1,721,092 research outputs found
Coronary in-stent restenosis in patients treated with thoracic external beam radiation for cancer
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Coronary in-stent restenosis in patients treated with thoracic external beam radiation for cancer
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Advances in mechanisms, imaging and management of the unstable plaque
No full textPost-mortem observations demonstrated that plaque fissure was the final event leading to coronary thrombosis and occlusion in about two-thirds of cases of sudden coronary death. Plaques prone to fissure have, therefore, been defined "vulnerable plaques" and are identified by specific anatomic features including thin inflamed fibrous cap, large lipidic core and positive remodeling. Accordingly, elegant imaging modalities have been developed in order to identify this "holy grail". However, the results of prognostic studies based on the identification of vulnerable plaques have not been encouraging because of the low positive predictive value for major cardiovascular events. This observation is not surprising as the pathogenesis of acute coronary syndromes is complex and multifactorial. In this review we propose a pathogenetic classification of acute coronary syndromes in the attempt to identify homogeneous groups of patients with a common mechanism of coronary instability which can be identified by using specific biomarkers and imaging techniques, and become a specific therapeutic target
Angina after percutaneous coronary intervention: The need for precision medicine
No full textPersistence or recurrence of angina after successful percutaneous coronary intervention (PCI) represent an important clinical issue involving from one fifth to one third of patients undergoing myocardial revascularization at one-year follow-up. A systematic approach to this syndrome is strongly needed. Precision medicine is particularly important in addressing angina after successful PCI because of the multiple underlying causes. Restenosis or coronary atherosclerosis progression explain symptom recurrence after successful PCI in some patients, while functional causes, including vasomotor abnormalities of epicardial coronary arteries and/or coronary microvascular dysfunction, explain symptoms in the remaining patients. In this review, we summarize the mechanisms of persistent or recurrent angina after PCI, proposing a diagnostic algorithm and a systematic therapeutic approach
Excimer laser for a highly stenotic saphenous vein graft: evidence of debulking by optical coherence tomography
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The evolving role of inflammatory biomarkers in risk assessment after stent implantation
No full textThe main adverse reactions to coronary stents are in-stent restenosis (ISR) and stent thrombosis. Along with procedural factors, individual susceptibility to these events plays an important role. In particular, inflammatory status, as assessed by C-reactive protein levels, predicts the risk of ISR after bare-metal stent implantation, although it does not predict the risk of stent thrombosis. Conversely, C-reactive protein levels fail to predict the risk of ISR after drug-eluting stent (DES) implantation, although they appear to predict the risk of stent thrombosis. Of note, DES have abated ISR rates occurring in the classical 1-year window, but new concern is emerging regarding late restenosis and thrombosis. The pathogenesis of these late events seems to be related to delayed healing and allergic reactions to polymers, a process in which eosinophils seem to play an important role by enhancing restenosis and thrombosis. The identification of high-risk individuals based on biomarker assessment may be important for the management of patients receiving stent implantation. In this report, we review the evolving role of inflammatory biomarkers in predicting the risk of ISR and stent thrombosis
Intracoronary bolus of glycoprotein IIB/IIIA inhibitor as bridging or adjunctive strategy to oral P2Y(12) inhibitor load in the modern setting of STEMI
No full textBackground: In the acute management of ST-elevation myocardial infarction (STEMI), glycoprotein IIb/IIIa inhibitors (GPIs) bolus not followed by intravenous infusion is potentially advantageous given their fast onset and offset of action, but clinical evidence in a contemporary setting is limited.
Methods: We collected data from consecutive STEMI patients admitted to the cardiac catheterization laboratory of the IRCCS A. Gemelli University Polyclinic Foundation from October 2017 to September 2019.
Results: Out of 423 consecutive STEMI patients, 297 met the inclusion and exclusion criteria and were included in the study. Of them, 107/297 (36%) received an intracoronary GPI bolus-only during primary percutaneous coronary intervention (PPCI) not followed by intravenous infusion and 190/297 (64%) received standard antithrombotic therapy. Of the 107 GPI-treated, 22/107 (21%) had P2Y12 inhibitor pretreatment (adjunctive strategy) and 85/107 (79%) did not (bridging strategy). During hospital staying, there was no difference in the primary safety endpoint of TIMI major+minor bleeding (P=0.283), TIMI major (P=0.267) or TIMI minor (P=0.685) bleeding between groups. No stroke event occurred in the GPI group. Despite patients receiving GPI having a significantly higher intraprocedural ischemic burden, no significant differences were found in the efficacy outcomes between groups. Consistent findings were observed for patients receiving GPIs bolus before (bridging strategy) or after (adjunctive strategy) P2Y12 inhibitors, compared to those receiving standard therapy. Multivariate logistic regression analyses did not find any independent predictors significantly associated to the primary and secondary composite endpoints.
Conclusions: In a contemporary real-world population of STEMI patients undergoing PPCI, the use of intracoronary GPIs bolus-only in selected patients at high ischemic risk is safe and could represent a useful antithrombotic strategy both in those pretreated and in those naïve to P2Y12 inhibitors
Diagnostic work-up and therapeutic implications in MINOCA: need for a personalized approach
No full textMyocardial infarction with non-obstructive coronaryartery(MINOCA) diseaserepresents a heterogeneous clinical conundrum accounting for about 6% of all acute myocardial infarction (MI) cases. Initially believed to be a benign condition, is now becoming clear that MINOCA is associated with a non-negligible risk of mortality, rehospitalization, disability and angina burden at follow-up, with high socioeconomic costs. To date, there are no prospective clinical trials in this population and cannot be assumed that benefits observed in patients suffering from MI with obstructive coronary artery disease maysuccessfully translate to this syndrome. Herein, we comment on the importance of the multimodality assessment to properly identify and treat the specific causes of MINOCA, in order to improve prognosis and the qualityof life in these patients
Optical coherence tomography features of angiographic complex and smooth lesions in acute coronary syndromes
No full textPlaque rupture (PR) and superimposed thrombosis have been shown as the most frequent underlying substrate in acute coronary syndromes (ACS). Coronary angiography is a luminogram not able to define in vivo features of the culprit plaques. The aim of the study was to use optical coherence tomography (OCT) to investigate the pathology underlying complex (CL) and non-complex angiographic lesions (NCL). We retrospectively enrolled 107 ACS patients admitted to our institution; 83 with non-ST elevation ACS (NSTE-ACS) and 24 with ST-elevation myocardial infarction. Coronary angiography was performed and culprit lesions were classified according to Ambrose criteria into NCL (n = 47) and CL (n = 60). OCT imaging was then performed to better identify plaque morphology; either PR or intact fibrous cap, the presence of superimposed thrombosis, lipid rich plaque, and thin cap fibroatheroma (TCFA). OCT analysis showed that 58 lesions (54.2%) were classified as PR and 48 lesions (44.9%) were associated with thrombi. Lipid rich plaques were identified in 62 lesions (57.9%). PR, intracoronary thrombi, lipid rich plaques and TCFA were more frequent in CL compared with NCL (71.7 vs 31.9%, 63.3 vs 21.3%, 71.7 vs 40.4% and 46.7 vs 21.3% respectively), but PR with superimposed thrombus may be also detected in NCL. OCT demonstrates PR and thrombosis in the majority of ACS patients presenting with CL. However, one-third of NCL show PR by OCT, suggesting that additional intracoronary imaging by OCT may better identify the underlying mechanism of coronary instability than coronary angiography alone
Direct Oral Anticoagulants versus Vitamin K Antagonists for the treatment of Left Ventricular Thrombosis: a systematic review of the literature and meta-analysis
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