Cardiovascular Journal of Africa: Vol 34 No 5 (NOVEMBER/DECEMBER 2023)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 5, November/December 2023 306 AFRICA of elevated perioperative neutrophil–lymphocyte ratio in predicting postoperative atrial fibrillation after cardiac surgery: a systematic review and meta-analysis. Heart Lung Circ 2020; 29(7): 1015–1024. 31. Horne BD, May HT, Kfoury AG, et al. The Intermountain Risk Score (including the red cell distribution width) predicts heart failure and other morbidity endpoints. Eur J Heart Fail 2010; 12: 1203–1213. 32. Providência R, Ferreira MJ, Gonçalves L, et al. Mean corpuscular volume and red cell distribution width as predictors of left atrial stasis in patients with non-valvular atrial fibrillation. Am J Cardiovasc Dis 2013; 3: 91–102. 33. Ertaş G, Aydin C, Sönmez O, et al. Red cell distribution width predicts new-onset atrial fibrillation after coronary artery bypass grafting. Scand Cardiovasc J 2013; 47: 132–135. 34. Korantzopoulos P, Sontis N, Liu T, et al. Association between red blood cell distribution width and postoperative atrial fibrillation after cardiac surgery: A pilot observational study. Int J Cardiol 2015; 185: 19–21. 35. Pilling LC, Atkins JL, Kuchel GA, et al. Red cell distribution width and common disease onsets in 240,477 healthy volunteers followed for up to 9 years. PLoS One 2018; 13: e0203504. 36. Jurin I, Hadžibegović I, Durlen I, et al. Left atrium size and red cell distribution width predict atrial fibrillation progression from paroxysmal or persistent to permanent. Acta Clinica Belgica 2020; 75(3): 205–211. 37. Sincer I, Gunes Y, Mansiroglu AK, et al. Association of mean platelet volume and red blood cell distribution width with coronary collateral development in stable coronary artery disease. Postepy Kardiol Interwencyjnej 2018; 14(3): 263–269. 38. Osadnik T, Strzelczyk J, Hawranek M, et al. Red cell distribution width is associated with long-term prognosis in patients with stable coronary artery disease. BMC Cardiovasc Disord 2013; 13: 113. 39. Rosas-Cabral A, Viana-Rojas JA, Prieto-Macías J, et al. [The association between red cell distribution width (RDW) and short-term mortality risk in patients with acute coronary syndrome (ACS)]. Gac Med Mex 2016; 152(1): 70–77. 40. Abrahan LL 4th, Ramos JDA, Cunanan EL, et al. Red cell distribution width and mortality in patients with acute coronary syndrome: a metaanalysis on prognosis. Cardiol Res 2018; 9(3): 144–152. … continued from page 277 been having chest pain before receiving the infusion but had not reported it. If the investigators had known, he would not have received the treatment. In a way, the treatment is a culmination of studies that began a decade ago when researchers discovered rare but healthy individuals with cholesterol levels that seemed impossibly low. The reason was that their PCSK9 gene was mutated and no longer functioned. As a result, these people were protected from heart disease. That led to the development of antibodies to block the gene. Patients inject themselves with the antibodies once a week. Then came a twice-yearly RNA injection that prevents PCSK9 from being made. It seemed possible that those treatments, as well as statins for those whose cholesterol is more easily controlled, could help solve the heart disease problem. But heart disease persists as a killer. Even after people are diagnosed with heart disease, less than 60% of all patients take a statin. Only a quarter take one of the more effective, high-intensity statins, Gulati said. ‘Patients take it initially, and then they forget or decide they don’t need it,’ she said. ‘That happens more than you’d think.’ Dr Michelle O’Donoghue, a cardiologist at Brigham and Women’s Hospital, said that because patients so often do not take their pills or injections, ‘there is a lot of interest, through gene editing, of a one and done – a single treatment and a lifetime response’. Family history was the inspiration for Kathiresan at Verve Therapeutics. His uncle and grandmother died of heart attacks. His father had a heart attack at 54 years. And then, on 12 September 2012, his 42-year-old brother returned from a run dizzy and sweaty. He was having a heart attack. He died nine days later. At that moment, Kathiresan said, he vowed to find a way to prevent what had happened to his brother from happening to anyone else. Of course, even if gene editing works, applying it to young people with heart risk is well into the future. But, Gulati said, early gene editing of younger patients with genetically high cholesterol levels might prevent arteries from hardening. ‘It could be an incredible medicine,’ she said. This all depends on success and safety of the gene editing and on its effects lasting. The first patient was treated just six months ago. But a previous study in monkeys lasted two and a half years, and the results of the gene editing persisted. Urnov, who said he has a genetic risk for heart disease, is optimistic for himself and his six-year-old daughter. ‘I honestly cannot wait for this medicine to become available for heart disease prevention,’ he said. ‘I love the idea of having gene editing as a vaccine for the prevention of heart disease.’ Source: MedicalBrief 2023

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