The relationship between electrocardiographic changes and early mortality rate in acute myocardial infarction

In 587 patients with acute myocardial infarction (AMI) and no previous MI, electrocardiographically estimated infarct size was related to three-month mortality. Mortality was found to be higher in patients with transmural MI (Q or R-wave changes in standard ECG) than in patients with subendocardial infarction (ST-T wave changes in standard ECG). In patients with anterior MI, precordial mapping with 24 chest electrodes was analyzed four days after arrival in hospital (n = 197). Neither the sum of R-waves, the sum of Q-waves, nor the number of Q-waves correlated significantly with early mortality, although there was a trend towards higher mortality among patients with more pronounced ECG changes. Finally, in patients with inferior AMI (n = 230), neither the sum of R-waves nor the sum of Q-waves in leads II, III and aVF on the fourth day influenced three-month mortality. However, when subtracting the sum of Q-waves from the sum of R-waves, there was a significant correlation between the estimated infarct size and the early mortality.     

Relationship between electrocardiographically estimated infarct size and clinical findings in anterior myocardial infarction

In 292 patients with anterior myocardial infarction (MI) and no previous MI the electrocardiographically estimated infarct size was correlated with clinical findings during hospitalization and 3-month follow-up. Patients with ECG-defined transmural MI had a higher incidence of different types of complications, such as congestive heart failure (CHF), hypotension, pericarditis, and a longer duration of hospitalization than patients with nontransmural MI. In a subgroup including 182 patients of the total series, a precordial map containing 24 electrodes was used. The sum of R waves (ΣR), the sum of Q waves (ΣQ), the number of Q waves, and ΣR-ΣQ were calculated 4 days after arrival in hospital to estimate the size of infarction. There was generally a correlation between these ECG variables and different clinical findings, such as incidence of CHF, hypotension, pericarditis, and the duration of hospitalization. It is concluded that the ECG determined infarct size in anterior MI in a majority of patients correlates with the incidence of different types of complications in acute myocardial infarction. In the individual patient, however, the risk of developing complications cannot be predicted by ECG changes.     

ST segment shifts are poor predictors of subsequent Q wave evolution in acute myocardial infarction. A natural history study of early non-Q wave infarction

Acute ST segment elevation is regarded generally as the sine qua non of evolving Q wave myocardial infarction (MI) because such electrocardiographic (ECG) injury is believed to be a marker of transmural ischemia and a forerunner of transmural necrosis. Alternatively, ST segment depression with or without T wave inversion is viewed as the dominant ECG feature of non-Q wave MI. However, this hypothesis has not been assessed prospectively in an acute MI population. We analyzed 2,304 serial ECGs at study entry (admission), day 2, day 3, and predischarge (mean, 10.2 +/- 2 days) from 576 patients with creatine kinase MB confirmed acute non-Q wave MI to determine what percentage of patients with early ST segment elevation culminated in subsequent Q wave development. Of this group, 187 patients (32%) exhibited 1 mm or greater ST segment elevation in two or more contiguous entry ECG leads. Of those patients whose non-Q wave MI could be localized on the basis of diagnostic admission ST segment shifts, the prevalence of early ST segment elevation was 43% (187 of 439). The sum total mean (+/- SD) peak ST segment elevation by lead group (anterior, inferior, lateral) was 4.0 +/- 2.4, 4.5 +/- 2.4, and 2.5 +/- 0.6 mm, respectively. Despite this, only 20% of patients with ST segment elevation (37 of 187) developed Q waves. Of 252 patients who exhibited early ST segment depression or T wave inversion or both, 39 (15%) evolved subsequent Q waves. Thus, while the prevalence of early ST segment elevation in acute evolving non-Q wave MI was higher than previously reported, 80% of patients with and 85% of patients without ST segment elevation and absent Q waves on the admission ECG did not develop subsequent Q waves during a 2-week period of observation (p = NS). In addition, when patients with ST segment elevation were compared with patients with ST segment depression or T wave inversions or both, there were no between-group differences in log peak creatine kinase (404 vs. 383 IU), reinfarction (6% vs. 8%), postinfarction angina (50% vs. 42%), or early recurrent ischemia (49% vs. 45%), defined as postinfarction angina with transient ECG changes. Thus, in patients who present with initial acute non-Q wave MI, ST segment shifts on admission are unreliable predictors of subsequent Q wave evolution and do not discriminate significant differences in postinfarction outcome. In particular, ST segment elevation during the early hours of evolving infarction is not an invariable harbinger of subsequent Q wave development.     

Q-wave prediction of myocardial infarct location, size and transmural extent at magnetic resonance imaging

OBJECTIVE: We investigated how pathologic Q waves or equivalents predict location, size and transmural extent of myocardial infarction (MI). METHODS: MI characteristics, detected by contrast-enhanced magnetic resonance imaging, were compared with 12-lead electrocardiogram in 79 patients with previous first MI. RESULTS: Q waves involved only the anterior leads (V1-V4) in 13 patients: in all patients MI involved the anterior and anteroseptal walls and apex; 81% of scar tissue was within these regions. Q waves involved only the inferior leads (II, III, aVF) in 13 patients: in 12 of these patients MI involved the inferior and inferoseptal walls; however, only 59% of scar occupied these regions. Q waves involved only lateral leads (V5, V6, I, aVL) in 11 patients: in nine of these patients MI involved the lateral wall but only 27% of scar tissue was within this wall. Q waves involved two electrocardiogram locations in 42 patients. In the 79 patients as a whole, the number of anterior Q waves was related to anterior MI size (r=0.70); however, the number of inferior and lateral Q waves was only weakly related to MI size in corresponding territories (r=0.35 and 0.33). A tall and broad R wave in V1-V2 was a more powerful predictor of lateral MI size than Q waves. Finally, the number of Q waves accurately reflected the transmural extent of the infarction (r=0.70) only in anterior infarctions. CONCLUSION: Q waves reliably predict MI location, size and transmural extent only in patients with anterior infarction. A tall and broad R wave in V1-V2 reflects a lateral MI.     

Prognostic significance of the electrocardiogram after Q wave myocardial infarction. The Framingham Study

The prognostic value of abnormalities on the electrocardiogram (ECG) present 1 year after initial myocardial infarction (MI) is examined in relation to reinfarction and coronary death throughout 32 years (mean, 10.1 years) of follow-up in the Framingham Heart Study. Resting 12-lead ECGs were available in 251 survivors (190 men and 61 women) of clinically recognized Q wave MI. The ECG reverted to normal in 31 (12.4%) cases and was abnormal but without Q waves in 37 (14.7%). Q waves persisted without other significant abnormalities in 108 (43.0%) and with other abnormalities in 75 (29.9%) cases. Electrocardiographic abnormalities at follow-up were more common in women and in those persons whose initial MI was anterior as compared with inferior. Nonspecific T wave, ST segment changes, and electrocardiographic left ventricular hypertrophy on the ECG before or after MI were powerful predictors (p less than 0.01) of coronary death. The relation of these residual post-MI electrocardiographic findings to reinfarction and coronary death was assessed by Cox regression analysis. The follow-up electrocardiographic status was unrelated to the risk of subsequent reinfarction. Subjects who lost Q wave evidence of MI but whose ECG continued to show evidence of repolarization abnormalities, left ventricular hypertrophy, or blocked intraventricular conduction were at a 3.5-fold increased risk (p less than 0.01) of coronary death as compared with those reverting to a normal ECG. Persons with a persistent Q wave MI accompanied by these abnormalities were at a 2.7-fold excess risk (p = 0.01) of coronary death as compared with those with a normalized ECG. These findings remained significant when considering age and standard coronary risk factors. The presence of other electrocardiographic abnormalities without persistent Q waves yields a worse prognosis than a Q wave persisting alone. The prognostic value of a follow-up ECG with abnormalities other than a persistent Q wave MI also remained after considering the effects of left ventricular hypertrophy and cardiac enlargement on x-ray, functional classification, and diuretic usage. Specific electrocardiographic abnormalities present before infarction, however, were potent indicators of long-term prognosis prognosis and diminished the importance of the follow-up ECG. Although survival after initial MI is improved only if the ECG reverts to normal, information on electrocardiographic abnormalities before MI can be especially useful in evaluating long-term risk.     

The time course in acute myocardial infarction evaluated with precordial mapping and standard ECG

Fifty-six patients with acute transmural anterior wall myocardial infarction (MI) were investigated with a 24-electrode grid and 34 patients with an acute transmural inferior wall MI were investigated with standard ECG leads II, III, and aVF in order to study the length of time after the onset of pain during which the development of Q waves and reduction of R waves progress. These ECG changes continued for 18-26 h after onset of pain but the majority appeared during the first 12 h.     

Correlation of electrocardiologic and pathologic findings in 100 cases of Q wave and non-Q wave myocardial infarction

Of 100 cases of acute myocardial infarction as shown on autopsy, 55 cases were transmural infarcts and 45 were subendocardial. Pathologic Q waves appeared in 67% of the cases of transmural infarct and in 30% of subendocardial infarct. In transmural infarcts, Q wave infarcts occurred twice as frequently as non-Q wave infarcts. In the cases of subendocardial infarcts just the opposite was observed: non-Q wave infarcts had double the frequency of Q wave infarcts. In spite of this, when a myocardial infarct is characterized strictly by electrocardiology, it should be described by only the accurate terminology of Q wave infarct or non-Q wave infarct. To distinguish with certitude between subendocardial infarct and transmural myocardial infarct on the basis of the ECG does not seem possible. Q wave infarct as "transmural" and non-Q wave infarct as "subendocardial" does not correspond to the pathologic evidence.     

Strain rate imaging differentiates transmural from non-transmural myocardial infarction: a validation study using delayed-enhancement magnetic resonance imaging

OBJECTIVES: The aim of this study was to determine if strain rate imaging (SRI) correlates with the transmural extent of myocardial infarction (MI) measured by contrast-enhanced magnetic resonance imaging (Ce-MRI). BACKGROUND: Identification of the transmural extent of myocardial necrosis and degree of non-viability after acute MI is clinically important. METHODS: Tissue Doppler echocardiography with SRI and Ce-MRI were performed in 47 consecutive patients with a first acute MI between days 2 and 6 and compared to 60 age-matched healthy volunteers. Peak myocardial velocities and peak myocardial deformation strain rates were measured. Location and size of the infarct zone was confirmed by Ce-MRI using the delayed enhancement technique with a 16-segment model. RESULTS: Contrast-enhanced MRI identified transmural infarction in 21 patients, non-transmural infarction in 15 (mean transmurality of infarct 72.3 +/- 10.6%), and another 11 patients with subendocardial infarction (<50% transmural extent of the left ventricular wall). Peak systolic strain rate (SRs) of the transmural infarction segments was significantly lower compared to normal myocardium or with non-transmural infarction segments (both p < 0.0005). A cutoff value of SRs >-0.59 s(-1) detected a transmural infarction with high sensitivity (90.9%) and high specificity (96.4%), and -0.98 s(-1) >SRs >-1.26 s(-1) distinguished subendocardial infarction from normal myocardium with a sensitivity of 81.3% and a specificity of 83.3%. CONCLUSIONS: Peak myocardial deformation by SRI can differentiate transmural from non-transmural MI, and it allows noninvasive determination of transmurality of the scar after MI and thereby the extent of non-viable myocardium.     

Changes in the QRS complex and ST segment in transmural and subendocardial myocardial infarctions. A clinicopathologic study.

The QRS complex and ST segment in the ECGs of 80 patients who died of an acute myocardial infarction (MI) were studied in relation to the extent of the MI (subendocardial vs. transmural). Changes in the QRS complex developed in nine out of the 15 cases with an acute subendocardial MI. Five of these cases fulfilled the conventional QRS criteria for a myocardial infarction. A definite ST segment depression (a J point depression of 2 mm. or more in at least one lead, and a horizontal or downward sloping ST segment with a minimum duration of 0.08 sec.) occurred most frequently in connection with a circumferential subendocardial MI (88 per cent), but it was also found in a regional subendocardial (43 per cent) and transmural MI (43 per cent). In 17 per cent of the cases with a transmural MI, this was the only ECG abnormality. It is concluded that cases with a subendocardial MI cannot always be distinguished from transmural MI on the basis of the presence or absence of the QRS changes, and that an ST segment depression, as defined in this study, can give additional information in the evaluation of an acute phase of an MI.     

Assessment of the accuracy of serial electrocardiograms in the diagnosis of myocardial infarction

The diagnostic accuracy of the 12-lead scalar electrocardiogram (ECG) for the presence or absence of acute transmural myocardial infarction (MI) was studied in 25 patients who died while in hospital for treatment of ischemic chest pain. Detailed autopsy studies revealed myocardial necrosis in 17 patients, with the ECG accurate in 11 (44%) of the 25 patients. None of the five pateints with autopsy-proven subendocardial infarction had abnormal Q waves. The admission ECG was diagnostic in only 4 of the 17 patients (24%) with infarction. The creatine kinase (CK) and CK-MB results agreed with the pathologic findings in 22 of the 25 patients (88%), were falsely negative in one patient, and falsely positive in two of the patients. In this selected population the most reliable diagnostic tests were CK or CK-MB isoenzymes. The ECG was frequently unhelpful (7 of 25 patients) because of left bundle branch block or paced rhythm, but when unaffected by these depolarization abnormalities it was useful in establishing the correct diagnosis.     

Abnormal Q waves on the admission electrocardiogram of patients with first acute myocardial infarction: Prognostic implications

Background: Q waves developed in the subacute and persisting into the chronic phase of myocardial infarction (MI) usually signify myocardial necrosis. However, the mechanism and significance of Q waves that appear very early in the course of acute MI (<6 h from onset of symptoms), especially if accompanied by ST elevation, are probably different. Hypothesis: This study assesses the prognostic implications of abnormal Q waves on admission in 2,370 patients with first acute MI treated with thrombolytic therapy <6 h of onset of symptoms. Results: Patients with abnormal Q waves in ≥2 leads with ST-segment elevation (n = 923) were older than patients without early Q waves (n = 1,447) (60.6 ±11.9 vs. 58.8 ±11.9 years, respectively; p = 0.0003), and had a greater incidence of hypertension (34.3 vs. 30.5% p = 0.05) and anterior MI (60.6 vs. 41.1 % p<0.0001). Time from onset of symptoms to therapy was longer in patients with Q waves upon admission (208 ± 196 vs. 183 ± 230 min; p = 0.01). Peak serum creatine kinase (2235 ± 1544 vs. 1622 ± 1536 IU; p<0.0001), prevalence of heart failure during hospitalization (13.8 vs. 7.0%, p<0.0002), hospital mortality (8.0 vs. 4.6% p = 0.02), and cardiac mortality (6.6 vs. 4.5%, p = 0.11) were higher in patients with anterior MI and with abnormal Q waves than in those without abnormal Q waves upon admission. There was no difference in peak creatine kinase, prevalence of heart failure, in-hospital mortality, and cardiac mortality between patients with and without abnormal Q waves in inferior MI. Multivariate regression analysis confirmed that mortality is independently associated with presence of Q waves on admission (odds ratio 1.61; 95% CI 1.04–2.49; p = 0.04 for all patients; odds ratio 1.65; 95% CI 0.97–2.83; p=0.09 for anterior wall MI. Conclusion: Abnormal Q waves on the admission electrocardiogram (ECG) are associated with higher peak creatine kinase, higher prevalence of heart failure, and increased mortality in patients with anterior MI. Abnormal Q waves on the admission ECG of patients with inferior MI are not associated with adverse prognosis.     

Insensitivity of the electrocardiogram in apical myocardial infarction

The ability of the standard ECG to identify myocardial infarction (MI) involving primarily the left ventricular (LV) apex is controversial. Therefore, the ECGs of 62 consecutive patients with acute infarction and isolated akinesia or dyskinesia of the LV apex on gated blood pool scintigraphy performed at rest 9 +/- 4 days after MI, were reviewed. The following distribution of Q waves was found: none, 26%; inferior leads only, 23%; anterior leads only, 32%; inferior + 1 or more V leads, 13%; lead I and/or aVL + 1 or more V leads, 6%. Only 12 patients (19%) demonstrated one of the "combination" Q-wave patterns thought to indicate apical infarction. Although the 20 patients with a history of MI did not differ in age or ejection fraction from those with a first MI, the combination of inferior and anterior Q waves was present in 6 of them (30%), vs only 2 of the remaining 42 patients (5%) (p less than 0.02). The 24 patients with apical dyskinesia had a lower ejection fraction (36 +/- 14 vs 48 +/- 12, p less than 0.001), a lower prevalence of isolated inferior Q waves (8 vs 32%, p less than 0.05) and a greater prevalence of isolated anterior Q waves (46 vs 24%, p = 0.09) than those with akinesia. Thus, in patients with recent MI localized to the LV apex on radionuclide ventriculography, pathologic Q waves are commonly confined to the anterior or inferior leads or absent altogether. The insensitivity of the various proposed criteria for the electrocardiographic diagnosis of apical MI emphasizes the value of imaging techniques in detecting this common clinical entity.     

Reliability of standard electrocardiogram in detecting left ventricular asynergy in 315 patients with recent myocardial infarction

The relationship between asynergy of the left ventricular wall detected by two-dimensional echocardiography and ECG signs of necrosis (number of Q waves greater than or equal to 40 ms, Wagner's score) was evaluated in 315 patients (NYHA I-II) 23-90 days after a first Q-wave myocardial infarction (MI). Poor correlations were found between asynergy and ECG parameters. An ECG anterior MI is an apicoseptal MI by echo (independently of the ECG extent of Q waves) and the ECG is of little or no help in predicting the extent of asynergy to the inferior wall and proximal segments of the septum. An ECG inferior MI is inferoposterior by echo and the ECG has very limited value in predicting the extent of asynergy to the apex and septum. Patients with Q waves in leads II, III, and aVF had more extensive asynergy than those with either 2Q or greater than 3Q. R/S greater than or equal to 1 in V1 and/or V2 was present in 44% of patients with inferior MI while asynergy of at least one segment of the posterior wall was observed in 94%. In conclusion, standard ECG is sensitive in identifying anterior versus inferior infarct but it is unreliable in predicting the real extent of asynergy of the left ventricle, particularly in inferior infarcts.     

Myocardial damage and left ventricular dysfunction in patients with and without persistent negative T waves after Q-wave anterior myocardial infarction

Persistent T-wave inversions during the chronic stage of Q-wave myocardial infarction (MI) indicate the presence of a transmural infarction with a fibrotic layer pathologically. The aim of the present study was to examine the relation between left ventricular (LV) damage and changes in polarity of the T waves from the acute to chronic phase in patients with Q-wave anterior wall MI. We studied 140 patients with persistent T-wave inversions in leads with Q waves (negative T-wave group) and 158 patients with positive T waves (positive T-wave group) at 12 months after anterior MI. In the positive T-wave group, the precordial T waves reverted from a negative to a positive morphology < 3 months after MI in 21 patients (3 M-positive T-wave subgroup), 3 to 6 months in 52 patients (6 M-positive T-wave subgroup), and 6 to 12 months in 75 patients (12 M-positive T-wave subgroup). Ten patients had persistent positive T waves without initial T-wave inversion (persistent positive T-wave group). Wall motion index and LV dimension were higher and the wall thickness for the infarct area and LV ejection fraction were lower in the negative T-wave than in the positive T-wave groups, except the persistent positive T-wave group in the chronic stage (p < 0.0001). Wall motion in the infarcted area improved over the course of 1 year in the 3 M-, 6 M-, and 12 M-positive T-wave subgroups (p < 0.0001), but not in the persistent positive T-wave group. Among the patients with T-wave inversions after admission, those who had persistent negative T waves after 12 months had worse LV function. In patients with initial T-wave inversion, earlier normalization of the precordial T waves was associated with greater improvement in LV function. Patients with persistent positive T waves without initial negative T waves had poorer recovery of LV function than patients with persistent negative T waves. We conclude that the presence of inverted T waves in leads with abnormal Q waves 12 months after MI and the time required for T-wave normalization can be used to assess the degree of LV dysfunction.     

Appearance of T-wave inversions without raised serum enzyme activity in suspected acute myocardial infarction: clinical outcome in relation to subendocardial infarction

In 67 patients with a clinical history of suspected acute myocardial infarction (MI) who developed T-wave inversions in standard ECG and had normal serum aspartate aminotransferase activity (possible MI) the clinical outcome was compared with that in patients fulfilling criteria for subendocardial infarction. Patients with possible MI had a lower mortality (p = 0.02) and also a lower reinfarction rate (p = 0.14) during the first 2 years as compared with those with subendocardial MI. Although patients with subendocardial MI had more problems with chest pain in the acute phase, angina pectoris occurred more frequently in patients with possible MI during a longer follow-up period. Congestive heart failure occurred more frequently in patients with subendocardial MI during initial hospitalization, whereas treatment for heart failure appeared similar in the two groups during a longer follow-up time. We conclude that the clinical course in patients with possible MI, here defined as chest pain and appearance of T-wave inversions without elevation of serum enzyme activity, seems to differ from that in patients with subendocardial MI, particularly regarding long-term survival and incidence of angina pectoris.     

So-called rudimentary or nontransmural myocardial infarction. Coronary lesions, course and prognosis

Eighty patients admitted to hospital between 1975 and 1980 for "non-transmural" myocardial infarction (72 men, 8 women, mean age 56 +/- 9 years) were studied. The diagnosis was based on a severe attack of pain of over 30 minutes duration, increased serum cardiac enzyme levels (CKMB greater than 24 U; SGOT greater than 60 U), pyrexia and signs of inflammation. The patients were divided into two groups according to their ECG changes: Group A: "rudimentary" infarction with prolonged T wave inversion from V1 to V5, narrow transient Q waves and reduction of R wave amplitude in the corresponding leads; Group B: persistant prolonged, intercritical ST depression greater than 2.5 mm (subendocardial infarct). All patients underwent selective coronary angiography and left ventriculography in the RAO projection within 15 days of admission. The angiographic data (coronary score, ejection fraction, alinetic perimeter) were compared to those of 2 randomly chosen control groups: Group C: 30 inferior wall infarcts with coronary angiography and regularly followed-up; Group D: 30 transmural anterior infarcts with coronary angiography, regularly followed-up. Four factors were analysed during follow-up: the incidence of death after discharge from hospital, transmural infarction, unstable angina and cardiac failure. All patients were treated medically (nitrate derivatives, betablockers, calcium antagonists). Sixteen patients in Group A (p less than 0,025) were operated and excluded from the prognostic study. The angiographic data showed a high incidence of isolated, severe LAD disease in Group A (59.2% of cases) and that multivessel disease was commoner in Group B (78.4%). A collateral circulation revascularising the LAD was observed in 42% of patients in Group A. (ABSTRACT TRUNCATED AT 250 WORDS)     

Fragmented QRS complexes are not hallmarks of myocardial injury as detected by cardiac magnetic resonance imaging in patients with acute myocardial infarction

Background

Q waves on a 12-lead electrocardiography (ECG) are considered to be classic hallmarks of prior myocardial infarction. However, one study suggested that the fragmented QRS complex (fQRS) on ECG is a highly sensitive and specific marker of myocardial scarring on a nuclear stress test. The study aimed to investigate the diagnostic accuracy of fragmented QRS complexes compared with Q waves for myocardial injury detected by delayed contrast-enhanced cardiovascular magnetic resonance imaging (DE-CMRI) in subjects with acute myocardial infarction.

Methods

Electrocardiograms of 190 subjects with myocardial infarction who underwent DE-CMR were analyzed. fQRS was defined by the presence of an additional R wave (R″), or notching of the S wave, or more than one R′ in two contiguous leads.

Results

Delayed enhancement was observed in 180 (94.7%) patients. Transmural enhancement was noted in 78 (43.3%) and subendocardial enhancement in 102 (56.7%) patients. The sensitivity and specificity of Q waved and fQRS for diagnosing delayed enhancement were 59.4% vs. 66.7% and 90.0% vs. 40.0%. The area under the receiver–operator characteristics curve of delayed enhancement was 0.75 for Q waves and 0.53 for fQRS (p = 0.04). The areas under the ROC curves of the transmurality of delayed enhancement were 0.44 for fQRS and 0.58 for Q waves (p = 0.73).

Conclusions

fQRS has poor accuracy for the detection of myocardial injury compared with Q waves. fQRS and Q waves are not valuable tools for the diagnosis transmural irreversible myocardial injury in acute myocardial infarction.     

Relationship between electrocardiographically estimated infarct size and morbidity during a two-year follow-up

In 587 patients with a first myocardial infarction (MI) the electrocardiographically (ECG) estimated infarct size was related to morbidity during a two-year follow-up. Patients with transmural MI (Q- or R-wave changes in standard ECG) were more often treated for heart failure and returned to work less frequently than patients with subendocardial MI (ST-T-wave changes only). There were trends indicating a higher reinfarction rate in patients with subendocardial MI, whereas angina pectoris was observed as frequently in both groups. In a subset of patients with anterior MI, infarct size was estimated from the total Q- and R-wave amplitude in 24 precordial leads 4 days after arrival in hospital. A positive relationship was observed between ECG-estimated infarct size and treatment for heart failure, and patients with smaller infarctions according to ECG criteria returned to work less frequently. A higher reinfarction rate was observed in patients with smaller infarctions. In patients with inferior MI there were mostly weaker correlations between ECG-estimated infarct size (Q- and R-wave changes in leads II, III, and a VF) and morbidity during the two-year follow-up.     

How reliable is electrocardiography in differentiating transmural from non-transmural myocardial infarction? A study with contrast magnetic resonance imaging as gold standard

Cardiovascular magnetic resonance (CMR) using contrast enhancement allows exact determination of the site and transmural extent of myocardial infarction (MI). We evaluated whether 12-lead electrocardiography can differentiate transmural from non-transmural MI or determine the site of MI by comparing the findings with those of contrast-enhanced CMR. A total of 27 patients (59.5+/-12.9 years) with a history of MI (6.4+/-2.9 months) underwent CMR (Magnetom, Siemens, Erlangen, Germany). Cine images were acquired in the horizontal and vertical long axes and short axis by TrueFISP. Contrast-enhanced CMR images were acquired in the same axes by segmented FLASH 15 min after administration of gadolinium-DTPA (0.15 mmol/kg). This showed the MI to be transmural in 11 patients and non-transmural in 16. An electrocardiogram (ECG) was recorded in all patients before CMR. T-wave alterations, descending ST-depression, pathological Q-waves and absent R waves were more frequent in non-transmural MI than transmural MI, as defined by contrast-enhanced CMR (p> or =0.618). However, none of the differences were statistically significant. R-wave reduction, q waves and horizontal ST-depression were more frequent in transmural than in non-transmural MI (p> or =0.157). Again, the differences were not significant. The sensitivity of the ECG for MI localization was highest in inferior infarctions (85.71%), the specificity was highest in anterior infarctions (100%), the best positive predictive value (80%) was achieved for anterolateral infarctions, and the best negative predictive value for lateral infarctions (95.83%). Transmural and non-transmural MI cannot be differentiated by ECG. The ECG is most accurate in detecting anterolateral MI.