Impact of Postprocedural Graft Flow on Outcomes Following Chronic Total Occlusion Intervention in Postcoronary Artery Bypass Graft Patients: A Detailed Angiographic Analysis.

Chronic total occlusions (CTOs) are frequent in patients with previous coronary artery bypass graft (CABG) surgery. Percutaneous coronary intervention (PCI) is the usual revascularization strategy. Whether or not the presence of a graft on a CTO vessel and post-PCI graft patency impacts outcomes after CTO-PCI is unknown. We sought to evaluate the impact of post-PCI graft patency on the durability of CTO-PCI. In total, 259 patients with previous CABG who underwent CTO-PCI in 12 international centers in 2019 to 2023 were categorized into "grafted" and "ungrafted" groups based on the presence of graft on a CTO vessel. The grafted group was subdivided into "graft-occluded" and "graft-patent" groups, depending on graft patency. The primary end points were (1) technical success rate, (2) target vessel failure, and (3) CTO failure rates at 1 year. CTO failure was defined as target vessel revascularization and/or significant in-stent restenosis. A total of 199 patients (77%) were in the grafted group. Grafted CTOs showed higher complexity and lower technical success rates (70% vs 80%, p = 0.004) than nongrafted CTOs. Of the grafted CTOs, 140 (70%) were in the grafted-occluded group and 59 (30%) were in the grafted-patent group. The technical success was lower in the former group (65% vs 81%, p = 0.022). An occluded graft was an independent predictor of technical failure (odds ratio 2.04, 95% confidence interval 1.03 to 4.76, p = 0.049) and persistent post-PCI graft patency was a strong independent predictor of CTO failure at 1 year (hazard ratio 5.6, 95% confidence interval 1.2 to 27.5, log-rank p = 0.033). In conclusion, in patients with previous CABG who underwent CTO-PCI, post-PCI graft patency was a significant predictor of CTO failure.

Comparison of Outcomes of Coronary Artery Bypass Grafting Using Internal Mammary Graft Versus Percutaneous Coronary Intervention for Isolated Proximal Left Anterior Descending Narrowing.

There are limited contemporary studies comparing coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) for isolated proximal left anterior descending (LAD) disease. Increasing stent length and decreasing stent diameters are associated with increased risk of restenosis and adverse outcomes after PCI. Whether these parameters influence outcomes when comparing CABG and PCI is unclear. We compared CABG and PCI in 3,473 patients who underwent revascularization for isolated proximal LAD disease from 2004 to 2015 at Harefield Hospital, UK; 3,078 patients (89%) had PCI and 384 patients had CABG (11%). We analyzed all-cause mortality at 3 years. The unadjusted mortality rates were similar (PCI vs CABG: 9.5% vs 7.0%, p = 0.109). PCI was associated with comparable mortality (hazard ratio [HR] 1.15, 95% confidence interval [CI] 0.70 to 1.89, p = 0.593), even when stratified to bare-metal stents (HR 1.58, 95% CI 0.89 to 2.80, p = 0.121); first-generation drug-eluting stents (FDES; HR 1.16, 95% CI 0.67 to 2.02, p = 0.597); and second-generation DES (SDES; HR 0.98, 95% CI 0.53 to 1.82, p = 0.946). Stent diameters did not influence outcomes, but PCI was associated with higher mortality when stent length ≥30 mm (HR 2.12, 95% CI 1.12 to 4.03, p = 0.022). There was a linear association between stent length and mortality, and for every 1-mm increase in stent length, the 3-year mortality increased by 0.32%. In conclusion, for patients with isolated proximal LAD disease, PCI and CABG were associated with similar mortality. Increasing stent length was progressively associated with worse outcomes with PCI. For longer segments of disease requiring stent lengths ≥30 mm, CABG may be associated with better outcomes.

Embolic protection device use and its association with procedural safety and long-term outcomes following saphenous vein graft intervention: An analysis from the British Columbia Cardiac registry.

BACKGROUND: Embolic protection devices (EPDs) have been designed and introduced to reduce distal embolization and peri-procedural myocardial infarction during saphenous vein graft (SVG) intervention. Current guidelines give a class I recommendation to EPD use during SVG intervention when technically feasible. However, the routine use of these devices has recently been debated. METHODS: We analyzed 1,359 patients undergoing isolated SVG intervention between 2008 and 2013 in the British Columbia Cardiac Registry. We analyzed (a) post-procedural TIMI flow; and (b) target vessel revascularization (TVR) and mortality at 1 and 2 years. RESULTS: EPD use was an independent predictor of post-procedural TIMI 2/3 flow (OR = 2.38, 95% CI: 1.51-3.74, P < 0.001). At 1 year, EPD use was an independent predictor for lower TVR (HR = 0.35, 95% CI: 0.14-0.85, P = 0.021) and a trend towards lower mortality (HR = 0.45, 95% CI: 0.18-1.10, P = 0.082). These associations were lost at 2 years where EPD use was not predictive of mortality (HR = 0.62, 95% CI: 0.33-1.17, P = 0.144) or TVR (HR = 0.70, 95% CI: 0.41-1.17, P = 0.176). These findings were confirmed in propensity-matched and inverse probability treatment weighted analyses. CONCLUSIONS: In this analysis of patients undergoing SVG intervention, EPD use was a strong predictor for improved post-procedural TIMI flow. Whilst EPD use was associated with lower TVR and a trend for lower mortality at 1 year, these associations were lost at 2 years. These findings would appear to support the use of EPD for SVG intervention. © 2015 Wiley Periodicals, Inc.

PARP-14 combines with tristetraprolin in the selective posttranscriptional control of macrophage tissue factor expression.

Tissue factor (TF) (CD142) is a 47 kDa transmembrane cell surface glycoprotein that triggers the extrinsic coagulation cascade and links thrombosis with inflammation. Although macrophage TF expression is known to be regulated at the RNA level, very little is known about the mechanisms involved. Poly(adenosine 5'-diphosphate [ADP]-ribose)-polymerase (PARP)-14 belongs to a family of intracellular proteins that generate ADP-ribose posttranslational adducts. Functional screening of PARP-14-deficient macrophages mice revealed that PARP-14 deficiency leads to increased TF expression and functional activity in macrophages after challenge with bacterial lipopolysaccharide. This was related to an increase in TF messenger RNA (mRNA) stability. Ribonucleoprotein complex immunoprecipitation and biotinylated RNA pull-down assays demonstrated that PARP-14 forms a complex with the mRNA-destabilizing protein tristetraprolin (TTP) and a conserved adenylate-uridylate-rich element in the TF mRNA 3' untranslated region. TF mRNA regulation by PARP-14 was selective, as tumor necrosis factor (TNF)α mRNA, which is also regulated by TTP, was not altered in PARP-14 deficient macrophages. Consistent with the in vitro data, TF expression and TF activity, but not TNFα expression, were increased in Parp14(-/-) mice in vivo. Our study provides a novel mechanism for the posttranscriptional regulation of TF expression, indicating that this is selectively regulated by PARP-14.

Solid-phase immunoglobulins IgG and IgM activate macrophages with solid-phase IgM acting via a novel scavenger receptor a pathway.

IgG may accelerate atherosclerosis via ligation of proinflammatory Fcγ receptors; however, IgM is unable to ligate FcγR and is often considered vasculoprotective. IgM aggravates ischemia-reperfusion injury, and solid-phase deposits of pure IgM, as seen with IgM-secreting neoplasms, are well known clinically to provoke vascular inflammation. We therefore examined the molecular mechanisms by which immunoglobulins can aggravate vascular inflammation, such as in atherosclerosis. We compared the ability of fluid- and solid-phase immunoglobulins to activate macrophages. Solid-phase immunoglobulins initiated prothrombotic and proinflammatory functions in human macrophages, including NF-κB p65 activation, H(2)O(2) secretion, macrophage-induced apoptosis, and tissue factor expression. Responses to solid-phase IgG (but not to IgM) were blocked by neutralizing antibodies to CD16 (FcγRIII), consistent with its known role. Macrophages from mice deficient in macrophage scavenger receptor A (SR-A; CD204) had absent IgM binding and no activation by solid-phase IgM. RNA interference-mediated knockdown of SR-A in human macrophages suppressed activation by solid-phase IgM. IgM binding to SR-A was demonstrated by both co-immunoprecipitation studies and the binding of fluorescently labeled IgM to SR-A-transfected cells. Immunoglobulins on solid-phase particles around macrophages were found in human plaques, increased in ruptured plaques compared with stable ones. These observations indicate that solid-phase IgM and IgG can activate macrophages and destabilize vulnerable plaques. Solid-phase IgM activates macrophages via a novel SR-A pathway.

A calcified cardiac mass.

Cardiac fibromas are benign tumours, often diagnosed in childhood, but rarely they may be diagnosed in adults or the elderly. We present an interesting case of a middle-aged lady presenting with exertional chest pain and breathlessness, who was found to have a heavily calcified mass within the myocardium. With a previous history of chest trauma, a calcified myocardial haematoma was initially suspected. Complete surgical excision led to a total resolution of symptoms. Histological examination confirmed the diagnosis of a cardiac fibroma. Complete excision of cardiac fibromas, where possible, is advised and is associated with excellent survival.