Purpose: To assess, by a European registry trial, the clinical event rate in patients with discrete stenotic lesions of coronary arteries (de novo or restenotic) in single or multiple vessels (native or bypass grafts) treated with β-radiation. Methods and materials: Between April 1999 and September 2000, 1098 consecutive patients treated in 46 centers in Europe and the Middle East with the Novoste Beta-Cath System were included in Registry Novoste (RENO). Results: Six-month follow-up data were obtained for 1085 patients. Of 1174 target lesions, 94.1% were located in native vessels and 5.9% in a bypass graft; 17.7% were de novo lesions, 4.1% were restenotic, and 77.7% were in-stent restenotic lesions. Intravascular brachytherapy was technically successful in 95.9% of lesions. Multisegmental irradiation, using a manual pullback stepping maneuver to treat longer lesions, was used in 16.3% of the procedures. The in-hospital rate of major adverse cardiac events was 1.8%. At 6 months, the rate was 18.7%. Angiographic follow-up was available for 70.4% of the patients. Nonocclusive restenosis was seen in 18.8% and total occlusion in 5.7% of patients. A combined end point for late (30–180 days) definitive or suspected target vessel closure was reached in 5.4%, but with only 2% of clinical events. Multivariate analysis was performed for major adverse cardiac events and late thrombosis. Conclusion: Data obtained from the multicenter RENO registry study, derived from a large cohort of unselected consecutive patients, suggest that the good results of recent randomized controlled clinical trials can be replicated in routine clinical practice.
No abstract is provided for this article.
No abstract is provided for this article.
The effect of posture on theophylline kinetics was examined in six healthy men who took 450 mg slow‐release aminophylline orally at the same time of day on two separate occasions. On one day they remained standing and on the other supine throughout. Plasma theophylline was measured hourly for 6 h from ingestion. Mean theophylline levels were significantly higher in the standing position at all times (P less than 0.01). We conclude that diurnal variation in theophylline kinetics can be explained, at least in part, by differences in posture.
The mechanism of bradykinin-induced bronchoconstriction was studied in anesthetized guinea pigs after both i.v. administration and direct airway instillation. We monitored airway opening pressure as an index of airway caliber, and the provocative dose of bradykinin required to produce 100% increase in airway opening pressure (PD100) was determined. Animals were pretreated with propranolol (1 mg/kg i.v.) to inhibit adrenergic bronchodilatation. After i.v. administration, the bronchoconstrictor dose-response curve to bradykinin (PD100 = 0.93 nmol/kg) was shifted significantly to the right by atropine (PD100 = 2.34 nmol/kg, P less than .05) and indomethacin (PD100 = 61.7 nmol/kg, P less than .05). Depletion of tachykinins by capsaicin pretreatment had no significant effect on the response to i.v. bradykinin. After tracheal instillation, the bronchoconstrictor dose-response curve to bradykinin (PD100 = 24.5 nmol) was shifted to the right by atropine (PD100 greater than 150 nmol, P less than .05) and capsaicin pretreatment (PD100 greater than 150 nmol, P less than .05). After atropine the response to instilled bradykinin was almost abolished in capsaicin-pretreated animals. Indomethacin had no effect on the bronchoconstrictor response to instilled bradykinin. We conclude that i.v. bradykinin causes bronchoconstriction predominantly by the release of cyclooxygenase products but that a cholinergic reflex is also involved, whereas sensory neuropeptides are not important. By contrast the bronchoconstrictor response to instilled bradykinin is mediated by neural mechanisms involving both cholinergic nerves and sensory neuropeptides but not by cyclooxygenase products.
Asthma and COPD are multidimensional diseases, with several systemic manifestations and associations with a number of comorbid diseases. The most likely link between asthma and COPD and these extrapulmonary conditions is the spillover of inflammatory mediators from the lung, as systemic inflammation is associated with skeletal muscle wasting and cachexia as well as with cardiovascular, metabolic, and bone diseases. Asthma is characterized by chronic airway inflammation, and infiltration of T-lymphocytes, mast cells, eosinophils and monocytes/macrophages. This is associated with the increased expression of several inflammatory proteins, including cytokines, enzymes, receptors and adhesion molecules. Chronic obstructive pulmonary disease (COPD) is currently a leading cause of morbidity and mortality worldwide, with the main cause being long-term cigarette smoking in the Western world. Accumulation of inflammatory mucous exudates in the lumen and infiltration of the wall by innate and adaptive inflammatory immune cells, such as CD4+ cells, CD8+ cells, B cells, macrophages, and neutrophils, and the formation of lymphoid follicles are all features of the observed inflammation that correlate with the severity of COPD. Previous studies have suggested that autoimmune mechanisms may contribute to the pathogenesis of COPD. Serum autoantibodies against elastin and bronchial epithelial cells along with corresponding IgG and complement (C3) deposition have been observed in COPD. In this regard, we have shown the presence of antibodies against carbonyl-modified protein neoepitopes in both COPD and a murine model of chronic exposure to oxidative stress. Thus, it seems that asthma and COPD are not only respiratory system dysfunctions but are also involved in multi-organ disorders. More research is needed to understand the links between these diseases and to search for common treatable components. It seems likely that treatments, such as statins, that are already used to manage cardiovascular and metabolic diseases might also provide benefit in COPD patients, although it is important that randomized placebo-controlled trials be conducted to confirm this possibility. It is important to consider how the existence of a comorbid disease may affect the management of a patient who also has COPD. Guidelines are needed that recognize the association of these various diseases and provide advice on management, as well as defining questions for future clinical research. In turn, it is important for specialists in nonpulmonary areas to recognize that COPD may commonly occur in association with certain diseases in their specialty and to make the diagnosis using spirometry so that appropriate treatment may be instituted. Treatments already used for COPD might also be beneficial in some comorbid diseases. New therapies should also be considered as potentially beneficial to systemic manifestations and comorbidities. For example, an effective inhaled anti-inflammatory therapy may improve comorbidities by reducing the overspill of inflammatory mediators from the lungs that contribute to systemic inflammation. Alternatively, an oral anti-inflammatory treatment, as well as suppressing inflammation on the respiratory tract, may directly reduce systemic inflammation. It is clear that much more clinical and basic research is needed to understand the complexity of COPD so that more effective management of COPD and its various comorbidities will be possible in the future.
