Publications

Background— Presently, no effective risk model exists to predict long-term mortality or other major adverse cardiovascular and cerebrovascular events (MACCE) in those patients undergoing percutaneous coronary intervention (PCI). This study aimed to assess whether the Clinical SYNTAX Score (CSS) calculated by multiplying the SYNTAX Score to a modified ACEF score (age/ejection fraction +1 for each 10 mL the creatinine clearance <60 mL/min per 1.73 m 2 ) would improve the ability of either score to predict mortality and MACCE. Methods and Results— The CSS was calculated in 512 patients enrolled in the ARTS-II study who had serum creatinine levels, ejection fraction, and body weight recorded at baseline. Clinical outcomes in terms of MACCE and mortality at 1- and 5-year follow-up were stratified according to CSS tertiles: CSS LOW ≤15.6 (n=170), 15.6<CSS MID ≤27.5 (n=171), and CSS HIGH >27.5 (n=171). At 1-year follow-up, rates of repeat revascularization and MACCE were significantly higher in the highest tertile group. At 5-year follow-up, CSS HIGH had a comparable rate of myocardial infarction, a trend toward a significantly higher rate of death, and significantly higher rates of repeat revascularization and overall MACCE compared with patients in the lower 2 tertiles. The respective C-statistics for the CSS, SYNTAX Score, and ACEF score for 5-year mortality were 0.69, 0.62, and 0.65 and for 5-year MACCE were 0.62, 0.59, and 0.57. Conclusions— An improvement in the ability of the SYNTAX Score to predict MACCE and mortality can be achieved by combining the SYNTAX Score with a simple clinical risk score incorporating age, ejection fraction, and creatinine clearance to produce the Clinical SYNTAX score. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00235170.

Most of the studies linking chronic obstructive pulmonary disease (COPD) with oxidative stress are in vitro, using invasive techniques, or measuring systemic oxidative stress. The aim of this study was to quantify oxidative stress in the lungs in patients with COPD and in healthy smokers, as reflected by 8-isoprostane concentrations in breath condensate. This is a noninvasive method to collect airway secretions. 8-Isoprostane is a prostaglandin-F(2alpha) isomer that is formed in vivo by free radical-catalyzed peroxidation of arachidonic acid. We also studied the acute effect of smoking on exhaled 8-isoprostane in healthy smokers. Exhaled 8-isoprostane was measured by a specific enzyme immunoassay in 10 healthy nonsmokers and 12 smokers, 25 COPD ex-smokers, and 15 COPD current smokers. 8-Isoprostane concentrations were similar in COPD ex-smokers (40 +/- 3.1 pg/ml) and current smokers (45 +/- 3.6 pg/ ml) and were increased about 1.8-fold compared with healthy smokers (24 +/- 2.6 pg/ml, p < 0.001), who had 2.2-fold higher 8-isoprostane than healthy nonsmokers (10.8 +/- 0.8 pg/ml, p < 0.05). Smoking caused an acute increase in exhaled 8-isoprostane by about 50%. Our study shows that free radical production is increased in patients with COPD and that smoking causes an acute increase in oxidative stress.

No abstract is provided for this article.

No abstract is provided for this article.

No abstract is provided for this article.

Background Local haemodynamic disturbances in coronary blood flow are associated with abnormal endothelial shear stress (ESS) and progressive atherosclerosis. However, standard techniques to estimate ESS lack the diagnostic specificity necessary for future clinical utility. Possible improvements include use of a more realistic non-Newtonian model of blood, which may provide more accurate ESS measurements and is further able to detect local variations in blood viscosity. Purpose To compare accuracy of ESS generated by Newtonian versus non-Newtonian rheological models to detect coronary plaque progression. To investigate local Reynolds number (ReL), a viscosity-based haemodynamic metric calculated by the non-Newtonian model, as an independent marker of plaque progression. Methods Sixteen patients with non-culprit plaques completely visualised in serial optical coherence tomography (OCT) imaging were identified. Plaques were analysed in 0.2mm intervals at each timepoint for lipid and calcium arc. Computational fluid dynamic simulations were performed using Newtonian and non-Newtonian models to calculate ESS, whereas ReL was calculated by the non-Newtonian simulations. Each haemodynamic index was compared to interval changes in lipid and calcium using multivariate regression. Results In total, 894 matched arterial segments from baseline and follow up imaging were analysed. In the Newtonian results, baseline segments exposed to ESS&gt;1.7Pa had a 12.5° increase in lipid arc (95% CI 2.2° to 22.8°, p=0.018) while segments exposed to ESS&lt;1.1Pa had an 8.1° decrease in calcium (95% CI −14.0° to −2.2°, p=0.007). In the non-Newtonian results, baseline regions exposed to ESS&gt;2.2Pa had a 14.4° increase in lipid (95% CI 4.2° to 24.7°, p=0.006) while areas with ESS&lt;1.4Pa had an 8.7° decrease in calcium (95% CI −14.6° to −2.8°, p=0.004). Baseline regions exposed to ReL&lt;34 showed an average 11.9° increase in lipid arc (95% CI 0.6° to 23.2°, p=0.039). Regions exposed to ReL&gt;55 had an average increase in lipid arc of 26.6° (95% CI 14.5° to 38.6°, p&lt;0.001). Conclusions Both Newtonian and non-Newtonian rheological models show that high ESS is associated with increased lipid while low ESS is associated with decreased calcium. ReL is independently associated with interval increases in lipid arc, suggesting a mechanistic role of local blood viscosity in lipid accumulation. ReL may serve as a novel haemodynamic marker of plaque progression.

Background To evaluate the long-term clinical performance, the impact of procedural configurations and post-procedure medications in atrial fibrillation patients with percutaneous left atrial appendage occlusion (LAAO). Methods The RECORD study was a prospective, all-comers registry conducted in 39 Chinese centers that consecutively enrolling patients who received LAAO between 1st April 2019 and 31st October 2020 with minimum inclusion and exclusion criteria. Events including any death, any stroke, systemic embolism and bleeding event were collected at 1 year and adjudicated by an independent clinical event committee. Cox proportional hazard models with multivariable adjustments were applied to estimate hazard ratios (HRs) for each outcome. Results Of the 3,096 participants, 3,082 successfully received an LAAO implant and 3,013 (97.8%) completed the 1-year follow-up. Participants had a high risk of stroke (mean CHA2DS2-VASc score of 4.0) and a moderate-to-high risk of bleeding (mean HAS-BLED score of 2.4). Local anesthetic was performed in 1,287 (41.6%) patients and fluoroscopy guidance in 492 (16.0%) patients. In 1295 (42.0%) cases, one-stage combination procedures of LAAO and radiofrequency ablation or cryoablation (CA) were performed. At 1 year, the composite ischemic endpoint of death, stroke, and systemic embolism occurred in 133 (4.51%) patients. Any life-threatening, disabling or major bleeding events occurred in 71 (2.36%) patients. There was no significant association between the type of anesthesia (general versus local), modality of image guidance (TEE, ICE, or fluoroscopy) with the ischemic or bleeding events. Combination procedures of LAAO plus CA was associated with a significantly lower rate of death, stroke, or systemic embolism than performing LAAO only (3.5% versus 5.2%, HRadjusted:0.69, 95%CI:0.48-0.98, P=0.041). The commonest antithrombotic strategy was OAC | APT | APT (38.1%; corresponded to medication prescribed at discharge | 45 days | 6 months), followed by OAC | OAC | APT (27.0%). Compared with OAC | APT | APT, the OAC | OAC | APT group was associated with a higher risk of life-threatening, disabling or major bleeding (1.2% versus 2.5%, HRadjusted:0.50, 95%CI: 0.25-0.99, P=0.47); whereas the risk of death, stroke and SE was numerically similar (2.9% versus 3.0%, HRadjusted:1.05, 95%CI: 0.61-1.78, P=0.867). There was no significant difference between OAC | APT | APT and OAC+APT | APT | APT groups regarding ischemic events; however, in patients with HAS-BLED ≥ 3, OAC | APT | APT was associated with lower rates of life-threatening, disabling or major bleeding events (1.1% versus 4.8%, HRadjusted:4.55, 95%CI: 1.31-15.81, P=0.017). Conclusion In Chinese centers, patients with a WATCHMAN LAAO device had low rates of ischemic and bleeding events at 1 year. One-stage combination procedures of LAAO and catheter ablation was associated with a significantly lower rate of ischemic events than performing LAAO only.Procedural configurations to outcomesPost-LAAO antithrombotic medications

Thrombosis is the main cause of acute coronary syndrome and myocardial infarction (Naghavi et al., 2003). The mechanism underlying thrombus formation is presently under debate, but several pathological conditions have been identified from human postmortem studies that correspond with the presence of thrombus. Of these conditions plaque rupture is the most common, but erosion of the endothelial layer and existence of calcified nodules without the existence of plaque rupture have also been identified. Plaques that have been ruptured have certain features in common (Falk, 1999; Virmani et al., 2002): (i) size of the lipid core (40% of the entire plaque), (ii) thickness of the fibrous cap (less than 65 µm), (iii) presence of inflammatory cells, (iv) amount of remodeling and extent of plaque-free vessel wall. Several terms have been identified focusing either on the pathological aspects ("thin-cap fibroatheroma") or on the possibility to rupture ("rupture-prone plaques") or on the possibility to induce thrombosis ("vulnerable plaque"). As vulnerable plaque is the term encompassing all other terms, therefore this term will be used throughout the chapter.