Why the study?
Does a 48-hour titrated intravenous infusion of nitroglycerin reduce ischaemic events and platelet/leucocyte activation in patients with unstable angina pectoris?
Does a 48-hour titrated intravenous infusion of nitroglycerin reduce ischaemic events and platelet/leucocyte activation in patients with unstable angina pectoris?
A 48-hour intravenous infusion of nitroglycerin significantly reduces the frequency and severity of ischemic chest pain episodes and inhibits platelet aggregation in patients with unstable angina pectoris.
Supports short-term IV nitroglycerin for fewer ischemic attacks in unstable angina; confirms symptom benefit in this RCT.
OBJECTIVE: To study whether intravenous nitroglycerin (NTG) reduces the incidence of ischaemic events and leucocyte activation, as well as inhibiting platelet aggregation in patients with unstable angina pectoris. DESIGN: Randomized double-blind placebo-controlled study. SUBJECTS: One hundred and sixty-two patients with a history and electrocardiographic changes suggesting unstable angina pectoris. INTERVENTIONS: A 48-hour titrated intravenous infusion of NTG or placebo. RESULTS: Of the 162 randomized patients, 19 were excluded because of an acute myocardial infarction on randomization (11 patients) or proven presence of a non-ischaemic cause of the pain (6 patients). Other causes (2 patients). No differences in the clinical findings were detected between the groups on randomization. In the comparison of NTG and placebo, fewer patients in the former group had more than two new attacks of chest pain lasting for < 20 min or one new attack of chest pain lasting > 20 min, despite sublingual NTG (13/25, P < 0.03). In addition, the attacks of pain lasting > 20 min in the NTG group were delayed compared to those in the placebo group (P < 0.05), suggesting a beneficial effect on these more severe episodes. Fewer patients in the NTG group required more than two sublingual NTG tablets (P < 0.005). NTG also reduced the rate-pressure product (P < 0.05), compared to placebo after 2 h but not after 24 h. Compared to baseline, platelet aggregation was inhibited in the patients who had received an NTG infusion for 2 h (P < 0.05). In both groups, leucocytes were activated at baseline, but remained unchanged thereafter. CONCLUSIONS: Intravenous NTG seems to reduce myocardial ischaemia in patients with unstable angina pectoris more than the placebo.
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Karlberg et al. (1998) studied this question.
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