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Biomedical subjects

Lars Rydén

Publications and source records attributed to Lars Rydén.

30 records · Page 2Linked to original sources
PubMed2003

The need for resources for clinical research: proceedings of a policy conference held at the European Heart House, 27-28 June 2002: executive summary.

The medical profession, in particular cardiologists, acknowledge the fact that during the last 30 years, much of the progress made in the field of medicine has resulted from fruitful and close collaboration between academia and the pharmaceutical industry. However, during the last decade, this relationship has changed considerably. The industry increasingly carries out its own research, development of drugs and trials, according to its own agenda. As a result, academia has lost its influence. This has led to a dramatic increase in the cost of clinical randomised trials. In the meantime, academic careers and research have become less attractive to physicians. Funding for research is increasingly devoted to basic science, in particular genomics, and little is left for clinical research. As a result, many important clinical trials in various areas of medicine, including cardiology, remain unfunded.

Cardiology↗
PubMed2003

Comparing multifactorial lifestyle interventions and stress management in coronary risk reduction.

The aim of this study was to compare the effects of residential multifactorial cardiac rehabilitation, outpatient multifactorial rehabilitation, stress management, and standard coronary rehabilitation, on cardiac risk reduction. Out of 144 eligible male patients recently treated with percantaneous transluminal coronary angiography (PTCA), coronary artery bypass graft (CABG), or acute myocardial infarction (AMI), 132 were randomized into this study. All interventions covered a 12-month active intervention, intense during the first months and subsequently leveled out. Main assessments were performed before randomization and after the intervention. Patients offered behavioral rehabilitation showed improved self-reported healthy diet habits and exercise frequency, and higher internal locus of control. Although blood lipids, exercise capacity, body mass, anxiety, depression, and Type A scores were changed in the expected direction, no significant difference emerged between active intervention and the standard care condition. Standard care of today appears to have great potential in particular if supplemented with some kind of stress management.

Angioplasty, Balloon, Coronary↗
PubMed2003

Diabetes, insulin resistance, and the metabolic syndrome in patients with acute myocardial infarction without previously known diabetes.

OBJECTIVE: Individuals with diabetes have an increased morbidity from acute myocardial infarction (AMI). Based on an oral glucose tolerance test (OGTT), 40-45% of patients with AMI have diabetes. The objective of this study was to characterize the glucometabolic profile of patients with AMI without known diabetes and to see if sustained glucometabolic perturbations are predictable during the hospital phase of the disease. RESEARCH DESIGN AND METHODS: A total of 145 patients with AMI and no previous diagnosis of diabetes were subjected to an OGTT at hospital discharge and 3 months thereafter. Based on the OGTT after 3 months, they were defined as having normal glucose tolerance (NGT; n = 50), impaired glucose tolerance (IGT; n = 59), or diabetes (n = 36). Components of the metabolic syndrome, including insulin resistance assessed by homeostasis model assessment (HOMA-IR), were recorded. RESULTS: Patients with AMI had no changes in insulin resistance from hospital discharge to follow-up. An OGTT and/or a single blood glucose taken 60 min (BG-60) after ingestion of 75 g glucose at hospital discharge were predictors of the outcome of the OGTT at follow-up. With a cutoff value for BG-60 of 8.6 mmol/l, 70% of the patients were correctly predicted as either belonging to the NGT group or the IGT/diabetes group after 3 months. Age, BMI, antihypertensive treatment, HbA(1c), fasting blood glucose, blood lipids, insulin, proinsulin, HOMA-IR, and plasminogen activator inhibitor 1 did not add predictive power. CONCLUSIONS: Patients with AMI and no previous diagnosis of diabetes have no changes in insulin resistance from hospital discharge to a 3-month follow-up. An OGTT or a single BG-60 performed at hospital discharge predicts the diagnosis of IGT or diabetes 3 months thereafter.

Acute Disease↗
PubMed2002

Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus: a prospective study.

BACKGROUND: Glycometabolic state at hospital admission is an important risk marker for long-term mortality in patients with acute myocardial infarction, whether or not they have known diabetes mellitus. Our aim was to ascertain the prevalence of impaired glucose metabolism in patients without diagnosed diabetes but with myocardial infarction, and to assess whether such abnormalities can be identified in the early course of a myocardial infarction. METHODS: We did a prospective study, in which we enrolled 181 consecutive patients admitted to the coronary care units of two hospitals in Sweden with acute myocardial infarction, no diagnosis of diabetes, and a blood glucose concentration of less than 11.1 mmol/L. We recorded glucose concentrations during the hospital stay, and did standardised oral glucose tolerance tests with 75 g of glucose at discharge and again 3 months later. FINDINGS: The mean age of our cohort was 63.5 years (SD 9) and the mean blood glucose concentration at admission was 6.5 mmol/L (1.4). The mean 2-h postload blood glucose concentration was 9.2 mmol/L (2.9) at hospital discharge, and 9.0 mmol/L (3.0) 3 months later. 58 of 164 (35%, 95% CI 28-43) and 58 of 144 (40%, 32-48) individuals had impaired glucose tolerance at discharge and after 3 months, respectively, and 51 of 164 (31%, 24-38) and 36 of 144 (25%, 18-32) had previously undiagnosed diabetes mellitus. Independent predictors of abnormal glucose tolerance at 3 months were concentrations of HbA(1c) at admission (p=0.024) and fasting blood glucose concentrations on day 4 (p=0.044). INTERPRETATION: Previously undiagnosed diabetes and impaired glucose tolerance are common in patients with an acute myocardial infarction. These abnormalities can be detected early in the postinfarction period. Our results suggest that fasting and postchallenge hyperglycaemia in the early phase of an acute myocardial infarction could be used as early markers of high-risk individuals.

Body Mass Index↗
PubMed2002

Pharmacological possibilities for protection against myocardial reperfusion injury.

Reperfusion through thrombolysis or percutananeous coronary angioplasty is standard treatment in impending acute myocardial infarction. Although restoration of blood flow to the jeopardised myocardial area is a perquisite for myocardial salvage, reperfusion itself may lead to accelerated and additional myocardial injury beyond that generated by ischemia alone. This is referred to as the "reperfusion injury". Since the reperfusion injury is initiated by the treatment of myocardial infarction, it is of importance to limit the extent of the injury. Several studies aimed at preventing reperfusion injury by means of pharmacological agents have therefore been conducted. The design of such studies is crucial for the results. Factors of importance are the timing of drug administration, animal species used, the degree of collateral flow and the duration of ischemia. A variety of pharmacological compounds have been investigated in different experimental models of myocardial ischemia and reperfusion. These include oxygen free radical scavengers, antioxidants, calcium channel blockers, inhibitors of neutrophils, nitric oxide, adenosine-related agents, inhibitors of the renin-angiotensin system, endothelin receptor antagonists, Na(+)/H(+) exchange inhibitors, and anti-apoptotic agents. All these groups of pharmacological agents have been demonstrated to protect from reperfusion injury determined as limitation of infarct size, improved myocardial and endothelial function, and reduced incidence of arrhythmias. The mechanism behind the protective effect may differ between different groups of compounds, but some compounds may exert cardioprotection via common pathways. Such a pathway may be via maintained bioavailability of nitric oxide.

Adenosine↗
PubMed2002

Recognising and treating the diabetic patient in cardiovascular care.

The global prevalence of diabetes mellitus has continuously and rapidly increased, and the number of diabetic people in the adult population is predicted to double within 30 years. The prevalence of and mortality from all forms of cardiovascular diseases is two- to eight-fold higher in diabetic individuals as compared with their non-diabetic counterparts. The excess of risk attributable to diabetes related heart disease accounts for 2.9% of the all cause annual mortality. Moreover, the cardiovascular risk increases continuously throughout a wide spectrum of glycaemia starting already at what, according to present definitions, is considered as normal blood glucose levels. Therefore, screening for diabetes and hyperglycaemia is recommended in various clinical settings. Criteria for classification of hyperglycaemic states are provided together with their relation to risk for cardiovascular events. The evidence-based treatment of cardiovascular disease in patients with concomitant diabetes is summarised. Degree of under-treatment of patients with diabetes and cardiovascular diseases is discussed. Finally, the potential impact that nurses may have on the quality and efficacy of care in the vulnerable patient with combined chronic diseases such as diabetes and cardiovascular disease and the improvement of the outcomes are discussed.

Cardiovascular Diseases↗
PubMed2002

Time-dependent cardioprotection with calcium antagonism and experimental studies with clevidipine in ischemic-reperfused pig hearts: part I.

Clevidipine is a new ultrashort-acting dihydropyridine calcium antagonist developed for blood pressure regulation during cardiac surgery. When given locally to the ischemic and reperfused myocardium, clevidipine exerts a cardioprotective effect that varies depending on the timing of administration during ischemia. The current study explored the pharmacokinetics of clevidipine when administered locally into the coronary circulation. Pentobarbital-anesthetized pigs were randomly divided into four groups, of which three were subjected to myocardial ischemia through ligation of the left anterior descending coronary artery (LAD) for 15, 35, or 45 minutes (n = 4 in each group). The fourth group (n = 4) was not subjected to LAD occlusion and acted as nonischemic controls. Clevidipine (0.3 nmol/kg per minute) was infused over a period of 5 minutes through a catheter distal to the LAD ligation in the ischemic pigs, or at the corresponding site of the nonligated LAD in the nonischemic pigs. Following release of the LAD ligation, or in the nonligated group following the drug infusion, the pigs were subjected to 60 minutes of reperfusion. Simultaneous blood samples were obtained for analysis of clevidipine from the femoral artery and the coronary vein during reperfusion and during drug infusion in the nonischemic pigs. Blood samples for estimating the in vitro hydrolysis rate both in whole blood and in plasma were also obtained. In nonischemic hearts, clevidipine reached a steady state level in the coronary venous blood of about 30 nM during the infusion. The concentration declined almost to the detection limit (1 nM) within 3 minutes of the end of infusion. The mean blood clearance of clevidipine was calculated to be 0.17 l/min per kilogram, and the estimated half-life was 0.5 minute. In animals subjected to different periods of ischemia, very low levels of clevidipine were detected in the coronary venous blood only during the first 2 minutes of reperfusion. There were no detectable levels in the arterial blood at any time. Blood concentration profiles of clevidipine did not differ with the length of myocardial ischemia. The in vitro half-life in pig blood was 13 minutes, and the corresponding half-life in plasma was 111 minutes. At a dose known to exert cardioprotection when given as an intracoronary injection, the systemic concentration of clevidipine does not reach pharmacologically active levels. Clevidipine has an ultrashort blood half-life, and ischemic duration of up to 45 minutes does not seem to change the cardiac metabolism of this drug. Thus, it represents a pharmacological tool well suited for the study of time windows in cardioprotection. Moreover, considering the possibility of exerting myocardioprotection without any systemic effects, it could be an interesting compound to test in a clinical setting.

Animals↗
PubMed2002

Time-dependent cardioprotection with calcium antagonism and experimental studies with clevidipine in ischemic-reperfused pig hearts: part II.

The intracellular calcium level is increased during ischemia and early reperfusion. The aim of this study was to study the role of the calcium influx in the development of myocardial ischemic and reperfusion injury during the early and late phases of ischemia and during early reperfusion. An ultrashort-acting calcium antagonist, clevidipine, was used as a tool for this investigation. Pentobarbital-anesthetized pigs were subjected to 45 minutes of LAD occlusion followed by 240 minutes of reperfusion. In the first set of experiments, clevidipine (0.3 nmol/kg per minute) was infused over 5 minutes into the ischemic myocardium via a catheter in the LAD, starting at 5, 35, or 44 minutes following the onset of ischemia (n = 6 in each group). The area at risk and the infarct size were determined after 240 minutes of reperfusion by staining with Evans blue dye and triphenyl tetrazolium chloride (TTC), respectively. In a second set of experiments, two groups of animals (n = 6 in each) were subjected to the same periods of ischemia and reperfusion; one group received no infusion during ischemia, whereas the other group received vehicle infusion during a 5-minute period between 5 and 10 minutes of ischemia. In the first set of experiments, there were no significant differences between the groups with regard to hemodynamic variables. The area at risk expressed as a percentage of the left ventricle was of similar magnitude in all three clevidipine-treated groups (about 18%). The infarct size, expressed as a percentage of the area at risk, was significantly smaller in pigs given clevidipine after 5 minutes (58 +/- 17%; p < 0.01) and after 44 minutes (42 +/- 6%; p < 0.01) of ischemia than in pigs receiving clevidipine after 35 minutes of ischemia (85 +/- 4%). The difference in infarct size between pigs given clevidipine after 5 or 44 minutes of ischemia was not significant. In the second set of experiments, there was a similar area at risk and no significant difference in infarct size between the noninfusion group and the 5-minute vehicle infusion group, indicating that the LAD infusion per se did not affect infarct size. The present results demonstrate that blockade of calcium influx by the short-acting dihydropyridine calcium antagonist clevidipine during the early phase of ischemia and at the time of reperfusion, but not during a late phase of ischemia, limits infarct size induced by ischemia and reperfusion. This indicates that the pathophysiological importance of calcium influx varies according to the different phases of myocardial ischemia and reperfusion.

Animals↗