الفهرس 
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Abstract
Coronary artery disease (CAD), a kind of cardiovascular disease, has been identified as the leading cause of death in both industrialised and developing countries. The four primary symptoms of CAD, an inflammatory atherosclerotic disease, are stable angina, unstable angina, myocardial infarction (MI), and sudden cardiac death (220, 221). Atherosclerosis and atherosclerotic occlusions of the coronary arteries cause coronary artery disease, a kind of cardiovascular illness (CAD). Atherosclerosis develops as a result of a buildup of lipoprotein droplets in the intima of the coronary vessels when the endothelial function of the arterial wall is compromised (15). Despite recent developments, the best way to treat ST segment elevation myocardial infarction (STEMI), which continues to be the leading cause of premature mortality worldwide, is still up for debate. The primary cause of STEMIs is the rupture of an atherosclerotic plaque with a subsequent thrombotic vascular occlusion; the size of the myocardium covered by the offending vessel, the length of the occlusion, and the existence of collaterals all affect how much myocardial damage results. Therefore, the treatment of this illness must focus on the swift restoration of vascular patency (222). Use of the ECG is necessary for early evaluation of people suspected of having acute coronary syndrome (ACS) (223). The most recent AHA/ACC and ESC recommendations state that the ECG from the acute phase, particularly in ST-segment elevation ACS, provides critical information on the location and size of the area at risk (224). The most appropriate therapy for each patient is selected using this information. The ECG is the sole objective diagnostic tool available in an emergency because serum markers don’t start to climb until necrosis has already occurred (225). An ECG may be used to pinpoint the causative coronary lesion’s location inside the infarct-related artery (IRA) in order to expedite reperfusion therapy and improve clinical decision-making (226). When the putative culprit artery is seen last with a guiding catheter and the nonculprit arteries are seen first with a diagnostic catheter, this catheter can remain in place for later coronary dilatation and stenting. However, the time to reperfusion has been shortened by rapid catheterization or opening of the likely culpable artery (227). Depending on the results of the 12-lead ECG, patients are categorised into one of three groups: those with ST segment elevation or new bundle branch block (suspicious for acute injury and possibly a candidate for acute reperfusion therapy with thrombolytics or primary PCI), those with ST segment depression or T wave inversion (suspicious for ischemia), and those with a so-called non-diagnostic or normal ECG. Aim of the study is to assess correlation between ST segment elevation in the12-lead ECG and the culprit coronary artery in patients with acute STEMI undergoing primary PCI. This is a prospective cohort study carried on patients presenting by ST-segment elevation of 1 mm or more in two or more contiguous leads, often with reciprocal ST-depression in the collateral leads within 24 hours and treated with primary PCI. Our study was carried out on 100 patients, 61 were males and 39 were females with a mean age of 59.23 ± 4.92 years. Kamal et al conducted a similar study to assess the accuracy of previously defined ECG criteria determined from ECG angiographic correlative studies in predicting not only the infarct-related artery but also the site of the culprit lesion within that artery. It consists of 2 study groups, the first with anterior STEMI 43 (86.0%) of them were males and seven (14.0%) were female patients. The mean age was 53.34 ± 10.54 years which is lower than our study participants, but the male gender is predominant as our study. The second group included patients with inferior STEMI, 40 (80%) male and 10 female (20%) patients. The mean age was 55.7 ± 12.5 years which is lower than our study with predominance of male gender as well (228). Regarding the type of infarction by ECG, our study reported that it was anterior MI in 26 (26.0%) patients, inferior MI in 26 (26.0%) patients, anterolateral MI in 19 (19.0%) patients, inferolateral MI in 14 (14.0%) patients, and Antero septal MI in 15 (15.0%) patients. In contrast to our study, Kamal et al and Joseph et al reported their findings on patients with anterior and inferior wall STEMI only (228, 229). In our study, the most common risk factor discovered in 35% of patients was hypertension, which was followed by smoking (33%), diabetes (22%), and dyslipidemia (19%). Contrary to our research, Joseph et al. (229) found that the top four risk factors for diabetes mellitus, each accounting for 39.8% of cases, were smoking, hypertension, and dyslipidemia. According to the INTERHEART-South Asia study, abnormal lipids, smoking, hypertension, diabetes, abdominal obesity, psychosocial factors, low fruit and vegetable consumption, and inactivity are the eight coronary risk factors that account for 89% of all acute MI cases in Indians (106, 230). In contrast to our findings and in agreement with Joseph et al., Kiani et al. found that the most common risk factors were hypertension, hyperlipidemia, and diabetes mellitus (229, 231). In a separate cross-sectional study with 100 STEMI patients conducted in India, diabetes (33%), hypertension (40%), and smoking (30%) were discovered to be the most common risk factors (232). The high frequency of concurrent risk factors in Indian CAD patients may be the cause of STEMI manifestation at a young age. Our study showed that there was no statistically significant difference in risk factors (HTN, DM, dyslipidemia, smoking, and family history) between patients with different types of STEMI. Similar to our findings, Kamal et al reported that there was no statistically significant difference in risk factors between patients with anterior or inferior STEMI (228). Fiol et al reported no difference among risk factors as well (233). Regarding the laboratory data of the studied patients, the average value of Hb was 13.07±1.24, for PLT was 215.78±53.42, for WBCs was 6.16±1.28, for S.cr was 0.969±0.18, for AST was 19.53±4.28, for ALT was 22.60±7.83, for TC was 195.07±27.21, for TGS was 140.88±22.49, for LDL was 117.29±8.72, and for HDL was 49.39±6.54. The troponin level was normal in 34 (34.0%) patients and was elevated in 66 (66.0%) patients. There was no significant difference in laboratory investigations (Hb, PLT, WBCs, S.cr, AST, ALT, TC, TGS, LDL, HDL, and troponin) between patients with different types of STEMI. Contrary to our results kamal et al reported the creatine kinase, creatine kinase-myoglobin, and troponin values only of the RCA and LCX patients. Contrast to our finding‘s troponin levels were elevated in all participants while in our study troponin was elevated in 66% only. Similar to our findings there was no statistically significant difference between ECG findings and the laboratory investigations in kamal et al findings(228). Our study showed that ECG findings in different types of myocardial infarctions are significant predictors of culprit artery defined by angiogram. This is consistent with Kamal et al as this study reported that there was a statistically significant relation found in the analysis of the relation between the ECG criteria and the angiographic findings in the four different group (228). Regarding relation between culprit artery and the location of STEMI, our study showed the following: LAD culprit lesion by angiogram was significantly higher in patients with anterior MI compared to inferior, anterolateral, and inferolateral MI, and was significantly higher in anteroseptal MI compared to inferior and inferolateral MI, and was significantly higher in inferolateral and anterolateral MI compared to inferior MI. RCA culprit lesion by angiogram was significantly higher in patients with inferior and inferolateral MI compared to patients with anterior, anterolateral and anteroseptal MI. RCA culprit lesion by angiogram was significantly higher in patients with anterolateral MI compared to patients with anterior MI. RCA was more common than LCX in inferior STEMI. Similar to our study, Kamal et al, Chia et al and Herz et al reported that the RCA is more common that LCX in patients with inferior STEMI (228, 234, 235). Similar to our study, Gaude et al (236) reported that LAD is the most common culprit artery in anterior wall STEMI. This was consistent with Engelen et al (237), and Ghosh et al (238) Regarding inferior wall STEMI, Gaude et al (236) reported that the culprit artery can be RCA or LCX as observed by our findings as well. This is in accordance with Gupta et al, Kosuge et al and Verouden et al (239-241). Regarding the relation between ejection fraction and location of STEMI, our study showed that EF was significantly lower in patients with inferolateral MI compared to patients with anterior, inferior, anterolateral, and anteroseptal MI. There was no significant difference in EF between patients with anterior, inferior, anterolateral, and anteroseptal MI. Different to our findings, as study carried out by Kiron et al showed that patients with anterior MI had a statistically significant lower LVEF than those with inferior and inferoposterior MI (39.3% vs. 48.6% vs. 47.6%, P = 0.04) (242). Donmez et al also reported significant lower ejection fraction in anterior STEMI compared to inferior STEMI which is similar to Kiron et al but different from our findings (243). Regarding the accuracy of different ECG findings to predict culprit artery defined by angiogram our study reported the following: ECG findings in different types of myocardial infarctions are significant predictors of culprit artery defined by angiogram. The ECG findings of LAD were significant predictors of LAD culprit artery by angiogram (AUC: 0.898, p <0.001). It had a sensitivity of 92.45%, specificity of 87.23%, PPV of 89.1% and NPV of 91.1%. The ECG findings of RCA were significant predictors of RCA culprit artery by angiogram (AUC: 0.852, p <0.001). It had a sensitivity of 73.3%, specificity of 97.1%, PPV of 91.7% and NPV of 89.5%. The ECG findings of LCx were significant predictors of LCx culprit artery by angiogram (AUC: 0.728, p <0.001). It had a sensitivity of 58.8%, specificity of 86.7%, PPV of 47.6% and NPV of 91.1%. Kamal et al reported the following: group A (anterior STEMI) the sensitivity of the ECG criteria in predicting the culprit artery was 76.92% and its specificity was 100%, with 100% PPV and 92.5% NPV. However, in group B (inferior STEMI), the sensitivity and specificity of the ECG criteria in predicting the culprit artery were 100 and 76.92%, respectively, with 92.5% PPV and 100% NPV (228). Ghosh et al reported that LAD artery prediction had sensitivity of 100%, 90.91% specificity, 100%PPV and 90.91 NPV. All these values are greater than those reported by our study except for the NPV (238). Regarding RCA, Ghosh et al reported 100% sensitivity, 91.67% specificity, 90% PPV and 100% NPV. Compared to our findings, sensitivity and NPV are greater than our findings while PPV and specificity are lower (238). Ghosh et al reported Sensitivity of LCX to be 0%, 100% specificity, no PPV and 90.48% NPV. Specificity is the only measured value to be higher than our findings (238).