An experimental and numerical study of ferritic stainless steel tubular cross sections under combined loading is presented in this paper. Two square hollow section (SHS) sizes—SHS 40×40×2 and SHS 50×50×2 made of Grade EN 1.4509 (AISI 441) stainless steel—were considered in the experimental program, which included 2 concentrically loaded stub column tests, 2 four-point bending tests, and 14 eccentrically loaded stub column tests. In parallel with the experimental investigation, a finite-element (FE) study was also conducted. Following validation of the FE models against the test results, parametric analyses were carried out to generate further structural performance data. The experimental and numerical results were analyzed and compared with the design strengths predicted by the current European stainless steel design code EN 1993-1-4 and American stainless steel design specification SEI/ASCE-8. The comparisons revealed that the codified capacity predictions for ferritic stainless steel cross sections under combined loading are unduly conservative. The deformation-based continuous strength method (CSM) has been extended to cover the case of combined loading. The applicability of CSM to the design of ferritic stainless steel cross sections under combined loading was also evaluated. The CSM was shown to offer substantial improvements in design efficiency over existing codified methods. Finally, the reliability of the proposals was confirmed by means of statistical analyses according to both the SEI/ASCE-8 requirements and those of EN 1990.
No abstract is provided for this article.
SummaryThe diastolic properties of the left ventricle (LV) are important determinants of cardiac function; alteration in diastolic function accounts for many of the clinical manifestations of congestive heart failure. Changes in myocardial relaxation and filling phases, changes in coronary blood flow, diastolic tone and ventricular shape all contribute to the abnormal diastolic compliance of the failing heart. To assess the short-term effects of a single oral dose (10 mg) of milrinone (M) on diastolic function, 14 patients (pts), mean age 59 ± 6 years, with severe congestive heart failure underwent this study. After baseline hemodynamic measurements, LV angiography with simultaneous recording of LV pressure (tip-manometry) and pressure-derived parameters was performed at paced heart rate (15 beats above spontaneous heart rate). After repeat baseline measurements, M was administered followed by LV pressure measurements at 10′ intervals to 50′ together with coronary blood flow measurement. Blood samples to determine the plasma concentration of M were withdrawn at the same intervals. Blood arterial and coronary sinus samples for catecholamine levels and oxygen saturations were withdrawn before and 50′ after M. LV angiography was repeated 60′ after M at matched atrial paced rates with simultaneous pressure recordings. During the first phase of the study, peak negative dP/dt progressively and significantly increased from 827 ± 209 to 904 ± 194mm Hg/sec (p < 0.01) whereas LV systolic pressure slightly decreased. The time constant of early relaxation, Tau1,(fit for the first 40 msec. after the occurrence of peak negative dP/dt), decreased progressively and significantly from 71 ± 17 to 58 ± 14 msec (p < 0.01). Minimal LV diastolic pressure and LV end-diastolic pressure (LVEDP) were significantly lowered after 50′ from 13 ± 4 to 10 ± 7 mm Hg (p < 0.05) and from 27 ± 7 to 20 ± 10 mm Hg (p < 0.01), respectively. Coronary blood flow rose progressively during the first 40′ but the increase failed to be significant at 50′. Coronary vascular resistance reciprocated these changes. Myocardial oxygen consumption remained unchanged over 50′. Noradrenaline, adrenaline and dopamine mean values also remained unchanged over 50′, thus demonstrating a lack of effect of M on the basal, elevated sympathetic tone. Mean plasma level of M rose progressively, achieving a therapeutic level after 30′. The analysis of LV volume, pressure and pressure-derived parameters during angiography showed an improved relaxation phase with an increase in peak filling rate from 290 ± 27 to 338 ± 55 ml sec. The constant of elastic chamber stiffness, measured by the simple elastic model, decreased but not significantly. Pressure-volume loops showed a downward shift in 10/14 pts, mainly because of a major reduction in LVEDP from 29 ± 10 to 20 ± 11 mm Hg (p < 0.001) while end-diastolic volume only slightly decreased. Conclusion: improvement in parameters of LV diastolic relaxation and filling with changes in chamber distensibility following oral M, suggest that improved diastolic function may contribute to the beneficial effects of M on the failing heart.During the last two years several investigators have demonstrated that the administration of milrinone in patients with congestive heart failure leads to an increased inotropism together with a vasodilation, in absence or with only slight changes in heart rate and aortic pressure (1, 7, 10, 16). Recently an improvement in diastolic left ventricular performance, occurring after intravenous milrinone, has been reported (14). In the present study we evaluated the effect of a single oral dose of milrinone on central hemodynamics and on systolic and diastolic mechanics in patients with congestive heart failure.
"Introductory Remarks." American Journal of Respiratory and Critical Care Medicine, 150(5_pt_2), p. S1
Cineangiograms of 138 patients who underwent percutaneous transluminal coronary angioplasty (PTCA) were analyzed with a computer-based coronary angiography analysis system. The results before and after dilatation are presented. In a first study group (120 patients), the severity of the obstructive lesions derived from the automatically detected contours was evaluated in absolute terms and in percent-diameter reduction. In a second group of patients, 18 coronary lesions were selected for their extreme severity and symmetric aspect before angioplasty as assessed from multiple views. In the second group, the densHometric percent-area stenosis was used to assess the changes in cross-sectional area after PTCA and was compared with the circular percent-area stenosis computed from the diameter measurements. Before PTCA, a good agreement exists between the densitometric percent-area stenosis and the circular percent-area stenosis. After PTCA, important discrepancies between these 2 types of measurements are observed. It is suggested that these discrepancies in results after PTCA can be accounted for by asymmetric morphologic changes in luminal cross section, which cannot be assessed accurately from diameter measurements in a single-plane view.
Background: Optical Coherence Tomography (OCT) is a high resolution imaging technique capable of accurate assessment of polymeric struts, changes in luminal and scaffold dimensions, and quantificat...
Aims The aim of the present investigation was to determine the long-term prognostic association of post-procedural cardiac enzyme elevation within the randomised Synergy between Percutaneous Coronary Intervention (PCI) with TAXUS and Cardiac Surgery (SYNTAX) Trial. Methods 1800 patients with unprotected left main or de novo three-vessel coronary artery disease were randomised to undergo coronary artery bypass graft (CABG) surgery or PCI. Per protocol patients underwent post-procedural blood sampling with creatine kinase (CK), and the cardiac specific MB iso-enzyme (CK-MB) only if the preceding CK ratio was ≥2× the upper limit of normal (ULN). An independent chemistry laboratory evaluated all collected blood samples. Results Post-procedural CK sampling was available in 1629 of 1800 patients (90.5%). As per protocol, CK-MB analyses were undertaken in 474 of 491 patients (96.5%) in the CABG arm, and 53 of 61 patients (86.9%) in the PCI arm. Within the CABG arm, despite the limitations of incomplete data, a post-procedural CK-MB ratio <3/≥3 ULN separated 4-year mortality into low- and high-risk groups (2.3% vs. 9.5%, p=0.03). Additionally, in the CABG arm, a post-procedural CK-MB ratio ≥3 ULN was associated with an increased frequency of a high SYNTAX Score (≥33) tertile (high [≥33] SYNTAX Score: 39.5%, intermediate [23–32] SYNTAX Score 31.0%, low [≤22] SYNTAX Score 29.5%, p=0.02). Within the PCI arm, a post-procedural CK ratio of <2 or ≥2 ULN separated 4-year mortality into low- and high-risk groups (10.8% vs. 23.3%, p=0.001). Notably, there was an early (within 6months) and late (after 2years) peak in mortality in patients with a post-PCI CK ratio of ≥2 ULN. Lack of pre-procedural thienopyridine, carotid artery disease, type 1 diabetes, and presence of coronary bifurcations were independent correlates of a CK ratio ≥2 ULN post-PCI. Conclusion Cardiac enzyme elevations post-CABG or post-PCI are associated with an adverse long-term mortality; the causes of which are multifactorial.
1. The effects of the muscarinic M2 receptor antagonist methoctramine, on contractions of airway smooth muscle induced by cholinergic nerve stimulation and by exogenously applied acetylcholine (ACh), have been investigated in vivo and in vitro in guinea-pigs. 2. Stimulation of the preganglionic cervical vagus nerve in anaesthetized guinea-pigs, caused bronchoconstriction and bradycardia which were mimicked by an intravenous dose of ACh. The muscarinic M2 antagonist, methoctramine (7-240 nmol kg-1), inhibited the bradycardia induced by both vagal stimulation and ACh (ED50: 38 +/- 5 and 38 +/- 9 nmol kg-1, respectively). In this dose-range, methoctramine facilitated vagally-induced bronchoconstriction (ED50: 58 +/- 5 nmol kg-1), despite some inhibition of ACh-induced bronchoconstriction (ED50: 81 +/- 11 nmol kg-1). The inhibition of ACh-induced bronchoconstriction and hypotension was dose-dependent, but was not statistically significant until doses of 120 nmol kg-1 and 240 nmol kg-1 respectively. 3. In the guinea-pig isolated, innervated tracheal tube preparation, methoctramine (0.01-1 microM) caused facilitation of contractions induced by both pre- and postganglionic nerve stimulation, whereas contractions induced by exogenously applied ACh were unaffected. Higher concentrations of methoctramine (greater than or equal to 10 microM), reduced responses to both nerve stimulation and exogenous ACh, indicating blockade of post-junctional muscarinic M3 receptors. 4 ACh caused a slow maintained increase in tone of the tracheal tube and at the same time reduced the contractions induced by nerve stimulation. This inhibitory effect of ACh on neuronally mediated responses was antagonized by methoctramine (0.01-1 microM) in a concentration-dependent manner. However, the ACh-induced tone change was unaffected by methoctramine in this concentration-range, indicating a lack of muscarinic M3 receptor antagonist activity in this concentration-range.5. The effect of methoctramine on responses induced by pre- and postganglionic nerve stimulation was not identical. At concentrations of methoctramine of 1 ,microM and greater, preganglionic stimulation-induced contractions were reduced when compared to those induced by postganglionic stimulation, suggesting an inhibitory effect of methoctramine on ganglionic transmission. This ganglion blocking action of methoctramine was not due to its reported M1 receptor antagonist activity (blocking facilitatory Ml receptors in the ganglia) since pirenzepine was without effect in this preparation. We believe that the ganglionic blocking action of metoctramine is due to its nicotinic receptor antagonist properties, since the concentration of methoctramine inhibiting ganglionic transmission in the tube preparation (1 microM) was shown to inhibit contractions induced by the nicotinic agonist, 1,1-dimethyl-4-phenyl-piperazine in tracheal strips.6. These results show that methoctramine is able to demonstrate adequately the presence of autoinhibitory receptors functionally both in vivo and in vitro and confirms their pre-junctional location on pulmonary cholinergic nerve terminals and their classification as muscarinic M2 subtypes. These results also indicate that while methoctramine is a potent muscarinic M2 receptor antagonist, it does not possess the required selectivity to discriminate between cholinoceptor subtypes in preparations, such as the airways, where mixed populations of muscarinic and nicotinic cholinoceptors exist.
