Correlation of Surface Ecg and 2d-Echo to Locate the Site of Infarction and Left Ventricular Ejection Fraction in Myocardial infarction
Dr. Lokesh Beerakayala*1, Dr Bakkuri Priyanka2
*Correspondence to: Dr. Lokesh Beerakayala, MD General Medicine, Hyderabad.
Copyright
© 2024 Dr. Lokesh Beerakayala. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received:17 February 2024
Published: 01 March 2024
Introduction
Cardiovascular diseases comprise the most prevalent serious disorders in industrialized nations and are a rapidly growing problem in developing nations. Cardiovascular diseases remain the most common causes of death, responsible for 35% of all deaths, almost 1 million deaths each year. Approximately one-fourth of these deaths are sudden.(1)
In addition, cardiovascular diseases are highly prevalent, diagnosed in 80 million adults, or ~35% of the adult population. The growing prevalence of obesity, type 2 diabetes mellitus, and metabolic syndrome ,which are important risk factors for atherosclerosis, now threatens to reverse the progress that has been made in the age-adjusted reduction in the mortality rate of coronary heart disease.(1)
Acute myocardial infarction (AMI) is one of the most common diagnosis in hospitalized patients in the industrialized countries, which is a serious complication of atherosclerotic coronary heart disease.
In most patients (80-95%) it results from thrombotic occlusion of the related vessel resulting in infarct. Myocardial ischemia and necrosis set in within about 20-40 minutes. This occurs as a wavefront starting from the sub-endocardial region and progressing to the sub epicardial region. The entire process usually takes 6 hours to complete.
Therefore any intervention for limiting infarct size should be initiated in this time window of 6 hours.(2)
It is observed that various risk factors such as age, male sex, smoking, obesity, hyperlipidemia, diabetes mellitus, hypertension, family history of IHD, type A personality, play a role in the occurrence of myocardial infarction.
Various methods such as QRS scoring index by electrocardiogram(ECG) & left ventricular ejection fraction (LVEF) and wall motion abnormality by 2 dimensional echocardiography (2D-Echo) help in diagnosis and prognostification of myocardial infarction.
These investigations are non invasive and can be done at less advanced centres. Hence, this study is undertaken to correlate the site of infarction and LVEF by ECG and 2D Echo and also to assess the severity and prognosis of myocardial infarction.
Materials And Methods
Place Of Study : Intensive Cardiac Care Unit(ICCU) Osmania General Hospital, Tertiary care hospital,Hyderabad
Collaborative Department : Cardiology
Study Design: Random control hospital based study
Study Sample: 100 Patients
Ethical committee clearance: Approved
Period Of Study : November 2016 to May 2018
Methodology
SOURCE OF DATA: Patients admitted in ICCU of Osmania General Hospital,Tertiary care hospital, Hyderabad who satisfy the inclusion criteria.
METHOD OF COLLECTION OF DATA: The study was conducted for a period of 18 months, from November 2016 to May 2018 in a 100 randomly selected patients. Data is collected by taking a detailed history from the patients (as per the proforma) particularly keeping the following points in view.
a) Time of onset of typical chest pain, nature of pain, radiating, increasing with exertion, not relieved by rest and associated symptoms like excessive sweating, vomiting, breathlessness, diarrhoea, giddiness, fatigue and abdominal pain. history of smoking, alcohol consumption, hypertension, diabetes mellitus, obesity according to BMI, personality type and family history of IHD
b)A thorough clinical examination was carried out in each case with special reference to pulse, BP, CVS and respiratory examination for the presence of any cardiac enlargement, S3 gallop, rub, murmur and basal crepitations in the lungs.
c) Investigations like fasting lipid profile & enzymes like CKMB and SGOT were done. (Serums LDL was calculated by Fried-Walds formula i.e., LDL = total cholesterol – [HDL + (TG/5)].
d) ECG is taken at the time of admission for the ECG diagnosis of myocardial infarction, the criteria consisting of ST segment elevation of ≥ 2mm, 0.08 second from J point in ≥2 related electric fields, with typical evolutionary changes or presence of new pathological Q waves.
Further patients were classified into subgroups.
i)Inferior wall myocardial infarction.
ii) Anterior wall myocardial infarction. iii)Global myocardial infarction.
e) Continuous cardiac monitoring was done and patients were treated with generally accepted methods of coronary care unit.
f) As soon as feasible, a 2D-Echo was performed by means of commercially available mechanical sector scanner. With the patient in left lateral decubitus position, multiple parasternal long axis views, short axis and apical views were taken to study regional wall motion abnormalities and for estimation of LVEF in all 100 patients of AMI.
g) ECG was recorded on a standard ECG machine at a paper speed of 25 mm/sec.
Artifactual recordings were eliminated. ECG showing the presence of first Q wave in post MI were taken and the day of evolution of Q waves noted.
From such a reading the EF was estimated using the QRS scoring of Palmeri and Wagner etal as indicated in the table . The scoring is based primarily on the duration of the ‘Q’ and ‘R’ waves on a 12 – lead ECG and secondarily on the magnitude of the R/Q and R/S with a maximum of 29 points possible.
Left ventricular Ejection Fraction (LVEF) has been estimated from the QRS score by means of the formula.
LVEF (%) = 60 – (3 x QRS score)
Echocardiographic correlation was obtained on the same day of ECG QRS scoring by direct estimation of Ejection Fraction in ‘Q’ wave infarction.
Example 1:
Example 2
Inclusion Criteria:
Patients above 25 years of age and WHO criteria for the diagnosis of acute MI are included
a)A history of ischemic type of chest pain
b)Evolutionary changes on serially obtained ECG tracings and
c)A rise and fall in serum cardiac markers.
Exclusion Criteria:
a)Patients above the age of 70 yrs were not considered for the study.
b)Patients presenting with:
Previous history of MI
•Subendocardial infarction, true posterior wall infarction.
• LVH, hemi-block, bundle branch blocks, intraventricular conduction defects and complete heart blocks.
•Valvular heart disease
•Cardiomyopathy
•Pericardial diseases
•Congenital heart disease
•Previous cardiac surgeries were excluded from the study
STATISTICAL ANALYSIS
The study involved 100 patients in the Department of Cardiology, Osmania General Hospital, Hyderabad. The data was collected, compiled and compared statistically by frequency distribution and percentage proportion.
Qualitative data variables were expressed by using frequency and Percentage (%). Quantitative data variables were expressed by using Descriptive statistics (Mean ± SD.).Chi-square (χ2) test was applied to know the statistically significant difference (p value) between different groups. Pearson’s correlation test was used to draw correlations between variables. P-values of < 0.05 were considered significant. Data analysis was performed by using SPSS Version 25.0 (Chicago, SPSS Inc.).
Observations And Results
All Tables(1-16) and Figures (1-17)
Please click here to view all tables and figures
Discussion
The present study was conducted in 100 patients who were selected from the cases admitted in ICCU, Osmania General Hospital, Hyderabad.
Age & Sex: Out of hundred patients studied,age ranging from 30 to 70 years,males were 69(69%) and females were31(31%). The maximum number of cases were noted in 51 – 60 years (37 cases). Less number of cases were noted in less than or equal to 30 years (2cases). The male to female ratio was 2.2:1.
Study conducted by Khanna et al, the mean age was 40 yrs ranging from 30 – 68 yrs. The male to female ratio was 11:2.In another study conducted by Shah et al, the mean age was 54. 4 yrs, male to female ratio was 11.3:1. The maximum number of cases noted in this study were between 51 – 60 yrs.
In Cole & Katz series 83% of cases came within the age group of 40 – 69 yrs.
They reported 25% incidence of infarction in females. The reported finding of male to female ratios was varied from 3.6:1 (Vakil, 1962) to 24:1 (Singh et al. 1977) (185). Our results correlate to these studies.
Symptoms: Malliani study shown that chest pain was the most common symptom and the associated symptom was excessive sweating. In the present study, chest pain is the commonest symptom (89%) & sweating is the most common associated symptom (82%). So there is no much difference between these studies.
Risk Factors: Among risk factors, the present study shows that smoking is the commonest risk factor (66%), followed by type A personality (55%), obesity (42%), family H/o IHD, DM, HTN (10%), hypertension 11%,DM and HTN (11%), hyperlipidemia (46%) and 8% for tobacco chewing.
In Kanitz et al study (186), (1996) showed that the major risk factors were tobacco use (81%), family history of IHD (40%), hypertension (26%), hyperlipidemia (20%) and diabetes was not a risk factor in his study. The study done by Sameer Thanavaro et al (187), found diabetes in 18 % of patients & hypertension 39%.
In another study Chinniah et al., 1979 smoking was seen in 76%, obesity in 25%,family history of IHD in 22%, hyperlipidemia in 32%. So there is no much significant difference noted when all the above studies were compared.
ECG & Echocardiography correlation for site of MI:According to Hegar et al. (188) (1979) echocardiography could evaluate regional asynergy associated with acute myocardial infarction. The location of segmental asynergy corresponded to ECG location of Q waves and pathological location of infarction but the echocardiogram also detected the segmental asynergy in the regions where the ECG showed no evidence of infarction
In our data, as shown in observation in TABLE 12 and TABLE 13, 46 patients out of 100 patients had extensive anterior wall myocardial infarction on ECG. Echocardiography in these patients further elaborated that 1 patients had extensive anterior wall infarction,37 patients had antero-septal and apical wall myocardial infarction, 5 had anterior & apical, 6 had anterior & septal infarction & 4 patient showed no regional wall motion abnormality, thus elaborating the extensive anterior infarction seen on echocardiography in great details.
29 patients, out of 100 patients had inferior wall myocardial infarction and inferior wall with right ventricle infarction on ECG. When echo was done in these patients, 31 patients had inferior wall myocardial infarction, 1 patients had inferior wall and left ventricle infarction,2 patients had global hypokinesia, 3 patients had inferior wall and anterior-septal myocardial infarction and 2 patient showed no regional wall motion abnormality, again giving a more lucid interpretation.
7 patients out of 100 patients had antero-septal infarction on ECG. On echocardiographic examination in these patients,6 patients had antero-septal myocardial infarction, 1 patient had anteroseptal apical infarction, 1patient had antero- septal and interventricular septum infarction & none showed no regional wall motion abnormality, thereby lending credence to the fact that echocardiography delineates ischemic changes more extensively.
6 patients out of 100 patients had antero-inferior wall myocardial infarction on ECG. When echo was done in these patients, 3 patients anteroseptal and apical, 1 each anterior wall and anteroseptal and inferior wall abnormality.
Ejection fraction by ECG & Echocardiographic Correlation: In our correlative study of EF with ECG & echocardiography we found that there was a good correlation in anterior wall MI & in inferior wall MI.
IN GENERAL
ECG showed EF of 47.95% (mean ± 6.59) when compared to EF by echo study which showed 48.23%(mean ± 9.33)
Inferior MI:
Our study has also shown that the index of ejection fraction in inferior wall infarction was better than anterior wall MI. EF by ECG was 54.55 ± 3.82. The EF by echocardiography was 56.25 ± 6.65 in inferior wall myocardial infarction. This correlates well with the study of Khanna et al., who found that left ventricular ejection fraction was better in inferior wall infarction than anterior wall infarction.
In our study out of 68 patients of anterior wall MI 3 patients expired of which 2 patients had low EF & out of 4 cases of global MI 3 cases had low EF in which 2 cases expired due to cardiogenic shock. This correlates well with the study of Nelson et al. In their analysis of mortality of 14 patients who died of shock subsequent to AMI, all patients had low ejection fraction.
Rudwan AW et al. showed that both techniques reflect the magnitude of damage sustained by the myocardium as reflected by the presence of Q wave in case of QRS score or regional wall motion abnormality in case of echo score.
In a study by Tateishi S et al. (1997) the QRS scoring system can be used as a simple & economical method for estimation of infarct size soon after reperfusion.
Barbagelata A. (189) (2004) concluded that in the reperfusion era, a 12-lead ECG provides a simple, economical means of risk stratification at discharge.
In the 45 patients out of 100 whose EF was repeated by QRS scoring system (7-20 days after the 1st ECG) showed a slightly improved EF after the 1st week.
The statistical analysis done on the basis of linear regression curve reveals a fair degree of correlation between ejection fraction as obtained by echocardiography with R2 – 0.716 and p>0.05.
However, better correlative values could not be obtained possibly because of certain limitations.
1) Equipment and techniques used in estimation of ejection fraction.
2) Standardization of ECG.
3) Ideally the ECG used for scoring should have been performed on the same day or nearest possible day as ejection fractions obtain the best correlation.
Summary
1) In the present study males outnumbered females (2.22 :1).
2) Majority of cases was seen in 51 – 60 years.
3) Smoking emerged as the main risk factor in acute myocardial infarction patients.
4) The most common type of myocardial infarction is anterior wall MI.
5) The lesions seen on ECG correlated broadly with those seen on echocardiography. Echo was able to elaborate regional wall motion abnormalities in detail than ECG.
6) LVEF (pump function) can be calculated from ECG at bedside in Q-wave infarction.
7) Can give a fair idea about pump function during the course in ICCU and at discharge.
8) LVEF in anterior wall MI was less compared to inferior wall MI.
9) Anterior & Global MI had lower LVEF.
10) ICCU mortality was 8%.
11) Correlative study of LVEF (pump function) by linear regression scale showed r = 0.84 p > 0.05. This indicates a fair correlation between EF as estimated by ECG & 2D- Echocardiography in MI as well as subgroups of AMI.
12) Hence the, QRS scoring system can be used as a simple and economical method for estimation of infarct size soon after reperfusion.
However, ejection fraction by QRS scoring system cannot be superior to LVEF obtained by echocardiography or even used as a substitute because of following limitation:
a) Cannot estimate infract size directly.
b)Cannot be used in –
- Non Q – wave infract
-Acute MI with conduction disturbance.
c)Scoring system cannot be used to exclude diagnosis of a prior or acute myocardial infarction.
d)Different equipment and techniques used in different institutions may have limitations on the scoring system.
Though the relative inadequacies of this study, relative fair correlation was obtained between ECG QRS scoring and echocardiographic LV pump function. Hence this can be used as an additional method of evaluating left ventricular function in ‘Q’ wave infarction.
Conclusion
•The location of MI seen on ECG correlated broadly with those seen on echocardiography. Echo was able to elaborate regional wall motion abnormalities in detail than ECG.
•LVEF (pump function) can be calculated from ECG at bedside in Q wave infarction, which correlated fairly to 2D-Echo findings.
•Anterior wall MI and Global MI had lower EF when compared to inferior wall MI.
Reference
1)Dennis Kasper, Anthony Fauci, Stephen Hauser, Dan Longo, J. Larry Jameson, Joseph Loscalzo. Harrison's Principles of Internal Medicine, 19e P-1439
2)Siddharth N. Shah. API Text book of Medicine. 7th Edn. Association of Physicians of India; P-441; 2003
3)DJ Weatherall, JGG Ledingham & DA Warrell. Oxford Text Book of Medicine. Vol. II, 3rd Edn, P – 2331; 1996.
4)Braunwald E. (ed) (1997), Heart Disease: A Textbook of Cardiovascular Medicine, Fifth Edition, p. 108, Philadelphia, W.B. Saunders Co
5) Rowbottom M, Ausskind C. Electricity and medicine: history of their interaction. USA: San Francisco Press, Inc; 1984. pp. 31–371.
6)Johansson BW. A history of the electrocardiogram. Dan Medicinhist Arbog. 2001:163–176.
7) Barold SS. Willem Einthoven and the birth of clinical electrocardiography a hundred years ago. Card Electrophysiol Rev. 2003;7:99–104.
8) Wolff L, Parkinson J, White PD. Bundle-branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. Am Heart J. 1930;5:685– 704.
9 )Sethi K K, Dhall A, Chadha D S, et al. WPW and preexcitation syndromes. J Assoc Physicians India. 2007;55:10–15.
10)Kent AFS. The structure of cardiac tissues at the auricular ventricular junction: proceedings of the Physiological Society. J Physiol. 1913;47:17–19.
11)Sethi KK, Dhall A, Chadha DS, et al. WPW and preexcitation syndromes. J Assoc Physicians India. 2007;55:10–15.
12)Armoundas AA, Tomaselli G F, Esperer H D. Pathophysiological basis and clinical application of T-wave alternans. J Am Coll Cardiol. 2002;40:207–217.
13) Adam DR, Powell AO, Gordon H, et al. Ventricular fibrillation and fluctuations in the magnitude of the repolarization vector. Comput Cardiol. 1982;8:241–244.
14)Hering HE. Das Wesen des Herzalternans. Munchen Med Wochenshr. 1908;4:1417–1421
15)Lewis T. Notes upon alternation of the heart. Q J Med. 1910;4:141–144.
16)Amerena JV. Update on the management of atrial fibrillation. Med J Aust. 2013;199:592–597.
17)Vohra J. The long QT syndrome. Heart Lung Circ. 2007;16:5–12.
18) Prinzmetal M, Kennamer R, Merliss R, et al. A variant form of angina pectoris. Am J Med. 1959;27:374.
19)Smirk FH, Palmer DG. A myocardial syndrome, with particular reference to the occurrence of sudden death and of premature systoles interrupting antecedent T waves. Am J Cardiol. 1960;6:620–629.
20 )Dessertenne F. La tachycardie ventriculaire a deux foyers opposes variables. Arch Mal Coeur Vaiss. 1966;59:263–272.
21 )Lown B. Electrical reversion of cardiac arrhythmias. Br Heart J. 1967;29:469– 489.
22) Thiene G, Buja G F, Canciani B. Ventricular fibrillation without apparent heart disease: description of six cases. Am Heart J. 1989;118:1203–1209.
23) Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol. 1992;20:1391–1396.
24) Brauwald E. Evolution of the management of acute myocardial infarction: a 20th century saga. Lancet. 1998;352:1771–1774
25) Haissaguerre M, Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med. 1998;339:659–666.
26 ) Ieva F, Paganoni A M, Zanini P. Detection of structural changes in tachogram series for the diagnosis of atrial fibrillation events. Comput Math Methods Med. 2013:84–104.
27) Gonna H, Gallagher MM, Guo XH. P-Wave abnormality predicts recurrence of atrial fibrillation after electrical cardioversion: a prospective study. Ann Noninvasive Electrocardiol. 2014;19:57–62.
28) Bazett HC. An analysis of the time-relations of electrocardiograms. Heart. 1920;7:353–370.
29) Abe Y, Kondo M, Matsuoka R, et al. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol. 2003;41:737–742.
30 )Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: a method for prognostication and therapeutic decision making. JAMA. 2000;284:835–842.
31 )Hare JM, Traverse JH, Henry TD, et al. A randomized, double-blind, placebo- controlled, dose-escalation study of intravenous adult human mesenchymal stem cells (prochymal) after acute myocardial infarction. J Am Coll Cardiol. 2009;54:2277–2286.
32) Hall AS, Barth JH. Universal definition of myocardial infarction. Heart. 2009;95:247–249.
33) Sarafoff N, Schuster T, Vochem R, et al. Association of ST-elevation and non- ST-elevation presentation on ECG with transmurality and size of myocardial infarction as assessed by contrast-enhanced magnetic resonance imaging. J Electrocardiol. 2013;46:100.
34) Schelbert EB, Cao J J, Sigurdsson S, et al. Prevalence and prognosis of unrecognized myocardial infarction determined by cardiac magnetic resonance in older adults. JAMA. 2012;308:890–896.
35 )Malik M, Bigger JT, Camm AJ, et al. Heart rate variability standards of measurement, physiological interpretation, and clinical use. Eur Heart J. 1996;17:354–381.
36 )Tang ZH, Zeng F, Yu X, et al. Bayesian estimation of cardiovascular autonomic neuropathy diagnostic test based on baroreflex sensitivity in the absence of a gold standard. Int J Cardiol. 2014;171:e78–e80.
37) Feigenbaum H. Evolution of echocardiography. Circulation. 1996;93:1321–7. PubMed PMID: 8641018.
38 ) Curie P, Curie J. Lois du degagement de l’electricite par pression, dans la tourmaline. Comptes Rendus. 1881;92:186–8.
39 ) Fraser AG. Inge Edler and the origins of clinical echocardiography. Eur J Echocardiogr. 2001;2:3–5.
40 )Edler I, Hertz CH. The use of ultrasonic reflectoscope for the continuous recording of the movements of heart walls. Clin Physiol Funct Imaging. 1954;24:118–36. PubMed PMID: 15165281.
41) Lindstrom K, Edler I. Ultrasonic Doppler technique used in heart disease: clinical application. Ultrasono Graphia Medica. 1969;3:455–61.
42) Feigenbaum H, Waldhausen JA, Hyde LP. Ultrasound Diagnosis of Pericardial Effusion. JAMA. 1965;191:711–4. PubMed PMID: 14245510.
43 )Gowda RM, Khan IA, Vasavada BC, Sacchi TJ, Patel R. History of the evolution of echocardiography. Int J Cardiol. 2004;97:1–6. doi: 10.1016/j.ijcard.2003.07.018. PubMed PMID: 15336798.
44) Gramiak R, Shah PM, Kramer DH. Ultrasound cardiography: contrast studies in anatomy and function. Radiology. 1969;92:939–48. PubMed PMID: 5771834.
45) Feigenbaum H, Stone JM, Lee DA, Nasser WK, Chang S. Identification of ultrasound echoes from the left ventricle by use of intracardiac injections of indocyanine green. Circulation. 1970;41:615–21. doi: 10.1161/01.CIR.41.4.615. PubMed PMID: 4245151.
46) Seward JB, Tajik AJ, Spangler JG, Ritter DG. Echocardiographic contrast studies: initial experience. Mayo Clin Proc. 1975;50:163–92. PubMed PMID: 1123933.
47 )Feinstein SB, Cheirif J, Ten CateFJ, Silverman PR, Heidenreich PA, Dick C, et al. Safety and efficacy of a new transpulmonary ultrasound contrast agent: initial multicenter clinical results. J Am Coll Cardiol. 1990;16:316–24. doi: 10.1016/0735- 1097(90)90580-I. PubMed PMID: 2197312.
48) Gowda RM, Khan IA, Vasavada BC, Sacchi TJ, Patel R. History of the evolution of echocardiography. Int J Cardiol. 2004;97:1–6. doi: 10.1016/j.ijcard.2003.07.018. PubMed PMID: 15336798.
49) Bom N, Lancée CT, Honkoop J, Hugenholtz PG. Ultrasonic viewer for cross- sectional analyses of moving cardiac structures. Biomed Eng. 1971;6:500–3. PubMed PMID: 5133281.
50) Griffith JM, Henry WL. A sector scanner for real time two-dimensional echocardiography. Circulation. 1974;49:1147–52. doi: 10.1161/01.CIR.49.6.1147. PubMed PMID: 4831657.
View all references in attached pdf