CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 4, September/October 2023 AFRICA 211 27. Glancy JM, Garratt CJ, de Bono D, Woods K. QT dispersion and mortality after myocardial infarction. Lancet 1995; 345: 945–948. 28. Okin PM, Devereux RB, Howard BV, Fabsitz RR, Lee ET, Welty TK. Assessment of QT interval and QT dispersion for prediction of all-cause and cardiovascular mortality in American Indians: The Strong Heart Study. Circulation 2000; 101: 61–66. 29. InanırM, Gunes Y, Sincer I, Erdal E. Evaluation of Electrocardiographic ventricular depolarization and repolarization variables in type 1 diabetes mellitus. Arquivos Brasileiros de Cardiologia 2020; 114: 275–280. 30. Vink AS, Neumann B, Lieve KV, Sinner MF, Hofman N, El Kadi S, et al. Determination and interpretation of the QT interval: Comprehensive analysis of a large cohort of long QT syndrome patients and controls. Circulation 2018; 138: 2345–2358. 31. Sen Ö, Yilmaz S, Sen F, Balcı KG, Akboga MK, Yayla C, et al. T‐peak to T‐end interval predicts appropriate shocks in patients with heart failure undergoing implantable cardioverter defibrillator implantation for primary prophylaxis. Ann Noninvasive Electrocardiol 2016, June 6. Ahead of print. 32. Hidayet Ş, Demir V, Turan Y, Gürel G, Taşolar MH. Evaluation of Tp–e interval, Tp–e/QT ratio, and Tp–e/QTc ratio in patients with Behçet’s disease. Anatolian J Cardiol 2019; 22: 85. 33. Zumhagen S, Zeidler EM, Stallmeyer B, Ernsting M, Eckardt L, Schulze-Bahr E. Tpeak–Tend interval and Tpeak–Tend/QT ratio in patients with Brugada syndrome. Ep Europace 2016; 18: 1866–1872. 34. Lellouche N, De Diego C, Akopyan G, Boyle NG, Mahajan A, Cesario DA, et al. Changes and predictive value of dispersion of repolarization parameters for appropriate therapy in patients with biventricular implantable cardioverter-defibrillators. Heart Rhythm 2007; 4: 1274–1283. 35. Kup A, Uslu A, Demir S, Gulsen K, Celik M, Bayam E, et al. Tp-Te interval and Tp-Te/QT ratio may be predictive of idiopathic ventricular tachycardia in patients with frequent outflow tract premature ventricular complexes. Acta Cardiologica 2021; 76: 605–610. 36. Tse G, Gong M, Li CKH, Leung KSK, Georgopoulos S, Bazoukis G, et al. Tpeak‐Tend, Tpeak‐Tend/QT ratio and Tpeak‐Tend dispersion for risk stratification in Brugada Syndrome: A systematic review and meta‐analysis. J Arrhythmia 2018; 34: 587–597. 37. Thomas D, Jex N, Thornley A. Ventricular arrhythmias in acute coronary syndromes – mechanisms and management. Contin Cardiol Ed 2017; 3: 22–29. 38. Allessie MA, Bonke F, Schopman F. Circus movement in rabbit atrial muscle as a mechanism of tachycardia. III. The ‘leading circle’ concept: a new model of circus movement in cardiac tissue without the involvement of an anatomical obstacle. Circ Res 1977; 41: 9–18. 39. Hariman RJ, Louie EK, Krahmer RL, Bremner SM, Euler D, Hwang MH, et al. Regional changes in blood flow, extracellular potassium and conduction during myocardial ischemia and reperfusion. J Am Coll Cardiol 1993; 21: 798–808. Genetic bad cholesterol drops 60% in Australian drug trial Australian researchers have found a potential oral medication developed to lower, by as much as 65%, levels of ‘bad’ cholesterol – lipoprotein(a) or Lp(a) – which affects some 20 to 25% of people around the world. Until now, there has been no cure or approved specific treatment for lowering these levels, reports Medical News Today, and because Lp(a) levels are genetically inherited, lifestyle changes such as diet and exercise that may benefit other types of cholesterol do not help. Now, researchers from Monash University’s Victorian Heart Institute and Victorian Heart Hospital have found that an experimental oral medication developed to target Lp(a) was able to lower its levels by more than half during a firstin-human phase one clinical trial. This study was recently published in the journal J Am Med Assoc. What is lipoprotein(a)? Lipoproteins are a type of protein that transports cholesterol through the blood. There are two main types of lipoproteins: high-density lipoprotein (HDL) cholesterol, considered ‘good’, and low-density lipoprotein (LDL) cholesterol, considered ‘bad’. Although the body needs some cholesterol for certain functions, too much LDL cholesterol can lead to atherosclerosis – where cholesterol builds up to form plaques on the inside walls of arteries, making it hard for blood to pump through. Lp(a) is a form of LDL cholesterol that is ‘stickier’ than other types, making it easier for the build-up to occur and arteries to become blocked. The amount of Lp(a) in a person’s system is determined by their genetic history and ethnicity. For example, African Americans are at an increased risk for high Lp(a) levels compared with other ethnic groups. Having a high level of Lp(a) can increase the risk of cardiovascular diseases such as coronary heart disease and stroke. Muvalaplin: a weapon against bad cholesterol? In this study, researchers conducted a clinical trial to assess an experimental medication called muvalaplin. ‘Genetic and population studies show us that high Lp(a) levels are associated with a high risk of heart disease,’ Dr Stephen Nicholls, cardiologist and director of Monash University’s Victorian Heart Institute and the Victorian Heart Hospital at Monash Health and lead author of this study, told Medical News Today. ‘As much as 20% of the population have high levels. We don’t currently have specific therapies that lower levels, which may be important in the prevention of heart disease.’ He and his team looked at how well the drug worked, as well as its safety and tolerability in humans. continued on page 216…
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