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Controversy exists as to whether the threshold for blood pressure-lowering treatment should differ between people with and without type 2 diabetes. We aimed to investigate the effects of blood pressure-lowering treatment on the risk of major cardiovascular events by type 2 diabetes status, as well as by baseline levels of systolic blood pressure.

Survival analysis is an important tool for assessing the outcome of total joint replacement. The Kaplan-Meier method is used to estimate the incidence of revision of a prosthesis over time, but does not account appropriately for competing events which preclude revision. In the presence of competing death, this method will lead to statistical bias and the curve will lose its interpretability. A valid comparison of survival results between studies using the method is impossible without accounting for different rates of competing events. An alternative and easily applicable approach, the cumulative incidence of competing risk, is proposed. Using three simulated data sets and realistic data from a cohort of 406 consecutive cementless total hip prostheses, followed up for a minimum of ten years, both approaches were compared and the magnitude of potential bias was highlighted. The Kaplan-Meier method overestimated the incidence of revision by almost 4% (60% relative difference) in the simulations and more than 1% (31.3% relative difference) in the realistic data set. The cumulative incidence of competing risk approach allows for appropriate accounting of competing risk and, as such, offers an improved ability to compare survival results across studies.

Two strategies for treatment of acute myocardial infarction were compared in a randomised trial of 533 patients admitted within 4 h of the onset of symptoms. 264 patients were allocated to conventional treatment and 269 patients to a strategy aimed at rapid recanalisation of the occluded coronary artery. At first, intracoronary streptokinase (up to 250 000 U) was given immediately after angiography. In the last 117 patients intracoronary administration was preceded by intravenous streptokinase (500 000 U). No angiography was done in 35 patients allocated to thrombolytic therapy. Among the 234 patients who underwent angiography the infarct-related coronary artery was patent on admission or recanalised in 198 (85%). The median time between onset of symptoms and angiographic confirmation of a patent infarct-related artery was 200 min. Mortality was lower in patients randomised to thrombolysis than in controls at 28 days (16 v31 patients) and at 8 months (23 v42); 1-year survival was higher after thrombolysis (91%) than conventional treatment (84%). The clinical course in hospital was more favourable in patients allocated to thrombolysis, with a lower incidence of ventricular fibrillation (38 v61), pericarditis (19 v46), and cardiogenic shock (13 v24), although they had a higher frequency of bleeding episodes (53 v7). Non-fatal reinfarction was commoner after thrombolysis than after conventional therapy (36 v16 patients). In both groups reinfarctions occurred predominantly in the same area as the initial infarct.

To assess the contribution of cardiovascular risk indicators to all-cause mortality, we used data from a follow-up study conducted in the Netherlands since 1975. Of 6,057 participants aged 20 years or over at the start of the study, 9.5% died during the 9 to 12 year follow-up period. Risk indicators independently related to all-cause mortality were age and diabetes mellitus in both sexes; pulse rate, smoking habits, antihypertensive drug use and a history of myocardial infarction most clearly in men; and body mass index and systolic blood pressure in women. A larger body mass index was associated with a gradual decrease in mortality probability. The risk of death for women in the highest quartile of body mass index (> 26.4 kg/m2) relative to those in the lowest quartile (< 21.9 kg/m2) was 0.56 (95% confidence limits 0.36 and 0.87). Serum cholesterol level showed no association with overall mortality.

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.

In addition to standard features of clinical trial design such as randomisation and double-blinding, sensitivity to drug effects is an important consideration when conducting exercise capacity trials in patients with heart failure. Two issues need to be addressed in this context. Firstly, it is important to enrol patients who are potential responders. Patients who have, for their age and sex, normal exercise capacity are unlikely to improve, even when given a drug that has a positive effect on exercise capacity. In addition, those patients who remain clinically stable following withdrawal of their previous drug therapy are unlikely to respond subsequently to an experimental drug with a similar mechanism of action. Secondly, failure to complete scheduled exercise tests during follow-up, prompting a ‘per-protocol’ analysis of results, may mask the drug’s actual effect. To avoid this, an ‘intention-to-treat’ approach to data collection and analysis, with appropriate allowance made for missing test data, should be adopted.