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Biomedical subjects

J Lubsen

Publications and source records attributed to J Lubsen.

At least 73 records · Page 4Linked to original sources
PubMed1988

[Randomized double-blind study comparing tissue-type plasminogen activator with placebo in acute myocardial infarct].

In a double-blind randomised trial 129 patients with first myocardial infarction of less than 6 h duration were allocated to treatment with human recombinant tissue-type plasminogen activator (rt-PA) given intravenously over 90 min, or to placebo infusion. Coronary angiography at the end of this infusion showed that the infarct-related vessel was patent in 61% of 62 assessable coronary angiograms in the rt-PA-treated group compared with 21% in the control group. Treatment with rt-PA was not accompanied by any major complications. In the rt-PA group the circulating fibrinogen level at the end of the catheterisation was 52 +/- 29% (mean +/- SD) of the starting value.

Adult↗
PubMed1987

[Thrombolytic therapy in fresh myocardial infarct].

In this overview the characteristics have been defined of those patients with acute myocardial infarction to whom early thrombolytic therapy would offer a major benefit. However, this concerns only the 20% of all patients who are admitted to the hospital with acute myocardial infarction within the specified time limit. It is still unclear whether later thrombolytic therapy with the newer agents might offer benefit to other patients with acute myocardial infarction. Presently, it seems unlikely that patients admitted to the hospital more than six hours after onset of symptoms will benefit from any reperfusion strategy. Patients admitted up to 24 hours after onset of symptoms with symptomatic and extensive ischemia (usually located anteriorly) or with signs of cardiogenic shock constitute a group of high risk patients who might derive further benefit from late reperfusion (42). It is likely that in the near future the new generation of thrombolytic agents (rt-PA, rscu-PA and APSAC) will become first choice for the intravenous initiation of thrombolytic therapy. Then, the indications for either acute or delayed angiography might be different from the present ones. Further cost/benefit analysis will certainly be required to assess the additional value of intracoronary thrombolysis and coronary angioplasty after intravenous administration of rt-PA, rscu-PA or APSAC. The required capacity of catheterization laboratories and facilities for coronary angioplasty and bypass surgery will depend on the results of those analyses.(ABSTRACT TRUNCATED AT 250 WORDS)

Combined Modality Therapy↗
PubMed1987

Acute coronary thrombolysis with recombinant human tissue-type plasminogen activator: initial patency and influence of maintained infusion on reocclusion rate.

An intravenous infusion of 40 mg of recombinant tissue-type plasminogen activator (rt-PA) was given intravenously over 90 minutes to 123 patients with acute myocardial infarction (AMI) of less than 4 hours' duration. A coronary angiogram was recorded at the end of the infusion in 119 patients. Central assessment of the angiograms revealed a patent infarct-related artery in 78 patients (patency rate 66%, 95% confidence limits 57 to 74%). Patients with a patent infarct-related artery at the first angiogram were randomized in a double-blind manner to receive a subsequent 6-hour infusion of either 30 mg of rt-PA or placebo. All patients had received an initial bolus of 5,000 IU of heparin and then 1,000 IU/hour until a second angiogram was recorded 6 to 24 hours after the start of the second perfusion. At central assessment of the second coronary angiogram the reocclusion rate was 2 of 36 patients who received rt-PA at the second infusion and 3 of 37 patients not receiving this drug (or the 2 groups combined 7%, 95% confidence limits 2 to 15%). Three of 60 patients (5%, 95% confidence limits 1 to 14%) with patent arteries on both previous angiograms had a later occlusion as judged on the angiogram recorded at hospital discharge. No difference in late reocclusion rates between the 2 treatment groups was observed.

Clinical Trials as Topic↗
PubMed1987

Efficacy of nifedipine and metoprolol in the early treatment of unstable angina in the coronary care unit: findings from the Holland Interuniversity Nifedipine/metoprolol Trial (HINT).

A multicenter, double-blind, placebo-controlled, randomized trial of nifedipine, metoprolol and their combination was conducted in 338 patients with unstable angina (hospital admission diagnosis) who had not previously received treatment with a beta blocker. In addition, nifedipine was compared with placebo in 177 patients who were receiving beta blockers upon hospital admission. The main outcome event was the recurrence of ischemia or progression to myocardial infarction within 48 hours. Trial medication effects are expressed as ratios of event rates relative to placebo, e.g., for nifedipine as the event rate under nifedipine divided by that under placebo; 95% confidence intervals are also given. In patients not pretreated with a beta blocker the rate ratio for nifedipine was 1.15 (0.83, 1.64), for metoprolol 0.76 (0.49, 1.16) and for the combination 0.80 (0.53, 1.19). In patients already receiving a beta blocker, the addition of nifedipine was favorable and the rate ratio was 0.68 (0.47, 0.97). Equal numbers of patients developed myocardial infarction and reversible ischemia. Most infarctions occurred early, within 6 hours of randomization. In patients who were not already taking a beta blocker, the nifedipine rate ratio for infarction only was 1.51 (0.87, 2.74). These results suggest that, in patients not previously receiving beta blockers, metoprolol has a beneficial short-term effect on unstable angina, that a fixed combination with nifedipine provides no further gain and that nifedipine may be ineffective or counterproductive. On the other hand, the addition of nifedipine to existing beta blockade when the patient becomes unstable seems beneficial.

Adrenergic beta-Antagonists↗
PubMed1987

Early termination of clinical trials with prolonged observation of individual patients: a case study.

Stopping rules for a placebo controlled clinical trial of anticoagulants after acute myocardial infarction were evaluated by means of computer simulation for the case of five interim analyses. The trial will be terminated and the null hypothesis of no treatment effect rejected when the one-sided P-value (logrank test) is lower than 0.005, 0.005, 0.005, 0.014, and 0.023 at the respective interim analyses, and 0.032 at final evaluation. This implies a total size alpha = 0.05 and a power close to that of fixed sample size testing. The trial will also be terminated, without rejecting the null hypothesis, when the one-sided P-value exceeds 0.95, 0.88, 0.81, 0.74, and 0.67 at the respective interim analyses. This modification hardly affects size and power.

Anticoagulants↗
PubMed1987

ST 567 (alinidine) in stable angina: a comparison with metoprolol.

Alinidine, a drug which reduces heart rate without depressing myocardial function was compared against metoprolol, a beta-blocking drug, in the treatment of stable angina pectoris in a double-blind cross-over trial. It was found that both drugs reduced anginal attacks and nitroglycerine consumption to a comparable degree. Exercise tolerance did not appear to be improved by either drug yet chest pain at ergometry was postponed by both drugs. In the doses used metoprolol was more effective in restraining heart rate, both at rest and even more during exertion. Both drugs were well tolerated and side-effects were few. It seems probable that the optimal dose of alinidine was not used in this trial and that the dosage could have been higher.

Angina Pectoris↗
PubMed1987

Effect of continued rt-PA administration on the residual stenosis after initially successful recanalization in acute myocardial infarction--a quantitative coronary angiography study of a randomized trial.

Quantitative angiography was performed in 68 out of 123 patients treated with intravenous rt-PA for acute myocardial infarction. At 90 min angiography, the median minimal cross-sectional area was 1.11 mm2 and the median percentage area stenosis was 80%. A percentage area stenosis greater than 70% was seen in 78% of the patients. Patients with a patient infarct related artery at the first angiogram were randomized to receive subsequent infusions either of rt-PA + heparin or placebo + heparin. There was a persistent trend of improvement in minimal lumen diameter and percentage diameter stenosis of the residual stenosis in the infarct related artery in both treatment groups when re-examined 6-24 hours later and at the time of hospital discharge. A reduction in 'plaque area', the area between the detected and the reference contours of the infarct related segment, was more frequently seen in patients receiving a second infusion of rt-PA than in patients with no prolonged thrombolytic therapy (83% versus 57%, P less than 0.025, chi square).

Cineangiography↗
PubMed1987

Prognostic value of predischarge 12 lead electrocardiogram after myocardial infarction compared with other routine clinical variables.

The prognostic value of QRS score (Selvester), ST depression, ST elevation, extrasystoles, P terminal force in V1, and QTc derived from the predischarge 12 lead electrocardiogram was assessed after myocardial infarction in 474 patients without intraventricular conduction defects, ventricular hypertrophy, or atrial fibrillation. The usefulness of these results in risk assessment was compared with that of other clinical data. During follow up 45 patients died. Logistic regression analysis showed that QRS score, ST depression, and QTc were independently predictive of cardiac mortality. When multivariate analysis was applied to clinical and electrocardiographic data together, however, the 12 lead electrocardiogram did not provide independent information additional to that provided by other routine clinical findings and laboratory tests such as a history of previous myocardial infarction, clinical signs of persistent heart failure, indication for digitalis or antiarrhythmic drugs at discharge, and enlarged heart on chest x ray. In conclusion, the electrocardiogram has important prognostic value; however, it is not powerful enough to further improve the risk assessment of post-infarction patients.

Aged↗
PubMed1987

Incidence, risk, and outcome of reintervention after aortocoronary bypass surgery.

Reintervention was required in 123 (12%) individuals during a follow up (mean 7.5 years, range 5-14.5) of 1041 patients with consecutive, isolated, first aortocoronary bypass operations. In 89 patients the intervention was a repeat bypass operation, in 24 it was angioplasty, and 10 had both. Procedure related mortality was significantly higher at reintervention (5.6%) than at the primary operation (1.2%). Survival probability after a single bypass procedure was 90% at six years and 82(3)% at nine years. Corresponding figures six and nine years after reintervention were 89(6)% and 87(7)% respectively. Stepwise multivariate analysis showed that survival was significantly correlated with left ventricular function (rate ratio 1.82) and with extent of vascular disease (rate ratio 1.80) but not with reintervention (rate ratio 1.45). Symptomatic improvement occurred in 89% of the survivors with or without reintervention. Repeat procedures are often necessary after coronary artery bypass grafting but they appear to provide appreciable relief of symptoms without reducing any long term improvement in survival brought about by the original operation.

Adult↗
PubMed1987

Clinical trials of antiarrhythmic therapy--an improper answer to a proper question?

Pharmacologic prevention of ventricular fibrillation (VF) and sudden cardiac death (SCD) is based on the assumption that the abnormal impulse that causes premature ventricular complexes (PVCs) may trigger VF and that antiarrhythmic drug therapy will thus inactivate the trigger. However, results available from secondary preventive trials of antiarrhythmic agents, including the Ghent-Rotterdam Aprindine (GRAP) study, have not established conclusively the value of antiarrhythmic therapy. A number of factors could explain this failure, e.g., PVCs and VF might not be causally related, thus, antiarrhythmic drugs might not prevent VF; the number of patients enrolled in investigations might have been too small to accommodate statistical proof of benefit; or the subjects might have been poorly selected. A serious design defect that could interfere with demonstrating a benefit for treatment might arise from the fact that all patients in the GRAP and similarly designed studies had to show complex ventricular arrhythmias at randomization and that antiarrhythmic treatment was usually continued regardless of its effect on the underlying arrhythmias. Given the variability of arrhythmias, it would be expected that arrhythmias would persist in only a fraction of patients randomized to placebo. However, arrhythmias also persisted, although to a lesser extent, in treated patients. If one considers that SCD risk may be reduced in the face of arrhythmia suppression but that it may be increased if the arrhythmia persists due to a toxic or proarrhythmic drug effect, any advantageous effects of successful antiarrhythmic drug therapy would be offset by the negative effects of unsuccessful arrhythmia suppression, which would distort the comparison with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1987

Nifedipine and metoprolol in unstable angina: findings from the Holland Interuniversity Nifedipine/Metoprolol Trial (HINT).

We conducted a multicenter, double-blind, placebo-controlled, randomized trial of nifedipine, metoprolol, and their combination in 338 patients whose hospital admission diagnosis was unstable angina and who were not pretreated with a beta-blocker, and of nifedipine in 177 patients who were treated with a beta-blocker. The main outcome event was the recurrence of ischemia or progression to myocardial infarction within 48 h. Trial medication effects are expressed as ratios of event rates relative to placebo, e.g., the ratio for nifedipine is the event rate under nifedipine divided by that under placebo. In addition, 95% confidence intervals are given. In patients not pretreated with a beta-blocker, the event rate ratio for nifedipine was 1.15 (0.83, 1.64), for metoprolol 0.76 (0.49, 1.16), and for the combination 0.80 (0.53, 1.19). In patients already on a beta-blocker, the addition of nifedipine was favorable; i.e., the rate ratio was 0.68 (0.47, 0.97). Equal numbers of patients developed myocardial infarction and reversible ischemia. Most infarctions occurred early, within 6 h of randomization. In patients not already on a beta-blocker, the nifedipine rate ratio for infarction was 1.51 (0.87, 2.74). These results suggest that, in patients not on previous beta-blockade, metoprolol has a beneficial short-term effect on unstable angina, a fixed combination with nifedipine provides no further gain, and nifedipine may be ineffective or counterproductive. On the other hand, the addition of nifedipine to existing beta-blockade when the patient becomes unstable seems beneficial.

Aged↗
PubMed1986

Quality of life after myocardial infarction: effect of long term metoprolol on mortality and morbidity.

A double blind randomised study of 154 patients with myocardial infarction assigned to metoprolol (100 mg twice daily) and 147 assigned to placebo compared the effects of treatment in relation to health state over three years. Health state was evaluated by a new method based on the average number of days spent in each of seven mutually exclusive categories of health. The scale took into account death, history of serious complications, functional state, and side effects of treatment. Of the maximum attainable 1095 days alive during the three years patients given metoprolol attained 992 days and those given placebo 964 days. During the period alive the metoprolol treated group spent an average of 278 days in an optimal functional state as compared with 176 days for the placebo treated group. This included 221 and 156 days respectively in a completely asymptomatic state (that is, without either cardiac symptoms or side effects of treatment). The time spent with a serious non-fatal complication was shortened by 56 days in the metoprolol group. The overall differences between the groups were statistically significant (p = 0.03). Aside from bringing an improved quality of life after myocardial infarction, metoprolol may add up to one month to life expectancy for three years of treatment.

Clinical Trials as Topic↗