Details

Autor(en) / Beteiligte

• Boden, William E
• van Gilst, Wiek H
• Scheldewaert, Rudy G
• Starkey, Ian R
• Carlier, Marc F
• Julian, Desmond G
• Whitehead, Anne
• Bertrand, Michel E
• Col, Jacques J
• Pedersen, Ole Lederballe
• Lie, Kong I
• Santoni, Jean-P
• Fox, Kim M

Titel

Diltiazem in acute myocardial infarction treated with thrombolytic agents: a randomised placebo-controlled trial

Ist Teil von

• The Lancet (British edition), 2000-05, Vol.355 (9217), p.1751-1756

Ort / Verlag

London: Elsevier Ltd

Erscheinungsjahr

2000

Quelle

Access via ScienceDirect (Elsevier)

Beschreibungen/Notizen

• Diltiazem reduces non-fatal reinfarction and refractory ischaemia after non-Q-wave myocardial infarction, an acute coronary syndrome similar to the incomplete infarction that occurs after successful reperfusion. We postulated that this agent would reduce cardiac events in patients after acute myocardial infarction treated initially with thrombolytic agents—a clinical application previously unexplored with heart-rate-lowering calcium antagonists. A prospective, randomised, double-blind, sequential trial was done in 874 patients with acute myocardial infarction, but without congestive heart failure, who first received thrombolytic agents. Patients received either 300 mg oral diltiazem once daily, or placebo, initiated within 36–96 h of infarct onset, and given for up to 6 months. The trial primary endpoint was the cumulative first event rate of cardiac death, non-fatal reinfarction, or refractory ischaemia. Additional prespecified endpoints included several composites of non-fatal cardiac events (non-fatal reinfarction combined with refractory ischaemia, all recurrent ischaemia, or the need for myocardial revascularisation). The diagnosis of ischaemia, whether refractory or recurrent, and the need for myocardial revascularisation, was always based on objective electrocardiographical evidence of ischaemia, either at rest or on exertion. For the trial primary endpoint, 131 events occurred in the 444 placebo patients and 97 events in the 430 diltiazem patients (hazard ratio 0·79; 95% Cl, 0·61–1·02; p=0·07). For non-fatal cardiac events, diltiazem treatment was associated with a relative decrease (0·76; 0·58–1·00) in the combined event rate of non-fatal reinfarction and refractory ischaemia. There was a similar decrease in the composite non-fatal endpoints of non-fatal reinfarction combined with all recurrent ischaemia (0·80; 0·64–1·00) and non-fatal reinfarction combined with the need for myocardial revascularisation (0·67; 0·46–0·96). The need for myocardial revascularisation alone was significantly reduced by 42% (0·61; 0·39–0·96). No major safety issues were encountered. Diltiazem did not reduce the cumulative occurrence of cardiac death, non-fatal reinfarction, or refractory ischaemia during a 6-month follow-up, but did reduce all composite endpoints of non-fatal cardiac events, especially the need for myocardial revascularisation.