ST-elevation myocardial infarction (STEMI) is most commonly caused by the total occlu sion of an epicardial coronary artery by a thrombus. [1] The cornerstone of STEMI management is early re vascularisation, either by primary percutaneous coronary intervention or fibrinolytic therapy, in conjunction with other adjunctive pharmaceutical agents.[1] The most important determinant of outcome, irrespective of which form of revascularisation is selected, is the time from symptom onset to restoration of flow in the obstructed artery.[2] The ideal reperfusion strategy for STEMI is primary percutaneous coronary intervention (PCI), provided it is performed in an experienced centre within 90 minutes of the time of hospital arrival or arrival of the emergency medical services (EMS).[1] Fibrinolytic therapy should be administered as an alternative within 30 minutes, if primary PCI is unavailable or transport times exceed 60 minutes to the nearest centre capable of performing PCI.[1] Randomised controlled trials of fibrinolytic therapy have demonstrated the benefit of initiating fibrinolytic therapy as early as possible after the onset of angina. [3,4] A myocardial infarction may be aborted and mortality dramatically reduced if fibrinolytic therapy is administered within the first 2 hours, and particularly within the first hour. [2] Delays relating to patient factors, emergency service and transport factors, and in-hospital factors broadly account for the delays in provision of appropriate reperfusion therapy. Globally, numerous studies have demonstrated that significant delays exist in the provision of any reperfusion strategy, including fibrinolytic therapy, to patients presenting with STEMI. [5][6][7][8][9][10] The largest time delay is attributed to delays by the patient in seeking medical attention. Further delays occur following the call for help and relate to delays in transportation, as well as in-hospital delays.In South Africa (SA) only a few tertiary public centres and selected private hospitals, almost exclusively in urban areas, are capable of performing primary PCI. The cardiology department at Steve Biko Academic Hospital (SBAH), Pretoria, was unable to perform routine primary PCI at the time of the study. Fibrinolytic therapy therefore constituted the primary revascularisation modality for patients presenting with STEMI. Furthermore, based on observation, few if any patients receive prehospital fibrinolytic therapy in SA, and there are minimal published data regarding the time to provision of fibrinolytic therapy (either prehospital or in-hospital). We therefore embarked on this study to systematically document the aforementioned observations in a tertiary hospital. Background. Fibrinolytic therapy is a time-critical intervention proven to reduce mortality and morbidity in patients with ST-elevation myocardial infarction (STEMI). Limited data exist in South Africa (SA) regarding time to fibrinolytic therapy for STEMI patients and reasons for delayed therapy. Objectives. To establish the proportion of STEMI pat...

A 25-year-old male presented after a motor vehicle accident with tricuspid valve (TV) regurgitation, due to a flail TV secondary to papillary muscle rupture. We highlight the importance of three-dimensional echocardiographic imaging of the tricuspid valve and its utility in aiding a successful surgical repair.

Invasion of the host cell via CD147 spike protein has emerged as a novel mechanism of direct myocardial injury. (6) CD147, also called Basigin, is a transmembrane glycoprotein and is involved in viral infection, tumour development and invasion by the malarial parasite. It is expressed in haematopoietic, epithelial and endothelial cells and is upregulated in early erythroblasts, cardiac tissue, the placenta and thyroid. (7) Interaction of the spike protein and ACE2 promotes invasion of the virus into host cells.It is unclear whether myocarditis is a result of direct viral invasion of the heart or whether it is secondary to the proinflammatory milieu. (8) Indirect effectsSystemic inflammatory response to the virus results in a cytokine-mediated storm culminating in multi-organ failure, including the heart. (9) Myocardial injury in the context of SARS-CoV-2 frequently results from impaired myocardial oxygen demand and supply ratio. (10) Injury to the myocardium results from a combination of hypoxia, sepsis with increased myocardial demand, and anaemia.Myocardial infarction secondary to plaque rupture is attributed to inflammatory response from the virus and possibly a pro-thrombotic state. (11) Arrhythmias have been noted -especially in patients hospitalised in intensive care units with severe disease. These may be attributed to effects of drugs and electrolyte imbalances. (12,13

Endomyocardial fibrosis remains a major public health problem worldwide. It is a restrictive cardiomyopathy, of uncertain aetiology, which may lead to right, left or biventricular heart failure. Progress continues to be made in understanding the prevalence and natural history of this disease. Specific treatment, apart from surgery, remains suboptimal. We report a case of advanced, biventricular EMF complicated by right ventricular outflow tract aneurysms.