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To determine the costs and cost-effectiveness of a diagnostic strategy including computed tomography coronary angiography (CTCA) in comparison with invasive conventional coronary angiography (CA) for the detection of significant coronary artery disease from the point of view of the healthcare provider.The average cost per CTCA was determined via a micro-costing method in four French hospitals, and the cost of CA was taken from the 2011 French National Cost Study that collects data at the patient level from a sample of 51 public or not-for-profit hospitals.The average cost of CTCA was estimated to be 180euro(95 % CI 162-206euro) based on the use of a 64-slice CT scanner active for 10 h per day. The average cost of CA was estimated to be 1,378euro(95 % CI 1,126-1,670euro). The incremental cost-effectiveness ratio of CA for all patients over a strategy including CTCA triage in the intermediate risk group, no imaging test in the low risk group, and CA in the high risk group, was estimated to be 6,380euro(95 % CI 4,714-8,965euro) for each additional correctly classified patient. This strategy correctly classifies 95.3 % (95 % CI 94.4-96.2) of all patients in the population studied.A strategy of CTCA triage in the intermediate-risk group, no imaging test in the low-risk group, and CA in the high-risk group, has good diagnostic accuracy and could significantly cut costs. Medium-term and long-term outcomes need to be evaluated in patients with coronary stenosis potentially misclassified by CTCA due to false negative examinations.

OBJECTIVES: Contrast-enhanced cardiac magnetic resonance (CMR) for infarct sizing has been validated in large animals, but studies and follow-up are restricted. We sought to (1) validate CMR for assessment of myocardial area at risk (MAR) and infarct size (IS) in a rabbit model of reperfused myocardial infarction (MI); (2) analyse the relation between ischaemic substrates and subsequent left ventricular (LV) remodelling. METHODS: Experimental reperfused acute MI was induced in 16 rabbits. Ten animals underwent cross-registered cine and contrast-enhanced CMR and histopathology at day 3 for assessment of MAR and IS (group 1). The remaining six rabbits underwent serial CMR for the study of LV remodelling (group 2). RESULTS: In group 1, mean IS was 12.7 +/- 6.4% and 12.7 +/- 6.9% of total LV myocardial mass on CMR (late-enhancement technique) and histopathology (P = 0.52; r = 0.93). No significant difference occurred between CMR and histopathology for the calculation of MAR and IS/MAR ratio (P = 0.18 and P = 0.17), whereas correlations were strong (r = 0.92 and r = 0.95). In group 2, mean LV end-diastolic, end-systolic volumes and LV mass were significantly increased at 3 weeks compared with measurements at day 3 (P < 0.01). Significant correlations between initial IS and the increase in LV end-diastolic volume (r = 0.66) and the increase in LV mass (r = 0.48) were observed, as well as correlations between initial MAR and the increase in LV end-diastolic volume (r = 0.70) and the increase in LV mass (r = 0.37). CONCLUSIONS: Comprehensive CMR provides accurate assessment of IS and MAR in reperfused rabbit MI. Infarct size is closely related to LV remodelling. Through the infarct size/MAR ratio, this approach has great potential for assessing interventions aimed at cardioprotection.

The long acting angiotensin-converting enzyme inhibitor enalapril was compared with the calcium channel blocker nifedipine as sustained-release formulation in 136 patients with mild to moderate hypertension. This multicentre study was carried out in a double-blind, double-dummy fashion by 28 cardiologists in private practice. After a 2-week placebo period, patients were randomly allocated to 2 treatment groups; the first group received enalapril 20 mg daily (n = 68), and the second group received sustained-release nifedipine 20 mg twice daily (n = 68). The duration of treatment was 12 weeks. In both groups, hydrochlorothiazide 25 mg was added at week 4 if diastolic blood pressure remained greater than 90 mm Hg. At week 8, if the target diastolic pressure of less than 90 mm Hg was not achieved, the dosage of hydrochlorothiazide was increased to 50mg. The clinical characteristics of the patients in each group were comparable. After 4 weeks of treatment, the reduction in supine diastolic blood pressure was similar in both groups (12.1 mm Hg in the enalapril group vs 10.3 mm Hg in the nifedipine group). Moreover, although the difference between the groups was more noticeable after 12 weeks of treatment (16.3 vs 13.9 mm Hg, respectively), it did not reach significance. The number of patients experiencing clinical adverse effects was significantly greater in the nifedipine group than in the enalapril group [33 (48.5%) vs 18 (26.5%), respectively]. The most common complaints of patients administered nifedipine included swollen ankles, flushing and headaches, whereas complaints in the enalapril group included cough, asthenia, and epigastralgia. Three patients were withdrawn from the study because of side effects in the enalapril group and 10 were withdrawn from the nifedipine group. These results indicate that enalapril and sustained-release nifedipine are equally effective in controlling mild to moderate hypertension. However, enalapril was much better tolerated in this study.

The aim of the study was to assess the duration of the haemodynamic effects of a new sustained-release oral formulation of isosorbide dinitrate (ISDN). Twenty patients (17 men and 3 women; mean age 60 years) with acute myocardial infarction (10 anterior, 10 inferior) complicated by moderate left ventricular failure took part in a randomized controlled trial. Ten patients were randomly assigned to the placebo group and 10 to the ISDN group, who received 40 mg sustained release isosorbide dinitrate. Haemodynamic variables were measured before treatment, after 0.5 and 1 h and then every 2 hours up to the 8th hour after treatment. There was no significant change in any haemodynamic parameter in the placebo group, during the study period. In the ISDN group there was a significant fall in pulmonary artery diastolic pressure at 4 and 8 h, from 19.0 +/- 1.0 mm Hg to 16.5 +/- 1.2 mm Hg and 15.5 +/- 0.8 mmHg, respectively. The mean pulmonary capillary wedge pressure fell progressively from 17.9 +/- 1.0 to 12.5 +/- 1.2 mmHg at 2 h (p less than 0.001 in comparison with the placebo group. The fall remained significant up to 8 h. There was no statistically significant change in heart rate, cardiac index, systemic blood pressure or systemic and pulmonary vascular resistances. On the whole the cardiac index remained unchanged. There were numerous individual variations of cardiac index in relation to the initial mean pulmonary capillary wedge pressure and the magnitude of its fall following administration of ISDN. The change in cardiac index was inversely correlated with the control cardiac index (r = -0.69, p less than 0.02).