1,721,168 research outputs found
Are Atherogenic Lipoprotein Phenotype and Inflammation Indicative of Plaque Phenotype and Clinical Stability in Coronary Artery Disease?-Reply
No full textShedding the optical coherence tomography light on the treatment of complex coronary bifurcation lesions
No full textThe European Trial on Optical Coherence Tomography Optimized Bifurcation Event Reduction (OCTOBER) was an investigator-initiated,
industry-funded, multicentre, open-label, randomized trial aiming to test the superiority of routine optical coherence tomography (OCT) guidance in percutaneous coronary intervention (PCI) of complex coronary bifurcation lesions as compared with angiographic guidance.1
• Patients with stable angina or non–ST-segment elevation acute coronary syndrome (NSTE-ACS) requiring PCI of a true bifurcation lesion (i.e.
bifurcation lesions with both the main vessel and side branch having significant disease) were enrolled. Eligible bifurcation lesions required a
main branch with a reference diameter ≥2.75 mm and a stenosis ≥50% on angiography and a side branch with a reference diameter ≥2.5 mm
and a stenosis ≥50% within 5 mm from the ostium. Left main bifurcation lesions were included. The functional significance of the main branch
stenosis required documentation by a noninvasive functional imaging test or a pressure wire–based method, unless an angiographic diameter
stenosis >80% was present. Patients with an estimated glomerular filtration rate <50 mL/min/1.73 m2 were excluded.
• Patients were randomized in a 1:1 ratio to OCT-guided PCI or angiography-guided PCI. In the OCT-guided PCI arm, a specific protocol defined the timing of OCT pullbacks (both in the main vessel and the side branch), as well as the recommended measurements, optimizations,
and treatment goals (i.e. optimal stent coverage of the target lesion, optimal stent expansion, and absence of stent malapposition or accidentally crushed/distorted stents). In the angiography-guided PCI arm, intravascular ultrasonography (IVUS) was not encouraged but was allowed
in case of left main bifurcation lesion. Conventional PCI bifurcation techniques were used,2 and the Xience everolimus-eluting stent was prespecified for implantation. The randomization was stratified based on the presence of a left main bifurcation lesion and on the PCI strategy (i.e.
provisional single-stent technique vs. two-stent technique).
• The primary endpoint was a composite of major adverse cardiac events (MACE), defined as cardiac death, target lesion myocardial infarction
(MI), or ischaemia-driven target lesion revascularization (TLR) at a median follow-up of 2 years. Secondary endpoints included the single components of the primary endpoint and a patient-oriented composite endpoint of all-cause death, MI, any coronary revascularization, or stroke.
• Between July 2017 and March 2022, a total of 1201 patients (mean age, 66 years; 21% female) were enrolled at 38 European institutions. A
total of 227 patients (19% of cases) had a lesion located at the left main bifurcation. In the angiography-guided PCI arm, 15% of the patients
underwent IVUS-guided PCI, of whom two-thirds had a lesion located in the left main bifurcation. The primary endpoint occurred less frequently in the OCT-guided PCI group than in the angiography-guided PCI group [10.1% vs. 14.1%; hazard ratio (HR), 0.70; 95% confidence
interval (CI), .50–.98; P = .035], driven by numerically lower rates of all the single endpoint components (cardiac death: 1.4% vs. 2.6%; target
lesion MI: 7.8% vs. 8.5%; ischaemia-driven TLR: 2.8% vs. 4.6%). The patient-oriented composite endpoint was less frequent in the OCT-guided
PCI than in the angiography-guided PCI group (13.6% vs. 17.7%, respectively). The median volume of contrast used was larger in the
OCT-guided PCI than in the angiography-guided PCI group {300 mL [interquartile range (IQR), 250–375] vs. 200 mL [IQR, 160–278]}, as
well as the median procedural time [113 min (IQR, 85–145) vs. 80 min (IQR, 60–110)
Weekly journal scan: do biodegradable polymer stents provide a durable benefit in patients with ST-segment elevation myocardial infarction?
No full textNo abstract availabl
Targeting inflammation with colchicine does not prevent atrial fibrillation after major non-cardiac thoracic surgery
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Atherosclerotic Plaque Healing
No full textAtherosclerotic plaques typically develop over a period of years or decades. In contrast, the thrombotic complications of atherosclerotic disease occur suddenly, often without warning.1 The notion that acute coronary syndromes develop from the rupture or superficial erosion of an atherosclerotic plaque is an oversimplification of a process involving plaque activity, blood thrombogenicity, and healing.2,3 Pathological studies have shown that many (if not most) atherosclerotic plaques destabilize without resulting in a clinical syndrome.4,5 The occurrence of an acute coronary syndrome probably depends on the disruption of a balance between instability ("activation") and healing ("passivation") of an atherosclerotic plaque. During the past 30 years, research efforts have mostly been focused on the mechanisms of plaque instability.2,3 Yet the risk of acute myocardial infarction or sudden death from coronary causes remains difficult to predict,6 suggesting that other pathogenic mechanisms should also be investigated. Recently, the notion that plaque healing may play a key role in the natural history of atherosclerotic disease has been gaining attention, in part because of the development of new imaging techniques, allowing in vivo study of the morphologic features of atherosclerotic plaque.7,8 This review examines the mechanisms of atherosclerotic plaque healing, their role in the progression of atherosclerotic disease and in the development of acute coronary syndromes, and the clinical and potential therapeutic implications of the healing process
Weekly journal scan: angina severity reduced by percutaneous coronary intervention in the ORBITA-2 trial
No full textNo abstract availabl
Chronic systemic glucocorticoid therapy is associated with increased risk of major vascular complications and cardiac tamponade after transcatheter aortic valve implantation: a systematic review and meta-analysis
No full textIntroduction: TAVI-related complications, such as conduction disturbances, vascular complications or death may be related to increased inflammatory response. The aim of this study was to elucidate the efficacy and safety of the systemic glucocorticoid therapy regarding the adverse events after TAVI deployment. Evidence acquisition: We conducted a systemic search of PubMed, a reference list of relevant articles, and Medline. The main efficacy outcomes of interest were all-cause death, cardiac and non-cardiac death, permanent pacemaker implantation (PPM), new left bundle branch block (LBBB), stroke, and myocardial infarction (MI). Safety endpoints were major vascular complications, major bleeding events, and cardiac tamponade. Evidence synthesis: A total of 7 studies including data from 3439 patients with a median follow-up was 30 days. Systemic glucocorticoid compared to the control group were associated with an increased risk of non-cardiac death (Relative Risk [RR] 5.90 95%CI [2.95; 11.80], P<0.001) major vascular complications (RR 1.78, 95%CI [1.22 - 2.61], P=0.003) and cardiac tamponade (RR 3.42, 95%CI [1.69 - 6.92], P<0.001). However, there were no differences in all-cause death, cardiac death, new LBBB, stroke, MI, or major bleeding events (all P values >0.05). Conclusions: Glucocorticoid therapy before the TAVI procedure was associated with an increase in non-cardiac death, major vascular events and cardiac tamponade. There were no differences in the risk of all-cause death, cardiac death, PPM or LBBB, stroke, or MI
Evaluation of culprit lesions by optical coherence tomography in patients with ST-elevation myocardial infarction
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