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Biomedical subjects

F W Verheugt

Publications and source records attributed to F W Verheugt.

At least 37 records · Page 2Linked to original sources
PubMed2001

Pravastatin in acute ischaemic syndromes: results of a randomised placebo-controlled trial.

Therapy with individual 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) has been shown conclusively to diminish coronary event rates and mortality in both primary and secondary prevention. To date, scant attention has been paid to whether initiation of such regimens in the hospital phase of acute coronary syndromes might confer cardioprotective benefits. The purpose of this study was to determine the safety and tolerability of early initiation of statin therapy in patients with acute coronary syndromes. In this randomised, double-blind, three-month, pilot study, 100 patients with acute myocardial infarction or unstable angina and low-density lipoprotein cholesterol > 3.5 mmol/l were randomly assigned to pravastatin 40 mg daily or placebo initiated within 48 hours of hospital admission. Pravastatin proved safe and well tolerated in these patients, who were well matched at baseline. No statistically significant differences in death, MI and drug-related adverse events were observed in the pravastatin group compared with control subjects. This pilot study shows that therapy with pravastatin early after an acute coronary event is safe and well tolerated. Larger, long-term studies are needed to confirm these findings.

Acute Disease↗
PubMed2000

[Acetylsalicylic acid versus coumarin derivatives in atrial fibrillation].

Atrial fibrillation is a chronic disorder, which significantly increases the risk of stroke. The risk of stroke largely depends on cardiac failure, age, sex, the presence of hypertension and a history of previousthromboembolism. In low risk patients with atrial fibrillation stroke can effectively be prevented with acetylsalicylic acid (100-200 mg/day). With increasing stroke risk coumarin derivatives are more effective than acetylsalicylic acid and its use has an acceptable bleeding risk. The target international normalized ratio (INR) should be between 2.0 and 3.0.

Adult↗
PubMed2000

[Aortocoronary bypass surgery; at least 6 months follow-up required for assessment of postoperative course].

OBJECTIVE: To determine how the mortality and morbidity after aortocoronary bypass surgery during the hospital stay correspond with those in the first 6 months after the operation. DESIGN: Prospective and retrospective. METHOD: Data of 563 patients undergoing isolated myocardial revascularization in 1998 in the Academic Hospital Nijmegen, the Netherlands, were collected on mortality and morbidity 180 days after the operation. The Parsonnet score was used to assess the operative risk of the patients. RESULTS: The patient group consisted of 422 males and 141 females, with a mean age of 64.3 years. The median Parsonnet score was 6 (range: 0-50). The mean hospital stay was 7.9 days (SD: 9.4). The hospital mortality was 3.9% (22/563). The follow-up was 100%. During the follow-up 11 patients died, 10 from cardiac causes. Six months postoperatively the mortality was 5.9% (22/563). The Kaplan-Meier curve of the survival probability rate showed a persistent decrease, mainly in the higher risk patients. Non-fatal cardiovascular events were registered in 9.6% of the surviving patients (51/530). CONCLUSION: The hospital mortality and morbidity after aortocoronary bypass surgery were considerably lower than the total postoperative mortality and morbidity during the first 6 months after the operation. For assessment of the postoperative course, systematic follow-up over 6 months is necessary.

Adult↗
PubMed2000

Effect of coumarins started before coronary angioplasty on acute complications and long-term follow-up: a randomized trial.

BACKGROUND: Coronary angioplasty frequently creates a thrombogenic surface, with subsequent mural thrombosis that may lead to acute complications and possibly stimulates the development of restenosis. Whether coumarins can prevent these complications is unclear. The objective of this open, randomized trial was to assess the clinical effect of coumarins started before coronary angioplasty and continued for 6 months. METHODS AND RESULTS: Before coronary angioplasty, 530 patients were randomly assigned to aspirin plus coumarins and 528 patients to aspirin alone. At the start of the angioplasty, the mean international normalized ratio was 2.7+/-1.1; during follow-up, it was 3.0+/-1.1. At 30 days, the composite end point of death, myocardial infarction, target-lesion revascularization, and stroke was observed in 18 patients (3.4%) treated with aspirin plus coumarin compared with 34 patients (6.4%) treated with aspirin alone (relative risk, 0.53; 95% CI, 0.30 to 0.92). At 1 year, these figures were 14.3% and 20.3%, respectively (relative risk, 0.71; 95% CI, 0.54 to 0.93). The incidence of major bleeding and false aneurysm during hospitalization was 3.2% and 1.0%, respectively (relative risk, 3.39; 95% CI, 1.26 to 9.11). The benefit of coumarins was observed in both stented and nonstented patients. CONCLUSIONS: Coumarins in addition to aspirin started before PTCA and continued for 6 months was more effective than aspirin alone in the prevention of acute and late complications after coronary angioplasty. This benefit was accompanied by a small but significant increase in bleeding complications.

Aged↗
PubMed2000

[Therapeutic angiogenesis as a new experimental treatment for vascular disease].

Currently, our treatment modalities for patients with severe coronary artery disease consist of combinations of medication, percutaneous transluminal coronary angioplasty (PTCA) and coronary revascularization operations. Still, the number of patients who cannot be treated adequately in these ways is growing. In recent years progress has been made in the field of angiogenesis: the process of the development of new capillaries. It is now known that blood vessel growth is an essential phenomenon in a range of disease. It is possible to inhibit or stimulate this process, offering hope for new treatments in a wide array of diseases. Stimulation of angiogenesis has already been successful in animal models of chronic peripheral and myocardial ischaemia. Results of experimental treatments of coronary patients have been reported since 1998. 'Therapeutic angiogenesis' may evolve as our fourth treatment modality for the treatment of coronary artery insufficiency.

Angiogenesis Inhibitors↗
PubMed2000

High dose heparin as pretreatment for primary angioplasty in acute myocardial infarction: the Heparin in Early Patency (HEAP) randomized trial.

OBJECTIVES: In the Heparin in Early Patency (HEAP) pilot study a beneficial effect of high-dose heparin on early patency in acute myocardial infarction (MI) was observed in a matched-control study. BACKGROUND: High dose bolus intravenous injection of heparin may achieve lysis of coronary thrombi and could enhance early patency of the infarct related vessel in patients with MI scheduled for primary angioplasty. METHODS: Before primary angioplasty, 584 patients with MI entered an open randomized trial of high dose (300 IU/kg) or low dose (0 or 5,000 IU) heparin. Of the 584 patients, 299 were randomized to high dose and 285 patients to low dose heparin. RESULTS: Thrombolysis In Myocardial Infarction (TIMI) flow grade 2 or 3 was observed before primary angioplasty in 65 patients (22%) in the high dose group and 60 patients (21%) in the low dose heparin group (p > 0.1), whereas TIMI flow grade 3 was observed in 38 (13%) and 24 patients (9%), respectively (p = 0.11). There were no differences in the clinical end points between the two groups. There were no hemorrhagic strokes, while 10% of the patients in the high dose group required blood transfusion versus 6% in the low dose/no heparin group (p = 0.07). No subsets of patients showed beneficial effects of high dose heparin, such as patients with longer delay between heparin administration and diagnostic angiogram or patients with short delay between symptom onset and admission. CONCLUSIONS: There is no benefit of high dose bolus heparin on early patency compared with no or low dose heparin.

Aged↗
PubMed2000

Scintigraphic detection of acute experimental endocarditis with the technetium-99m labelled glycoprotein IIb/IIIa receptor antagonist DMP444.

Bacterial endocarditis is an important clinical problem that may result in persistent bacteraemia and irreversible cardiac damage. Since endocarditis is characterized by aggregation of activated platelets, fibrin and bacteria, we studied DMP444, a technetium-99m labelled high-affinity antagonist of the GP IIb/IIIa receptor that is expressed on activated platelets. In seven Beagle dogs (11-15 kg), the left ventricle was catheterized via the right carotid artery. One hour later, 5x10(7) colony forming units of Staphylococcus aureus were injected intracardially. Half an hour later, the catheter was removed. Two extra dogs underwent a complete sham procedure. One day after the intervention, five infected and the two non-infected dogs were injected with 37 MBq/kg 99mTc-DMP444 and two infected dogs with 37 MBq/kg 99mTc-IgG (used as a non-specific control agent) and imaged up to 4 h after injection. Samples were obtained for tissue counting, microbiology and histology. From 1 to 2 h post injection onward, there was clear focal accumulation of DMP444 in the aortic valve region when endocarditis was present, and this accumulation increased with time. The non-infected and the 99mTc-IgG injected dogs showed only persisting blood pool activity without any focal abnormality. At 4 h post injection, the in vivo valve-to-blood pool ratios were 1.87+/-0.18 in endocarditis, 1.01+/-0.05 in non-infected controls and 1.09+/-0.02 in 99mTc-IgG injected dogs (P<0.05). It is concluded that targeting activated platelets with the 99mTc-labelled GP IIb/IIIa antagonist DMP444 allows a final diagnosis of experimental bacterial endocarditis within 4 h owing to high, specific and fast in vivo uptake.

Acute Disease↗
PubMed2000

Successful out-of-hospital cardiopulmonary resuscitation: what is the optimal in-hospital treatment strategy?

UNLABELLED: The aim of the study was to evaluate prognostic factors in patients after successful out-of-hospital resuscitation (sOHR) within 30 min after admission. A prognostic scoring scale in patients surviving OHR was analysed. We also studied the effect of these predictive factors and the in-hospital treatment (percutaneous transluminal coronary angioplasty (PTCA) vs. thrombolysis) on mortality. We performed a retrospective analysis of the emergency medical system forms and medical files of 72 consecutive patients aged > or =18 years with sOHR. Of these 72 patients 37 (51%) met the electrocardiographic and enzymatic criteria for acute myocardial infarction (AMI). Ten of the 37 AMI patients (27%) underwent acute PTCA as primary treatment and seven patients (19%) received thrombolytic therapy for AMI despite prolonged (mean 24+/-13 min) cardiopulmonary resuscitation (CPR). The remaining 20 patients had no specific infarct treatment. Despite successful PTCA, in eight out of ten patients, their mortality in hospital was 60% (6/10). Mortality in the thrombolysis group was 57% (4/7). For the remaining 20 MI-patients the mortality was 65% (13/20). Univariate and multivariate analyses were performed to design a weighted prognostic scoring system. The Glasgow coma scale (GCS) was the strongest independent predictor (r=0.76, P< or =0.001) for in-hospital death. CONCLUSIONS: in-hospital mortality after successful OHR seems to largely depend on neurological status at admission and much less on the specific treatment of myocardial infarction. The prognostic scoring system accurately predicted the in-hospital mortality and can be used for early treatment stratification; however, it should be proven in a prospective study.

Adult↗
PubMed2000

Low-molecular-weight heparin and other antithrombotic agents in the setting of a primarily medical treatment of unstable coronary artery disease.

Antithrombotic treatment of acute coronary syndromes (ACS) comprises aspirin and (low-molecular-weight) heparin. Adjunctive treatment with intravenous glycoprotein IIb/IIIa receptor antagonists may be used in high-risk individuals, especially when they undergo percutaneous coronary interventions. Results from large-scale trials studying the efficacy and safety of oral glycoprotein IIb/IIIa blockers in patients with ACS have been disappointing. Thrombolytic therapy is not indicated in ACS.

Acute Disease↗
PubMed1999

[Acute coronary syndrome: technological improvements in diagnostics and therapy].

Unstable angina pectoris and non-Q wave infarction are difficult to distinguish clinically and electrocardiographically and currently are often called 'acute coronary syndrome'. In the technology of diagnosis and treatment there have been a number of innovations. The early diagnosis can be improved by means of plasma assays of the highly sensitive and specific cardiac markers troponin I and T. Both the pharmacotherapy (new platelet aggregation inhibitors) and the invasive treatment (use of coronary stents and arterial bypasses) have undergone major--expensive--innovations. Randomized trials have not yet made it clear whether invasive or conservative therapy is the optimal initial treatment. Both invasive treatment and pharmacotherapy are changing rapidly, so that the results of the randomized trials are already less relevant to the cardiological practice of 1999.

Angina Pectoris↗
PubMed1999

Effect of prehospital thrombolysis on aborting acute myocardial infarction.

On administering thrombolysis in a prehospital setting, we found a threefold increase in the incidence of abortion of myocardial infarction, compared with the in-hospital program of a nearby hospital. Assessment of aborted myocardial infarction may be a better criterion for the efficacy of early thrombolysis than mortality data.

Emergency Medical Services↗
PubMed1999

Improvement in three-month angiographic outcome suggested after primary angioplasty for acute myocardial infarction (Zwolle trial) compared with successful thrombolysis (APRICOT trial). Antithrombotics in the Prevention of Reocclusion In COronary Thrombolysis.

It has been shown that primary percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction results in higher patency rates than thrombolytic therapy. However, no data are available on differences in long-term angiographic outcome after successful primary PTCA compared with successful thrombolysis. Therefore, we compared angiographic data of the Antithrombotics in the Prevention of Reocclusion In COronary Thrombolysis (APRICOT) trial and the Zwolle primary PTCA trial. In the APRICOT trial 248 patients underwent coronary angiography at a mean of 24 hours after thrombolysis and had a patent infarct-related vessel (Thrombolysis In Myocardial Infarction-3 trial flow) when entering the study. Reocclusion rates were assessed at a second angiography after 3 months. In the Zwolle trial 136 patients had a successful primary PTCA. At 3 months 131 patients underwent a second angiography. Quantitative coronary angiography showed a significant lower mean diameter stenosis of the infarct-related vessel after primary PTCA (27 +/- 12% vs 57 +/-12%; p = 0.00001). At 3 months this difference was sustained (35 +/- 22% vs 63 +/- 26%; p = 0.00001). After thrombolysis the reocclusion rate at 3 months was 29% compared with 5% after primary PTCA (p = 0.0001). Results show that compared with successful thrombolytic therapy, primary PTCA for acute myocardial infarction results in an improved infarct-related vessel status not only short term but also long term, with a low reocclusion rate.

Aged↗
PubMed1999

C-reactive protein as a cardiovascular risk factor: more than an epiphenomenon?

BACKGROUND: Circulating levels of C-reactive protein (CRP) may constitute an independent risk factor for cardiovascular disease. How CRP as a risk factor is involved in cardiovascular disease is still unclear. METHODS AND RESULTS: By reviewing available studies, we discuss explanations for the associations between CRP and cardiovascular disease. CRP levels within the upper quartile/quintile of the normal range constitute an increased risk for cardiovascular events, both in apparently healthy persons and in persons with preexisting angina pectoris. High CRP responses after acute myocardial infarction indicate an unfavorable outcome, even after correction for other risk factors. This link between CRP and cardiovascular disease has been considered to reflect the response of the body to the inflammatory reactions in the atherosclerotic (coronary) vessels and adjacent myocardium. However, because CRP localizes in infarcted myocardium (with colocalization of activated complement), we hypothesize that CRP may directly interact with atherosclerotic vessels or ischemic myocardium by activation of the complement system, thereby promoting inflammation and thrombosis. CONCLUSIONS: CRP constitutes an independent cardiovascular risk factor. Unraveling the molecular background of this association may provide new directions for prevention of cardiovascular events.

Adult↗