Among subjects with first-time anterior STEMI due to a proximal or mid LAD lesion who undergo successful PCI, administration of MTP-131 was safe and well tolerated. Treatment with MTP-131 was not associated with a decrease in myocardial infarct size as assessed by AUC0-72 of CK-MB.
d-Dimer is a biomarker of fibrin formation and degradation. While a d-dimer within normal limits is used to rule out the diagnosis of deep venous thrombosis and pulmonary embolism among patients with a low clinical probability of venous thromboembolism (VTE), the prognostic association of an elevated d-dimer with adverse outcomes has received far less emphasis. An elevated d-dimer is independently associated with an increased risk for incident VTE, recurrent VTE, and mortality. An elevated d-dimer is an independent correlate of increased mortality and subsequent VTE across a broad variety of disease states. Therefore, medically ill subjects in whom the d-dimer is elevated constitute a high risk subgroup in which the prospective evaluation of the efficacy and safety of antithrombotic therapy is warranted.
Background
Obstructive sleep apnea (OSA) is associated with atrial remodeling, atrial fibrillation (AF), and increased incidence of arrhythmia recurrence following pulmonary vein isolation (PVI). We aimed to characterize the atrial substrate, including AF triggers in patients with paroxysmal AF (PAF) and OSA.
Methods and Results
In 86 patients with PAF (43 with ≥ moderate OSA [apnea-hypopnea index ≥15] and 43 without OSA [apnea-hypopnea index <5]) right atrial (RA) and left atrial (LA) voltage distribution, conduction velocities, and electrogram characteristics were analyzed during atrial pacing. AF triggers were examined before and after PVI and targeted for ablation. Patients with OSA had lower atrial voltage amplitude (RA, p=0.0005; LA, p=0.0001), slower conduction velocities (RA, p=0.02; LA, p=0.0002), and higher prevalence of electrogram fractionation (p=0.0001). The areas of atrial abnormality were consistent among patients, most commonly involving the LA septum (32/43; 74.4%). At baseline, the PVs were the most frequent triggers for AF in both groups, however following PVI patients with OSA had increased incidence of additional extra-PV triggers (41.8% vs. 11.6%; p=0.003). The 1-year arrhythmia-free survival was similar between patients with and without OSA (83.7% and 81.4%, respectively; p=0.59). In comparison, control patients with PAF and OSA who underwent PVI alone without ablation on extra-PV triggers had increased risk of arrhythmia recurrence (83.7% vs. 64.0%; p=0.003)
Conclusions
OSA is associated with structural and functional atrial remodeling and increased incidence of extra-PV triggers. Elimination of these triggers resulted in improved arrhythmia-free survival.
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