Version May 2024
INTRODUCTION — The electrocardiogram (ECG) is a mainstay in the diagnosis of acute and chronic syndromes due to coronary artery disease. The findings depend upon a number of key factors, including the duration (hyperacute/acute versus evolving/chronic), extent (Q wave versus non-Q wave), localization (anterior-lateral versus inferior-posterior and the size of the ischemic or infarcted region) of ischemia or infarction, and the presence of other underlying abnormalities [1-3]. The ECG also provides information on prognosis. Serial ECGs should always be evaluated in the fullest clinical context, including cardiac enzyme biomarkers and imaging studies.
The use of the ECG for prognosis in myocardial infarction (MI) or unstable angina will be reviewed here.
The use of the ECG for diagnosis is discussed separately. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction".)
Additional prognostic factors in acute MI are discussed elsewhere. (See "Prognosis after myocardial infarction".)
GENERAL ISSUES OF RISK STRATIFICATION — The process of risk stratification in a patient who has had an acute MI has several components:
●Early in-hospital identification of patients at increased risk for recurrent ischemic events.
●Identification of patients at increased risk for arrhythmic or nonarrhythmic death; arrhythmias, for example, are the most frequent cause of death during the first year after an MI.
●Identification of patients at high risk of developing other complications such as heart failure and shock.
These issues are discussed elsewhere in a variety of topics:
●For early risk stratification after an ST-elevation (Q wave) MI (STEMI). (See "Risk stratification after acute ST-elevation myocardial infarction".).
●For early risk stratification after a non-ST-elevation (non-Q wave) MI (NSTEMI) or unstable angina. (See "Risk factors for adverse outcomes after non-ST elevation acute coronary syndromes".)
●For risk stratification for late cardiovascular mortality. (See "Incidence of and risk stratification for sudden cardiac death after myocardial infarction".)
●For general prognosis after an MI. (See "Prognosis after myocardial infarction".).
STEMI VERSUS NSTEMI AND UNSTABLE ANGINA — The extent and severity of ischemia are the primary determinant of ST changes that occur in an acute coronary syndrome. Primary ST elevation is generally associated with transmural ischemia while ST depression (not related to reciprocal changes) is associated with ischemia limited to the subendocardium. As will be described below, marked ST elevation or depression in multiple leads usually indicates very severe and widespread ischemia and therefore a worse outcome. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction".)
Necrosis of sufficient myocardial tissue can lead to decreased R wave amplitude or frank Q waves due to loss of electromotive forces in the infarcted area. Thus, the reason why Q waves do or do not develop following coronary occlusion is related to the duration of occlusion, the area of myocardium at risk, and the extent to which myocardial viability is maintained during occlusion by remaining anterograde blood flow and the function of collaterals. The infarct-related artery is occluded in over 90 percent of cases. In contrast, coronary arteriography performed in the acute period of NSTEMI has shown that the infarct-related artery is not occluded in 60 to 85 percent of patients [3-6]. (See "Pathogenesis and diagnosis of Q waves on the electrocardiogram".)
Prognosis — Short- and long-term outcomes are better in patients with unstable angina than in those with an MI. Among patients with an MI, NSTEMI is associated with lower in-hospital mortality but a similar or worse long-term outcome than ST-elevation infarcts. The worse short-term outcome with STEMI reflects a larger infarction that is presumably due to the much higher rate of complete occlusion of the infarct-related artery with STEMI than with NSTEMI. The similar or worse late prognosis with NSTEMI is in part related to a more than 50 percent prevalence of multivessel disease in patients with an NSTEMI [3] and a higher rate of recurrent ischemia and infarction than with STEMI [7]. Thus, a significant amount of myocardium remains at risk.
ECG FOR PROGNOSIS IN STEMI — Prognostic factors for STEMI and NSTEMI differ. In addition to identifying the location of the infarction, the initial ECG can give important information regarding severity and prognosis in patients with an STEMI.
Extent of myocardial injury — A multivariate analysis from the GUSTO-I database of 41,021 patients found that the following ECG variables were predictive of 30-day mortality [8]:
●Sum of the absolute ST-segment deviation, both elevation and depression, ≥19 mm (odds ratio 1.53)
●Evidence of prior infarction for new inferior infarction (odds ratio 2.47)
●Heart rate >84 beats per min (odds ratio 1.49)
●QRS duration ≥100 msec for anterior infarction (odds ratio 1.55)
Each of these parameters, particularly the first two, is at least in part related to the extent of myocardial injury. This issue was addressed more directly in an analysis from the historic GISSI-1 trial, which confirmed the value of ST-segment elevations observed on the admission ECG in predicting in-hospital mortality, as well as mortality at both 30 days and long term in patients with a first MI [9]. Four distinct severity groups were defined based upon the number of ECG leads with ST elevation: two to three leads, four to five leads, six to seven leads, and more than eight leads. In-hospital, 30-day, and 10-year mortality increased progressively as the number of ECG leads with ST elevation increased, although not all differences were statistically significant. Furthermore, patients with more extensive disease showed greater benefit from thrombolytic therapy.
Anterior MI — Anterior wall infarction is associated with a worse prognosis than inferior wall infarction, mostly because of larger infarct size [10-14]. In one report that included both ST-elevation and non-ST-elevation infarctions, anterior infarcts had the following significant differences from inferior infarcts: a lower admission left ventricular ejection fraction (38 versus 55 percent), higher incidences of heart failure (41 versus 15 percent), serious ventricular arrhythmias, in-hospital mortality (11.9 versus 2.8 percent), and, at a mean duration of 30 months, total cardiac mortality (27 versus 11 percent) [10].
Similar findings were noted in a report from the SPRINT registry of patients with a first NSTEMI [11]. Patients with an anterior infarction had a higher rate of in-hospital complications (heart failure and cardiogenic shock) and a higher in-hospital mortality (15 versus 10 percent) when compared to those with less extensive inferior/lateral wall infarctions. They also had a higher one-year rate of recurrent infarction or cardiac death (14.2 versus 4.8 percent) and a higher five-year mortality (36 versus 22 percent). After adjustment for other risk factors, most of these differences did not reach statistical significance except for a higher one-year cardiac event rate (odds ratio 3.15, 95% confidence interval 1.59-6.78).
As a result of these and other findings, anterior wall infarction has been included as a risk factor in the TIMI risk scores for both STEMI (calculator 1) and non-ST-elevation acute coronary syndrome (calculator 2) [15-17]. (See "Risk stratification after acute ST-elevation myocardial infarction" and "Risk stratification after non-ST elevation acute coronary syndrome", section on 'TIMI risk score'.)
Inferior MI — The importance of the extent of injury also applies to inferior infarcts. A report from the GUSTO-I trial evaluated 16,521 patients with an acute inferior wall STEMI [18]. The following findings were noted:
●Precordial ST-segment depressions were associated with larger infarctions, more post-infarction complications (heart failure, second- or third-degree heart block, or shock) and a small but significant increase in mortality rate at 30 days and one year when compared to the absence of these changes. After adjustment for clinical risk factors, the magnitude of the ST depression (sum of leads V1-V6) added significant independent prognostic information, as the 30-day mortality increased by 36 percent for every 0.5 mV (5 mm) increment in summed precordial ST-segment depression.
●Patients with concomitant ST-segment depression in leads V4-V6 were more likely to have three-vessel disease than those with ST depression in leads V1-V3 or those without precordial ST-segment depression (36 versus 16 and 14 percent) [19]. Such patients derive greater absolute benefit from reperfusion therapy with thrombolytic agents or percutaneous coronary intervention because they have a larger amount of myocardium at risk [20].
QRS morphology — Distinct QRS morphologies may also provide information relating to infarct size and prognosis. Data from the TIMI-4 trial suggested that the following distortion of the terminal portion of the QRS complex in two or more adjacent leads may be particularly informative [21]:
●Tall symmetric upright T waves and ST-segment elevation accompanied, in leads with an initial QR configuration, by the J point at ≥50 percent of the R wave amplitude (measured from the isoelectric line).
●Disappearance of the S wave in leads with an Rs configuration on admission ECG.
Patients with either of these findings had larger infarct sizes and larger defects on nuclear imaging technetium sestamibi scans than those without these findings. Patients with this type of terminal QRS distortion had a higher mortality at one year (18 versus 6 percent, p = 0.03) and an increasing trend for the end points of death, reinfarction, heart failure, and an ejection fraction of less than 40 percent. The risk was greatest in patients who had an anterior wall infarction.
Presence or absence of new Q waves — Although STEMI is typically associated with the evolution of pathologic Q waves, some patients do not develop new Q waves. This is an important issue since the appearance of new Q waves in the setting of STEMI predicts both a larger infarct and increased mortality.
●In an initial report of 150 patients presenting with STEMI, 115 (77 percent) developed Q waves during the hospitalization; none of the patients were treated with reperfusion (thrombolytic therapy or primary percutaneous coronary intervention [PCI]) [22]. The patients who developed Q waves had a significantly lower rate of patency of the infarct-related artery (24 versus 57 percent) and a larger infarction as demonstrated by higher peak serum cardiac biomarkers and a lower left ventricular ejection fraction before discharge.
●In a cohort of 4530 patients with STEMI treated with primary PCI, 56 percent had Q waves on presentation [23]. Patients with Q waves had a significantly higher mortality at 90 days compared with those who did not develop Q waves (5.3 versus 2.1 percent). The presence or absence of Q waves was a better predictor of mortality at 90 days than time from symptom onset to PCI.
Persistent absence of Q waves after thrombolytic therapy also predicts a less severe infarction and better outcomes [24-27].
●Among 21,570 patients enrolled in the GUSTO-I trial of thrombolysis who did not have confounding ECG factors or a prior MI, Q waves did not develop in 4601 (21.3 percent) [24]. Compared to the Q wave group, patients with a non-Q wave STEMI had a significantly lower rate of heart failure (8.5 versus 13.9 percent) and significant reductions in mortality in-hospital and at 30 days (adjusted mortality 4.8 versus 5.3 percent) and one year.
●In a second subset analysis from GUSTO-I, patients without Q waves had a significantly higher left ventricular ejection fraction (66 versus 57 percent) and higher rates of survival at all time points, including two years (6.3 versus 10.1 percent) [25]. The infarct-related artery was significantly less likely to be anterior (33 versus 42 percent) and more likely to be distal. The degree of reperfusion was greater, as evidenced by a higher likelihood of early (77 versus 65 percent at 90 minutes) and complete patency in the infarct-related artery (54 versus 44 percent).
R waves — Extensive loss of R waves on the ECG is usually seen in patients with an anterior MI, and there is a rough correlation between the sum of R wave voltages in all 12 ECG leads and the left ventricular ejection fraction (LVEF). Patients with diminished total R wave voltage, defined as less than 4 mm total in ECG leads AVL, AVF, and V1-V6 in the absence of bundle branch block, have significantly reduced LV dysfunction and a worse prognosis [28]. More complex formulae employing summated R waves and Q waves that produce a more accurate prediction of LVEF exist [29].
Resolution of ST- and T-wave changes — The outcome after acute STEMI is improved in patients who have resolution of ST- and T-wave changes.
ST-segment elevation — In the era of PCI and fibrinolytic therapy, resolution of ST-segment elevation in patients with an STEMI [30] is a marker of reperfusion and coronary artery patency (as estimated from TIMI flow grade) [31] and is associated with smaller infarct size [32]. Lack of ST-segment resolution by 90 to 180 minutes and the amount of ST deviation persisting at 90 minutes are powerful clinical predictors of 35-day, six-month, one-year, and long-term mortality (figure 1A-B) [31,33]. The importance of ST-segment elevation resolution is reviewed in detail elsewhere. (See "Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinants of outcome", section on 'Prognosis after primary PCI' and "Diagnosis and management of failed fibrinolysis or threatened reocclusion in acute ST-elevation myocardial infarction", section on 'Primary failure'.)
ST-segment depression — ST-segment depression (in leads other than those initially showing ST-segment elevation) is commonly seen in patients with an ST-segment elevation infarction. This may reflect ischemia in a second myocardial region or reciprocal changes from the region with ST elevation. As indicated above, the presence of concomitant ST-segment depression is associated with a larger infarct and a poorer prognosis [8,18,19]. The course of these changes after an MI is also of prognostic importance.
The importance of serial changes was illustrated in a series of 261 patients presenting with an acute MI that evaluated the timing of ST-segment depression resolution relative to the resolution of ST-segment elevation [34]. In-hospital mortality was significantly higher in patients who had ST-segment depression that persisted after resolution of ST-segment elevation compared to those with simultaneous resolution of ST-segment depression and elevation or those without ST-segment depression (13 versus 1 and 0 percent, respectively, p = 0.002). The incidence of recurrent angina, reinfarction, and heart failure was similar among the three groups.
In another report, persistence of ST-segment depression in V5 to V6 for more than six months after an anterior infarction was associated with diastolic dysfunction [35].
T-wave inversion — Serial ECG changes may also predict post-infarction "remodeling" [36]. Lack of negative T-wave resolution and late appearance of new negative T waves predict more pronounced left ventricular enlargement and progressive deterioration of ventricular function. In contrast, normalization of T waves is related to functional recovery of viable myocardium and may be more predictive than QRS changes.
Conduction abnormalities — A variety of conduction abnormalities, including atrioventricular block and bundle branch block, are associated with acute MI and may have prognostic significance [37]. This issue is discussed in detail elsewhere. (See "Conduction abnormalities after myocardial infarction".)
ECG FOR PROGNOSIS IN UNSTABLE ANGINA AND NSTEMI — As mentioned above, patients with NSTEMI have lower in-hospital mortality but similar or worse long-term outcomes than those with ST-elevation infarcts. Patients with unstable angina without evidence of infarction have a better prognosis than do either infarct group (figure 2) [7,10,38,39]. Among patients with a non-ST-elevation acute coronary syndrome (ACS), the ECG can identify patients in different risk categories. The major factors are the presence, extent, and location of ST-segment depression. (See "Risk stratification after non-ST elevation acute coronary syndrome".)
ST-segment depression — ST-segment depression is associated with a worse outcome than T-wave inversion alone or no ECG changes, and it is one of the adverse risk factors in the TIMI risk score (calculator 1) [17,40-44]. ST-segment depression also identifies patients who are more likely to benefit from an early invasive strategy [45,46]. (See "Non-ST-elevation acute coronary syndromes: Selecting an approach to revascularization".)
The importance of ST depression for prognosis was demonstrated in an analysis from GUSTO-IIb of over 12,000 patients presenting with symptoms of cardiac ischemia at rest that was confirmed by ECG; only about one-third underwent revascularization, a value much lower than current clinical practice [40]. The 30-day incidence of death or MI was significantly higher in patients with ST depression (10.5 versus 5.5 percent in those with T-wave inversion alone, adjusted odds ratio 1.62). This difference in mortality persisted at six months (15.4 versus 8.1 percent).
ST-segment depression also has long-term adverse predictive value [41-43,47]. This was illustrated in a review of 1416 patients with a non-ST-elevation ACS in the TIMI-III study registry [41]:
●Death or recurrent MI at one year was significantly more common in patients with ST-segment deviation (depression or elevation) ≥1 mm compared to those with isolated T-wave inversions or no ECG changes (11 versus 6.8 and 8.2 percent).
●Anterior ST-segment changes carried the worst prognosis, while the location of T-wave inversions did not correlate with outcome.
●Patients with left bundle branch block or those with the presence of only 0.5 mm ST-segment deviation were also at increased risk.
In addition to its presence, the extent of ST-segment depression also has prognostic value. (See 'Extent of myocardial ischemia' below.)
Recurrence or persistence of ST-segment depression also appears to predict a poorer outcome [48]. In a review of 515 patients who survived hospitalization after a confirmed NSTEMI, mortality during one-year follow-up was 5.5 percent in patients with no ST depression, 10 percent in those with ST depression at baseline or discharge, and 22 percent in those with ST depression at baseline and discharge (persistent ST-segment depression) [49].
T-wave inversion — Among patients with a non-ST-elevation ACS, the short-term prognosis appears to be better in those who present with T-wave inversion alone compared to ST-segment depression [40,43,50]. This was illustrated in an analysis from GUSTO-IIb in which the 30-day incidence of death or reinfarction in patients with T-wave inversion alone on the initial ECG (22 percent of patients) was significantly lower than in those with ST depression (5.5 versus 10.5 percent, adjusted odds ratio 0.62) [40].
Extent of myocardial ischemia — Among patients with unstable angina or NSTEMI, the magnitude, location, and extent of ST-segment depression, a reflection of the extent of myocardial ischemia, are associated with increased mortality. This was demonstrated in a logistic regression model that used data from the PARAGON-A trial and was then applied to 8001 patients in GUSTO-IIb trial [42]. The presence of ≥2 mm ST-segment depression was associated with a significant increase in the risk of death at one year (14 versus 4.4 percent for no ST-segment depression, adjusted odds ratio 5.73) (figure 3), while its presence in more than one region was associated with a mortality of 20 percent (adjusted odds ratio 9.2).
Additional short-term prognostic indicators related to the extent of myocardial ischemia have been identified in other studies:
●In a review of admission ECGs from almost 5200 patients in the GUSTO-IIb trial, the sum of ST-segment depression in all leads was a powerful independent predictor of 30-day mortality [44]. The risk increased continuously with increasing ST-segment depression: 30-day mortality in the top quartile (>6 mm) compared to the bottom quartile (0 to 2 mm) was 6.3 and 1.6 percent, respectively. Even minimal (<1 mm) ST-segment elevation in anterior or inferior leads was also an adverse predictor.
●In a series of 516 patients with unstable coronary disease, ST-segment depression or inverted T waves in five or more leads at the time of hospital admission was the only independent predictor of death or MI at 30 days [51].
●In a report of 432 patients with a first acute NSTEMI, the only ECG finding predictive of in-hospital outcome was ST-segment depression in two or more lateral leads (I, aVL, V5, or V6) [52]. Such patients had much higher rates of in-hospital mortality (14.3 versus 2.6 percent without lateral ST-segment depression), severe heart failure (14.3 versus 4.1 percent), and left main or three-vessel coronary disease in those who were catheterized (60 versus 22 percent). (See "Left main coronary artery disease".)
The extent of myocardial ischemia as determined by measurement of ST-segment depression also predicts which patients with a non-ST-elevation ACS will benefit most from an invasive treatment strategy. In an analysis of ECGs from 2201 patients participating in the FRISC-II trial, patients were stratified according to the sum of ST-segment deviation in all leads (0 to 2.5 mm, 3 to 5.5 mm, or ≥6 mm) and according to the number of leads with ST-segment deviation (0 to 4, 5 to 7, or ≥8 leads) [53]. At one year, the rate of death or MI was significantly lower with an invasive strategy for those patients with the greatest extent of myocardial ischemia by ST-segment sum (9.5 versus 19.4 percent) or by number of affected leads (8.5 versus 19.2 percent); there was no statistical benefit from invasive therapy in patients with the least extent of ischemia by ST-segment scoring.
AV block — Earlier reports that have assessed the incidence and prognostic significance of high degree atrioventricular (AV) block after MI have not distinguished between STEMI and NSTEMI. In a review of 610 patients with a first non-Q wave MI, second or third degree AV block developed in 7 percent [54]. High degree AV block was associated with larger and more complicated infarctions, similar to the observation in ST-elevation infarcts (see 'Conduction abnormalities' above). In the era of percutaneous coronary interventions, high degree AV block continues to be a marker of adverse outcomes [55,56].
New Q waves — Patients with non-ST-elevation ACS can develop new Q waves, which are associated with a worse prognosis. These relationships were illustrated in a review of 10,501 such patients who had survived 30 days: the 30-day ECG (compared to the baseline ECG) revealed new 30 to 40 msec Q waves in 7 percent and new ≥40 msec Q waves in 3 percent [47]. At six months, there was a nonsignificant increase in mortality in the patients with new 30 to 40 msec Q waves (3.4 versus 2.4 percent with no new Q waves, adjusted odds ratio 1.30, 95% CI 0.85-1.30) and a significant increase in mortality in those with new ≥40 msec Q waves (5.3 versus 2.4 percent, adjusted odds ratio 1.87, 95% CI 1.13-3.09). (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Significance of Q waves'.)
SUMMARY
In patients with ST-elevation myocardial infarction (STEMI), the following ECG features appear to predict a worse outcome:
●The extent of myocardial injury as estimated by the sum of the absolute ST-segment deviation, evidence of prior infarction, heart rate >84 beats per minute, and prolonged QRS duration. (See 'Extent of myocardial injury' above.)
●Presence of new Q waves. (See 'Presence or absence of new Q waves' above.)
●Lack of resolution of ST- and T-wave changes. (See 'Resolution of ST- and T-wave changes' above.)
In patients with non-ST-elevation acute coronary syndromes, the following ECG features appear to predict a worse outcome:
●ST-segment depression compared with just T-wave inversion. (See 'ST-segment depression' above and 'T-wave inversion' above.)
●Magnitude and extent of the ST-segment depression. (See 'ST-segment depression' above.)
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