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Biomedical subjects

F W Verheugt

Publications and source records attributed to F W Verheugt.

At least 55 records · Page 3Linked to original sources
PubMed1999

Management strategies in unstable coronary artery disease--current problems and future directions. The UCAD Council.

Unstable coronary artery disease continues to pose a major challenge to clinicians. The advent of new therapies, such as percutaneous transluminal coronary angioplasty, low-molecular-weight heparins, and glycoprotein IIb/IIIa inhibitors, provides new management options for this indication but also raises new questions with regard to optimal management. Prospective randomized trials with well-defined, long-term outcome measures and a means of identifying which patients will derive most benefit from each treatment, together with a means of rapid and clear dissemination of study results and implications, are required in order to advance the management of unstable coronary artery disease.

Angina, Unstable↗
PubMed1999

Thrombolysis with saruplase versus streptokinase in acute myocardial infarction: five-year results of the PRIMI trial.

BACKGROUND: Short-term safety and efficacy of thrombolysis with saruplase in acute myocardial infarction have been shown in several trials. To assess long-term outcome of patients treated with saruplase or streptokinase for myocardial infarction, a 5-year follow-up of patients included in the Pro-Urokinase in Myocardial Infarction Trial was performed. METHODS AND RESULTS: Follow-up data are available from 8 centers on 255 (92.4%) of 276 included patients. The 5-year mortality rate was comparable with 20.8% of patients in the saruplase group and 16.9% in the streptokinase group (odds ratio 1.29, 95% confidence interval 0.69 to 2.42). In both groups, a considerable number of fatal cardiovascular events occurred more than 1 year after study inclusion. Rates of percutaneous transluminal coronary angioplasty and coronary artery bypass grafting were comparable in both groups. Reinfarction within 5 years occurred in 19.0% of patients in the saruplase group and tended to be less frequent at 10.8% after streptokinase treatment (odds ratio 1.94, 95% confidence interval 0.98 to 3.84). In both groups, the majority of reinfarctions took place more than 3 months after study inclusion. The 5-year stroke rate was 3.6% and 7.2% in the saruplase and streptokinase groups, respectively (odds ratio 0.49, 95% confidence interval 0.16 to 1.47). Subjective symptoms of heart failure and angina pectoris were comparable in both groups. CONCLUSIONS: Our data are consistent with a similar long-term outcome for patients treated with saruplase or streptokinase. Despite the low-risk profile of the patient cohort, there were considerable adverse event rates over a 5-year period.

Aged↗
PubMed1999

Abciximab in the treatment of acute myocardial infarction eligible for primary percutaneous transluminal coronary angioplasty. Results of the Glycoprotein Receptor Antagonist Patency Evaluation (GRAPE) pilot study.

OBJECTIVES: We sought to study the effect of early infusion of abciximab on coronary patency before primary angioplasty in patients with acute myocardial infarction. BACKGROUND: Glycoprotein IIb/IIIa antagonists have proved to be effective in reducing ischemic events associated with coronary angioplasty. The present study explores whether abciximab alone, without administration of thrombolytic therapy, may induce reperfusion in patients with acute myocardial infarction. METHODS: In the Glycoprotein Receptor Antagonist Patency Evaluation pilot study 60 patients with less than 6 h signs and symptoms of acute myocardial infarction eligible for primary angioplasty received in the emergency room a bolus of abciximab 250 microg/kg followed by a 12-h infusion of 10 microg/min. All patients were also treated with an oral dose of 160 mg aspirin and 5,000 IU of heparin intravenously. As soon as possible a diagnostic angiography was performed to evaluate the patency of the infarct-related artery. RESULTS: The median time between onset of symptoms and the administration of the abciximab bolus was 150 min (range 45 to 345), and the median time between abciximab bolus and first contrast injection in the infarct-related artery was 45 min (range 10 to 150). In 24 patients (40%, 95% confidence interval 28% to 52%) Thrombolysis in Myocardial Infarction (TIMI) flow grade 2 or 3 was observed at a median time of 45 min (range 10 to 150) after abciximab bolus; TIMI flow grade 3 was observed in 11 patients (18%, 95% confidence interval 9% to 28%). There was no difference in percentage of TIMI flow grade 2 or 3 between patients who received abciximab within 2.5 h after onset of symptoms or thereafter. CONCLUSIONS: Abciximab therapy given in the emergency room in patients awaiting primary angioplasty is associated with full reperfusion (TIMI flow grade 3) in about 20% and with TIMI flow grade 2 or 3 in about 40% of the patients at a median time of 45 min. These figures are higher than those in primary angioplasty trials without such pretreatment. Randomized controlled trials of very early infusion of abciximab, either prehospital or in-hospital, in patients eligible for angioplasty are warranted.

Abciximab↗
PubMed1999

What an interventional cardiologist should know about the pharmacological treatment of acute myocardial infarction.

The treatment of acute myocardial infarction consists of pain and anxiety relief, anti-ischaemic treatment and antithrombotic therapy. Due to its bleeding complications and, in some cases, procoagulant effects, antithrombotic therapy has consequences for coronary procedures in the setting of acute myocardial infarction. Antiplatelet therapy has no procoagulant effects, and its bleeding complications can easily be managed. Antithrombin therapy has rebound effects, for which no clear solution is available. Thrombolytic therapy has also procoagulant effects, which may interfere with coronary procedures in the early hours of acute myocardial infarction. Heparin may counteract the thrombolysis-induced thrombin generation, but has an unpredictable effect. Postprocedural therapy after angioplasty in the setting of acute myocardial infarction should consist of antiplatelet therapy.

Angioplasty, Balloon, Coronary↗
PubMed1999

Anticoagulation after artificial valve replacement with or without atrial fibrillation: how much is really needed?

Insertion of a mechanical artificial heart valve is an absolute indication for the use of lifelong oral anticoagulation, irrespective the presence or absence of atrial fibrillation. Depending on the type and position of the artificial valve the optimal International Normalized Ratio (INR) for these patients is between 2.5 and 4.5, although more prospective studies on the optimal range of oral anticoagulation are necessary. Addition of low dose antiplatelet therapy may further decrease the rate of thromboembolism, but also here more studies are needed. Patients with a bioprosthesis need only oral anticoagulation for the first three months following surgery in the absence of an indication for anticoagulation for other conditions. Atrial fibrillation is often seen in patients with artificial heart valves. Stroke prevention can be instituted by the mandatory oral anticoagulant therapy. The presence of atrial fibrillation and the use of oral anticoagulation prior to heart valve surgery support the indication for the insertion of a mechanical artificial heart valve. However, relative contraindications to oral anticoagulation and the presence of sinus rhythm may favor the use of a bioprosthesis.

Anticoagulants↗
PubMed1998

[The systolic heart murmur].

The abnormality most often found at physical examination of the heart is a systolic murmur. Aortic valve stenosis is a feared cause of systolic murmurs, which is also well evaluated with respect to the predictive value of physical diagnostic findings. Auscultatory characteristics of the murmur and palpatory findings of the carotid arteries show an acceptable predictive value and can be used by the general practitioner in the referral or reassurance of individuals with a systolic murmur. The different forms of the systolic murmur can be heard on the Internet address of this journal (http:@appendix.niwi. knaw.nl).

Aortic Valve Stenosis↗
PubMed1998

Management strategies for a better outcome in unstable coronary artery disease.

Unstable coronary artery disease is a term encompassing both unstable angina and non-Q-wave (non-ST-segment elevation) myocardial infarction. Patients with these conditions are at risk of early progression to acute myocardial infarction and death. Thus, management of these conditions must aim to reduce long-term mortality and morbidity. Risk stratification is crucial for the identification of patients whose risk of early progression is high; they may require coronary angiography and (if suitable) either percutaneous transluminal coronary angioplasty or coronary artery bypass surgery. No single variable can accurately predict risk, but considerable data are emerging to show that biochemical markers of myocardial injury, such as troponin-T and troponin-I, are valuable in combination with electrocardiographic findings and clinical features. Routine early invasive procedures (coronary angiography with or without revascularization) have not yet been shown to have any significant advantage over conservative regimens for the majority of patients. Antiplatelet, anticoagulant, and anti-ischemic agents remain the mainstay of treatment in the acute phase. New agents, such as glycoprotein IIb/IIIa receptor inhibitors and low-molecular-weight heparins, as well as antithrombins and Factor Xa inhibitors add to the treatments currently available. Thrombolytic agents are contraindicated in the absence of ST-segment elevation. After clinical stabilization, ongoing assessment should include exercise testing for all patients who are able; other imaging techniques should be used for patients unable to exercise. A profile indicating a high risk of future events is an indication for elective angiography and consideration for revascularization.

Algorithms↗
PubMed1998

High dose bolus heparin as initial therapy before primary angioplasty for acute myocardial infarction: results of the Heparin in Early Patency (HEAP) pilot study.

OBJECTIVES: We sought to determine the effect of high dose intravenous bolus heparin on early coronary patency before primary angioplasty. BACKGROUND: Early coronary angiography after thrombolysis for acute myocardial infarction has shown better patency when intravenous heparin is used as an adjunct. The present study explores whether heparin alone can induce reperfusion. METHODS: In the Heparin in Early Patency (HEAP) pilot study, 108 patients with signs and symptoms of acute myocardial infarction < 6 h eligible for primary angioplasty received a single intravenous bolus of 300 U/kg of heparin together with aspirin (160 mg chewed) in the emergency room. The median dose of bolus heparin given was 27,000 U. Patency of the infarct-related artery (IRA) was assessed by coronary angiography at a median of 85 min after the heparin bolus. RESULTS: In 55 patients (51%, 95% confidence interval 38% to 64%), Thrombolysis in Myocardial Infarction (TIMI) flow grade 2 or 3 was observed at 90 min: TIMI flow grade 3 in 33 patients (31%); TIMI flow grade 2 in 22 (20%). Thirty-two (64%) of 50 patients with symptoms < or = 2 h had TIMI flow grade 2 or 3 versus 23 (40%) of 58 patients with symptoms > 2 h (p = 0.02). No significant bleeding was seen. Two patients (2%) died in the hospital. The patency results obtained in patients treated with the high dose bolus heparin were compared with those in 108 patients from a large primary angioplasty database, who were treated with standard therapy, including aspirin but not intravenous heparin, and were matched for clinical and angiographic characteristics with the HEAP pilot study patients. They showed an 18% patency rate (p < 0.001) of the IRA (TIMI flow grade 3 in 9%, TIMI flow grade 2 in 9%) before primary angioplasty. CONCLUSIONS: Early therapy with high dose heparin is associated with full coronary reperfusion in a considerable number of patients with acute myocardial infarction, especially in those treated early (< 2 h). This simple, inexpensive, probably safe and easily antagonizable treatment may be an attractive first treatment of acute myocardial infarction both before and during the hospital stay in conjunction with primary angioplasty.

Administration, Oral↗
PubMed1998

The early risk of thrombolytic therapy for acute myocardial infarction: incidence, mechanisms and possible prevention.

By restoring coronary flow, thrombolytic therapy for acute myocardial infarction diminishes infarct size and left ventricular dysfunction, resulting in better early and late outcome. Thrombolytic therapy has, however, an inherent early risk, that of intracranial hemorrhage and, possibly, myocardial rupture. An effective strategy in reducing this early risk has not so far been available, but lowering of blood pressure and reduction of myocardial contractility may be candidates for further study aiming to fight these often fatal complications of a life-saving therapy for acute myocardial infarction.

Blood Pressure↗
PubMed1997

[Antithrombotic treatment following acute ischemic heart disease: acetylsalicylic acid and (or) oral anticoagulants?; ASPECT-II, a new study].

In order to compare the efficacy and safety of three regimens of long-term antithrombotic treatment in patients with acute ischaemic syndromes, a prospective, randomized, open-label, multicentre study is being conducted in which 60-70 Dutch hospitals will participate. Eligible patients discharged following hospitalization for acute myocardial infarction or unstable angina pectoris are randomly assigned to receive either (a) adjusted full intensity oral anticoagulation (target range: 3.0-4.0 International Normalised Ratio (INR), (b) low dose aspirin or (c) combined therapy of low dose aspirin and adjusted low intensity oral anticoagulation (target range INR: 2.0-2.5). It is planned to enroll 8,700 patients within three years. During an estimated mean follow-up of 2.5 years the evolutions of total mortality, non-fatal myocardial infarction, non-fatal stroke and major bleeding complication will be assessed.

Anticoagulants↗
PubMed1997

Thermolabile methylenetetrahydrofolate reductase in coronary artery disease.

BACKGROUND: Hyperhomocysteinemia, an independent and graded risk factor for coronary artery disease (CAD), may result from both environmental and hereditary factors. Methylenetetrahydrofolate reductase (MTHFR) catalyzes the conversion of methylenetetrahydrofolate to methyltetrahydrofolate, the methyl donor in the remethylation of homocysteine to methionine. A 677C-->T mutation in the MTHFR gene has been associated with elevated homocysteine concentrations in homozygous (+/+) individuals. METHODS AND RESULTS: We assessed the frequency of this common mutation in 735 CAD patients from the Regression Growth Evaluation Statin Study (REGRESS), a lipid-lowering coronary-regression trial, and in 1250 population-based control subjects. Furthermore, the association between the mutation and serum homocysteine concentrations was studied. The frequency of the homozygous (+/+) mutation was 9.5% among patients versus 8.5% among control subjects, resulting in an odds ratio of 1.21 (95% confidence interval [CI], 0.87 to 1.68), relative to the (-/-) genotype. Homocysteine concentrations were significantly elevated in both (+/+) and (+/-) individuals compared with (-/-) individuals (median homocysteine levels, 15.4, 13.4, and 12.6 micromol/L, for (+/+), (+/-), and (-/-) individuals, respectively). For a summary estimation of the risk of the (+/+) genotype for CAD, we performed a meta-analysis on 8 different case-control studies on thermolabile MTHFR in CAD. In the meta-analysis, the homozygous (+/+) genotype was present in 299 of 2476 patients (12.1%) and in 257 (10.4%) of 2481 control subjects, resulting in a significant odds ratio of 1.22 (95% CI, 1.01 to 1.47) relative to the (-/-) genotype. CONCLUSIONS: Both the homozygous (+/+) and heterozygous (+/-) genotype result in elevated homocysteine concentrations. From our meta-analysis, we conclude that the homozygous (+/+) genotype is a modest but significant risk factor for CAD.

Coronary Disease↗