Cardiovascular Journal of Africa: Vol 33 No 6 (NOVEMBER/DECEMBER 2022)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 6, November/December 2022 312 AFRICA on ventricular arrhythmias in response to left ventricular afterload increase and microRNA expression profiles in Wistar rats. Peer J 2018; 6: e6110. 21. Franz MR, Burkhoff D, Yue DT, Sagawa K. Mechanically induced action potential changes and arrhythmia in isolated and in situ canine hearts. Cardiovasc Res 1989; 23(3): 213–223. 22. Sadoshima J, Izumo S. Mechanical stretch rapidly activates multiple signal transduction pathways in cardiac myocytes: potential involvement of an autocrine/paracrine mechanism. EMBO J 1993; 12(4): 1681–1692. 23. Ning W, Wit A. Comparison of the direct effects of nifedipine and verapamil on the electrical activity of the sinoatrial and atrioventricular nodes of the rabbit heart. Am Heart J 1983; 106(2): 345–355. 24. Zeltser D, Justo D, Halkin A, Rosso R, Ish-Shalom M, Hochenberg M, et al. 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New light on potentially damaging effects of standard heart attack treatment A common treatment given to patients experiencing heart attack may not be as successful in halting muscle damage as once thought, found a study in the Journal of the American College of Cardiology. In heart attack patients, the amount of heart muscle that is irreversibly damaged is directly linked to how much time elapses between the onset of heart attack symptoms and when the blockage is opened up. More damage means higher risk of complications such as heart failure after a heart attack. Therefore, treating heart attacks focuses on opening up the coronary arteries as quickly as possible through a procedure called reperfusion, often with a stent. The common belief in reperfusion therapy is that once the coronary arteries are opened, the damage to the heart muscle is stopped. However, according to the study team, led by Rohan Dharmakumar, of the Indiana University School of Medicine, that is not always the case. ‘In our work, we demonstrate that if reperfusion results in internal bleeding or haemorrhage within the heart muscle, the heart muscle can continue to die even after the culprit coronary artery is opened,’ said Dharmakumar, executive director of the Krannert Cardiovascular Research Centre at IU School of Medicine. ‘Haemorrhage is known to occur in heart muscle of around half of all heart attack patients who undergo reperfusion. We sought to determine what effect that internal bleeding has on progressive heart muscle damage after reperfusion.’ Dharmakumar and his team studied blood samples of heart attack patients obtained before and after they received reperfusion therapy. Using cardiac magnetic resonance imaging (cardiac MRI), they non-invasively identified which patients experienced haemorrhage within their heart muscle after reperfusion. A key protein called troponin is known to go up with heart muscle damage. In patients with heart muscle haemorrhage, troponin values rose more rapidly reaching higher values when compared with patients without haemorrhage. The team also used a large animal model to prove that haemorrhage is directly involved in the extent of infarction after reperfusion. Serial cardiac MRIs non-invasively tracked infarct size in animals with and without haemorrhage; similar findings to those seen in patients means that the team can use the animal model to develop new treatments to reduce haemorrhage, which can be brought back to help patients. In the modern era of revascularisation, Dharmakumar asserts in his study that infarct size is not only determined by restricted blood supply to the heart, but also by the effects continued on page 316…

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