Computed tomography coronary angiography (CTCA) has been successfully integrated with the magnetic navigation system (MNS) to facilitate a roadmap-assisted percutaneous coronary intervention (PCI). The aim of this study was to compare this new approach of PCI versus conventional PCI regarding the difference of contrast usage, X-ray exposure, procedure success and the in-hospital expenses.
Methods
Thirty-eight patients with stable coronary artery disease and coronary artery lesions of ≥ 70% diameter stenosis diagnosed by both pre-procedure CTCA and coronary angiography (CAG) were enrolled to receive the MNS and CT roadmap-assisted PCI. Another 38 patients were consecutively recruited to receive conventional PCI, matched with the MNS group by the vessel and lesion type base on ACC/AHA criteria.
Results
Regarding the process of the guidewire placement where the technical difference of the two procedures exists in, the median contrast usage for guidewire crossing was significantly lower in the MNS group than that in the conventional group [0.0 (0.0, 3.0) vs. 5.0 (3.1, 6.8) mL; P < 0.001], with zero contrast usage in 25 of the 44 guidewire placements in the MNS group, but in none of the conventional group; the radiation dosage for guidewire crossing in the MNS group was also significantly lower than that in the conventional group [235.8 (134.9, 455.1) vs. 364.4 (223.4, 547.2) μGym2; P = 0.033]. There were no significant differences between the two groups concerning the total contrast usage, total radiation dosage of the PCI, the procedural fees, or the overall in-hospital expenses. All of the enrolled vessels were successfully intervened in both groups.
Conclusions
In PCI of simple lesions, the applicaiton of CT guidance and magnetic navigation had modest impacts on radiation dosage and contrast usage for wire crossing, but no impact on overall radiation dosage or contrast usage for the procedure. In addition, the use of CT roadmap and MNS was likely more expensive compared to PCI using conventional radiographic technique.
Abstract Objective This study was aimed to investigate an optimal therapeutic window for platelet reactivity (PR) to predict the lowest ischemic and bleeding events in patients underwent percutaneous coronary intervention (PCI) and treated with dual antiplatelet agents. Design A total of 1709 patients who had received coronary stent implantation and had taken aspirin 100 mg in combination with clopidogrel 75 mg daily for >5 days were consecutively recruited and their platelet reactivity was determined by light transmittance aggregometry (LTA). All patients were followed up for 12 months. The primary end-point was the net adverse clinical events (NACE) of cardiovascular death, nonfatal myocardial infarction (MI), target vessel revascularization (TVR) , stent thrombosis (ST) and any bleeding. Result By using the receiver-operating curve (ROC) analysis, the optimal cutoff values were found to be 37.5% and 25.5% respectively in predicting ischemic and bleeding events. Patients were classified into 2 groups according to PR: inside the window group (IW) [adenosine diphosphate (ADP) induced platelet aggregation (PL ADP ) 25.5%-37.4%)] and outside the window group (OW) (PL ADP <25.5% or ≥37.5%). The incidence of NACE was 16.8% and 23.1% respectively in the IW and OW group. The hazard ratio of NACE in IW-group was significantly lower [0.69 (95% CI: 0.54–0.89; P = 0.004)] than that in the OW-group during 12 month follow-up. Conclusion An optimal therapeutic window of 25.5%-37.4% for PL ADP predicts the lowest risk of NACE, which could be referred for tailored antiplatelet treatment while using LTA assay. Trial and clinical registry Trial registration number: ClinicalTrials.gov NCT01968499. Registered 18 October 2013 - Retrospectively registered.
Objective The relationship between admission serum calcium levels and in-hospital mortality in patients with acute ST-segment elevation myocardial infarction (STEMI) has not been well definitively explored. The objective was to assess the predictive value of serum calcium levels on in-hospital mortality in STEMI patients. Methods From 2003 to 2010, 1431 consecutive STEMI patients admitted to the First Affiliated Hospital of Nanjing Medical University were enrolled in the present study. Patients were stratified according to quartiles of serum calcium from the blood samples collected in the emergency room after admission. Between the aforementioned groups,the baseline characteristics, in-hospital management, and in-hospital mortality were analyzed. The association of serum calcium level with in-hospital mortality was calculated by a multivariable Cox regression analysis. Results Among 1431 included patients, 79% were male and the median age was 65 years (range, 55–74). Patients in the lower quartiles of serum calcium, as compared to the upper quartiles of serum calcium, were older, had more cardiovascular risk factors, lower rate of emergency revascularization,and higher in-hospital mortality. According to univariate Cox proportional analysis, patients with lower serum calcium level (hazard ratio 0.267, 95% confidence interval 0.164–0.433, p<0.001) was associated with higher in-hospital mortality. The result of multivariable Cox proportional hazard regression analyses showed that the Killip's class≥3 (HR = 2.192, p = 0.026), aspartate aminotransferase (HR = 1.001, p<0.001), neutrophil count (HR = 1.123, p<0.001), serum calcium level (HR = 0.255, p = 0.001), and emergency revascularization (HR = 0.122, p<0.001) were significantly and independently associated with in-hospital mortality in STEMI patients. Conclusions Serum calcium was an independent predictor for in-hospital mortality in patients with STEMI. This widely available serum biochemical index may be incorporated into the current established risk stratification model of STEMI patients. Further studies are required to determine the actual mechanism and whether patients with hypocalcaemia could benefit from calcium supplement.
Background Vascular calcification (VC), associated with enhanced cardiovascular morbidity and mortality, is characterized by the osteogenic transdifferentiation of vascular smooth muscle cells. Inflammation promotes VC initiation and progression. Interleukin (IL)-29, a newly discovered member of type III interferon, has recently been implicated in the pathogenesis of autoimmune diseases. Here we evaluated the role of IL-29 in the VC process and underlying inflammatory mechanisms. Methods and Results The mRNA expression of IL-29 was significantly increased and positively associated with an increase in BMP2 (bone morphogenetic protein 2) mRNA level in calcified carotid arteries from patients with coronary artery disease or chronic kidney disease. IL-29 and BMP2 proteins are colocalized in human calcified arteries. IL-29 binding to its specific receptor IL-28Rα (IL-28 receptor α) (IL-29/IL-28Rα) inhibited the proliferation of rat vascular smooth muscle cells without altering cell apoptosis or migration. IL-29 promoted the calcification of rat vascular smooth muscle cells and their osteogenic transdifferentiation in vitro as well as the rat aortic ring calcification ex vivo, induced by the calcification medium or osteogenic medium. The procalcification effect of IL-29 was reduced by pharmacological inhibition of IL-29/IL-28Rα binding as well as suppression of janus kinase 2/signal transducer and activator of transcription pathway activation, accompanied by decreased BMP2 expression in the cultured rat vascular smooth muscle cells. Conclusions These results suggest an important role of IL-29 in VC development, at least partly, via activating the janus kinase 2/signal transducer and activator of transcription 3 signaling. Inhibition of IL-29 or its specific receptor, IL-28Rα, may provide a novel strategy to reduce VC in patients with vascular diseases.
Objective:To observe the thrombolytic efficacy of recombinant staphylokinase (r SAK) in patients with acute myocardial infarction (AMI) .Method:Five AMI patients were enrolled with the age less than 60 years old and the onset of chest pain less than 6 hours. After angiography of the infarct related arteries was performed, 15 mg r SAK was administered intravenously in combination with intravenous heparin. Coronary artery angiography (CAG) was re performed at 15, 30, 45, 60, 90 minutes and 1 or 2 weeks post thrombolysis. The thrombolytic in myocardial infarction (TIMI) perfusion grade and the residual stenosis of the culprit vessels post thrombolysis were recorded. The relief of chest pain, appearance of reperfusion arrhythmia, alteration of ST segment and time to peak plasma level of myocardial enzymes were noticed. In addition, the related complications and cardiac events were followed up whenever it pressented.Result:CAG showed that the culprit vessels were proximal right coronary artery in one case, first diagonal branch in another, and proximal left anterior descending branch in the next three cases. All the culprit vessels were totally occluded prior to thrombolysis. After r SAK thrombolysis, all occluded arteries recanalized with the TIMI flow in two patients reached grade 3 and in the next three patients, between 2 and 3, the averaged time to reperfusion was ( 34.0 ± 14.7 ) minutes. Five patients were all clinically evaluated reperfusion. There was no severe bleeding or cardiac events pressent in any of the patients.Conclusion:A favorable efficacy/safety of intravenous 15 mg dose of r SAK is approved in this study, and further investigation is warranted.
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