Active clinical trials for "Myocardial Ischemia"

We will compare three study groups receiving metoprolol, esmolol, or placebo. Level of anesthesia will be titrated to achieve the same range of BIS value in all groups. Our hypothesis is that the metoprolol and esmolol groups will require a lower level of anesthetic agent to achieve the targeted BIS range, compared to the placebo group. Our objective is to clarify if metoprolol, in a dose range used for perioperative cardiac protection, decreases anesthetic requirement.

The purpose of this study is to collect and analyze additional information about the safety and effectiveness of the Presillion™ Stent System in the treatment of de novo stenotic lesions in native coronary arteries.

In a previous randomized comparison oral sirolimus plus bare metal stent compared to bare metal stent implantation alone demonstrated at one year of follow up a significant reduction of angiographic and clinical parameters of restenosis (ANMAT resolution number 3366 from June 2004 and Rodriguez A et al JACC,2006,47,1522-1529). In addition previous reported registries from our group with Drug Eluting Stents showed similar amount of reduction in clinical parameters (not angiographic)of restenosis (ERACI III, Rodriguez A et al EuroIntervention 2006,2:53-60). Taking in account that 8.3% of patients treated with oral rapamycin plus Bare Metal Stents(ORAR II Trial JACC 2006)and 8.8% of patients treated with DES developed clinical restenosis (ERACI III Registry, EuroIntervention 2006) the investigators sought to compare differences in overall cost with both revascularization strategies at 1, 2, 3 and 5 years of follow up assuming that safety and efficacy clinical end points would be similar.

A pilot study of 15 subjects will be conducted to confirm an acute effect of grape seed extract on endothelial function. We then will perform a a randomized, double blind, placebo controlled crossover study designed to investigate the benefit of grape seed extract/vitamin C treatment on endothelial function. Participants (n=40) will take a food supplement containing 450 mg of grape seed extract and 1500 mg of vitamin C or matching placebo for four weeks and then cross over to the alternative treatment (active supplement or placebo) for four weeks. We will examine endothelial function before and after each of the two treatment periods. The study will provide information about the vascular effects of these compounds.

The purpose of this study was to determine the effects of exercise training on insulin resistance in subjects with coronary artery disease independent of changes in weight, diet, or the effect of an acute bout of exercise. We hypothesized that subjects with CAD and high normal or impaired glucose tolerance performing 12 weeks of aerobic exercise training while on a non weight-reducing diet, would have a greater decrease in insulin resistance than controls measured at 72 hours following their last bout of exercise.

Aim: To investigate the quality of history taking by physician and computer-based system. Patients: 100 inpatients presenting at the RBK for the first time and treated in the departments of nephrology and cardiology. Methods: The information obtained by the computer based system is compared with the information acquired by conventional history taking. Study endpoint is the comparison of historical data organized according to the elements in a standard medical history on a patient-by-patient basis. Study procedure History taking is performed by physicians according to the guidelines of the RBK. Within 2 days thereafter the patient is interviewed with help of the CLEOS system with the support of a study nurse.

This study will examine whether a twelve-week intervention with one ounce (28 g) per day of walnuts improves endothelial function measured non-invasively using finger probe (EndoPat-2000) in people with coronary heart disease or type 2 diabetes.

The aim of this study is to explore the role of Canonical β-catenin/Wnt and forkhead box O (FOXO) pathways by means of investigating their target genes in coronary artery disease (CAD) pathogenesis and to examine the effects of resveratrol (RES) on these pathways in CAD patients.

Coronary artery disease (CAD) is the leading cause of morbidity and mortality in industrialized countries despite advances in medical, interventional, and surgical revascularization therapies. In both, acute myocardial infarction (AMI) and chronic stable disease, standard therapeutic approaches may fail to restore tissue perfusion. Indeed, a substantial number of chronic CAD patients may not be amenable to standard revascularization therapies or percutaneous coronary intervention (PCI) may fail to restore coronary artery patency following an acute vessel occlusion (no-reflow phenomenon, microvascular obstruction). As a consequence, the long pursued strategy of augmenting myocardial perfusion by diverting blood from the coronary venous system to an ischemic region (venous retroperfusion) has again gained attention during recent years. Occlusion of the coronary sinus (CSO) was introduced to provide retroperfusion by transient augmentation of coronary venous pressure. Different devices using CSO have been invented and evaluated in animal models and small clinical trials, e.g. intermittent CSO (ICSO) and pressure-controlled intermittent CSO (PICSO) which seem to be effective for myocardial salvage. However, they are not yet employed in clinical routine, and importantly, the exact underlying mechanisms by which retroperfusion due to CSO may reduce myocardial ischemia are not yet understood. As "natural bypasses", coronary collaterals are anastomoses without an intervening capillary bed between portions of the same coronary artery or between different coronary arteries that represent an alternative source of blood supply to a myocardial area jeopardized by ischemia. Collaterals of the heart can be assessed quantitatively by coronary pressure measurements, which have become the gold standard (collateral flow index, CFI=[Poccl-CVP]/[Pao-CVP]). Theoretically, augmentation of coronary sinus pressure by CSO with an increase of venous backflow reaches the upstream collateral circulation, which in turn could lead to improved collateral flow from non-ischemic area(s) to an occluded, ischemic myocardial region by upstream flow diversion. On the other hand, when considering the formula to calculate pressure-derived CFI, it seems that augmentation of coronary back pressure would rather impair collateral flow (since central venous pressure is coronary sinus pressure). However, the regional effect of a global increase in coronary sinus pressure is unlikely to be as uniform as the above formula implies, i.e., the response is more pronounced in some than in other vascular territories. In experimental studies using dogs (with abundant collaterals), elevation of coronary sinus pressure caused an augmentation of regional myocardial blood flow in the collateralized area. In contrast, when ICSO was performed in pigs (which possess no preformed collaterals), it increased the pressure distal of an occluded LAD but did not improve blood flow or left ventricular function. In conclusion, experimental studies and pathophysiologic considerations suggest a necessary role of the collateral circulation for the beneficial effects of coronary sinus occlusion (CSO) observed in animals and humans; however, no clinical data are available so far on the effect of CSO on myocardial ischemia in the presence of varying collateral flow. Study hypotheses CSO decreases intra-coronary ECG ST-segment elevation during a 2-minute coronary occlusion. The decrease in occlusive intra-coronary ECG ST elevation during CSO is directly proportional to CFI. Coronary sinus oxygen saturation during coronary occlusion with CSO is directly proportional to CFI.

The underlying hypothesis is that whole body cholesterol - including cholesterol present in tissues that cannot be measured by standard blood tests - is related to heart disease risk. Endogenous cholesterol will be labeled with an intravenous infusion of one type of cholesterol tracer and dietary cholesterol will be labeled with another. These tracers will be used to measure how fast cholesterol is synthesized and excreted using mass spectrometry to distinguish the tracers. Data will be related to circulating biomarkers (blood tests) and to the thickness of the lining of the carotid artery. The effect of the drug ezetimibe on these processes will also be determined. Successful completion of this study will give us more knowledge about cholesterol metabolism that may be useful in designing new drugs and treatments for patients with heart disease, especially those that are already receiving maximum amounts of current medications.