Prevalence of Coronary Artery Calcification on Pre-Atrial Fibrillation Ablation CT Pulmonary Venograms and its Impact on Selection for Statin Therapy.

Atherosclerotic cardiovascular disease (ASCVD) shares many risk factors with atrial fibrillation (AF). Obtaining computed tomography images of the pulmonary veins (CTPV) before AF ablation procedures is common and can incidentally detect coronary artery calcification (CAC). The purpose of this study was to investigate the prevalence of CAC on pre-ablation CTPV, the frequency of CAC reporting on CTPV reports, and its impact on statin therapy among patients hospitalized for AF procedures. We retrospectively evaluated consecutive patients undergoing CTPV and AF procedures from October 2016 to December 2017 in a single-center tertiary hospital. The patients' demographic and clinical characteristics were analyzed. The CAC presence on CTPV was visually assessed. The severity was classified qualitatively. The statin therapy status was evaluated using the patient's admission and discharge medication lists. A total of 638 subjects were included in our study, with 34.5% female. The mean age was 63.3 ± 10.8 years. CAC was detected in 70.1% of all patients, and in 58.1% of patients without a history of ASCVD. When present, CAC was documented in 92.6% of the clinical CTPV reports. While coronary artery atherosclerosis was present in a majority of AF patients, and its presence was widely reported, it was not associated with increased statin therapy at discharge.

Molecular Regulation of Toll-like Receptors in Asthma and COPD.

Asthma and chronic obstructive pulmonary disease (COPD) have both been historically associated with significant morbidity and financial burden. These diseases can be induced by several exogenous factors, such as pathogen-associated molecular patterns (PAMPs) (e.g., allergens and microbes). Endogenous factors, including reactive oxygen species, and damage-associated molecular patterns (DAMPs) recognized by toll-like receptors (TLRs), can also result in airway inflammation. Asthma is characterized by the dominant presence of eosinophils, mast cells, and clusters of differentiation (CD)4(+) T cells in the airways, while COPD typically results in the excessive formation of neutrophils, macrophages, and CD8(+) T cells in the airways. In both asthma and COPD, in the respiratory tract, TLRs are the primary proteins of interest associated with the innate and adaptive immune responses; hence, multiple treatment options targeting TLRs are being explored in an effort to reduce the severity of the symptoms of these disorders. TLR-mediated pathways for both COPD and asthma have their similarities and differences with regards to cell types and the pro-inflammatory cytotoxins present in the airway. Because of the complex TLR cascade, a variety of treatments have been used to minimize airway hypersensitivity and promote bronchodilation. Although unsuccessful at completely alleviating COPD and severe asthmatic symptoms, new studies are focused on possible targets within the TLR cascade to ameliorate airway inflammation.