density lipoprotein cholesterol (LDL-C) is associated with endothelial dysfunction, inflammation and increased vasoconstriction, which are involved in the development of contrast-induced acute kidney injury (CI-AKI). However, whether LDL-C is an independent risk factor of CI-AKI in patients undergoing percutaneous coronary intervention (PCI) is unknown. METHODS: We prospectively enrolled 3236 consecutive patients undergoing PCI between January 2010 and September 2012. Multivariate logistic regression analysis was used to determine whether LDL-C is an independent risk factor of CI-AKI. CI-AKI was defined as an absolute increase in serum creatinine of ≥ 0.5 mg/dL or ≥ 25% over the baseline value within 48-72 h after contrast exposure. RESULTS: CI-AKI was observed in 338 patients (10.4%). Patients with CI-AKI had a significantly higher rate of in hospital mortality (4.4% vs. 0.5%, p < 0.001), and significantly higher rates of other in hospital complications compared with those without CI-AKI. The LDL-C quartiles were as follows: Q1 (<2.04 mmol/L), Q2 (2.04-2.61 mmol/L), Q3 (2.61-3.21 mmol/L) and Q4 (>3.21 mmol/L). Patients with high baseline LDL-C levels were more likely to develop CI-AKI and composite end points including all-cause mortality, renal replacement therapy, non-fatal myocardial infarction, acute heart failure, target vessel revascularization or cerebrovascular accident during the observation period of hospitalization (8.9%, 9.9%, 10.5%, 12.6%, p = 0.001, and 5.0%, 5.2%, 6.1%, 8.1%, respectively; p = 0.007). Univariate logistic analysis showed that LDL-C levels (increment 1 mmol/L) were significantly associated with CI-AKI (odds ratio = 1.25, 95% confidence interval (CI), 1.11-1.39, p < 0.001). Furthermore, LDL-C remained a significant risk factor of CI-AKI (odds ratio = 1.23, 95% CI, 1.04-1.45, p = 0.014), even after adjusting for potential confounding risk factors. CONCLUSIONS: Measurement of plasma LDL-C concentrations in patients undergoing PCI may be helpful to identify those who are at risk of CI-AKI and poor in hospital outcomes.

Comparison of the efficacy of rosuvastatin versus atorvastatin in preventing contrast induced nephropathy in patient with chronic kidney disease undergoing percutaneous coronary intervention.

OBJECTIVES: We prospectively compared the preventive effects of rosuvastatin and atorvastatin on contrast-induced nephropathy (CIN) in patients with chronic kidney disease (CKD) undergoing percutaneous coronary intervention (PCI). METHODS: We enrolled 1078 consecutive patients with CKD undergoing elective PCI. Patients in Group 1 (n = 273) received rosuvastatin (10 mg), and those in group 2 (n = 805) received atorvastatin (20 mg). The primary end-point was the development of CIN, defined as an absolute increase in serum creatinine ≥0.5 mg/dL, or an increase ≥25% from baseline within 48-72 h after contrast medium exposure. RESULTS: CIN was observed in 58 (5.4%) patients. The incidence of CIN was similar in patients pretreated with either rosuvastatin or atorvastatin (5.9% vs. 5.2%, p = 0.684). The same results were also observed when using other definitions of CIN. Clinical and procedural characteristics did not show significant differences between the two groups (p>0.05). Additionally, there were no significant inter-group differences with respect to in-hospital mortality rates (0.4% vs. 1.5%, p = 0.141), or other in-hospital complications. Multivariate logistic regression analysis revealed that rosuvastatin and atorvastatin demonstrated similar efficacies for preventing CIN, after adjusting for potential confounding risk factors (odds ratio = 1.17, 95% confidence interval, 0.62-2.20, p = 0.623). A Kaplan-Meier survival analysis showed that patients taking either rosuvastatin or atorvastatin had similar incidences of all-cause mortality (9.4% vs. 7.1%, respectively; p = 0.290) and major adverse cardiovascular events (29.32% vs. 23.14%, respectively; p = 0.135) during follow-up. CONCLUSIONS: Rosuvastatin and atorvastatin have similar efficacies for preventing CIN in patients with CKD undergoing PCI.

Changes of cerebrospinal fluid pressure after thoracic endovascular aortic repair.

BACKGROUND: Decreasing the intracranial pressure has been advocated as one of the major protective strategies to prevent spinal cord ischemia after endovascular aortic repair. However, the actual changes of cerebrospinal fluid (CSF) pressure and its relation with spinal cord ischemia have been poorly understood. We performed CSF pressure measurements and provisional CSF withdrawal after thoracic endovascular aortic repair, and compared the changes of CSF pressure in high risk patients and in patients with new onset paraplegia and paraparesis. METHODS: Four hundred and nineteen patients were evaluated for the risk of spinal cord ischemia after thoracic endovascular aortic repair. Patients with identified risk factors before the procedure constituted group H and received prophylactic sequential CSF pressure measurement and CSF withdrawal. Patients who actually developed spinal cord ischemia constituted group P and received rescue CSF pressure measurements and CSF withdrawal. RESULTS: Among the 419 patients evaluated, 17 were graded as high risk. Four patients actually developed spinal cord ischemia after endovascular repair. The incidence of spinal cord ischemia in this investigation was 0.9%. The patients who actually developed spinal cord ischemia had no identified risk factors and had elevated CSF pressure, ranging from 15.4 to 30.0 mmHg. Six of the 17 patients graded as high risk had elevated CSF pressure: >20 mmHg in two patients and >15 mmHg in four patients. Sequential CSF pressure measurements and provisional withdrawal successfully decrease CSF pressure and prevented symptomatic spinal cord ischemia in high-risk patients. However, these measurements could only successfully reverse the neurologic deficit in two of the patients who actually developed spinal cord ischemia. CONCLUSIONS: Cerebrospinal fluid pressure was elevated in patients with spinal cord ischemia after thoracic endovascular aortic repair. Sequential measurements of CSF pressure and provisional withdrawal of CSF decreased CSF pressure effectively in high risk patients and provided effective prevention of spinal cord ischemia. Risk factor identification and prophylactic measurements play the key role in prevention of spinal cord ischemia after thoracic endovascular aortic repair.

[Analysis of coronary rotational atherectomy related complications].

OBJECTIVE: To analysis the complications of coronary rotational atherectomy and evaluate the safety of this procedure. METHOD: A total of 250 rotational atherectomy cases from April 1994 to February 2012 were screened retrospectively and 22 cases patients (8.8%) with rotational atherectomy-related complications were included in this analysis. RESULTS: Among these 22 patients, all lesions were either type B2 or C calcified lesions as evidenced by coronary angiography. After the rotation procedure, there were seven cases (2.8%) with slow reflow and two (0.8%) cases with no reflow. Seven cases (2.8%) developed severe coronary spasm and two cases (0.8%) had sinus bradycardia. Coronary dissection occurred in two cases (0.8%), while one case (0.4%) had coronary perforation and cardiac tamponade. Burr entrapment happened in one case (0.4%). There was no malignant arrhythmia, acute myocardial infarction, emergent coronary artery bypass graft or device related death during and post procedure. Comparison with baseline data, the concentration of CK-MB elevated significantly after the rotational atherectomy [(31.2 ± 4.8) mmol/L vs. (11.4 ± 6.5) mmol/L, P < 0.05]. CONCLUSION: Coronary rotational atherectomy is safe and procedure-related complications are rare.

Perioperative aortic dissection rupture after endovascular stent graft placement for treatment of type B dissection.

BACKGROUND: The perioperative aortic dissection (AD) rupture is a severe event after endovascular stent graft placement for treatment of type B AD. However, this life-threatening complication has not undergone systematic investigation. The aim of the study is to discuss the reasons of AD rupture after the procedure. METHODS: The medical record data of 563 Stanford type B AD patients who received thoracic endovascular repair from 2004 to December 2011 at our institution were collected and analyzed. Double entry and consistency checking were performed with Epidata software. RESULTS: Twelve patients died during the perioperation after thoracic endovascular repair, with an incidence of 2.1%, 66.6% were caused by aortic rupture and half of the aortic rupture deaths were caused by retrograde type A AD. In our study, 74% of the non-rupture surviving patients had the free-flow bare spring proximal stent implanted, compared with 100% of the aortic rupture patients (74% vs. 100%, P = 0.213). The aortic rupture patients are more likely to have ascending aortic diameters = 4 cm (62.5% vs. 9.0%, P = 0.032), involvement the aortic arch concavity (62% vs. 27%, P = 0.041) and have had multiple stents placed (P = 0.039). CONCLUSIONS: Thoracic AD endovascular repair is a safe and effective treatment option for AD with relative low in-hospital mortality. AD rupture may be more common in arch stent-graft patients with an ascending aortic diameter = 4 cm and with severe dissection that needs multi-stent placement. Attention should be paid to a proximal bare spring stent that has a higher probability of inducing an AD rupture. Post balloon dilation should be performed with serious caution, particularly for the migration during dilation.

Transradial artery intervention: an alternative approach for renal artery stent implantation?

BACKGROUND: Transfemoral artery access is the main approach for the interventional treatment of renal artery stenosis (RAS). This study aimed to investigate the technical feasibility of a transradial interventional (TRI) treatment of renal artery stenosis. METHODS: A series of 23 patients who underwent transradial renal artery stenting from October 2010 to October 2011 were studied. Radial sheath system (Terumo, Japan) was used to get access to the radial artery. Radial tourniquet (Terumo) was used to stop bleeding. A 5Fr MPA (COOK, USA) was used to perform selective renal arteriography. Percutaneous renal artery stent systems were used to perform renal artery stenting. RESULTS: Renal artery angiography showed that 15 patients had unilateral renal artery stenosis and eight patients had bilateral renal artery stenosis. The descending aorta could not be catheterized in one patient because of the type III aortic arch. Twenty-two patients successfully underwent transradial renal artery angiography and the technical success rate was 95.7%. There was no puncture site hematoma or pseudoaneurysm. Mean procedure time was (38.4 ± 7.2) minutes, the mean amount of contrast agent used was (93.2 ± 6.3) ml, and the mean postprocedure bleeding time was (3.2 ± 1.9) minutes. CONCLUSION: Transradial renal artery intervention is technically reliable with less invasion, rapid recovery, fewer complications and may become an alternative intervention approach for the treatment of renal artery stenosis.

[MicroRNAs expression in normal and dissected aortic tissue].

OBJECTIVES: To investigate if there is altered microRNAs (miRNAs) expression in aortic dissection (Debakey Type A) and normal aorta tissue. METHODS: Total RNA was exacted from aorta of 5 patients with aortic dissection (AD) and four patients without aortic diseases (NA). miRNAs of the aortic tissues were analyzed by miRNA microarray. Reverse transcription polymerase chain reaction (RT-PCR) was performed to verify the expression of miRNAs in larger sample size (AD = 11 and NA = 9). RESULTS: hsa-miR-146b-5p_st, hsa-miR-19a_st and hsa-miR-505_st were significantly upregulated while hsa-miR-1268_st and hsa-miR-939_st were significantly downregulated [fold change > 2, q-value (%) ≤ 5] in AD group compared with NA group. RT-PCR verified hsa-miR-146b-5p_st miRNAs change in AD group. CONCLUSIONS: Altered miRNAs expression might play an essential role in the pathogenesis of aortic dissection formation and hsa-miR-146b-5p_st might serve as a new diagnosis biomarker of aortic dissection.

Contrast medium volume to creatinine clearance ratio: a predictor of contrast-induced nephropathy in the first 72 hours following percutaneous coronary intervention.

OBJECTIVES: To investigate the predictive value of the contrast media volume to creatinine clearance (V/CrCl) ratio for the risk of contrast-induced nephropathy (CIN) (i.e., within 48-72 hr) and to determine a relatively safe V/CrCl cut-off value to avoid CIN in patients following percutaneous coronary intervention (PCI). BACKGROUND: The V/CrCl ratio is a pharmacokinetic risk factor for an early abnormal increase in serum creatinine (i.e., within 24 hr) after PCI. METHODS: V/CrCl ratios were obtained from 1,140 consecutive consenting patients after unselective PCI. Receiver-operator characteristic (ROC) curves were used to identify the optimal sensitivity for the observed range of V/CrCl. The predictive value of V/CrCl for the risk of CIN was assessed using multivariate logistic regression. RESULTS: Fifty-five (4.8%) patients out of 1,140 developed CIN. There was a significant association between higher V/CrCl ratio values and risk of CIN in the overall population: 1.4%, 1.4%, 5.7%, and 10.9% for quartile 1 (Q1) of the V/CrCl value (<1.56, n = 283), Q2 (1.56-2.27, n = 289), Q3 (2.28-3.42, n = 282), and Q4 (>3.42, n = 285) of contrast, respectively (P < 0.001). ROC curve analysis indicated that a V/CrCl ratio of 2.62 was a fair discriminator for CIN (C-statistic 0.73). After adjusting for other known predictors of CIN, V/CrCl ratios > 2.62 remained significantly associated with CIN (odds ratio: 2.20; 95% confidence interval: 1.00-4.81, P < 0.05). CONCLUSION: A V/CrCl ratio > 2.62 was a significant and independent predictor of CIN after PCI in unselected patients.

High-sensitivity C-reactive protein predicts contrast-induced nephropathy after primary percutaneous coronary intervention.

BACKGROUND: Few studies have investigated hs-CRP as a risk factor for contrast-induced nephropathy (CIN). The aim of this study was to evaluate the predictive value of high-sensitivity C-reactive protein (hs-CRP) for risk of CIN in patients with acute ST-segment elevation myocardial infarction (STEMI) who were undergoing primary percutaneous coronary intervention (PCI). METHODS: We prospectively observed 165 consenting patients with STEMI undergoing primary PCI. An increase in serum creatinine of more than 0.5 mg/dL from baseline within 48-72 hours of contrast media exposure was defined as CIN. Demographics, traditional risk factors, CIN incidence and other in-hospital clinical outcomes were compared among hs-CRP quartiles. Receiver operator characteristic curves were used to identify the optimal sensitivity for the observed range of hs-CRP. The predictive value of hs-CRP for the risk of CIN was assessed using multivariate logistic regression. RESULTS: CIN occurred in 17 patients (10%). Univariate analysis revealed CIN incidence was significantly associated with hs-CRP, with 2.4% for quartile Q1 (<6.00 mg/L), 2.3% for Q2 (6.00-13.90), 12.5% for Q3 (13.91-32.75) and 24.4% for Q4 (>32.75) (P-trend <0.001), as was in-hospital death (0% for Q1, 2.3% for Q2, 5% for Q3 and 12.2% for Q4; P-trend = 0.009). Receiver operator characteristic curve analysis showed that an hs-CRP of 16.10 mg/L was a fair discriminator for the early creatinine increase (C statistic 0.78). After adjusting for potential confounding predictors, hs-CRP >16.10 mg/L remained significantly associated with CIN (odds ratio = 6.51; 95% confidence interval, 1.26-33.61). CONCLUSION: An hs-CRP >16.10 was a significant and independent predictor of CIN after primary PCI in patients with STEMI.