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Objective: To investigate whether a very early invasive strategy (IS)±revascularisation improves clinical outcomes compared with standard care IS in higher risk patients with non-ST-elevation acute coronary syndrome (NSTE-ACS)., Methods: Multicentre, randomised, controlled, pragmatic strategy trial of higher risk patients with NSTE-ACS, defined by Global Registry of Acute Coronary Events 2.0 score of ≥118, or ≥90 with at least one additional high-risk feature. Participants were randomly assigned to very early IS±revascularisation (<90 min from randomisation) or standard care IS±revascularisation (<72 hours). The primary outcome was a composite of all-cause mortality, new myocardial infarction or hospitalisation for heart failure at 12 months., Results: The trial was discontinued early by the funder due to slow recruitment during the COVID-19 pandemic. 425 patients were randomised, of whom 413 underwent an IS: 204 to very early IS (median time from randomisation: 1.5 hours (IQR: 0.9-2.0)) and 209 to standard care IS (median: 44.0 hours (IQR: 22.9-72.6)). At 12 months, there was no significant difference in the primary outcome between the early IS (5.9%) and standard IS (6.7%) groups (OR 0.93, 95% CI 0.42 to 2.09; p=0.86). The incidence of stroke and major bleeding was similar. The length of hospital stay was reduced with a very early IS (3.9 days (SD 6.5) vs 6.3 days (SD 7.6), p<0.01)., Conclusions: A strategy of very early IS did not improve clinical outcomes compared with a standard care IS in higher risk patients with NSTE-ACS. However, the primary outcome rate was low and the trial was underpowered to detect such a difference., Trial Registration Number: NCT03707314., Competing Interests: Competing interests: NC has received unrestricted grants from HeartFlow, Boston Scientific, Haemonetics and Beckman Coulter; speaker fees from Abbott and Boston Scientific; and travel sponsorship from Edwards Lifesciences, Boston Scientific, Abbott and Biosensors., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY. Published by BMJ.)

Objective: To determine whether the changes in the manifestations of myocardial ischaemia during sequential angina episodes caused by exercise or coronary artery occlusion are collateral dependent., Methods: 40 patients awaiting percutaneous transluminal coronary angioplasty for an isolated left anterior descending artery stenosis underwent three sequential treadmill exercise tests, with the second exertion separated from the first by 15 minutes, and from the third by 90 minutes; 28 patients subsequently completed two (> 180 s) sequential intracoronary balloon inflations with measurement of collateral flow index from mean coronary artery wedge, aortic, and coronary sinus pressures., Results: On second compared with first exercise, time to 0.1 mV ST depression (mean (SD): 340 (27) v 266 (25) s) and rate-pressure product at 0.1 mV ST depression (22 068 (725) v 19 586 (584) beats/min/mm Hg) were increased (all p < 0.005), while angina and ventricular ectopic beat frequency were diminished (p < 0.05). This advantage, which had waned by the third effort, was independent of collateral flow index. Similarly, at the end of the second compared with the first coronary occlusion, ventricular tachycardia (21% v 0%, p < 0.05), ST elevation (0.47 (0.07) v 0.33 (0.05) mV, p < 0.005), and angina severity (6.1 (0.7) v 4.6 (0.7) units, p < 0.005) were reduced despite similar collateral flow indices., Conclusions: In patients with coronary artery disease, ventricular arrhythmias, ST deviation, and angina are reduced during a second exertion or during a second coronary occlusion. This protective effect can occur independently of collateral recruitment. These characteristics, together with the breadth and temporal pattern of protection, are consistent with ischaemic preconditioning.

Background: Pericardial thickening is an uncommon complication of cardiac surgery., Objectives: To study pericardial thickening as the cause of severe postoperative venous congestion., Subjects: Two men, one with severe aortic stenosis and single coronary artery disease, and one with coronary artery disease after an old inferior infarction. Both had coronary artery bypass grafting surgery., Methods: Magnetic resonance imaging (MRI), Doppler echocardiography, and cardiac catheterisation., Results: Venous pressure was raised in both patients. MRI showed mildly thickened pericardium, and cardiac catheterisation indicated diastolic equalization of pressures in the four chambers. Jugular venous pulse showed a dominant "Y" descent coinciding with early diastolic flow in the superior vena cava, and mitral and tricuspid Doppler forward flow proved restrictive physiology. The clinical background suggested pericardial disease so both patients had pericardiectomy. This proved the pericardium to be thickened; the extent of fibrosis also involved the epicardium., Conclusions: Although rare, restrictive pericarditis (restrictive ventricular physiology resulting from pericardial disease) should be considered to be a separate diagnostic entity because its pathological basis and treatment are different from intrinsic myocardial disease. This diagnosis may be confirmed by standard investigational techniques or may require diagnostic thoracotomy.

Coagulation is triggered during the onset of myocardial infarction, resulting in vascular occlusion. However, a causal role for individual haemostatic factors in the development of thrombotic occlusion is not established. Three cases (all relatively young women) are reported of raised factor VIII associated with myocardial infarction. Two patients presented acutely with myocardial infarction at a relatively young age with no preceding history of angina. The other patient had had venous thrombosis when young and activated protein C resistance (APCR), without the presence of factor V Leiden. A functional relation exists between APCR and factor VIII; therefore, raised factor VIII may contribute to APCR and the increased thrombotic risk in patients without factor V Leiden. Factor VIII is an important risk factor for atherothrombotic events, including sudden death, in patients with vascular disease. These cases support the association of raised factor VIII with acute thrombotic events, even in patients without significant underlying atheromatous disease.