Prophylactic veno-arterial extracorporeal membrane oxygenation in patients undergoing high-risk percutaneous coronary intervention

Netherlands Heart Journal - Complex high-risk percutaneous coronary intervention (PCI) is challenging and frequently accompanied by haemodynamic instability. Veno-arterial extracorporeal membrane...     

A computed tomography algorithm for crossing coronary chronic total occlusions: riding on the wave of the proximal cap and distal vessel segment

With wider adoption of coronary computed tomography angiography (coronary CTA), chronic total occlusions (CTOs) are being increasingly identified and characterised by non-invasive angiography. In particular, the ability of coronary CTA to clearly delineate atherosclerotic plaque, as well as to display three-dimensional vessel trajectories, has garnered particular attention in the context of preprocedural planning and periprocedural guidance of CTO percutaneous coronary intervention (PCI). Single CTO features and combined scoring systems derived from CTA (mostly exceeding the diagnostic performance of the angiographic J‑CTO score) have been used to predict time-efficient guidewire crossing, and thus grade the CTO difficulty level prior to PCI. In addition, the introduction of three-dimensional CTA/fluoroscopy co-registration for periprocedural navigation during CTO PCI offers the unprecedented opportunity to resolve proximal cap ambiguity and clearly visualise the distal CTO segment, thereby potentially influencing CTO PCI strategies and techniques. In this review, the potential advantages of non-invasive evaluation of CTO by coronary CTA are described, and a CTA-based hybrid algorithm is introduced for further enhancing the efficiency of CTO PCI. Further studies are clearly needed to verify the proposed approach. However, several luminary operators have already implemented coronary CTA for planning and periprocedural guidance of CTO interventions using the hybrid algorithm.

     

Oxidant-induced DNA damage by quartz in alveolar epithelial cells

Respirable quartz has recently been classified as a human carcinogen. Although, studies with quartz using naked DNA as a target suggest that formation of oxyradicals by particles may play a role in the DNA-damaging properties of quartz, it is not known whether this pathway is important for DNA damage in the target cells for quartz carcinogenesis, i.e. alveolar epithelial cells. Therefore, we determined in vitro DNA damage by DQ12 quartz particles in rat and human and alveolar epithelial cells (RLE, A549) using the single cell gel electrophoresis/comet assay. The radical generation capacity of quartz was analysed by electron spin resonance (ESR) and by immunocytochemical analysis of the hydroxyl radical-specific DNA lesion 8-hydroxydeoxyguanosine (8-OHdG) in the epithelial cells. Quartz particles as well as the positive control hydrogen peroxide, caused a dose-dependent increase in DNA strand breaks in both cell lines. DNA damage by quartz was significantly reduced in the presence of the hydroxyl-radical scavengers mannitol or DMSO. The involvement of hydroxyl radicals was further established by ESR measurements and was also demonstrated by the ability of the quartz to induce formation of 8-OHdG. In conclusion, our data show that quartz elicits DNA damage in rat and human alveolar epithelial cells and indicate that these effects are driven by hydroxyl radical-generating properties of the particles.     

Magnetic resonance imaging,pacemakers and implantable cardioverter-defibrillators: current situation and clinical perspective

New developments and expanding indications have resulted in a significant increase in the number of patients with pacemakers and internal cardioverterdefibrillators (ICDs). Because of its unique capabilities, magnetic resonance imaging (MRI) has become one of the most important imaging modalities for evaluation of the central nervous system, tumours, musculoskeletal disorders and some cardiovascular diseases. As a consequence of these developments, an increasing number of patients with implanted devices meet the standard indications for MRI examination. Due to the presence of potential life-threatening risks and interactions, however, pacemakers and ICDs are currently not approved by the Food and Drug Administration (FDA) for use in an MRI scanner. Despite these limitations and restrictions, a limited but still growing number of studies reporting on the effects and safety issues of MRI and implanted devices have been published. Because physicians will be increasingly confronted with the issue of MRI in patients with implanted devices, this overview is given. The effects of MRI on an implanted pacemaker and/or ICDs and vice versa are described and, based on the current literature, a strategy for safe performance of MRI in these patients is proposed. (Neth Heart J 2010;18:31-7.)     

Long-term Clinical Outcome and MIBI SPECT Parameters in Percutaneous Coronary Interventions

Background and Aim

Primary percutaneous coronary intervention (PCI) is the preferred treatment option for acute myocardial infarction (MI). Off-site PCI reduces time-to-treatment, which could potentially lead to enhanced clinical outcomes. Therefore, we investigated whether off-site PCI improves 5-year clinical outcomes compared with on-site PCI and whether this is related to in-hospital ^99mTc-sestamibi single photon emission computed tomography (MIBI SPECT) parameters.

Methods

We describe the 5-year follow-up for a combined endpoint of death or re-infarction in 128 patients with acute MI who were randomly assigned to undergo primary PCI at the off-site centre (n = 68) or to transferral to an on-site centre (n = 60). Three days after PCI, MIBI SPECT was performed to estimate infarct size. A multivariate Cox regression model was created to study the relation between MIBI SPECT parameters and long-term clinical outcomes.

Results

After a mean follow-up of 5.8 ± 1.1 years, 25 events occurred. Off-site PCI significantly reduced door-to-balloon time compared with on-site PCI (94 ± 54 versus 125 ± 59 min, p = 0.003). However, infarct size (17 ± 15 versus 14 ± 12%, p = 0.34) and 5-year death or infarct rate (21% versus 18%, p = 0.75) were comparable between treatment centres. With multivariate analysis, only Killip class ≥2 and Q wave MI, but not scintigraphic data, predicted long-term clinical outcomes.

Conclusion

Off-site PCI reduced door-to-balloon time with a comparable 5-year death or infarct rate. Parameters from resting MIBI SPECT on day 3 after MI did not predict long-term clinical outcomes.     

Oxidative stress and calcium signaling in the adverse effects of environmental particles (PM10)

This review focuses on the potential role that oxidative stress plays in the adverse effects of PM(10). The central hypothesis is that the ability of PM(10) to cause oxidative stress underlies the association between increased exposure to PM(10) and both exacerbations of lung disease and lung cancer. Pulmonary inflammation may also underlie the cardiovascular effects seen following increased PM(10), although the mechanisms of the cardiovascular effects of PM(10) are not well understood. PM(10) is a complex mix of various particle types and several of the components of PM(10) are likely to be involved in the induction of oxidative stress. The most likely of these are transition metals, ultrafine particle surfaces, and organic compounds. In support of this hypothesis, oxidative stress arising from PM(10) has been shown to activate a number of redox-responsive signaling pathways in lung target cells. These pathways are involved in expression of genes that play a role in responses relevant to inflammation and pathological change, including MAPKs, NF-kappaB, AP-1, and histone acetylation. Oxidative stress from particles is also likely to play an important role in the carcinogenic effects associated with PM(10) and hydroxyl radicals from PM(10) cause DNA damage in vitro.     

Autophagy in cardiovascular disease

Autophagy is a major cytoprotective pathway that eukaryotic cells use to degrade and recycle cytoplasmic contents. Recent evidence indicates that autophagy under baseline conditions represents an important homeostatic mechanism for the maintenance of normal cardiovascular function and morphology. By contrast, excessive induction of the autophagic process by environmental or intracellular stress has an important role in several types of cardiomyopathy by functioning as a death pathway. As a consequence, enhanced autophagy represents one of the mechanisms underlying the cardiomyocyte dropout responsible for the worsening of heart failure. Successful therapeutic approaches that regulate autophagy have been reported recently, suggesting that the autophagic machinery can be manipulated to treat heart failure or to prevent rupture of atherosclerotic plaques and sudden death.     

Soluble metals as well as the insoluble particle fraction are involved in cellular DNA damage induced by particulate matter

Exposure to ambient particulate matter has been reported to be associated with increased rates of lung cancer. Previously we showed that total suspended particulate matter (PM) induces oxidative DNA damage in epithelial lung cells. The aim of the present study was to further investigate the mechanism of PM-induced DNA damage, in which soluble iron-mediated hydroxyl radical (.OH) formation is thought to play a crucial role. Using electron spin resonance (ESR) we showed that PM suspensions as well as their particle-free, water-soluble fractions can generate .OH in the presence of hydrogen peroxide (H2O2), an effect which was abrogated by both deferoxamine and catalase. In addition, PM was also found to induce the .OH-specific DNA lesion 8-hydroxydeoxyguanosine (8-OHdG) in the presence of H2O2 as assessed by dot-blot analysis of calf thymus DNA using an 8-OHdG antibody. In human alveolar epithelial cells (A549), both PM suspensions and the particle-free soluble fraction elicited formation of DNA strand breaks (comet-assay). Unlike the acellular DNA assay, in epithelial cells the DNA-damaging capacity of the particle suspensions appeared to be stronger than that of their corresponding particle-free filtrates. In conclusion, our findings demonstrate that the water-soluble fraction of PM elicits DNA damage via transition metal-dependent .OH formation, implicating an important role of H2O2. Moreover, our data indicate that direct 'particle' effects contribute to the genotoxic hazard of ambient particulate matter in lung target cells.