A real-world multicenter study on left atrial appendage occlusion: The Italian multi-device experience.

Background: Transcatheter left atrial appendage occlusion (LAAO) has emerged as an alternative treatment for stroke prevention in patients with atrial fibrillation (AF) at high risk of thromboembolism, who cannot tolerate long-term oral anticoagulation (OAC). Questions persist regarding effectiveness and safety of this treatment and the optimal post-interventional antithrombotic regimen after LAAO. Methods: We retrospectively gathered data from 428 patients who underwent percutaneous LAAO in 6 Italian high-volume centres, aimed at describing the real-world utilization, safety, and effectiveness of LAAO procedures, also assessing the clinical outcomes associated with different antithrombotic strategies. Results: Among the entire population, 20 (4.7 %) patients experienced a combination of pericardial effusion and periprocedural major bleeding: 8 (1.9 %) pericardial effusion, 1 (0.3 %) fatal bleeding, and 3 (0.7 %) non-fatal procedural major bleeding. Patients were discharged with different antithrombotic regimens: dual (DAPT) (27 %) or single (SAPT) (26 %) antiplatelet therapy, OAC (27 %), other antithrombotic regimens (14 %). Very few patients were not prescribed with antithrombotic drugs (6 %). At a medium 523 ± 58 days follow-up, 14 patients (3.3 %) experienced all-cause death, 6 patients (1.4 %) cardiovascular death, 3 patients (0.7 %) major bleeding, 10 patients (2.6 %) clinically relevant non-major bleeding, and 3 patients (0.7 %) ischemic stroke. At survival analysis, with DAPT as the reference group, OAC therapy was associated with better outcomes. Conclusions: Our findings confirm that LAAO is a safe procedure. Different individualized post-discharge antithrombotic regimens are now adopted, likely driven by the perceived thrombotic and hemorrhagic risk. The incidence of both ischemic and bleeding events tends to be low.

Nonfluoroscopic mapping reduces radiation exposure in ablation of atrial fibrillation.

BACKGROUND: Radiofrequency catheter ablation (RFCA) of atrial fibrillation is an effective and definitive treatment. The methods used to guide RFCA have evolved over the years from a purely electrophysiological approach, in which anatomical lesions were guided solely by fluoroscopy and angiographic imaging of the pulmonary veins, to an approach guided by modern nonfluoroscopic electroanatomical mapping, integrated or not with computed tomography (CT). The aim of this study was, therefore, to compare radiation exposure of RFCA based on a fast three-dimensional nonfluoroscopic mapping system with 'traditional' mapping integrated with CT imaging. METHODS: Thirty consecutive patients with atrial fibrillation who underwent RFCA were treated with two different approaches: 3D-Fast-Anatomical-Mapping and One-Map tool (FAM-One Map group, 21 patients) vs. 3D-Fast-Anatomical-Mapping integrated with CT images (MERGE-CT group, nine patients). Fluoroscopy time and radiation doses (expressed in milliGray) were compared. RESULTS: No statistically significant difference was detectable between FAM-One Map group and MERGE-CT group considering RFCA success rates and fluoroscopy times. Radiation exposure was higher in the MERGE-CT group (965 ±â€Š138  mGy MERGE-CT group vs. 532 ±â€Š216  mGy FAM-One Map group, P < 0.001) because of supplemental radiation exposures due to CT imaging (470 ±â€Š126  mGy). CONCLUSION: A fast nonfluoroscopic electroanatomical mapping system may reduce radiation exposure in RFCA of atrial fibrillation, with preserved success rates.

Facilitated PCI: rationale, current evidence, open questions, and future directions.

Both thrombolysis and primary percutaneous coronary intervention (PCI) are validated therapies in the treatment of ST-elevation acute myocardial infarction (STEMI). Primary PCI appears now to be more effective, provided the vessel patency is restored within 120 minutes. An approach combining the possibility of quickly starting a clot-dissolving medication with a subsequent PCI of the culprit lesion has therefore recently gained considerable interest. Facilitated percutaneous coronary intervention (PCI) refers to a pretreatment with any pharmacological agent allowing the achievement of some recanalization and possibly myocardial reperfusion, which might translate into an improved clinical outcome. Many drugs reduce the thrombus burden; however, the term "facilitated" is currently operatively restricted to glycoprotein GP-IIb-IIIa inhibitors, thrombolytic drugs, and their combination. Several earlier clinical trials tested the hypothesis that facilitated PCI in the setting of STEMI allows the achievement of a better myocardial reperfusion compared with primary PCI and that this benefit translates into an improved clinical outcome. However, after the first promising results, the recent ASSENT-4 trial has been prematurely interrupted because of higher in-hospital mortality in the group of patients who underwent full-dose tenecteplase followed by PCI compared with subjects undergoing primary PCI alone. After a critical review of the current knowledge, and pending the completion of ongoing trials, no clear evidence currently exists on the benefit of any systemic pharmacological facilitation of PCI beyond the upfront administration of dual oral antiplatelet therapy with aspirin and clopidogrel. While awaiting the results of a few other currently ongoing trials, facilitated PCI should now probably be restricted to the administration of glycoprotein IIb-IIIa inhibitors for patients at high risk of cardiovascular events and at low risk of bleeding when a more than 60-minute delay to primary PCI is anticipated. In patients having first medical contact within 3 hours, with an anticipated absolute delay to PCI of more than 90 minutes, thrombolysis can be safely recommended.

Celecoxib, ibuprofen, and the antiplatelet effect of aspirin in patients with osteoarthritis and ischemic heart disease.

BACKGROUND AND OBJECTIVE: We performed a placebo-controlled, randomized study to address whether celecoxib or ibuprofen undermines the functional range of inhibition of platelet cyclooxygenase (COX)-1 activity by aspirin in patients with osteoarthritis and stable ischemic heart disease. METHODS: Twenty-four patients who were undergoing long-term treatment with aspirin (100 mg daily) for cardioprotection were coadministered celecoxib, 200 mg twice daily, ibuprofen, 600 mg 3 times daily, or placebo for 7 days. RESULTS: The coadministration of placebo or celecoxib did not undermine the aspirin-related inhibition of platelet COX-1 activity, as assessed by measurements of serum thromboxane B(2) (TXB(2)) levels, as well as platelet function. In contrast, a significant (P < .001) increase in serum TXB(2) level was detected on day 7 before drug administration (median, 19.13 ng/mL [range, 1-47.5 ng/mL]) and at 24 hours after the coadministration of aspirin and ibuprofen (median, 22.28 ng/mL [range, 4.9-44.4 ng/mL]) versus baseline (median, 1.65 ng/mL [range, 0.55-79.8 ng/mL]); this was associated with a significant increase in arachidonic acid-induced platelet aggregation (P < .01) and adenosine diphosphate-induced platelet aggregation (P < .05) and a decrease in the time to form an occlusive thrombus in the platelet function analyzer (P < .01). The urinary excretion of 11-dehydro-TXB(2), an index of systemic thromboxane biosynthesis, was not significantly affected by the coadministration of treatment drugs. At steady state, a comparable and persistent inhibition of lipopolysaccharide-stimulated prostaglandin E(2) generation, a marker of COX-2 activity ex vivo, was caused by ibuprofen (>or=80%) or celecoxib (>or=70%) but not placebo. CONCLUSIONS: Unlike ibuprofen, celecoxib did not interfere with the inhibition of platelet COX-1 activity and function by aspirin despite a comparable suppression of COX-2 ex vivo in patients with osteoarthritis and stable ischemic heart disease.