Deadbeat-fuzzy controller for the power control of a Doubly Fed Induction Generator based wind power system.

This paper proposes a Fuzzy Logic Controller for improvement of the steady-state response of a Doubly Fed Induction Generator used in a wind energy system, and governed by means of a Deadbeat Power Controller. The generator mathematical model is consistent with the Stator Flux oriented strategy in the synchronous reference frame. Different simulation scenarios were developed in Matlab/Simulink to evaluate the dynamic and the steady-state responses. In order to obtain experimental results, the simulated scenarios were repeated by means of a test bench and a Digital Signal Processor board. These results demonstrate that the response still follows the power references imposed, despite the fact that the generator parameters ( Rr, Ls and Lm) were varied in a 30%. A lower steady-state error is also achieved when compared with a Deadbeat and a classical PI controller. All the aforementioned evidence the proper application of this Fuzzy Controller in a wind power system based on a Doubly Fed Induction Generator.

Cyclooxygenase-2--specific inhibitors and cardiorenal function: a randomized, controlled trial of celecoxib and rofecoxib in older hypertensive osteoarthritis patients.

BACKGROUND: Arthritis and hypertension are common comorbid conditions affecting elderly adults. Use of nonsteroidal anti-inflammatory drugs in patients treated with antihypertensive medication can lead to destabilization of blood pressure control and other cardiorenal events. The potential for similar interactions with cyclooxygenase-2-specific inhibitors has not been fully explored. The authors evaluated the cardiorenal safety of two new cyclooxygenase-2-specific inhibitors, celecoxib and rofecoxib. METHODS: This study was a 6-week, randomized, parallel-group, double-blind trial in patients with osteoarthritis who were > or =65 years of age and were taking antihypertensive agents. Patients received once-daily celecoxib 200 mg or rofecoxib 25 mg. The primary endpoints were the development of edema, changes in systolic blood pressure, and changes in diastolic blood pressure as measured at any time point in the study. Measurements occurred at baseline and after 1, 2, and 6 weeks of treatment. FINDINGS: Eight hundred ten patients received study medication (celecoxib, n = 411; rofecoxib, n = 399). Nearly twice as many rofecoxib- compared with celecoxib-treated patients experienced edema (9.5% vs. 4.9%, P = 0.014). Systolic blood pressure increased significantly in 17% of rofecoxib- compared with 11% of celecoxib-treated patients (P = 0.032) at any study time point. Diastolic blood pressure increased in 2.3% of rofecoxib- compared with 1.5% of celecoxib-treated patients (P = 0.44). At week 6, the change from baseline in mean systolic blood pressure was +2.6 mmHg for rofecoxib compared with -0.5 mmHg for celecoxib (P = 0.007). CONCLUSIONS: Patients taking antihypertensive therapy and receiving cyclooxygenase-2-specific inhibitors should be monitored for the development of cardiorenal events. Patients receiving celecoxib experienced less edema and less destabilization of blood pressure control compared with those receiving rofecoxib.

Comparison of medicine alone, coronary angioplasty, and left internal mammary artery-coronary artery bypass for one-vessel proximal left anterior descending coronary artery disease.

Despite the deleterious and sometimes catastrophic consequences of proximal left anterior descending (LAD) artery occlusion, there is a paucity of data to guide the treatment of patients with such disease. Our aim was to describe outcomes with medical therapy, angioplasty, or left internal mammary artery (LIMA) bypass grafting in patients with 1-vessel, proximal LAD disease. We retrospectively analyzed prospectively collected data from 1,188 patients first presenting only with proximal LAD disease at 1 center over 9 years. We assessed the rates of death, acute myocardial infarction, and repeat intervention by initial treatment over a median 5.7 years of follow-up. Patients undergoing angioplasty or LIMA bypass were more often men and had progressive or unstable angina; those receiving medical therapy had a lower median ejection fraction. Both revascularization procedures offered slightly better adjusted survival versus medicine (hazard ratio for angioplasty, 0.82; 95% confidence interval, 0.60 to 1.11; hazard ratio for bypass, 0.74; 95% confidence interval, 0.44 to 1.23). Bypass, but not angioplasty, was associated with significantly fewer composite end point events (death, infarction, or reintervention, p <0.0001), and angioplasty was associated with a higher composite event rate than bypass or medical therapy (p <0.0001 and p = 0.0003, respectively). The initial advantages of bypass and medicine over angioplasty diminished over time; angioplasty became more advantageous than medicine after 1 year (p = 0.05) and not significantly different from bypass. Treatment of 1-vessel, proximal LAD disease with medicine, angioplasty, or UMA bypass resulted in comparable adjusted survival. However, LIMA bypass alone reduced the long-term incidence of infarctions and repeat procedures.

Thrombolytic, antithrombin, and antiplatelet treatment of acute coronary syndromes.

Acute coronary syndromes are a major public health problem and the leading cause of death in the western world. Acute coronary syndromes consist of unstable angina pectoris, non-ST-segment-elevation myocardial infarction, and ST-segment-elevation myocardial infarction. These diseases represent a continuum of increasing severity and are pathophysiologically linked to intracoronary thrombus formation that is nonocclusive, transiently occlusive, or completely occlusive, respectively. Antiplatelet treatment with aspirin is the cornerstone of treatment for all acute coronary syndromes. Newer intravenous antiplatelet agents reduce 30-day mortality and myocardial infarction in unstable angina and non-ST-segment-elevation myocardial infarction. Adenosine diphosphate antagonist antiplatelet agents have an ill-defined role in the treatment of acute coronary syndromes. Fibrinolytic therapy has been shown to reduce mortality in ST-segment-elevation myocardial infarction but may pose a hazard in other acute coronary syndromes.

Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction: results of a multicenter, randomized, placebo-controlled trial: the Acute Myocardial Infarction STudy of ADenosine (AMISTAD) trial.

OBJECTIVES: The Acute Myocardial Infarction STudy of ADenosine (AMISTAD) trial was designed to test the hypothesis that adenosine as an adjunct to thrombolysis would reduce myocardial infarct size. BACKGROUND: Reperfusion therapy for acute myocardial infarction (MI) has been shown to reduce mortality, but reperfusion itself also may have deleterious effects. METHODS: The AMISTAD trial was a prospective, open-label trial of thrombolysis with randomization to adenosine or placebo in 236 patients within 6 h of infarction onset. The primary end point was infarct size as determined by Tc-99 m sestamibi single-photon emission computed tomography (SPECT) imaging 6+/-1 days after enrollment based on multivariable regression modeling to adjust for covariates. Secondary end points were myocardial salvage index and a composite of in-hospital clinical outcomes (death, reinfarction, shock, congestive heart failure or stroke). RESULTS: In all, 236 patients were enrolled. Final infarct size was assessed in 197 (83%) patients. There was a 33% relative reduction in infarct size (p = 0.03) with adenosine. There was a 67% relative reduction in infarct size in patients with anterior infarction (15% in the adenosine group vs. 45.5% in the placebo group) but no reduction in patients with infarcts located elsewhere (11.5% for both groups). Patients randomized to adenosine tended to reach the composite clinical end point more often than those assigned to placebo (22% vs. 16%; odds ratio, 1.43; 95% confidence interval, 0.71 to 2.89). CONCLUSIONS: Many agents thought to attenuate reperfusion injury have been unsuccessful in clinical investigation. In this study, adenosine resulted in a significant reduction in infarct size. These data support the need for a large clinical outcome trial.

Support for the open-artery hypothesis in survivors of acute myocardial infarction: analysis of 11,228 patients treated with thrombolytic therapy.

We examined the possible benefits of achieving and maintaining infarct-related artery potency beyond the time when preservation of left ventricular function would be expected. The open-artery hypothesis suggests that a patent infarct-related artery confers a survival benefit greater than that expected from myocardial salvage alone, which extends beyond the time when preservation of left ventricular function is expected. We examined the survival experience of patients undergoing thrombolysis in the Global Utilization of Streptokinase and TPA for Occluded Arteries (GUSTO-I) trial for whom data on the potency of the infarct artery were available. Univariable analysis was used to determine the unadjusted relations of angiographic variables and revascularization procedures to both 30-day and 1-year mortality in 30-day survivors. Multivariable analysis was used to test for interactions between patency and each characteristic and to adjust both for all other variables and for baseline characteristics known to predict mortality. In both univariable and multivariable analysis, patients with an open rather than a closed infarct-related artery had significantly lower 30-day mortality (p <0.001). This benefit cannot be accounted for by myocardial salvage alone, because it remained after adjustment for left ventricular ejection fraction. Patency was also associated with lower 1-year mortality in 30-day survivors, but not after adjustment for other variables affecting late mortality. Having an open infarct-related artery at the time of first catheterization confers a survival advantage that extends beyond the benefit of myocardial salvage from thrombolytic therapy, and is independent of ejection fraction.