ObjectiveTo review the results of uncomplicated coronary artery bypass graft surgery and to identify factors which influence operative mortality (OM) and postoperative myocardial infarction (PMI). DesignAn analysis of the outcome in patients having coronary artery bypass graft surgery for the first time from 1978 to 1990 inclusive. SettingThe Cardiothoracic Surgery Unit at the Royal Adelaide Hospital. ParticipantsTwelve thousand and twenty‐two patients had coronary artery bypass graft surgery only. Complete data were available for 12 003 patients. ResultsThere was an overall mortality rate of 0.99% and a postoperative myocardial infarction rate of 1.34%. Older patients and women had a higher operative mortality rate. Both unstable angina and poor ventricular function increased the mortality rate. The only significant operative factor was the perfusion time. There was a more than 16‐fold increase in mortality in patients who had an average bypass time (48 minutes) compared with those whose bypass time was 100 minutes or more (0.63% v. 10.3%). The PMI rate changed over the study period, and was also influenced by the presence of unstable angina and the duration of bypass: unstable angina doubled the rate from 0.86% to 1.91 %, and with an average bypass time the PMI rate was 0.56% whereas with a bypass time of 100 minutes or more the rate increased to 7.7%. ConclusionsThe outcome after coronary artery bypass graft surgery is strongly dependent on the perfusion time and the presence of unstable angina. Older patients and women are more likely to die during the operation.

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CRISPR/Cas9 can be used to inactivate or modify genes by inducing double-stranded DNA breaks. As a protective cellular response, DNA breaks result in p53-mediated cell cycle arrest and activation of cell death programs. Inactivating p53 mutations are the most commonly found genetic alterations in cancer, highlighting the important role of the gene. Here, we show that cells deficient in p53, as well as in genes of a core CRISPR-p53 tumor suppressor interactome, are enriched in a cell population when CRISPR is applied. Such enrichment could pose a challenge for clinical CRISPR use. Importantly, we identify that transient p53 inhibition suppresses the enrichment of cells with these mutations. Furthermore, in a data set of >800 human cancer cell lines, we identify parameters influencing the enrichment of p53 mutated cells, including strong baseline CDKN1A expression as a predictor for an active CRISPR-p53 axis. Taken together, our data identify strategies enabling safe CRISPR use.