Search

Evidence from a recent trial has shown that the antiinflammatory effects of colchicine reduce the risk of cardiovascular events in patients with recent myocardial infarction, but evidence of such a risk reduction in patients with chronic coronary disease is limited.In a randomized, controlled, double-blind trial, we assigned patients with chronic coronary disease to receive 0.5 mg of colchicine once daily or matching placebo. The primary end point was a composite of cardiovascular death, spontaneous (nonprocedural) myocardial infarction, ischemic stroke, or ischemia-driven coronary revascularization. The key secondary end point was a composite of cardiovascular death, spontaneous myocardial infarction, or ischemic stroke.A total of 5522 patients underwent randomization; 2762 were assigned to the colchicine group and 2760 to the placebo group. The median duration of follow-up was 28.6 months. A primary end-point event occurred in 187 patients (6.8%) in the colchicine group and in 264 patients (9.6%) in the placebo group (incidence, 2.5 vs. 3.6 events per 100 person-years; hazard ratio, 0.69; 95% confidence interval [CI], 0.57 to 0.83; P0.001). A key secondary end-point event occurred in 115 patients (4.2%) in the colchicine group and in 157 patients (5.7%) in the placebo group (incidence, 1.5 vs. 2.1 events per 100 person-years; hazard ratio, 0.72; 95% CI, 0.57 to 0.92; P = 0.007). The incidence rates of spontaneous myocardial infarction or ischemia-driven coronary revascularization (composite end point), cardiovascular death or spontaneous myocardial infarction (composite end point), ischemia-driven coronary revascularization, and spontaneous myocardial infarction were also significantly lower with colchicine than with placebo. The incidence of death from noncardiovascular causes was higher in the colchicine group than in the placebo group (incidence, 0.7 vs. 0.5 events per 100 person-years; hazard ratio, 1.51; 95% CI, 0.99 to 2.31).In a randomized trial involving patients with chronic coronary disease, the risk of cardiovascular events was significantly lower among those who received 0.5 mg of colchicine once daily than among those who received placebo. (Funded by the National Health Medical Research Council of Australia and others; LoDoCo2 Australian New Zealand Clinical Trials Registry number, ACTRN12614000093684.).

About half of all patients who experience an acute coronary syndrome (ACS) in Australia have their conditions managed non-invasively - that is, they do not undergo coronary angiography and revascularisation in hospital. ACS patients whose conditions are managed non-invasively may not receive the same level of evidence-based care as those who receive coronary revascularisation. This article reviews the optimal pharmacological management of ACS managed non-invasively. There is strong evidence to support the prescription of dual antiplatelet therapy (DAPT; aspirin with a P2Y12 inhibitor). DAPT should continue for 12 months after an ACS, then aspirin should be continued indefinitely. Anticoagulation with warfarin or a novel oral anticoagulant may be needed if atrial fibrillation occurs; the combination with DAPT increases the risk of bleeding. Unless contraindicated, high-intensity statin therapy should be prescribed for all post-ACS patients irrespective of their cholesterol level. Non-statin lipid therapy has not been shown to improve outcomes. Use of β-adrenergic blockers is recommended in most guidelines, but the clinical trials to support this recommendation were performed more than 30 years ago, and routine long-term use may not be relevant to modern treatment, except when there is cardiac failure or left ventricular dysfunction. Angiotensin-converting enzyme inhibitors or angiotensin receptor blockers are also widely recommended, but the evidence for benefit is stronger when there is left ventricular dysfunction. Calcium-channel blockers, nitrates, antiarrhythmic drugs, digoxin and diuretics do not improve outcomes in post-ACS patients.

We report a case of successful resuscitation after cardiac arrest associated with obstruction of the airway by chewing gum. In December 2005, in Port Hedland, Western Australia, a 57-year-old electrician was found unconscious by workmates 5 minutes after he was seen working normally. He was not breathing and had no pulse. Bystander cardiopulmonary resuscitation (CPR) was commenced immediately and an ambulance arrived within 3 minutes. Cardiac monitoring showed the patient was in ventricular fibrillation. Direct-current defibrillation was performed three times, resulting in reversion to ventricular tachycardia, rapid atrial fibrillation and, within minutes, spontaneous reversion to sinus rhythm.