PubMed Health⌕ Search

Biomedical subjects

F W Verheugt

Publications and source records attributed to F W Verheugt.

At least 73 records · Page 4Linked to original sources
PubMed1997

[Left ventricular hypertrophy; differences in the diagnostic and prognostic value of electrocardiography and echocardiography].

OBJECTIVE: To compare the electrocardiogram (ECG) and the echocardiogram for demonstration of left ventricular hypertrophy (LVH) and the prognostic values of these methods. DESIGN: Literature study. SETTING: Department of General Practice, Social and Nursing Home Medicine, R.C. University of Nijmegen, the Netherlands. METHOD: Using articles retrieved by means of a search action in Medline (1962-January 1996), a study was made of the differences between determination of LVH by ECG and by echocardiography with regard to the sensitivities and specificities for measuring anatomical LVH, and their predictive values concerning cardiovascular morbidity and mortality. RESULTS: The sensitivity of echocardiography for the prediction of anatomical LVH (88-93%) exceeded that of ECG (21-54%), while both methods had a high specificity (77-97%). ECG-LVH seemed a better predictor of cardiovascular complications than echo-LVH. CONCLUSION: Echocardiography is the better instrument for screening for LVH, but ECG should keep its place in the diagnostics of LVH in view of its high predictive value for morbidity and mortality and its availability to primary health care. In regard to LVH, echocardiography measures only morphological disorders, while ECG also detects functional disorders.

Electrocardiography↗
PubMed1997

Long-term implications of reocclusion on left ventricular size and function after successful thrombolysis for first anterior myocardial infarction.

BACKGROUND: Successful thrombolysis can prevent left ventricular dilatation after acute myocardial infarction. However, in almost 30% of patients, reocclusion occurs. The aim of this study was to assess the long-term implications of reocclusion on left ventricular size and function. METHODS AND RESULTS: Fifty-six patients were studied with two-dimensional echocardiography at baseline (2 +/- 1.6 days) and 5.0 +/- 1.4 years after first anterior myocardial infarction. All patients (a subset of those enrolled in the APRICOT trial) had a patent infarct-related artery when studied < 48 hours after thrombolysis and underwent repeat coronary angiography at 3 months. Baseline characteristics were comparable in patients with (n = 17) and without reocclusion (n = 39). Left ventricular volume indexes were stable in patients without reocclusion. Patients with reocclusion, however, showed a significant increase in end-diastolic volume index (EDVI; P = .008) and end-systolic volume index (ESVI; P = .039). Furthermore, patients without reocclusion demonstrated improvement in wall motion score index (WMSI; P = .0001) and ejection fraction (EF; P = .016), whereas patients with reocclusion did not. After 5 years, patients with reocclusion had significantly larger volume indexes (EDVI, 99 +/- 41 versus 76 +/- 22 mL/m2, P = .007; ESVI, 59 +/- 40 versus 39 +/- 20 mL/m2, P = .017) and more compromised left ventricular function (WMSI, 1.63 +/- 0.33 versus 1.39 +/- 0.32, P = .013; EF, 45 +/- 13% versus 51 +/- 11%, P = .077) than patients without reocclusion. Multivariate analysis identified baseline WMSI and reocclusion as significant independent predictors of left ventricular dilatation. CONCLUSIONS: Reocclusion of the infarct-related artery within 3 months of successful thrombolysis is associated with left ventricular dilatation and is detrimental to functional recovery of left ventricular function 5 years after first anterior myocardial infarction.

Coronary Disease↗
PubMed1997

C-reactive protein colocalizes with complement in human hearts during acute myocardial infarction.

BACKGROUND: Rises in circulating C-reactive protein (CRP), the prototypical acute-phase protein in humans, correlate with clinical outcome in patients with myocardial ischemia and infarction. We hypothesized that these correlations might reflect active participation of CRP in the local inflammatory response ensuing in the jeopardized myocardium because on binding to a ligand, CRP is able to activate the classic pathway of complement, and in addition, complement activation has been shown to occur locally in infarcted myocardium. METHODS AND RESULTS: To verify our hypothesis, we investigated localization of CRP in relation to deposition of complement in tissue specimens of infarcted and healthy heart tissue obtained from 17 patients who had died after acute myocardial infarction. CRP was found to be deposited only in infarcted regions and not in normal-appearing areas of the myocardium, being colocalized with depositions of C4 and C3 activation fragments of the complement system. Deposition of CRP and complement in infarcted myocardium appeared to be time dependent, because it was found in all infarctions except for one of young age (< 12 hours old) and two of greater age (> 1 year old), whereas another tissue specimen of an infarct < 12 hours old showed only moderate but positive staining for both CRP and complement in comparison with older infarctions. CONCLUSIONS: We conclude that in humans, CRP may localize in infarcted heart tissue and suggest that this acute-phase protein promotes local complement activation, and hence tissue damage, in acute myocardial infarction.

Aged↗
PubMed1997

ATP content measured by 31P NMR correlates with post-ischaemic recovery of external work output in an isolated rat heart perfused with erythrocyte suspension.

The limited capacity of the heart to survive ischaemia presents a recognized problem during open-heart surgery. In order to provide a baseline for the study of cardioprotection we subjected a series of isolated rat hearts to periods of ischaemia of increasing duration, and sought correlations between phosphate metabolite levels as measured by 11P NMR and post-ischaemic recovery of external work output. A strong linear correlation was found between the fraction of ATP measured after reperfusion expressed as a ratio. RATP to the pre-ischaemic level, and the fractional recovery of external work output, RW: Rw = 1.06 (SE 0.27) RATP + 0.01 (SE 0.21) (Spearman rank correlation coefficient 0.72, two-tailed P value 0.006).

Adenosine Triphosphate↗
PubMed1997

Post-ischemic 31P NMR determination of myocardial intracellular pH in vivo using ATP peak.

31P NMR allows non-invasive measurement of intracellular pH, which drops during tissue hypoxia or ischemia. Determination is usually based on the chemical shift between the inorganic phosphate (P(i)) and phosphocreatine (PCr) peaks. During reperfusion, P(i) is taken up to form PCr and ATP, and in our model at least (an isolated, working rat heart perfused with an erythrocyte suspension), the level of P(i) reduces well below the pre-ischemic level, making pH determination difficult. The chemical shifts of the three ATP peaks also depend on pH, and the level of ATP remains high during reperfusion, so these might be used to determine pH. The results of one experiment are presented in detail, showing the time course of high energy phosphate levels before, during and after a 32 min ischemic insult, and close agreement between the pH determinations from the Pi and gamma-ATP peaks can be seen. The formula used to calculate pH from the ATP peak was: pH (ATP) = 0.59 delta 2-5.0 delta + 15.9 where delta is the shift in ppm between PCr and gamma-ATP. All pH readings by both methods from a series of seven experiments were compared and a 1:1 agreement demonstrated (correlation coefficient 0.63, p < 0.0001). Although the ATP shifts also depend on magnesium complexation which we have ignored, this appears to be justifiable within the errors of the method; the good agreement between the results of the two methods, and the ability to determine pH during reperfusion suggest that calculation of intracellular pH from the chemical shift of gamma-ATP is a useful technique.

Adenosine Triphosphate↗
PubMed1996

Influence of early prehospital thrombolysis on mortality and event-free survival (the Myocardial Infarction Triage and Intervention [MITI] Randomized Trial). MITI Project Investigators.

The Myocardial Infarction Triage and Intervention Trial of prehospital versus hospital administration of thrombolytic therapy markedly reduced hospital treatment times, but the 2 groups had similar outcomes. However, patients treated < 70 minutes from symptom onset had better short-term outcomes. The purpose of this study was to determine the long-term influence of very early thrombolytic treatment for acute myocardial infarction. A total of 360 patients were followed for vital status and cardiac-related hospital admissions over a period of 34 +/- 16 months. Patients enrolled in the trial had symptoms for < or = 6 hours, ST-segment elevation on the prehospital electrocardiogram, and no risk factors for serious bleeding. They received aspirin and recombinant tissue plasminogen activator either before or after hospital arrival. Primary end points in this study included long-term survival and survival free of death or readmission to the hospital for angina, myocardial infarction, congestive heart failure, or revascularization. Two-year survival was 89% for prehospital- and 91% for hospital-treated patients (p = 0.46). Event-free survival at 2 years was 56% and 64% for prehospital- and hospital-treated patients, respectively (p = 0.42). In patients treated < 70 minutes from symptom onset, 2-year survival was 98%, and it was 88% for those treated later (p = 0.12). Two-year event-free survival was 65% for patients treated early and 59% for patients treated later (p = 0.80). In this trial, poorer long-term survival was associated with advanced age, history of congestive heart failure, and coronary artery bypass surgery performed before the index hospitalization, but not with time to treatment.

Aged↗
PubMed1996

Reocclusion: the flip side of coronary thrombolysis.

Since the introduction of thrombolytic therapy for acute myocardial infarction, the incidence of coronary artery reocclusion has been intensively studied. Also, the prediction and diagnosis of reocclusion by angiographic and clinical variables, as well its invasive and pharmacologic prevention, have gained much attention. By angiographic definition, reocclusion requires three angiographic observations: one with an occluded artery, one with a reperfused artery and a third for the assessment of subsequent occlusion (true reocclusion). Since the introduction of early intravenous reperfusion therapy, most studies use only two angiograms: one with a patent and one with a nonpatent infarct-related artery. A search for all published reocclusion studies revealed 61 studies (6,061 patients) with at least two angiograms. The median time interval between the first angiogram after thrombolysis and the second was 16 days (range 0.1 to 365). Reocclusion was observed in 666 (11%) of 6,061 cases. Interestingly, the 28 true reocclusion studies showed an incidence of reocclusion of 16 +/- 10% (mean +/- SD), and the 33 studies with only two angiograms 10 +/- 8% (p=0.04), suggesting that proven initial occlusion of the infarct-related artery is a risk factor for reocclusion after successful thrombolysis. The other predictors for reocclusion are probably severity of residual stenosis of the infarct-related artery after thrombolysis and perhaps the flow state after lysis. Reocclusion is most frequently seen in the early weeks after thrombolysis. The clinical course in patients with reocclusion is more complicated than in those without this complication. Left ventricular contractile recovery after thrombolysis is hampered by reocclusion. Routine invasive strategies have not been proven effective against reocclusion. In the prevention of reocclusion, both antiplatelet and antithrombin strategies have been tested, including hirudin and hirulog, but the safety of these agents in thrombolysis is still questionable. Thus, reocclusion after thrombolysis is an early phenomenon and is more frequent after proven initial occlusion of the infarct-related artery. Reocclusion can be predicted by angiography after thrombolysis. Because reocclusion is detrimental, strategies to prevent it should be developed and carried out after thrombolytic therapy for acute myocardial infarction as soon as they are deemed safe.

Antithrombins↗
PubMed1996

Bleeding risk of combined oral anticoagulant and antiplatelet therapy in cardiovascular disease.

BACKGROUND: In controlled clinical trials with patients with cardiovascular disease, both antiplatelet and oral anticoagulant therapy have proved effective in reducing thrombotic and thromboembolic complications. The combination of both therapeutic strategies has been evaluated in several cardiovascular conditions. METHODS: A meta-analysis was performed on the bleeding risk in six published trials of combined oral anticoagulant and antiplatelet therapy. RESULTS: The results of clinical trials (in patients with artificial heart valves and in patients with unstable angina or non-Q myocardial infarction) suggest that combined oral anticoagulant and antiplatelet therapy may be as safe as oral anticoagulation alone. Also, in a large study of healthy subjects the safety of combined oral anticoagulant and low-dose antiplatelet therapy was acceptable at one to two major bleedings per 100 person-years more than with oral anticoagulation alone. CONCLUSIONS: The safety of combined oral anticoagulant and antiplatelet therapy is probably acceptable, provided the antiplatelet therapy is given in a low dose. These results warrant an efficacy and safety evaluation of combined oral anticoagulant and low-dose antiplatelet therapy in large clinical trials.

Administration, Oral↗
PubMed1995

Adverse long-term effects of reocclusion after coronary thrombolysis.

OBJECTIVES: This study sought to assess the long-term clinical consequences of reocclusion after coronary thrombolysis. BACKGROUND: After acute myocardial infarction successfully treated with thrombolysis, reocclusion occurs in approximately 30% of patients and leads to poorer in-hospital outcome. However, the long-term effects of reocclusion are unknown. METHODS: Three hundred patients with no history of coronary surgery and with a patent infarct-related artery at coronary angiography within 48 h after thrombolysis were enrolled in the Antithrombotics in the Prevention of Reocclusion in Coronary Thrombolysis (APRICOT) trial. At a mean (+/- SD) of 77 +/- 23 days after thrombolysis, 248 patients (87%) underwent follow-up angiography. Reocclusion was observed in 71 (29%) of 248 patients. To compare outcome between 71 patients with and 177 without reocclusion an analysis of event-free survival, defined as a clinical course without death, reinfarction and revascularization, was performed. RESULTS: Over a 3-year follow-up period, event-free survival was significantly better in patients without reocclusion: At 1 year it was 63% for patients with and 83% for those without reocclusion (p < 0.001). In the first year, two or more cardiac-related events occurred in 24% of patients with and 6% of those without reocclusion (p < 0.001). Patients with reocclusion had a markedly higher reinfarction and revascularization rate. At 1 year the reinfarction rate was 23% for patients with and 5% for those without reocclusion (p < 0.001). CONCLUSIONS: This analysis shows the adverse influence of reocclusion on long-term clinical outcome in relation to reinfarction and need for revascularization. To further optimize prognosis after thrombolysis, prevention of reocclusion should become a main priority. Future research should focus on the criteria and timing of elective revascularization procedures in the prevention of coronary reocclusion.

Aged↗