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Anatomical scoring systems for coronary artery disease, such as the SYNTAX (Synergy Between Percutaneous Coronary Intervention [PCI] With Taxus and Cardiac Surgery) score, are well established tools for understanding patient risk. However, they are cumbersome to compute manually for large data sets, limiting their use across broad and varied cohorts.To adapt an anatomical scoring system for use with registry data, allowing facile and automatic calculation of scores and association with clinical outcomes among patients undergoing percutaneous or surgical revascularization.This cross-sectional observational cohort study involved procedures performed in all cardiac catheterization laboratories in the largest integrated health care system in the United States, the Veterans Affairs (VA) Healthcare System. Patients undergoing coronary angiography in the VA Healthcare System followed by percutaneous or surgical revascularization within 90 days were observed and data were analyzed from January 1, 2010, through September 30, 2017.An anatomical scoring system for coronary artery disease complexity before revascularization was simplified and adapted to data from the VA Clinical Assessment, Reporting, and Tracking Program. The adjusted association between quantified anatomical complexity and major adverse cardiovascular and cerebrovascular events (MACCEs), including death, myocardial infarction, stroke, and repeat revascularization, was assessed for patients undergoing percutaneous or surgical revascularization.A total of 50 226 patients (49 359 men [98.3%]; mean [SD] age, 66 [9] years) underwent revascularization during the study period, with 34 322 undergoing PCI and 15 904 undergoing coronary artery bypass grafting (CABG). After adjustment, the highest tertile of anatomical complexity was associated with increased hazard of MACCEs (adjusted hazard ratio [HR], 2.12; 95% CI, 2.01-2.23). In contrast, the highest tertile of anatomical complexity among patients undergoing CABG was not independently associated with overall MACCEs (adjusted HR, 1.04; 95% CI, 0.92-1.17), and only repeat revascularization was associated with increasing complexity (adjusted HR, 1.34; 95% CI, 1.06-1.70) in this subgroup.These findings suggest that an automatically computed score assessing anatomical complexity can be used to assess longitudinal risk for patients undergoing revascularization. This simplified scoring system appears to be an alternative tool for understanding longitudinal risk across large data sets.

BACKGROUND. The European Cooperative Study Group conducted two randomized trials in patients with suspected myocardial infarction to assess the effect of 100 mg single-chain recombinant tissue-type plasminogen activator (rt-PA, alteplase) on enzymatic infarct size, left ventricular function, morbidity and mortality relative to placebo (alteplase/placebo trial) and to assess the effect of immediate percutaneous transluminal coronary angioplasty (PTCA) in addition to alteplase (alteplase/PTCA trial). One-year follow-up results are reported. METHODS AND RESULTS. In the alteplase/placebo trial, 721 patients with chest pain of less than 5 hours and extensive ST-segment elevation were allocated at random to 100 mg alteplase or placebo (double-blind) over 3 hours. In the alteplase/PTCA trial, 367 similar patients received alteplase and subsequently were allocated at random to immediate coronary angiography and angioplasty of the infarct-related vessel or control. All patients received aspirin and intravenous heparin. In the alteplase/placebo trial, mortality during the first year was reduced by 36% with alteplase (from 9.3% to 5.6%; difference, -3.7%; 95% confidence interval, -7.5% to 0.2%). Revascularization was performed more frequently after alteplase, and more patients in the alteplase group were in New York Heart Association functional class I or II. Reinfarction tended to occur more frequently after alteplase than after placebo. In the alteplase/PTCA trial, reinfarction was less common after immediate PTCA, and revascularization procedures were less frequent. However, this benefit was offset by a high rate of immediate reocclusion and early recurrent ischemia and by higher mortality at 1 year (9.3% versus 5.4%; difference, 3.9%; 95% confidence interval, -1.5% to 9.2%) in the invasive group. In a multivariate analysis of 1,043 hospital survivors, mortality after discharge was related to coronary anatomy, left ventricular function, age, and previous infarction but not to initial treatment allocation. Reinfarction after hospital discharge tended to be more common after alteplase and related to coronary anatomy. CONCLUSIONS. Benefit from treatment with alteplase, heparin, and aspirin is not diminished at 1 year. Routine immediate PTCA does not confer additional benefit. Prognosis after hospital discharge mainly is determined by coronary anatomy and residual left ventricular function and is unrelated to initial treatment assignment.

Conference Abstract| December 01 1994 Nitric Oxide Synthase (NOS) is Induced in Main Pulmonary Arteries (PA) following in VIVO Treatment of Rats with Bacterial Endotoxin (LPS) Mjd Griffiths; Mjd Griffiths 1Unit of Critical Care, Department of Thoracic Medicine, National Heart & Lung Institute, London SW3 6NY, UK Search for other works by this author on: This Site PubMed Google Scholar M Messent; M Messent 1Unit of Critical Care, Department of Thoracic Medicine, National Heart & Lung Institute, London SW3 6NY, UK Search for other works by this author on: This Site PubMed Google Scholar SF Liu; SF Liu 1Unit of Critical Care, Department of Thoracic Medicine, National Heart & Lung Institute, London SW3 6NY, UK Search for other works by this author on: This Site PubMed Google Scholar PJ Barnes; PJ Barnes 1Unit of Critical Care, Department of Thoracic Medicine, National Heart & Lung Institute, London SW3 6NY, UK Search for other works by this author on: This Site PubMed Google Scholar TW Evans TW Evans 1Unit of Critical Care, Department of Thoracic Medicine, National Heart & Lung Institute, London SW3 6NY, UK Search for other works by this author on: This Site PubMed Google Scholar Author and article information Publisher: Portland Press Ltd Online ISSN: 1470-8736 Print ISSN: 0143-5221 © 1994 The Biochemical Society and the Medical Research Society1994 Clin Sci (Lond) (1994) 87 (s31): 37P–38P. https://doi.org/10.1042/cs045037Pb_pt2 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Cite Icon Cite Get Permissions Citation Mjd Griffiths, M Messent, SF Liu, PJ Barnes, TW Evans; Nitric Oxide Synthase (NOS) is Induced in Main Pulmonary Arteries (PA) following in VIVO Treatment of Rats with Bacterial Endotoxin (LPS). Clin Sci (Lond) 1 December 1994; 87 (s31): 37P–38P. doi: https://doi.org/10.1042/cs045037Pb_pt2 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1994 The Biochemical Society and the Medical Research Society1994 Article PDF first page preview Close Modal You do not currently have access to this content.

The American Thoracic Society/European Respiratory Society jointly created a Task Force on “Outcomes for COPD pharmacological trials: from lung function to biomarkers” to inform the chronic obstructive pulmonary disease research community about the possible use and limitations of current outcomes and markers when evaluating the impact of a pharmacological therapy. Based on their review of the published literature, the following document has been prepared with individual sections that address specific outcomes and markers, and a final section that summarises their recommendations.

No abstract is provided for this article.

In industrialised nations, cigarette smoking is the major risk factor for COPD, but in the developing world, exposure to biomass smoke (BMS) particles accounts for ∼50% of COPD deaths. COPD is associated with an increase in macrophages, albeit functionally defective. We hypothesise that exposure to BMS particles will elicit an inflammatory response and decrease phagocytosis of bacteria by monocyte derived macrophages (MDM). BMS particles were collected from a rural kitchen in India by burning wood and animal dung in a standard 3-stone cookstove using a high volume sampler. MDM from non-smoker (NS n=2-4) and COPD (n=2-5) subjects were exposed to BMS (1-300μg/ml) ± polymyxin B (10μg/ml) for 24h to eliminate LPS contamination. MDM were then incubated for 4h with fluorescently labelled heat killed H. influenzae (HI), S. pneumoniae (SP) or inert beads. Phagocytosis was measured by fluorimetry, cytokine release by ELISA and viability by MTT. BMS particles caused a concentration-dependent increase in CXCL8 (max release NS: 54±13.8 ng/ml; COPD: 42±1.1ng/ml) and IL-6 (max release NS: 6.2±0.7ng/ml; COPD: 7.3±3.3ng/ml) and TNFα (max release NS: 1.5±0.5ng/ml, COPD no stim). BMS particles stimulated release of IL-10 from COPD MDM (0.3±0.1ng/ml) but not from NS MDM. Polymyxin B had minimal effect on BMS particle-induced cytokine release. BMS particles had no effect on phagocytosis of HI, SP or beads by MDM from NS subjects. However, BMS particles reduced phagocytosis of HI by 55.1±2.7% and SP by 36.9±28.1% by COPD MDM. Viability was not affected. BMS particles are pro-inflammatory independent of LPS contamination and may drive defective macrophage phagocytosis in COPD.

Animal experimentation has shown that the instantaneous pressure-velocity of coronary blood flow in the hyperaemic phase has a linear relationship. The slope of this regression evaluates coronary reserve independently of haemodynamic variables and the X-intercept (zero flow pressure or Pf = 0) determines the intra-myocardial back pressure which could influence the regulation of coronary flow. The object of this study was to evaluate the instantaneous pressure-velocity relationship of coronary flow in clinical practice and to analyse the reproducibility of this parameter. Forty-nine patients were divided into two groups, depending on whether their coronary arteries were angiographically normal (n = 34) or atheromatous with stenosis > or = 35% of the reference diameter (n = 15). Recordings of coronary flow velocity were made with a Doppler transducer mounted on a 0.018 inch guide wire. The slope of the diastolic linear segment of the pressure-velocity relationship was determined at the peak of papaverine-induced vasodilation from 4 consecutive cycles by a regression analysis. The pressure value at 0 flow was obtained by extrapolation of the regression slope to the axis of aortic perfusion pressure. A good quality spectral recording allowing reliable analysis of the velocity profile was obtained in 88% of cases (44/49). The high values of the correlation coefficient observed with each measurement of the slope confirm the applicability of linear regression analysis to the pressure-velocity relationship. The slope of the pressure-velocity relationship was significantly lower in patients with coronary stenosis (1.7 +/- 0.7 cm/s/mmHg in normal vessels versus 0.7 +/- 0.3 cm/s/mmHg in stenotic arteries, p < 10(-4)), and, similarly, the pressure at zero flow was also reduced (36.9 +/- 16 mmHg versus 25.5 +/- 12 mmHg, p = 0.03). A statistically significant correlation was observed between the slope values and coronary flow reserve but no correlation was demonstrated between the slope and intraluminal surface area of angiographically normal coronary arteries or the slope and degree of stenosis of atheromatous vessels. The linear regression slope and the pressure at zero flow were lower when the pressure-velocity relationship was measured during long diastolic periods induced by the injection of adenosine. In addition, the curvilinear appearances of the pressure-velocity relationship observed during these long periods suggest that the linear regression model is not applicable throughout the whole range of pressures and velocities, especially for the lowest values.(ABSTRACT TRUNCATED AT 400 WORDS)

We have studied the contractile response and phosphoinositide hydrolysis induced by substance P (SP), neurokinin A (NKA), neurokinin B (NKB), and Alp-Phe-Phe(R)-Gly[ANC-2]-Leu-Met-NH2 (L 363851), a selective NK2-receptor agonist, in guinea pig tracheal smooth muscle. The four tachykinins elicited a concentration-dependent contraction in tracheal smooth muscle devoid of epithelium, with the following order of potency: NKA greater than L 363851 greater than NKB greater than SP, (EC50 1.0 x 10(-9) M, 3.2 x 10(-9) M, 7.5 x 10(-9) M and 1.2 x 10(-7) M, respectively), which suggests that NK2 receptors predominate in airway smooth muscle. In the presence of epithelium, the sensitivity of airway smooth muscle to tachykinins was decreased, and the concentration response curves to tachykinins were shifted rightward by 30-fold for SP, 9-fold for NKA, and 5-fold for NKB. The concentration response curve to L 363851 was not significantly shifted in the presence of epithelium. This suggests that epithelium may release a relaxant factor in response to tachykinins via an NK1 receptor. In airway smooth muscle, we found that tachykinins elicited phosphoinositide breakdown with an order of potency similar to that for contractile response (EC50 2.2 x 10(-5) M, 3.6 x 10(-5) M, 4.4 x 10(-5) M, and 5.9 x 10(-5) M). In epithelium, SP alone elicited a significant phosphoinositide breakdown, suggesting that epithelial receptors to tachykinins may be of the NK1 subtype. Since it is established that phosphoinositide derivatives can elicit mobilization of intracellular calcium, our results suggest that phosphoinositide breakdown is the coupling mechanism for tachykinin-induced contraction of airway smooth muscle.