CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 4, September/October 2023 AFRICA 209 Studies on the prognosis of MINOCA patients have shown variables results. The significant determinants of these results are that a single aetiology for MINOCA does not exist and there was a limited number of participants.17 However, current data and guidelines have reported that the prognosis might worsen, as with MI with obstructive CAD. In these studies, groups were generally compared with regard to mortality, angina frequency, recurrent MI and quality of life.6,7 Approximately 25% of patients with MINOCA will experience angina in the subsequent 12 months, similar to the frequency reported in patients with MI with obstructive CAD.18 In addition, the study reporting that the risk of arrhythmia may increase in MINOCA patients during hospitalisation or out-patient follow up is limited. Biere et al. showed in their study that MINOCA patients with an ischaemic late gadolinium enhancement (LGE) pattern on cardiac magnetic resonance imaging (MRI) experience more frequent ventricular arrhythmias during hospitalisation than patients without LGE in cardiac MRI.19 There was no difference in the incidence of arrhythmia between the two groups at the end of the one-year follow up.19 AF is the most common cardiac arrhythmia. However, no studies show an increased incidence and risk of AF in MINOCA patients during and after hospitalisation. Although the underlying pathophysiological mechanisms can be very different in MINOCA patients, it can be expected that the frequency of AF may increase due to the resulting myocardial ischaemia, as with MI with obstructive CAD. Furthermore, it has been previously reported that AF may be expected more frequently in MINOCA patients than in patients with MI with obstructive CAD (14.7 vs 7.3%).20 However, an increased frequency of AF at follow up was not reported in the same study.20 In order to predict the risk of AF on the surface ECG, many studies have been conducted.21 Alexander et al. recently developed the MVP ECG score as a novel scoring method for AF risk prediction.12 The MVP ECG score, which incorporates P-wave characteristics such as P-wave duration, inter-atrial block and P-wave voltage, represents atrial electrical and structural remodelling.12 According to MVP ECG scores, Alexander et al. classified study populations as low, medium or high risk and reported that the risk of AF increased 2.4 times in those with high MVP ECG scores.12 In 2019, after the article by Alexander et al., a few more studies on MVP scores were published. Yang et al. showed that this score could predict AF recurrence after pulmonary vein isolation.13 In one of these, Kahyaoğlu et al. showed a correlation between left atrial dysfunction demonstrated by speckle tracking echocardiography and MVP risk score in patients with hypertension.22 In another study, Hayiroglu et al. reported that ischaemic stroke patients with higher MVP ECG scores had higher AF incidence in index hospitalisation.23 A longer and strict follow up of these patients may be beneficial. As a result of our study, we found that according to the MVP ECG risk score of MINOCA patients, 55 (66.2%) were in the low-risk group, 25 patients (32.5) were in the intermediate-risk group and only one patient (1.2%) was in the high-risk group. We did not find an increased risk of AF in the MINOCA patients compared to that of the control group. Several ECG markers related to increased risk of ventricular arrhythmias and sudden cardiac death have been proposed.24 In various clinical situations and especially in patients with MI and heart failure, many studies have shown that QT, corrected QT and QT dispersion, which are markers of ventricular repolarisation, are associated with an increased frequency of ventricular arrhythmic episodes and may predict sudden cardiac death.9,25-29 The QT interval is between the beginning and end of ventricular repolarisation. The heart rate-corrected QT interval has been proposed as a more accurate QT measure because QT is typically altered by heart rate.30 Although the QT interval was not statistically significantly different between the groups in our study, the corrected QT interval was statistically significantly different between the groups. We attributed this to the fact that MINOCA patients were more tachycardic due to their intensive care unit admission and acute ischaemic cardiac condition. Other recently proposed ECG markers of ventricular repolarisation, the Tpeak–Tend, Tpeak–Tend/QT interval ratio and Tpeak– Tend/corrected QT interval ratio have been shown to predict ventricular arrhythmic events and sudden cardiac death in many studies.14,31-34 T peak–Tend/corrected QT ratio is a new measure for predicting cardiac arrhythmias that incorporates both transmural (Tpeak–Tend) and spatial (QT) ventricular repolarisationdispersion. 14,35 Transmural repolarisation is caused by the different action potential durations of epicardial cells, M cells and endocardial cells.14 T peak–Tend indicates transmural dispersion of repolarisation, and this pathophysiological mechanism is generally thought to represent an increased risk of re-entry arrhythmias.36 The risk and mechanism of ventricular arrhythmia in MINOCA patients have not been previously investigated. However, similar arrhythmia mechanisms can be expected in these patients as they have similar pathophysiology mechanisms as patients with MI with obstructed CAD. During the first 10 minutes after MI, ventricular tachycardia is due to re-entry within the ischaemic myocardium.37,38 This is caused by a minimal decrease in conduction velocity and delayed recovery of excitability in relatively large circuits.38 In the reperfusion period, K+, Na+, and Ca2+ imbalance occurs in intracellular and extracellular components of the myocardium and leads to dispersion of refractoriness, which forms the substrate for re-entry.37,39 In the subacute phase of MI, the primary mechanisms of ventricular arrhythmia are automaticity in surviving Purkinje fibres and triggered activity due to delayed after-depolarisation.37 In the chronic phase, the primary mechanism, electrically inactive scar tissue forms a focus around which re-entrant circuits form.37 Table 3. Comparison of ventricular arrhythmia predictors in electrocardiography Predictors MINOCA (n =77) Control (n = 78) p-value QRS complex duration, ms 90.21 ± 14.87 82.99 ± 21.59 0.017 ST segment, ms 113.61 ± 40.09 131.15 ± 46.12 0.130 ST interval, ms 271.95 ± 45.91 302.31 ± 38.40 < 0.001 QT interval, ms 389.03 ± 37.08 390.71 ± 29.12 0.754 Corrected QT interval, ms 438.17 ± 43.80 421.41 ± 28.39 0.005 QT dispersion 60.75 ± 22.77 34.19 ± 12.95 < 0.001 Tpeak–Tend interval 89.53 ± 32.16 65.22 ± 18.11 < 0.001 Tpeak–Tend interval/QT interval 0.2306 ± 0.0813 0.1676 ± 0.0470 < 0.001 Tpeak–Tend interval/corrected QT interval 0.2043 ± 0.6997 0.1551 ± 0.4310 < 0.001 Numerical variables with normal distribution were shown as mean ± standard deviation. Categorical variables are shown as numbers (%). MVP ECG: morphology–voltage–P‐wave duration electrocardiography.
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