CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 2, May/June 2023 AFRICA 103 16. Hunt SA, Abraham WT, Chin MH, et a1. 2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 2010; 121: e391–479. 17. Ronco C, Mc Cullogh P, Anker SD, et al. Cardiorenal syndromes: report from the consensus conference of the Acute Dialysis Quality Initiative. Eur Heart J 2010; 31: 703–711. 18. Ronco C, Haapio M, House AA, et al. Cardiorenal syndrome. J Am Coll Cardiol 2008; 52: 1527–1539. 19. Heywood JT, Fonarow GC. High prevalence of renal dysfunction and its impact on outcome in 118,465 patients hospitalized with acute decompensated heart failure: A report from the ADHERE Database. J Card Fail 2007; 13: 422–430. 20. Rayner KJ, Esau CC, Hussain FN, et al. Inhibition of miR-33a/b in non-human primates raises plasma HDL and lowers VLDL triglycerides. Nature 2011; 478: 404–407. 21. Yang J, Nie Y, Wang F, et al. Reciprocal regulation of miR-23a and lysopliospliatidic acid receptor signaling in cardiomyocyte hypertrophy. Biochim Biophys Acta 2013; 1831: 1386–1394. 22. Li C, Li X, Gao X, et al. MicroRNA-328 as a regulator of cardiac hypertrophy. Int J Cardiol 2014; 173: 268–276. 23. Wang D, Zhai G, Ji Y, et al. microRNA-10a targets T-box 5 to inhibit the development of cardiac hypertrophy. Int Heart J 2017; 58: 100–106. 24. Kumarswamy R, Bauters C, Volkmann I, et al. Circulating long noncoding RNA, LIPCAR, predicts survival in patients with heart failure. Circ Res 2014; 114: 1569–1575. 25. Lu X, Yin D, Zhou B, et al. MiR-135a promotes inflammatory responses of vascular smooth muscle cells from db/db mice via downregulation of FOXO1. Int Heart J 2018; 59: 170–179. 26. Morceau F, Chateauvieux S, Gaigneaux A, Dicato M, Diederich M. Long and short non-coding RNAs as regulators of hematopoietic differentiation. Int J Mol Sci 2013, 14(7): 14744–14770. 27. Daniel L, Bardin N, Moal V, et al. Tubular CD146 expression in nephropathies isrelated tochronic renal failure. Nephron Exp Nephrol 2005; 99(4): e105–e111. Scientists find 16 genes that increase women’s heart attack risk Researchers who conducted a genome-wide association meta-analysis of eight studies into spontaneous coronary artery dissection (SCAD), which can lead to heart attacks, particularly in women under 60 years, found 16 gene variants linked to an increased risk of the condition. SCAD can occur suddenly, with no warning and often affects people who are otherwise healthy, making it difficult to detect early, reports Medical News Today. The team, from the United Kingdom, France, Australia, Canada and USA, had collaborated to examine whether there were genetic factors contributing to someone developing SCAD, and to learn more about what causes it. The study, published in Nature Genetics, identified 16 genes, including those involved in artery integrity and blood clotting that are associated with an increased risk. Conducting a meta-analysis The researchers compared a group of 1 917 people with SCAD to a control group of 9 292: included were patients with SCAD who had similar clinical characteristics and met diagnostic criteria. They then analysed genes that were possibly ‘regulated in vascular smooth muscle cells’, as well as genes involved in blood coagulation. This is significant because blood coagulation, or blood clotting, prevents an injured vessel from bleeding profusely. An injured blood vessel can lead to a heart attack in SCAD. The research team also investigated the causal relationships between cardiovascular disease risk factors (predicted based on genetics) and SCAD and coronary artery disease (CAD). In their combined genetic analysis of the eight studies, they found 16 genes that factor into SCAD. They found that lower expression of the tissue factor gene F3, involved in blood coagulation, is associated with a higher risk of SCAD, and a ‘novel association signal with SCAD’ with the gene THSD4 that is associated with fibrillin, which regulates heart functioning. The team also found causal genes involved in maintaining arterial wall integrity and function, including genes HTRA1, TIMP3, ADAMTSL4, LRP1, COL4A1 and COL4A2. ‘This research confirms there are multiple genes involved in determining the risk of a person having a SCAD,’ said lead study author Dr David Adlam, associate professor of acute and interventional cardiology at the University of Leicester in England. The team also found that some of the genetic variants in SCAD and CAD are connected but have an opposite impact. ‘Several associated variants have diametrically opposite associations with CAD, suggesting that shared biological processes contribute to both diseases, but through different mechanisms,’ wrote the authors. What is SCAD? SCAD happens when a tear spontaneously occurs within the artery wall and causes blood to get trapped. This narrows or blocks the artery and can cause a heart attack because blood flow can’t reach the heart muscle. While typical CAD often affects people with certain risk factors (such as a family history of it or people with high cholesterol levels), SCAD can occur without warning and in people who are healthy. SCAD mostly affects young women and is the cause of 25% of acute coronary syndrome cases in women under 50 years. Additionally, SCAD can cause heart attacks in pregnant women. While symptoms can vary, they may resemble symptoms of a heart attack and may include chest pain, shortness of breath, profuse sweating and dizziness. Source: MedicalBrief 2023
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