Exercise-provoked ST-segment depression and prognosis in patients recovering from acute myocardial infarction. Significance and pitfalls.

The importance of maximal versus submaximal exercise testing and the significance of heart failure on the prognostic value of exercise-provoked ST-segment depression > or = 0.1 mV was studied in 143 patients recovering from acute myocardial infarction. Patients were exercise tested prior to discharge and follow up lasted for up to 18 months (mean 17 months). End-point was first major event (i.e. first non-fatal reinfarction or death). A symptom-limited exercise test was superior to a heart-rate-limited test in detecting ST-segment depressions (27% vs. 20%: P < 0.5), and patients with ST-segment depression at lower heart rates did not have an increased risk of subsequent events compared with patients with ST-segment depression at higher heart rates (14% vs. 27%; NS). Heart failure surpassed ST-segment depression as a risk predictor (34% vs. 18%). Based on a meta-analysis including 13 studies (1987 patients) exercise-provoked ST-segment depression possessed an increased risk of subsequent major events (P < 0.0001; risk ratio = 1.90; 95% confidence limits 1.43,2.51). Thus, ST-segment depression provoked by a symptom-limited test selects patients with an increased risk of subsequent major events. In patients with a history of heart failure exercise-provoked ST-segment depression is of limited value.

Does exercise-induced ST-segment depression predict benefit of medical intervention in patients recovering from acute myocardial infarction? The Danish Study Group on Verapamil in Myocardial Infarction.

The present study tested the hypothesis that the increased risk in patients with exercise-provoked ST-segment depression recovering from acute myocardial infarction could by abolished by anti-ischaemic medical intervention. Prior to discharge a symptom-limited exercise test was carried out. Patients were then double-blindly randomized to treatment with either verapamil 120 mg t.i.d. or placebo, and observed for up to 18 months (mean 17 months). End-point was first major event; i.e. non-fatal reinfarction or death. Two-hundred-and-ninety-eight patients were included. Forty-four patients with and 111 without exercise-induced ischaemia were randomized to verapamil and 39 and 104 respectively, to placebo. The overall number of events was 12.5%. In patients without ST-segment depression, 12.5% in the placebo group (hazard = 1) and 12.6% in the verapamil group (hazard = 1.13) had an event (NS). In patients with ST-segment depression 15.4% in the placebo group (hazard = 1.20) and 9.1% in the verapamil group (hazard = 0.85) had an event (NS). The latter reduction (41%) supports the hypothesis that patients with ST-segment depression, i.e. residual myocardial ischaemia, are those who benefit from anti-ischaemic intervention after myocardial infarction.

[Effect of 1-year long-term treatment with sucralfate on symptomatic recurrence of duodenal ulcer]. / Effekt af ét års langtidsbehandling med sukralfat på symptomatisk recidiv af duodenalt ulcus.

One hundred and two patients, who obtained relief from their duodenal ulcer symptoms with sucralfate (Antepsin R) in a dosage of 2 g b.i.d. for four weeks, were randomized to maintenance therapy with sucralfate 2 g at bedtime or a placebo for one year or until possible recurrence of symptoms. Ninety-four patients completed the study, 46 on sucralfate and 48 on the placebo. Eighteen of the sucralfate-treated patients (39%) experienced relapse of symptoms, as did 36 (75%) of the placebo treated patients. This difference was significant (p = 0.0008). In the sucralfate group most of the symptoms recurred within three months after randomisation, whereas the relapse rate seemed constant in the placebo group. It is concluded that 2 g sucralfate at bedtime is effective in preventing recurrence of duodenal ulcer symptoms.

Antihypertensive effect of atenolol (100 mg once a day) and methyldopa (250 mg thrice a day). A double-blind cross-over multicentre study.

In a double-blind cross-over multicentre study lasting for 16 weeks, the antihypertensive effect of atenolol (100 mg once a day) was compared with that of methyldopa (250 mg thrice a day) in 48 patients with mild to moderately severe hypertension. At the end of the trial, atenolol was superior to methyldopa in achieving clinically relevant BP levels, less than 150/95 mmHg (p less than 0.001), and in respect to patients' drug preference (p less than 0.04). The BP levels after the first 2 weeks of treatment with either drug were identical but, in contrast to methyldopa, atenolol caused further significant reduction in BP during the following 4 weeks. This finding implies that one should hesitate to start additional therapy until after at least six weeks of atenolol treatment, whereas no further reduction in BP can be expected after the first 2 weeks of treatment with methyldopa. Two patients had to be withdrawn from the study during treatment with atenolol, as they developed severe bradycardia and dyspnoea, respectively. Other side-effects were few and of minor clinical importance.