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ORIGINAL ARTICLE |
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Year : 2018 | Volume
: 6
| Issue : 4 | Page : 115-122 |
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Study of coronary angiographic correlation with electrocardiography in patients of acute coronary syndrome-ST-elevation myocardial infarction
Rohit Prabha Gaude1, Deepak Kumar Gautam1, Dharmendra Jain2, Gyan Prakash Singh3, Pritam Das1, Ashis Kumar Choudhury1, Sankha Shubhra Chakrabarti1, Kailash Kumar1, Indrajeet Singh Gambhir4
1 Department of General Medicine, Institute of Medical Sciences, BHU, Varanasi, Uttar Pradesh, India 2 Department of Cardiology, Institute of Medical Sciences, BHU, Varanasi, Uttar Pradesh, India 3 Department of Statistics, Institute of Science, BHU, Varanasi, Uttar Pradesh, India 4 Department of General Medicine (MD) and Former Head of Division of Geriatric Medicine, Institute of Medical Sciences, BHU, Varanasi, Uttar Pradesh, India
Date of Web Publication | 17-Dec-2018 |
Correspondence Address: Dr. Deepak Kumar Gautam Institute of Medical Sciences, BHU, Varanasi, Uttar Pradesh India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/heartindia.heartindia_41_18
Background: Abnormalities in the 12-lead electrocardiography (ECG) are often used to localize the anatomic site of myocardial infarction (MI) and ischemia in patients with coronary artery disease. The same ECG findings are often assumed to correlate with anatomy of coronary arteries as well as the site of occlusion. Unfortunately, there is only limited documentation for correlation between the location of coronary artery occlusion and the finding of Q-waves during MI, thus tending to compromise the predictive value of ECG. Aims and Objectives: The objective of this study is to correlate the accuracy of ECG in localization of culprit coronary vessels involved in acute coronary syndrome-ST-elevation myocardial infarction (ACS-STEMI) and to combine various ECG criteria for localization of culprit vessel and the occlusion site to assess the diagnostic accuracy of ECG as compared to coronary angiographic findings. Materials and Methods: ECGs of patients with MI events, symptomatic or silent, were analyzed for STEMI or non-STEMI. One hundred patients with STEMI satisfying the inclusion and exclusion criteria were included as participants for the study. Coronary angiography was done after an event of acute MI or within 3 months after an event. ECG changes in various leads were used to localize the vessel involved and were correlated with dominant vessel involved in coronary angiography in development of MI. ECG criteria were used to localize the vessel involved. The statistical analysis was done using SPSS for windows version 16.0 software. Results and conclusions: We found that anterior wall myocardial infarction was more common than inferior wall myocardial infarction. Incidence of MI correlated positively with age. Acute MI was more common in males than females. Diabetes was more common risk factor for acute MI. ECG criteria utilized in our study were found to have high sensitivity and specificity, when combined together, in localizing culprit vessel in ACS-STEMI in left anterior descending artery, right coronary artery, and left circumflex coronary artery and this is in accordance with the studies conducted in other populations.
Keywords: Coronary angiography, correlation, electrocardiography, localization, predictive value, sensitivity, specificity, ST-elevation myocardial infarction
How to cite this article: Gaude RP, Gautam DK, Jain D, Singh GP, Das P, Choudhury AK, Chakrabarti SS, Kumar K, Gambhir IS. Study of coronary angiographic correlation with electrocardiography in patients of acute coronary syndrome-ST-elevation myocardial infarction. Heart India 2018;6:115-22 |
How to cite this URL: Gaude RP, Gautam DK, Jain D, Singh GP, Das P, Choudhury AK, Chakrabarti SS, Kumar K, Gambhir IS. Study of coronary angiographic correlation with electrocardiography in patients of acute coronary syndrome-ST-elevation myocardial infarction. Heart India [serial online] 2018 [cited 2023 May 31];6:115-22. Available from: https://www.heartindia.net/text.asp?2018/6/4/115/247576 |
Introduction | |  |
Abnormalities in the 12-lead electrocardiography (ECG) are often used to localize the anatomic site of myocardial infarction and ischemia in patients with coronary artery disease. This practice is based largely on autopsy series correlating the site of myocardial infarction with the location of Q-waves on ante-mortem ECGs. Q-waves in the precordial Leads V1–V4 appear to reflect anterior wall infarction; in Leads II, III, and aVF inferior wall infarction; and in Leads I, aVL, V5, and V6 lateral wall infarction. The same ECG findings are often assumed to correlate with coronary artery anatomy as well. Anterior wall infarction is usually attributed to disease of the left anterior descending (LAD) coronary artery. Inferior wall infarction is attributed to disease of the right coronary artery (RCA) except in patients with left-dominant systems and lateral wall infarction in whom it is due to disease of the left circumflex (LCX) coronary artery. Unfortunately, there is only limited documentation for these correlations between the location of coronary artery narrowing or occlusions and the findings of Q-waves during myocardial infarction. Studies are often confounded by the inclusion of patients with multi-vessel coronary artery disease, which makes it difficult to determine that the symptoms are due to which vascular distribution. Nonetheless, patients who develop ST depression (STD) in Leads II, III, and aVF during angina are commonly referred to as having “inferior wall ischemia” and are often presumed to have RCA disease. Similar associations are often drawn between STD in anterior precordial leads and LAD artery disease and between STD in so-called lateral Leads I and aVL and LCX disease.
Aims and objectives
- To correlate the accuracy of ECG in localization of culprit coronary vessels involved in acute coronary syndrome ST-elevation myocardial infarction (STEMI)
- To combine various ECG criteria for localization of culprit vessel and the occlusion site and to assess its diagnostic accuracy as compared to coronary angiographic findings.
Materials and Methods | |  |
Sample size
One hundred patients with STEMI satisfying inclusion and exclusion criteria were included as participants for this study.
Population on which study conducted
The study was conducted on patients visiting Cardiology Outpatient Department (OPD) or Inpatient Department (IPD) and General Medicine OPD or IPD of Sir Sunderlal Hospital, BHU, Varanasi, India, during June 2017 to July 2018. The newly diagnosed patients of acute coronary syndrome with ST elevation (STE) in their ECG were included in the study. Written and informed consent was taken. Patients were subjected to detailed clinical examination. ECG of these patients was taken, and on the basis of ECG, patients were differentiated into STEMI and non-STEMI. The coronary angiographic study of patients with STEMI was analyzed.
Patients satisfying the following inclusion criteria were included in the study.
Inclusion criteria
- Newly diagnosed patients
- Chest pain lasting more than 30 min or patients having symptoms of angina equivalents accompanied by ST-segment elevation
- Patients with confirmed enzymatic changes
- Patients suitable for angiography having no contraindications to the administration of iodinated contrast
- Patients without implanted pacemakers or valve prostheses.
Exclusion criteria
- Those with evolving MI defined by established pathological Q-waves
- Patients with signs of reperfusion by negative or biphasic T-waves were excluded
- Previous angioplasty of coronary vessels
- Prior coronary artery bypass graft surgery
- Presence of right or left bundle branch block
- Left ventricular hypertrophy
- Patients with severe valvular heart disease other than ischemic mitral regurgitation and congenital cardiac anomaly
- Patients with implanted pacemakers or valve prostheses.
Details of procedures and methods used
ECGs of patients with MI events, symptomatic or silent, were taken and analyzed whether STEMI or NSTEMI. Only the STEMI patients fulfilling inclusion criteria were included in the study. These patients were evaluated for risk factors such as diabetes, hypertension, smoking, and other addictions. Percentage of association was seen with risk factors in the development of STEMI. Coronary angiography was done after event of acute myocardial infarction or within 3 months after an event. ECG changes in various leads were used to localize the vessel involved and were correlated with dominant vessel involved in coronary angiography in development of MI. ECG criteria were used to localize the vessel involved [Table 1], [Table 2], [Table 3]. | Table 1: Electrocardiography criteria to identify site of occlusion in left anterior descending (in anterior wall myocardial infarction)
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 | Table 2: Electrocardiography criteria to identify whether site of occlusion is in right coronary artery or left circumflex (in inferior wall myocardial infarction)
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 | Table 3: Electrocardiography criteria for site of occlusion in right coronary artery
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In inferior wall myocardial infarction (IWMI), several ECG criteria identify RCA or LCX as the artery containing the culprit lesion. Each of these criteria is based on one of two anatomic facts.
Patients were divided into three groups, namely Groups I, II, and III according to the localization of occlusion site in LAD, RCA, and LCX coronary arteries, respectively. Group I was further divided into four subgroups: Ia, Ib, Ic, and Id according to whether occlusion in LAD was proximal to S1, LAD proximal to D1, LAD distal to S1, and LAD distal to D1.
Group II was further divided into two subgroups: IIa and IIb according to whether occlusion in RCA was proximal or distal to right ventricular (RV) branch, respectively.
Statistical analysis of study
The statistical analysis was done using SPSS for windows version 16.0 software by IBM Inc., Armonk, New York, US. For categorical data, Chi-square, and Fischer's exact test was used. For comparing mean of two groups, Student's t-test and, for comparing median, Mann–Whitney U-test were used. For paired samples, paired t-test and Wilcoxon signed-rank test were applied. One-way analysis of variance test was used to compare differences among group means. The critical value of “P” indicating the probability of significant difference was taken as <0.05 for comparison.
Demographic profile of participants is depicted in the form of graphical representations in [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]. | Figure 3: Distribution of patients with diabetes, hypertension, and obesity in acute myocardial infarction
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 | Figure 4: Distribution of patients with positive family history and addiction in acute myocardial infarction
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 | Figure 5: Distribution of anterior wall myocardial infarction and inferior wall myocardial infarction in acute myocardial infarction
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Results and Discussion | |  |
ECG is one of the most convenient, noninvasive, and inexpensive tools widely available even in rural areas and peripheral health care. It is highly sensitive for detecting acute myocardial infarction. Majority of ECG changes correlate well with coronary angiographic lesions in accordance with basic physiology and the principles of ECG. However, there can be false-positive and false-negative ECG findings due to wrong placement of leads, limb movements, hairy chest, and lack of electrolyte gel between electrode and skin and in conditions of severe dyselectrolytemia causing muscle twitching and fasciculation including motor neuron disease. In addition, there can be ST-T changes due to nonischemic conditions such as acute pericarditis and subarachnoid hemorrhage. Apart from these modifiable factors, noncorrelation between ECG and coronary angiography is also due to anatomical variation in branching pattern of coronary arteries, and ethnic or racial differences can play a role in it. This study was planned in North Indian population to study and re-establish sensitivity and specificity of ECG with coronary angiography in cases of STEMI.
In this study, it was found that in cases of anterior wall myocardial infarction (AWMI), the occlusion is in the LAD coronary artery which is in accordance with the study conducted by Engelen et al.,[1] Ghosh et al.,[2] and Gorgels et al.[3] With IWMI, occlusion can be either in the RCA or the LCX coronary artery, and this is in accordance with a study conducted by Gupta et al.,[4] Kosuge et al.,[5] Verouden et al.,[6] and Ghosh et al.[2] In AWMI, ST-segment elevation in precordial leads (mainly V1, V2, V3, and V4) indicates occlusion of the LAD coronary artery. ST-segment elevation in precordial leads (mainly V1, V2, V3, and V4) and in Lead aVL in association with ST-segment depression of >1 mm in Leads II, III, and aVF indicates occlusion of the LAD artery proximal to first septal branch and first diagonal branch. In this case, the ST-segment vector is directed upward, toward Leads V1, V2, V3, V4, aVL, and aVR and away from the inferior leads. Hence, ST-segment elevation is present in leads V1, V2, V3, and V4, aVL, aVR, and ST-segment depression in inferior leads, i.e., Lead II, Lead III, and Lead aVF. ST-segment elevation in Leads V1, V2, V3, V4 with absence of ST-segment depression in inferior leads, i.e., Lead II, Lead III, and Lead aVF suggests occlusion of the LAD artery distal to first septal branch and first diagonal branch.
According to a study conducted by Verouden et al.,[6] the myocardial distribution of the RCA is slightly rightward in the frontal plane, and consequently, the current of injury resulting from its occlusion will be reflected more in Lead III than in Lead II and STD will be more in Lead aVL than in Lead I. Similarly, the distribution of the LCX is slightly leftward in the frontal plane, and the current of injury from its closure will be seen more in Lead II than in Lead III. As per a study conducted by Bairey et al.,[7] an injury vector leftward causing ST-segment elevation in Lead I is common with LCX occlusion but rare with RCA occlusion.
Mortality and morbidity in part are determined by the location of the occlusion. For example, in patients with inferior wall MI who have RV infarction, the culprit artery virtually always is the RCA. Such patients, including those in whom ECG evidence of RV MI is masked, are at increased risk of death, shock, and arrhythmias, including atrioventricular block. Thus, identifying the culprit artery in acute IWMI helps define those in whom aggressive reperfusion strategies are likely to yield the most benefit. Coronary angiography is the best means of determining the culprit artery in acute IWMI. When both the RCA and LCX are severely diseased, however, deciding which one is the culprit can be difficult and having an independent predictor of the culprit artery such as the ECG can be very helpful.
In a study conducted by Engelen et al.[1] entitled “Value of the ECG in localizing the occlusion site in the LAD coronary artery in acute anterior myocardial infarction,” published in the Journal of the American College of Cardiology in August 1999, the following results were obtained [Table 4], [Table 5], [Table 6], [Table 7]. | Table 4: Predictors of left anterior descending occlusion proximal to S1
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 | Table 5: Predictors of left anterior descending occlusion proximal to D1
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Electrocardiographic predictors of LAD coronary artery occlusion proximal to the first septal perforator (S1) and/or the first diagonal branch (D1) are shown in [Table 4] and [Table 5].
Electrocardiographic predictors of LAD artery occlusion distal to S1 and/or D1 are shown in [Table 6] and [Table 7].
In our study, to diagnose a lesion proximal to S1, we used ECG criteria – STE in aVR and STD in Lead II >1 mm – which had sensitivity, specificity, positive predictive accuracy (PPA), and negative predictive accuracy (NPA) of 43%, 95%, 86%, and 70% and 36%, 100%, 100%, and 68%, respectively, according to Engelen et al.[1] study. We found ECG criteria – STE in aVR and STD in Lead II >1 mm to diagnose lesion in LAD proximal to S1 – which had sensitivity, specificity, PPA, and NPA of 50%, 77%, 45%, and 87.3% and 33%, 60%, 5.1%, and 93.4%, respectively. Specificity and NPA of our study were similar to a study done by Gorgels et al.[8] published in the Journal of the American College of Cardiology in 2001 but sensitivity and PPA were low.
In our study, to diagnose lesion proximal to D1, we used STD in Lead II >1 mm to diagnose lesion in LAD proximal to D1 which had sensitivity, specificity, PPA, and NPA of 34%, 98%, 93%, and 68%, respectively, according to Engelen et al.[1] study. In our study, we found ECG criteria – STD in Lead II >1 mm – which had sensitivity, specificity, PPA, and NPA of 57.1%, 68.3%, 10.25%, and 95.08%, respectively. Sensitivity and specificity in these two studies varied widely, one of the reasons being – only ten patients had coronary angiography showing occlusion in LAD proximal to D1.
In our study, to diagnose lesion distal to S1, we used ECG criteria – absence of STD in Lead III and Q-wave in V5 – which had sensitivity, specificity, PPA, and NPA of 34%, 86%, 77%, and 49% and 24%, 93%, 82%, and 47%, respectively, according to Engelen et al.[1] study. We found ECG criteria – absence of STD in Lead III and Q-wave in V5 – which had sensitivity, specificity, PPA, and NPA of 57%, 81%, 19%, and 96% and 50%, 95%, 42%, and 96%, respectively. Sensitivity, specificity, PPA, and NPA varied in these two studies.
In our study, to diagnose lesion distal to D1, we used ECG criteria – absence of STD in Lead III and STD in aVL – which had sensitivity, specificity, PPA, and NPA of 41%, 95%, 92%, and 53% and 22%, 95%, 87%, and 46%, respectively, according to Engelen et al.[1] study. We found ECG criteria – absence of STD in Lead III and STD in aVL – which had sensitivity, specificity, PPA, and NPA of 50%, 82.2%, 23.8%, and 93.6% and 40%, 61.1%, 10.25%, and 90.1%, respectively. Sensitivity, specificity, PPA, and NPA varied in two studies. Most likely reason for variability in results could be ethnicity and racial differences. Engelen et al.[1] study was conducted in American population whereas our study was conducted in Indian population. There could be anatomic variation in branching pattern of left main coronary artery in two populations.
In a study conducted by Gupta et al. entitled “Electrocardiographic differentiation between right coronary and LCX coronary arterial occlusion in isolated IWMI” published in Indian Heart Journal in July 1999, with the objective to study ST-segment elevation in Leads II and III, in order to differentiate between RCA and LCX coronary artery with inferior myocardial infarction who subsequently underwent coronary angiography, results showed that ST-segment elevation was greater in Lead III than in Lead II when the RCA was the culprit vessel and vice versa when the LCX was the culprit vessel (P < 0.001). ST-segment elevation in Lead III was higher than in Lead II with a sensitivity of 99% and a specificity of 100% for diagnosing RCA as the culprit vessel. ST-segment elevation in Lead II was higher than in Lead III with a sensitivity of 93% and a specificity of 100% in identifying the LCX as the culprit vessel. In our study, we found ECG criteria – STE in Lead III > STE in Lead II for diagnosing RCA – which had sensitivity and specificity of 100% and 98.6%, respectively. Similarly, ECG criteria – STE in Lead II > STE in Lead III for diagnosing LCX artery – had sensitivity and specificity of 100%. Our study agreed with results of Gupta et al.[4]
In a study conducted by Kosuge et al.,[5] entitled “New electrocardiographic criteria for predicting the site of coronary artery occlusion in inferior wall acute myocardial infarction” published in December 1998 in American Journal of Cardiology, standard 12-lead ECGs were used to identify the site of coronary artery occlusion i.e., a site proximal to the origin of the RV branch of the RCA, a site distal to the origin of the RV branch of the RCA, or a site in the LCX. The ratio of STD in Lead V3 to STE in Lead III (V3/III ratio) was evaluated. Results of the study were following: V3/III ratio <0.5 identified proximal RCA occlusion, 0.5<V3/III ratio < or = 1.2 identified distal RCA occlusion and 1.2<V3/III ratio identified LCX occlusion with sensitivities of 91%, 84%, and 84%, and specificities of 91%, 93%, and 95%, respectively. In our study we found that, V3/III ratio <0.5 identified proximal RCA occlusion, 0.5 <V3/III ratio < or = 1.2 identified distal RCA occlusion, and 1.2<V3/III ratio identified LCX occlusion with sensitivities of 100%, 100%, 100% and specificities of 95%, 95%, 100% respectively. Our study agreed with the results of Kosuge et al.[5]
A study was conducted by Verouden et al. entitled “Distinguishing the RCA from the LCX coronary artery as the infarct-related artery in patients undergoing primary percutaneous coronary intervention for acute inferior myocardial infarction” was published in August 2009 in EP Europace. The objective of this study was to investigate the diagnostic accuracy of ECG criteria – STE in Lead III > STE in Lead II for identification of lesion in RCA. This ECG criteria in localizing RCA had sensitivity of 70% and specificity of 72%. We found that this ECG criterion has sensitivity and specificity both of 100%, which were higher than that found in the study by Verouden et al.[6]
In a study by Ghosh et al.[2] entitled “ECG-a simple noninvasive tool to localize culprit vessel occlusion site in acute STEMI” published in Indian Journal of Clinical Practice in March 2013. In this study, combination of ECG criteria was used to localize LAD territory. Results of this study are given in [Table 8]. | Table 8: Correlation of electrocardiography criteria with coronary angiography
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In our study, we found the results [Table 9] which were similar to the one mentioned above. | Table 9: Correlation of electrocardiography criteria with coronary angiography
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Limitations of this study
The present study has two major limitations. Its sample size is small and coronary angiography was not done immediately on presentation but at a later date. It may be sometimes difficult to attribute a lesion as culprit lesion if angiography is done later in the course after thrombolytic therapy has been given or if multivessel disease is present.
Conclusions | |  |
- Sixty-three percent (n = 63) patients had anterior wall MI; 37% (n = 37) patients had inferior wall MI
- Incidence of MI correlated positively with age
- Most of the patients were male (n = 82) as compared to female (n = 18). In our setting, male: female disparity is commonly seen for most disease conditions suggesting a gender bias in health-care-seeking behavior of population
- Forty-nine percent (n = 49) had diabetes, 44% (n = 44) had hypertension and 30% (n = 30) patients were obese
- Twenty-four percent (n = 24) were smoker and 42% (n = 42) had family history of similar illness
- Eighty-eight percent (n = 88) presented with chest pain and 41% (n = 41) with breathlessness
- Sensitivity, specificity, PPA and NPA of ECG in localizing culprit vessel in IWMI involving RCA is 100%, 98%, 96.5% and 100%, respectively
- Sensitivity, specificity, PPA and NPA of ECG in localizing culprit vessel in AWMI involving LAD artery is 100%, 98%, 98.41% and 100%, respectively
- Sensitivity, specificity, PPA and NPA of ECG in localizing culprit vessel in IWMI involving LCX is 100%
- Sensitivity, specificity, PPA and NPA of ECG in localizing culprit vessel in IWMI involving distal RCA is 100%
- Sensitivity, specificity, PPA and NPA of ECG in localizing culprit vessel in IWMI involving proximal RCA is 100%, 95%, 83.3% and 100%, respectively
- Sensitivity, specificity, PPA and NPA of ECG in localizing culprit vessel in AWMI involving LAD distal to D1 artery is 70%, 90%, 43.7% and 96.4%, respectively
- Sensitivity, specificity, PPA and NPA of ECG in localizing culprit vessel in AWMI involving LAD distal to S1 artery is 66%, 96%, 43.7% and 96.4%, respectively
- Sensitivity, specificity, PPA and NPA of ECG in localizing culprit vessel in AWMI involving LAD proximal to S1 artery is 76%, 75%, 45.7% and 92.3%, respectively
- Sensitivity, specificity, PPA and NPA of ECG in localizing culprit vessel in AWMI involving LAD proximal to D1 artery is 0%, 96.6%, 0% and 89.6%, respectively
- Sensitivity, specificity, PPA and NPA of ECG criteria – STD in Lead II for AWMI involving LAD proximal to S1 artery – is 33%, 60%, 5.1% and 93.4%, respectively
- Sensitivity, specificity, PPA and NPA of ECG criteria – STE in Lead aVR for AWMI involving LAD proximal to S1 artery – is 50%, 77%, 45% and 87.3%, respectively
- Sensitivity, specificity, PPA and NPA of ECG criteria – STD in Lead II for AWMI involving LAD proximal to D1 artery – is 57.1%, 62.3%, 10.25% and 95.08%, respectively
- Sensitivity, specificity, PPA and NPA of ECG criteria – absence of STD in Lead III and STD in aVL for AWMI involving LAD distal to D1 artery – is 50%, 82.2%, 23.8% and 93.67%, respectively
- Sensitivity, specificity, PPA and NPA of ECG criteria – STD in aVL for AWMI involving LAD distal to D1 artery – is 40%, 61.1%, 10.25% and 90.16%, respectively
- Sensitivity, specificity, PPA and NPA of ECG criteria – absence of STD in Lead III for AWMI involving LAD distal to S1 artery – is 57.1%, 81.7%, 19.04% and 96.2%, respectively
- Sensitivity, specificity, PPA and NPA of ECG criteria – Q-wave in Lead V5 for AWMI involving LAD distal to S1 artery – is 50%, 95.7%, 42.8% and 96.7%, respectively
- Sensitivity, specificity, PPA and NPA of ECG criteria – STE in Lead III > STE in Lead II for IWMI involving proximal RCA – is 100%, 98.6%, 96.5% and 100%, respectively
- Sensitivity, specificity, PPA and NPA of ECG criteria – STE in Lead II > STE in Lead III for IWMI involving LCX coronary artery – is 100%
- Sensitivity, specificity, PPA and NPA of ECG criteria – ratio of STD in Lead V3 to STE in Lead III ≤ 0.5 for IWMI involving proximal RCA – is 100%, 95.0%, 83.3% and 100%, respectively
- Sensitivity, specificity, PPA and NPA of ECG criteria – ratio of STD in Lead V3 to STE in Lead III = 0.5–1.2 for IWMI involving distal RCA – is 100%, 95%, 100% and 100%, respectively
- Sensitivity, specificity, PPA, and NPA of ECG criteria – ratio of STD in Lead V3 to STE in Lead III >1.2 for IWMI involving LCX coronary artery – is 100%.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Engelen DJ, Gorgels AP, Cheriex EC, De Muinck ED, Ophuis AJ, Dassen WR, et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol 1999;34:389-95. |
2. | Ghosh B, Indurkar M, Jain MK. ECG: A simple noninvasive tool to localize culprit vessel occlusion site in acute STEMI. Indian J Clin Pract 2013;23:590-5. |
3. | Gorgels AP, Engelen DJ, Wellens HJ. The electrocardiogram in acute myocardial infarction. In: Fuster V, Alexander RW, O'Rourke RA, editors. Hurst's The Heart. 11 th ed. New York: McGraw-Hill; 2004. p. 1351-60. |
4. | Gupta A, Lokhandwala YY, Kerkar PG, Vora AM. Electrocardiographic differentiation between right coronary and left circumflex coronary arterial occlusion in isolated inferior wall myocardial infarction. Indian Heart J 1999;51:281-4. |
5. | Kosuge M, Kimura K, Ishikawa T, Hongo Y, Mochida Y, Sugiyama M, et al. New electrocardiographic criteria for predicting the site of coronary artery occlusion in inferior wall acute myocardial infarction. Am J Cardiol 1998;82:1318-22. |
6. | Verouden NJ, Barwari K, Koch KT, Henriques JP, Baan J, van der Schaaf RJ, et al. Distinguishing the right coronary artery from the left circumflex coronary artery as the infarct-related artery in patients undergoing primary percutaneous coronary intervention for acute inferior myocardial infarction. Europace 2009;11:1517-21. |
7. | Bairey CN, Shah PK, Lew AS, Hulse S. Electrocardiographic differentiation of occlusion of the left circumflex versus the right coronary artery as a cause of inferior acute myocardial infarction. Am J Cardiol 1987;60:456-9. |
8. | Gorgels AP, Engelen DJ, Wellens HJ. Lead aVR, a mostly ignored but very valuable lead in clinical electrocardiography. J Am Coll Cardiol 2001;38:1355-6. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9]
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