RESUMO
Out-of-hospital cardiac arrest (OHCA) is a major cause of death. Although the aetiology of cardiac arrest can be diverse, the most common cause is ischaemic heart disease. Coronary angiography and percutaneous coronary intervention, if indicated, has been associated with improved long-term survival for patients with initial shockable rhythm. However, in patients without ST-segment elevation on the post-resuscitation electrocardiogram, the optimal timing of performing this invasive procedure is uncertain. One important challenge that clinicians face is to appropriately select patients that will benefit from immediate coronary angiography, yet avoid unnecessary delay of intensive care support and targeted temperature management. Observational studies have reported contradictory results and until recently, randomised trials were lacking. The Coronary Angiography after Cardiac Arrest without ST-segment elevation (COACT) was the first randomised trial that provided comparative information between coronary angiography treatment strategies. This literature review will provide the current knowledge and gaps in the literature regarding optimal care for patients successfully resuscitated from OHCA in the absence of ST-segment elevation and will primarily focus on the role and timing of coronary angiography in this high-risk patient population.
RESUMO
OBJECTIVE: Well-developed collaterals provide survival benefit in patients with obstructive coronary artery disease (CAD). Therefore, in this study we sought to determine which clinical variables are associated with arteriogenesis. DESIGN: Clinical and laboratory variables were collected before percutaneous coronary intervention. Multivariate analysis was performed to determine which variables are associated with the collateral flow index (CFI). PATIENTS: Data from 295 chronic total occlusion (CTO) patients (Bern, Switzerland, Amsterdam, the Netherlands and Jena, Germany) were pooled. In earlier studies, patients had varying degrees of stenosis. Therefore, different stages of development of the collaterals were used. In our study, a unique group of patients with CTO was analysed. INTERVENTIONS: Instead of angiography used earlier, we used a more accurate method to determine CFI using intracoronary pressure measurements. CFI was calculated from the occlusive pressure distal of the coronary lesion, the aortic pressure and central venous pressure. RESULTS: The mean CFI was 0.39 ± 0.14. After multivariate analysis, ß blockers, hypertension and angina pectoris duration were positively associated with CFI (B: correlation coefficient ß=0.07, SE=0.03, p=0.02, B=0.040, SE=0.02, p=0.042 and B=0.001, SE=0.000, p=0.02). Furthermore also after multivariate analysis, high serum leucocytes, prior myocardial infarction and high diastolic blood pressure were negatively associated with CFI (B=-0.01, SE=0.005, p=0.03, B=-0.04, SE=0.02, p=0.03 and B=-0.002, SE=0.001, p=0.011). CONCLUSIONS: In this unique cohort, high serum leucocytes and high diastolic blood pressure are associated with poorly developed collaterals. Interestingly, the use of ß blockers is associated with well-developed collaterals, shedding new light on the potential action mode of this drug in patients with CAD.