CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 3, July/August 2023 AFRICA 133 with ICM and NICM and compare it to the prognostic value of the LVEF in the same study population. Methods This study included 154 patients who were diagnosed to have cardiomyopathy (both ischaemic and non-ischaemic) using cardiac MRI (1.5 tesla). The patients were either referred from heart failure clinics or recruited directly after having been diagnosed by cardiac MRI. All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. The study protocol got the approval of the Committee of Ethics of the Alexandria University. CMR was performed using the 1.5-T machine. Sequences were ECG-triggered and performed in breath-hold technique using a body array coil. Myocardial function was assessed with cine steady-state free-precession (SSFP) pulse sequences that were acquired in stacks of short-axis slices covering the whole left ventricle with eight to 10 contiguous sections. LGE was acquired 10 minutes after intravenous gadolinium contrast (0.2 mmol/kg) by using a gradient-spoiled turbo fast low-angle shot sequence with phase-sensitive inversion recovery technique in four- and two-chamber views and a series of left ventricular short axes (section thickness 6 mm). The cardiac MRI study analysis included (1) ventricular function assessment (LVEF) though volume measurements in short-axis cine images; (2) detection of any myocardial scar or fibrosis using short-axis, two-, three- and four-chamber LGE images; (3) quantification of myocardial scar/fibrosis using three methods: manual quantification of the LGE mass in each slice of the short-axis LGE sequence; number of segments involved in the scar tissue (segments involving LGE); percentage of the scarred myocardium (summation of the percentage of the scarred myocardium in each segment of the 17 myocardial segments in relation to the total left ventricular mass). All 154 patients were followed up for at least six months for any clinical cardiac events. These events were scaled according to severity, from one (less severe) to seven (most severe); ranging from mild chest pain (non-acute coronary syndrome), mild dyspnoea (New York Heart Association stage I–II), and including hospital admission due to decompensated heart failure and up to syncope, documented ventricular arrhythmia and sudden cardiac arrest/death, respectively. Follow-up details were collected from hospital records and arranged phone calls with patients. Statistical correlation between the amount of the scarred myocardium in both ICM and NICN patients and the severity of the clinical events during the period of the follow up was performed. If any patient had experienced more than one event, the most serious one was considered the main event for this patient. Details of clinical events were collected from hospital records. Additional phone calls were arranged to get more details about the patient’s symptoms. Statistical analysis Data were fed into the computer and analysed using IBM SPSS software package version 20.0. (Armonk, NY: IBM Corp). The Kolmogorov–Smirnov test was used to verify the normality of distribution of variables. The Spearman coefficient was used to correlate between quantitative variables. Significance of the obtained results was judged at the 5% level. Results One hundred and fifty-four patients were included in the study, and 87 patients (56%) were male and 69 (44%) were female, with a mean age of 61 ± 15 years (range 20–87). The time of the clinical follow up was variable, with a minimum of six months and a mean of 10 months (from six to 40 months). Our patients were divided into two groups; 89 (58%) were diagnosed with ICM and 65 (42%) with NICM. The NICM subgroup included a variety of different aetiologies of cardiomyopathies: 41 patients were diagnosed to have dilated cardiomyopathy (DCM), seven with Takotsubo cardiomyopathy, five with left ventricular non-compaction, four with apical non-obstructive hypertrophic cardiomyopathy (HCM), three with amyloidosis, two with sarcoidosis, two with arrhythmogenic left ventricular dysplasia and one patient with endomyocardial fibrosis. Of the 154 patients, 52 (34%) had LVEF < 45% (28 patients in group I and 24 in group II) and 102 (66%) patients had LVEF ≥ 45% (61 patients in group I and 41 in group II). All the 154 patients were followed up clinically for at least six months. The clinical presentation ranged from eventless (no events) in 16 patients (six in group I, 10 in group II), chest pain in 28 (18%) patients (19 in group I, nine in group II), heart failure in 23 (15%) (12 in group I, 11 in group II), hospitalisation in 54 (35%) patients (35 in group I, 19 in group II), syncope in 14 (1%) (six in group I, eight in group II), ventricular tachycardia in nine (< 1%) patients (five in group I, four in group II) and cardiac arrest in 10 (< 1%) patients (six in group I, four in group II). Our main concern in this study was to determine whether there was a relationship between the scar size detected in the LGE CMR and the severity of clinical presentation of the patient during the follow up. In our study, a direct relationship between the absolute size of the myocardial scar (g) and event severity was observed (p < 0.001, rs = 0.464), as shown in Table 1 and Fig 1. When the two subgroups were compared, the scar mass was larger in size in group I (19.5 ± 18.9 g) than in group II (11.3 ± 19.9 g) but still with a linear relationship between scar size and event severity (p < 0.001) in both groups (Fig. 1). The size of the scar was also assessed by the total number of segments involved in the scar. Again, there was a significant direct relationship between the number of segments involved in this scar and event severity in both subgroups (group I, p < 0.001, rs = 0.490; group II, p < 0.001, rs = 0.536). The third method to evaluate the myocardial scar mass was through calculation of the percentage of myocardial scar to the total myocardial mass (by estimating the percentage of scar tissue in each segment of the 17 myocardial segments separately, each myocardial segment representing 1/17th of the total myocardial mass). The mean scar percentage was 17 ± 15% in the ICM patients and 8 ± 13% in the NICM patients. There was also a direct relationship observed between the estimated percentage of scarred myocardium and event severity (group I, p < 0.001, rs = 0.468; group II, p < 0.001, rs = 0.558) (Fig. 2).
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