6,963 publications from this institution
To investigate in terms of clinical, haemodynamic and biochemical profile the safety and efficacy of the Impella Recover(R) LP 2.5 left ventricular assist device during elective high risk percutaneous coronary interventions (HR-PCI).Ten out of twelve patients were initially enrolled to receive PCI supported by the Impella catheter; eight underwent pressure-volume (PV) loop analysis while one patient was monitored by intra-cardiac echocardiographic. Free haemoglobin (fHb), B-type natriuretic pepetide, catecholamines, aldosterone, angiotensin II, and endothelin were assessed before, every 40 minutes as average during the procedure and at 3, 12, 24 and 48 hours after intervention. The Impella catheter was used for 144+/-88 min [median (IQR) 108 (85-198)], and was removed immediately after the procedure in all but one patients. In 6, 3 and 2 patients, fHb levels increased above 1, 5 and 10 times the upper limit of normal (ULN), respectively. No significant effect was found on the tested biomarkers in Impella-supported procedures. The PV analysis showed the occurrence of an acute volume increase in the majority of patients immediately after Impella insertion that tended to persist even at maximal pump speed. This was confirmed by the intracardiac echocardiography that was performed in one patient.Our data, although preliminary due to the limited sample size, does not encourage the routine use of Impella Recover(R) LP 2.5 in HR-PCI. Additional studies are required to confirm and elucidate the mechanisms responsible for the acute LV volume loading and to quantify the degree of haemolysis induced by the pump in a broader set of patients.
The time course of the development of airway hyperresponsiveness (AHR) to inhaled acetylcholine (ACh) and the associated inflammatory cell recovery in bronchoalveolar lavage fluid (BAL) in actively sensitised Brown-Norway rats was studied following challenge with inhaled ovalbumin (OA). IgE for OA was detected in serum obtained from sensitised rats using passive cutaneous anaphylaxis, at titres of 1:10 to 1:30; none was detected in unsensitised animals. There was no significant change in either airway responsiveness to inhaled ACh or in BAL cell counts in rats challenged with saline over the 24 h. Following challenge with a 1% OA aerosol, airway responsiveness to inhaled ACh increased over the 24-hour period, maximal at 18–24 h (saline-challenged group mean ––log PC200 1.95 ± 0.07 M; OA-challenged group mean –log PC200 2.30 ± 0.05 M; p < 0.01). The composition of the inflammatory cells in the BAL fluid after allergen inhalation varied over the 24-hour period, with an initial neutrophilia at 5––8 h (p < 0.01), followed at 18–24 h by an increase in lymphocytes (p < 0.01) and marked eosinophilia (p < 0.01). There was a significant correlation between airway responsiveness and eosinophil recovery at 5–8 h (p < 0.05), and at 18-24 h after allergen exposure (p < 0.05). At 18–24 h there was also a significant correlation between neutrophils and airway responsiveness (p < 0.05). There was no difference between baseline lung resistance in matched saline- or OA-challenged animals at each time point. This animal model may be useful to study the cells and mediators involved in the development of allergen-induced AHR.
Background Clinical restenosis after balloon angioplasty can be categorized by use of dichotomous terms based on the presence or absence of recurrent myocardial ischemia. In contrast, recent investigations have concluded that late luminal renarrowing, documented through angiographic imaging, occurs to a variable extent in nearly all stenoses. This process has been characterized by a gaussian or normal frequency distribution, with restenosis simply representing an extreme form of this delayed remodeling. In the current study, frequency distribution analysis was used to examine the process of coronary restenosis in a large cohort of patients at risk. Methods and Results Quantitative coronary angiographic analysis was applied to 9279 cineangiograms obtained in 3093 patients before and immediately after angioplasty and after 6-month follow-up. Late loss, defined as the change in minimum lumen diameter of the target stenosis from postdilation to follow-up, did not statistically conform to a normal distribution ( P <.0001 by both χ 2 statistic and Kolmogorov-Smirnov test), even after the exclusion of the 236 stenoses that displayed total occlusions at follow-up angiography. Examination of deviations from a normal curve revealed an excessively high frequency of stenoses that experienced either little change (0.0±0.3 mm) or marked change (1.0 to 2.0 mm) in late loss, with a low frequency of stenoses with intermediate values (0.3 to 1.0 mm). Similarly, although the distribution of percent diameter stenosis of the target lesion was statistically normal immediately after dilation, this gaussian distribution disappeared during the follow-up period. Other angiographic indexes of restenosis also failed to approximate a normal curve. In an attempt to improve the goodness of fit, a probabilistic model of late loss was created on the basis of deconvolution of the observed data distribution. Two theoretical, discrete populations of stenoses were identified, one with and one without overall late luminal narrowing. Unlike the gaussian distribution, this model provided a good representation of the observed data ( P =NS for lack of fit). Conclusions The frequency distributions of angiographic indexes of restenosis often superficially resemble a gaussian curve, an appearance that is artifactually enhanced by the measurement imprecision of current quantitative techniques. Nevertheless, standard indexes of coronary restenosis fail to conform statistically to a normal distribution. The pattern of deviations observed supports the possible existence of discrete subpopulations of lesions, each with a different propensity toward the development of restenosis after coronary intervention.
In bovine tracheal smooth muscle the presence of airway epithelium significantly reduced the sensitivity and maximum contractile response to histamine, 5-hydroxytryptamine (5-HT) or acetylcholine. Muscle contraction induced by K+ and electrical field stimulation was of similar magnitude both in the presence or absence of adherent epithelium. The effect of epithelium on smooth muscle contractility was unaffected by pretreatment with indomethacin (10(-6) M) or mepacrine (5 X 10(-5) M). The relaxant response to isoprenaline was enhanced in the presence of epithelium, although this was significant only in the case of precontraction with 5-HT. It is concluded that the bronchial epithelium may produce a relaxant factor which is not a cyclooxygenase or lipoxygenase product. The production of this factor may be reduced or lost following epithelial damage and this may be important in the pathogenesis of bronchial hyperresponsiveness in asthma.
