Angiographically demonstrable changes in bypass status and their relation to the disease in the native coronary circulation were studied in 221 patients one year and three years after coronary artery bypass graft surgery.The extent of coronary artery disease was scored according to the recommendations of the American Heart Association and quantified following the method of Leaman.Patency in 570 grafts at one year was 79-6% and at three years 76-5%.The majority of grafts (83-5%) showed no change from one year to three years, 1144% showed progression in disease, and 5-1% showed regression.The majority of grafts which occlude do so in the first year after surgery.After the first year, the graft attrition rate is 1*6% of grafts per year.The coronary score (0, no disease; >30, serious three vessel disease) before surgery was 14 2+ 1.92 (mean +95% confidence) and dropped to 5 3+0 76 at one year when corrected for patent grafts.The coronary score remains greater than zero because of early graft closure and/or untreated lesions.By three years the corrected coronary score increased to 7-2 t1*06 primarily because of progression of disease in the native coronary circulation.Two subgroups, formed on the basis of angina pectoris at three years, showed that progression of disease in the native circulation was identical, but that return of angina was highly correlated with whether or not this disease occurred in segments perfused by patent grafts.Those factors known to be risk factors for coronary artery disease do not appear to have a bearing on progression or regression of disease in the graft, nor does the extent of coronary artery disease at the time of surgery correlate with eventual graft patency.
We compared inhibitory nonadrenergic noncholinergic (i-NANC) neural relaxations, evoked by electrical field stimulation (EFS), at three levels (main [MA], proximal [PA], and distal [DA] airways) of isolated human airways and correlated these with nitric oxide synthase-immunoreactive (NOS-IR) nerves, using antiserum raised to rat cerebellar NOS. Maximal relaxations to papaverine (100 microM) were reduced in PA and DA (MA: 1,712 +/- 219 mg, n = 12; DA: 862 +/- 69 mg, n = 5, P < 0.05 versus MA); hence, subsequent relaxations were expressed as a percentage of the papaverine maximum. EFS elicited frequency-dependent relaxations that were largest in MA and reduced in PA and DA, especially at high stimulation frequencies (10 Hz EFS: MA: 51.6 +/- 3.7%, n = 12; PA: 30.5 +/- 6.0%, n = 6, P < 0.01 versus MA; DA: 17.8 +/- 3.6%, n = 5, P < 0.001 versus MA). The NOS inhibitor L-NG-nitroarginine methyl ester (L-NAME) (100 microM) and tetrodotoxin (3 microM) significantly inhibited i-NANC responses at all frequencies, leaving an L-NAME-resistant non-neural relaxation at frequencies > 5 Hz which was reduced in PA and DA. Cumulative concentration-response studies to sodium nitroprusside (1 nM to 0.1 mM) and the NO donor 3-morpholinosydnonimine (1 nM to 1 mM) were not significantly different in PA and DA, suggesting impaired relaxation is not caused by impaired guanylyl cyclase activity. Total nerve density, shown by protein gene product 9.5 staining, was not significantly different in PA and DA; however, NOS-IR nerve density was reduced in PA and DA (NOS-IR [intercepts/mm2]: MA: 705 +/- 98, n = 6; DA: 284 +/- 32, n = 6, P < 0.01 versus MA). These studies demonstrate that i NANC neural relaxations are reduced in DA, apparently due to a decrease in the density of nitrergic innervation.
In 1981 we initiated a randomized trial at the Thoraxcenter in Rotterdam which was later extended to include four other hospitals cooperating in the Netherlands Interuniversity Cardiology Institute: the Zuiderziekenhuis in Rotterdam, the Free University in Amsterdam, the St. Annadal Hospital in Maastricht and the Leiden University Hospital. Since the global results of the study have been published in the Lancet (4) and in other journals (3, 5) we present a summary of the findings and discuss the clinical consequences of the trial.
No abstract is provided for this article.
Objectives: To evaluate the safety and efficacy of the XIENCE V everolimus‐eluting stent compared to the TAXUS paclitaxel‐eluting stent in small vessels. Backgroud: The XIENCE V everolimus‐eluting stent (EES) has been shown to improve angiographic and clinical outcomes after percutaneous myocardial revascularization, but its performance in small coronary arteries has not been investigated. Methods: In this pooled analysis, we studied a cohort of 541 patients with small coronary vessels (reference diameter <2.765 mm) by using patient and lesion level data from the SPIRIT II and SPIRIT III studies. TAXUS Express (73% of lesions) and TAXUS Liberté (27% of lesions) paclitaxel‐eluting stents (PES) were used as controls in SPIRIT II. In SPIRIT III, Taxus Express 2 PES was the control. Results: Mean angiographic in‐stent and in‐segment late loss was significantly less in the EES group compared with the PES group, (0.15 ± 0.37 mm vs. 0.30 ± 0.44 mm; P = 0.011 for in‐stent; 0.10 ± 0.38 mm vs. 0.21 ± 0.34 mm; P = 0.034 for in‐segment). EES also resulted in a significant reduction in composite major adverse cardiac events at 1 year (19/366 [5.2%] vs. 17/159 [10.7%]; P = 0.037), due to fewer non‐Q‐wave myocardial infarctions and target lesion revascularizations. At 1 year, the rate of non‐Q‐wave myocardial infarction was significantly lower in the EES group compared with that of the PES group (6/366 [1.6%] vs. 8/159 [5.0%]; P = 0.037). Conclusions: In patients with small vessel coronary arteries, the XIENCE V EES was superior to the TAXUS PES. © 2010 Wiley‐Liss, Inc.
No abstract is provided for this article.
Assembly 5 of the European Respiratory Society (ERS) is the Inflammatory Airway Diseases and Clinical Allergy Assembly and consists of three Scientific Groups: 1) Airway Pharmacology and Treatment; 2) Monitoring Airway Diseases; and 3) Allergy and Immunology. The original focus of the Assembly was mostly on asthma, but in recent years, it has increasingly begun to encompass chronic obstructive pulmonary disease (COPD). A substantial number of pharmacologists and basic scientists have joined clinicians to work together to unravel mechanisms of and improve diagnosis and treatment of these common chronic airway diseases. The Airway Pharmacology and Treatment Group focuses its activities on the pharmacology of the drugs used in asthma and COPD, and the development of scientific rationales for new drugs. The Monitoring Airway Disease Group evolved from the Airway Regulation and Provocation Group. Initially, focus was on the evaluation of bronchial responsiveness but in the past 20 years, important new technologies have developed, such as sputum induction, and measurement of exhaled nitric oxide (eNO) and exhaled breath condensate for noninvasive evaluation of airways inflammation. The Allergy and Immunology Group focuses mainly on airway and lung immunology, a rapidly advancing field that is crucial to our understanding of cellular and molecular backgrounds of allergy and inflammatory airways diseases. The majority of adult asthma patients can now be treated by a combination of inhaled corticosteroids and long-acting inhaled β2-agonists. Combination inhalers are highly effective, relatively inexpensive and safe. The scientific rationale is based on knowledge derived from both basic science and landmark clinical trials, in which prominent members of our Assembly have taken the lead 1–3. More recently, the …