CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 3, July/August 2023 136 AFRICA Our study included both the ischaemic and non-ischaemic spectrum, studied independently and also compared to each other. Moreover, the follow up included a wider spectrum of clinical events ranging from mild chest pain or shortness of breath, passing through hospitalisation due to decompensated heart failure and up to malignant arrhythmia and sudden cardiac arrest. We were concerned about the clinical pattern of the patients regarding their morbidity, hospitalisation and quality of life. The mean LVEF was 51 ± 14% (18–77) in group I (32% of group I with LVEF < 45% and 69% with LVEF > 45%) and 48 ± 16% (9–77) in group II (37% of group II with LVEF < 45% and 63% with LVEF > 45%). There was a statistically significant linear relationship between left ventricular systolic dysfunction represented by LVEF and event severity in group I (p = 0.013). On the other hand, for group II patients, there was no clear relationship between LVEF and event severity (p = 0.150). In this non-ischaemic group, the main predictor of cardiac events was scar mass. For example, in the four patients in group II who experienced sudden cardiac arrest, the LVEF was > 45% but with a high scar mass average (13.99 ± 13.77 g). It was also observed in group I that the lower LVEF was more linked with hospitalisation due to decompensated heart failure (63% of the hospital admissions had LVEF < 45%). On the other hand, most of the patients with no events or mild chest pain or dyspnoea had LVEF > 45%. This could be explained by the fact that in ischaemic patients, the amount of scarred myocardium was directly linked to the severity of the underlying coronary artery disease, and the amount of scar mass and its distribution may also indicate the number of coronary territory affected. In non-ischaemic patients, the preserved LVEF is misleading because it does not indicate the degree of underlying myocardial pathology. However, LGE in cardiac MRI is more precise in tissue characterisation and spotting unhealthy myocardium that is usually a substrate for serious arrhythmogenic events and subsequently sudden cardiac arrest, even in cases of preserved LVEF.12 In the report by Dokainish et al.,13 they had a similar outcome to ours when they evaluated the prognostic implications of left ventricular systolic and diastolic dysfunction early post-acute ST-segment elevation myocardial infarction. Patients with LVEF ≤ 45% and restrictive diastolic function (RDF) were at greatly increased risk of major adverse cardiovascular events (MACE) (HR 8.85, 95% CI: 4.21–18.60) compared to patients with LVEF ≥ 45% and without RDF. RDF remained a strong predictor for MACE in patients with LVEF ≥ 45% (HR 4.38, 95% CI: 1.52–12.60), and in multivariate models adjusted for LVEF, left ventricular end-systolic volume and clinical variables. 90 80 70 60 50 40 30 20 10 0 LVEF Event severity 1 2 3 4 5 6 7 rs = 0.263* p < 0.013* 90 80 70 60 50 40 30 20 10 0 LVEF Event severity 1 2 3 4 5 6 7 rs = 0.180 p < 0.150 80 60 40 20 0 LVEF Asympt CP HF HA Syncope VT Arrest Event 80 60 40 20 0 LVEF Asympt CP HF HA Syncope VT Arrest Event Fig. 3. Relationship between event severity and LVEF; A and C for group I, and B and D for group II. Asympt, asymptomatic; CP, chest pain; HF, heart failure; HA, hospitalisation; VT, ventricular tachycardia. A C B D
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