Early and 1-Year Clinical Outcome of Patients’ Evolving Non–Q-Wave Versus Q-Wave Myocardial Infarction After Thrombolysis
Results From the TIMI II Study
Background There are few data comparing clinical outcome and potential indications for routine post–myocardial infarction cardiac catheterization and revascularization of patients who sustain a non–Q-wave versus Q-wave infarct after thrombolytic therapy.
Methods and Results A secondary analysis of 2634 patients enrolled in the TIMI II trial with a first myocardial infarction was performed to determine 6-week and 1-year cardiac event rates and identify clinical and angiographic differences between the 1867 patients (70.9%) who evolved a Q-wave infarct and the 767 patients (29.1%) who sustained a non–Q-wave infarct after treatment with intravenous thrombolytic therapy. Male sex (85.3% versus 75.6%; P<.001) and anterior wall infarcts (53.8% versus 43.7%; P<.001) were more frequent in the Q-wave versus the non–Q-wave group. During recombinant tissue-type plasminogen activator (rTPA) infusion, a greater percentage of non–Q-wave patients (37.3% versus 23.5%; P=.001) had normalization of initial ST-segment elevation. Infarct-related artery patency (TIMI flow grade 2 or 3) (P=.02), complete infarct-related artery reperfusion (TIMI 3 flow grade) (P<.001), and the percentage of patients with a predischarge resting left ventricular ejection fraction >55% (P<.001) were greater in the non–Q-wave group. New congestive heart failure during hospitalization developed more frequently in Q-wave patients (18.9% versus 11.6%; P<.001). After 42 days, the occurrences of reinfarction (P=.76), death (P=.76), and combined death or reinfarction (P=.43) were similar in patients assigned to the invasive or conservative postlytic management strategy, regardless of infarct type. One-year mortality was 3.4% versus 4.4% for non–Q-wave versus Q-wave infarct type, respectively (P=.25).
Conclusions Angiographic and clinical differences were observed between patients who present with initial ST-segment elevation and evolve early non–Q-wave versus Q-wave myocardial infarcts after treatment with rTPA, heparin, and aspirin. Early mortality and adverse clinical cardiac events in these patients are not significantly different after a conservative compared with an invasive treatment strategy, regardless of whether the infarct type is non–Q wave or Q wave.
The differing pathogeneses and prognoses of Q-wave and non–Q-wave myocardial infarctions were established in the prethrombolytic era.1 2 Non–Q-wave infarct patients have a relatively high prevalence of spontaneous infarct artery reperfusion,1 2 3 4 smaller infarct size,1 5 and relatively low in-hospital mortality1 2 6 but a higher rate of postinfarction recurrent ischemic events compared with patients with Q-wave infarcts.1 2 7 A greater residual ischemic burden attributed to a “limited” infarction among patients evolving a non–Q-wave infarction has led some clinicians to recommend a more aggressive postinfarction evaluation, including routine cardiac catheterization and coronary revascularization in patients with non–Q-wave infarction.8
In the past decade, thrombolytic therapy has evolved as the standard treatment for appropriately selected patients with acute myocardial infarction presenting with ECG ST-segment elevation.9 10 Results of placebo-controlled trials of intravenous thrombolytic therapy have indicated that pharmacological reperfusion limits infarct size and reduces in-hospital and 1-year mortality rates, producing clinical outcomes similar to those observed in patients with non–Q-wave infarction in the prethrombolytic era.10 11 The majority of patients with acute infarction who present with ST-segment elevation evolve Q-wave infarcts even though thrombolytic therapy reduces infarct size and enhances infarct artery reperfusion.12
Patients receiving thrombolytic therapy are a selected population compared with nonselected consecutive patients with myocardial infarction. However, there are few data comparing the clinical features of patients with non–Q-wave and Q-wave infarcts after thrombolytic therapy. The aims of the present study were to determine the prevalence of non–Q-wave and Q-wave infarctions in patients treated with thrombolytic therapy who present with initial ST-segment elevation; compare 21-day, 42-day, and 1-year clinical outcomes of both patient groups; and determine whether an invasive strategy applied to patients evolving a non–Q-wave myocardial infarction after thrombolysis results in fewer adverse cardiac events than a conservative strategy.
Study Design and Study Population
The inclusion and exclusion criteria for the TIMI II study have been previously described.13 In brief, eligible patients <76 years old with ischemic cardiac pain for >30 minutes who gave informed consent within 4 hours of symptom onset received thrombolytic therapy if they had ST-segment elevation of ≥0.1 mV in two or more contiguous ECG leads and no contraindication to thrombolytic therapy. Patients received intravenous recombinant tissue-type plasminogen activator (rTPA) and concomitant intravenous heparin and oral aspirin as previously described.13
To avoid misclassification of the qualifying event as non–Q-wave versus Q-wave infarction due to the presence of old Q waves on ECGs or Q waves resulting from reinfarction after the initial event, this analysis was restricted to TIMI II patients who met the following criteria: enzymatically and electrocardiographically confirmed first myocardial infarction, an interpretable day-2 ECG, and freedom from reinfarction before the day-2 ECG.
The magnitude and extent of ST-segment elevation of abnormal leads were measured from the qualifying ECG in the TIMI II Central ECG Laboratory. Normalization of ST-segment elevation was assessed and defined as return of ST segments to or close to baseline during infusion of rTPA. Infarct site was classified from the qualifying ECG as either anterior (ST-segment elevation of ≥0.1 mV in two or more adjacent V1 to V6 leads)or nonanterior.
The determination of non–Q-wave and Q-wave infarct ECG patterns was assessed in the TIMI II Central Exercise ECG Laboratory at St Louis University by analysis of the day-2 ECG. Measurements included Q-wave depth and duration, R-wave amplitude, S-wave depth, and degree of ST-segment displacement determined using a three-power–calibrated magnifying loupe. Averaged measurements were determined. Standard Minnesota Q-wave codes were generated using Q-wave width, depth, and Q-to-R ratio for the anterior (V1 to V5), inferior (II, III, and aVF), and lateral (I, aVL, and V6) lead groups, respectively (“Appendix”).14
Patients were classified as having a Q-wave infarct if new Q-wave criteria were present on the day-2 ECG. The remaining patients were classified as having a non–Q-wave infarct. The day-2 ECG was obtained at a mean±1 SD of 24.5±49.6 hours and 24.2±33.0 hours after study entry for the Q-wave and non–Q-wave groups, respectively (P=.83).
At study entry, patients were defined as being “not low risk” if any of the following criteria were present: age ≥70 years, anterior infarct location, rales involving ≥one third of the lung fields, systemic hypotension with sinus tachycardia, atrial fibrillation or flutter, pulmonary edema, or cardiogenic shock.
Invasive Versus Conservative Postlytic Management Strategies
At study entry, patients were randomly assigned to either an invasive or a conservative treatment strategy.13 The invasive strategy consisted of coronary angiography, contrast left ventriculography, and percutaneous transluminal coronary angioplasty (PTCA), if feasible, within 18 to 48 hours of the start of rTPA administration. The protocol PTCA was not performed if the infarct-related artery was occluded, had a residual stenosis <60%, or had unsuitable anatomy or abrupt closure of the vessel was likely to cause catastrophic hemodynamic consequences. Coronary artery bypass graft surgery (CABG) was recommended when clinically indicated or the coronary anatomy was considered unsuitable for protocol coronary angioplasty. In the conservative strategy, the protocol specified coronary angiography and revascularization for recurrent spontaneous or exercise-induced myocardial ischemia.
Before hospital discharge, radionuclide ventriculography (RVG) was performed at rest and during supine exercise to a heart rate of 120 beats per minute or to a maximum workload of 400 kilopound meter. The RVGs were analyzed at a central radionuclide core laboratory.13
Cardiac Catheterization Analysis
Coronary angiographic findings were analyzed at an angiographic core laboratory and are reported for the invasive strategy patients who received protocol catheterization. Obstructive coronary artery disease was considered present when there was a stenosis of ≥60% of the luminal diameter as assessed by visual and caliper-assisted methods. An occluded infarct artery was defined by either TIMI 0 (no perfusion) or TIMI 1 (penetration without perfusion) grade flow. A patent infarct artery was defined by either TIMI 2 (partial perfusion) or TIMI 3 (complete perfusion) grade flow.15
Clinical End Points
Death and recurrent fatal and nonfatal reinfarctions are reported for 21 days, 42 days, and 1 year after study enrollment. Myocardial infarction and cause of death were classified by a Morbidity and Mortality Classification Committee who had no knowledge of treatment assignment according to established criteria.13 Recurrent painful ischemic events before hospital discharge were defined as either definite myocardial infarction, suspected recurrent myocardial infarction, or other recurrent ischemic pain. New congestive heart failure before hospital discharge was defined by the appearance of clinical signs or symptoms of heart failure in patients without heart failure at enrollment.
The results are based on an analysis file created by the TIMI II Coordinating Center in January 1991. Comparisons of baseline characteristics between patient groups were carried out using χ2 tests or Fisher’s exact test for differences in proportions of categorical variables and Student’s t test for differences in mean values of continuous variables. The cumulative probability of events (eg, death, death or myocardial infarction, fatal and nonfatal recurrent myocardial infarction) was determined by the Kaplan-Meier method,16 and differences in the distribution of events during the first year after study entry were evaluated with the log-rank test.17 The effects of treatment strategy on 42-day outcomes were compared between patients with non–Q-wave versus Q-wave myocardial infarction using the Breslow-Day test for the homogeneity of the odds ratio.18 To account for potential biases due to nonrandomly missing data, outcomes on the hospital discharge resting RVGs were compared between patient subgroups using a composite unfavorable end point of death by 14 days, failure to complete a study, or a study with abnormal findings (ie, rest ejection fraction <55%). To account for the multiple statistical hypothesis tested in this analysis, P values <.01 were required to show evidence of a difference, and P values <.001 showed strong evidence.
Of 3339 patients enrolled in the TIMI II study, 705 (21.1%) were excluded from analysis due to history of prior myocardial infarction (n=468), no enzymatic confirmation of myocardial infarction (n=138), no day-2 ECG (n=55), reinfarction before day-2 ECG (n=23), or uninterpretable day-2 ECG (n=21). Of the remaining 2634 patients, 1867 (70.9%) were classified as having Q-wave and 767 (29.1%) as having non–Q-wave myocardial infarction.
Baseline Characteristics of Postlytic Q-Wave Versus Non–Q-Wave Infarction Groups
A greater percentage of the Q-wave patients were male (85.3% versus 75.6%; P<.001) and presented with ST-segment elevation in the anterior leads (53.8% versus 43.7%, P<.001, Table 1⇓). Atrial fibrillation or flutter and the use of nitrates during the week before study entry were more common among the non–Q-wave group (each P<.01). The baseline mean diastolic blood pressure was slightly greater (2 mm Hg) in the non–Q-wave group (P<.01). The mean±SD time from symptom onset to treatment with rTPA was 2.7±0.8 and 2.6±0.8 hours for Q-wave and non–Q-wave patients, respectively (P=.09). Infusion of rTPA began less than 2 hours after symptom onset in 27.1% of patients with non–Q-wave myocardial infarction and in 24.4% of patients with Q-wave myocardial infarction (P=.14) (Table 1⇓).
Qualifying ECG Findings
ECG indicators of infarct severity were fewer and of less magnitude in non–Q-wave patients compared with those who developed Q waves: the mean number of leads with ST-segment elevation of ≥0.l mV was 3.6 versus 4.2 leads (P<.001); the mean of the maximal ST-segment elevation in any ECG lead was 0.33±0.22 versus 0.43±0.28 mV (P<.001); and the percentage of patients with ≥0.3 mV of ST-segment elevation in any individual ECG lead was 41% versus 65%, respectively (P<.001). Non–Q-wave patients were more likely to have normalization of ST-segment elevation during the rTPA infusion than the Q-wave group (37.3% versus 23.5%; P<.001).
Cardiac Catheterization Findings
Among invasive strategy patients receiving protocol catheterization, the percentage of patients with two or more coronary arteries with ≥60% diameter stenosis (27.5% versus 29.2%, respectively, P=.27), the percentage of patients with collateral blood flow to the infarct-related artery, and the mean percent residual stenosis of the infarct-related artery were similar in the non–Q-wave and Q-wave groups (Table 2⇓). TIMI grade 3 flow was more frequent in non–Q-wave patients (P<.001).
The circumflex coronary artery was more commonly classified as the infarct-related vessel in patients who evolved a non–Q-wave infarction (20.6% versus 9.9%, P<.001; Table 2⇑). In a multivariate logistic model, both occlusion of the infarct artery (TIMI grade 0 or I) and location of the infarct artery were significant (P=.01) predictors of Q-wave versus non–Q-wave myocardial infarction. The odds ratio for Q-wave myocardial infarction was 1.6 for an occluded versus a patent infarct artery; the odds ratio for Q-wave myocardial infarction was 2.3 for an infarct in the right coronary artery compared with the left circumflex artery, 2.5 for the left anterior descending coronary artery compared with the left circumflex artery, and 1.1 for the left anterior descending versus the right coronary artery (P=NS).
Predischarge Rest and Exercise ECG and RVG
The mean resting left ventricular ejection fraction was 56.4% and 48.6% for the non–Q-wave and Q-wave groups, respectively. A greater percentage of patients evolving a non–Q-wave infarct had a left ventricular ejection fraction >55% (43.4% versus 24.1%; P=.001); severe left ventricular dysfunction (ie, ejection fraction ≤35%) was approximately threefold higher (11.1% versus 3.0%) in Q-wave infarction patients (Table 3⇓).
The percentages of patients with an increase in exercise ejection fraction ≥5% and without exercise-induced ST-segment depression were similar in the two groups (Table 3⇑).
The development of new congestive heart failure by hospital discharge occurred in a greater percentage of the Q-wave patients, whereas in-hospital recurrent cardiac ischemic pain occurred in a similar percentage of patients (Table 4⇓). A trend toward more frequent reinfarction by 21 days (5.9% versus 4.0%), 42 days (6.0% versus 4.6%), and 1 year (9.4% versus 7.4%) after study entry was observed in the non–Q-wave compared with the Q-wave group (P=.07). The odds ratio for reinfarction by 1 year was 1.3 (99% confidence interval [CI], 0.9 to 1.9). Fatal reinfarctions occurred in 1.0% of both the non–Q-wave and Q-wave groups, respectively.
The cumulative 1-year mortality was 3.4% among non–Q-wave and 4.4% among Q-wave patients (P=.25). The 1-year combined end point of death or reinfarction was also similar for the two groups (P=.24; Figure⇓). The odds ratio for 1-year mortality was 0.8 (99% CI, 0.4 to 1.4).
To assess whether lack of sensitivity of ECGs for detection of posterior infarction could lead to bias in comparison of prognosis of non–Q-wave versus Q-wave infarction, we compared 1-year prevalence of events according to infarction type among invasive strategy patients after excluding patients with circumflex artery infarctions. One-year mortality (3.1% versus 3.8%), reinfarction (7.6% versus 7.3%), and death or reinfarction (9.3% versus 9.8%) for non–Q-wave versus Q-wave patients, respectively, were not significantly different.
Approximately half of the patients in each infarct group were randomly assigned to either the invasive or conservative strategy (Table 5⇓). Of the 1867 Q-wave patients, 929 and 938 were randomly assigned to the invasive and conservative strategies, respectively. Of the 767 non–Q-wave patients, 395 and 372 were assigned to the invasive and conservative postlytic strategies.
By 42 days after study entry, a similar percentage of Q-wave and non–Q-wave infarct patients assigned to the invasive strategy underwent revascularization (Table 5⇑). Protocol PTCA was performed on 248 (62.8%) and 523 (56.3%) of non–Q-wave and Q-wave patients, respectively. The protocol PTCA was considered partially or fully successful in 237 (95.6%) and 473 (90.4%) of patients in whom it was attempted, respectively. The occurrence of clinical complications related to the protocol catheterization was similar for the two infarct groups (P=.80).
Among patients randomly assigned to the conservative strategy, cardiac catheterization and revascularization were performed, respectively, in 47.5% and 27.6% of non–Q-wave patients and in 51.8% and 24.3% of Q-wave patients by 42 days after study entry. Among the 143 (38.4%) non–Q-wave and 373 (39.8%) Q-wave patients undergoing cardiac catheterization before discharge, recurrent ischemic pain (46.2% versus 42.6%), suspected reinfarction (5.6% versus 4.6%), and an abnormal exercise test (2.1% versus 2.9%) accounted for the majority of reasons for cardiac catheterization.
Among conservative strategy patients not receiving catheterization during the initial hospitalization who completed a hospital discharge exercise test, 74 of 140 patients (52.8%) with a positive exercise test, 169 of 621 patients (27.2%) with a negative test, and 58 of 167 patients (37.7%) with an equivocal test had received cardiac catheterization by 42 days after study entry. The percentage of patients with a clearly positive or negative test receiving cardiac catheterization by 42 days was nearly identical for non–Q-wave and Q-wave patients; among patients with an equivocal test, a slightly higher percentage of Q-wave patients (38.8%) than non–Q-wave patients (23.9%) received cardiac catheterization.
Within 42 days of study entry, the occurrence of death (P=.76), fatal or nonfatal reinfarction (P=.81), or death or reinfarction (P=.43) was similar in the invasively and conservatively treated patients regardless of Q-wave or non–Q-wave infarct type (Table 5⇑). Subgroup analyses did not indicate evidence for differences in the effect of treatment strategy in Q-wave versus non–Q-wave patients in either the low-risk or not-low-risk patient groups.
In the thrombolytic era, the prevalence rates and prognoses of postlytic non–Q-wave and Q-wave myocardial infarction types are incompletely defined and have the potential to have different prognoses compared with prethrombolytic studies since the majority of fibrinolytically treated patients present with ECG ST-segment elevation.
In TIMI II, 29.1% of the 2632 patients with a first myocardial infarction who were eligible for this analysis and presented with ST-segment elevation were classified as evolving a non–Q-wave infarct pattern within 24 hours of treatment with intravenous rTPA. Similar findings have recently been observed in another large thrombolytic trial enrolling patients with ST-segment elevation.19 In TIMI II, non–Q-wave infarction was more frequently associated with circumflex artery occlusions, more brisk perfusion of the infarct-related vessel, enhanced predischarge left ventricular function, and a lower frequency of developing new congestive heart failure during the index hospitalization.
Clinical Outcome of Q-Wave and Non–Q-Wave Infarct Types After Thrombolysis: Infarct Size
In the TIMI II study, non–Q-wave infarct patients were more frequently observed to have resolution of ST-segment elevation during rTPA infusion, suggesting successful infarct artery reperfusion.20 The greater percentage of non–Q-wave patients observed to have TIMI grade 3 flow of the infarct-related vessel may have in part contributed to the observed differences in left ventricular function and the lower prevalence of new congestive heart failure occurring during hospitalization in postlytic non–Q-wave infarct patients, supporting earlier studies.21 22 Alternatively, the greater preservation of postinfarct left ventricular function among non–Q-wave patients may be in part attributable to a smaller initial ischemic myocardial burden, as reflected by the finding of fewer ECG leads with ST-segment elevation and more frequent circumflex artery infarcts.
Reinfarction and Mortality
A trend was present (P=.07) toward slightly more frequent recurrent myocardial infarctions in non–Q-wave compared with Q-wave patients during the year after study entry. Mortality rates were low at both 21 days and 1 year after study entry and were similar for the two infarct groups. These findings are in contrast to prethrombolytic studies23 24 25 and a recent report from the TPA/SK Mortality investigators.19 The latter study group have made a preliminary report of a significantly higher 6-month frequency of postdischarge reinfarction (6.2% versus 3.6%; odds ratio [95% CI], 1.8 [1.22 to 2.66]) and mortality (4.6% versus 3.5%) among patients evolving a postlytic non–Q-wave compared with Q-wave myocardial infarction. The higher event rate in TIMI II compared with the TPA/SK report for Q-wave and non–Q-wave patients may be accounted for by (1) differences in reporting (ie, this report includes all events after the day-2 ECG, whereas the TPA/SK report includes only the lower-risk period after hospital discharge); (2) exclusion of patients with prior myocardial infarction, enhancing the ability to detect new Q-wave versus non–Q-wave items on the surface ECG; and (3) differences in postlytic treatment strategies (ie, greater use of coronary revascularization and the use of adjunctive intravenous heparin) in the TIMI II study. The TIMI II study had limited power to detect modest differences in mortality and reinfarction rates according to infarct type, and the odds ratios in this report do not exclude risks for death or reinfarction similar to those in the TPA/SK study among the non–Q-wave patients.
Comparison of Postlytic Management Strategies Among the Q-Wave and Non–Q-Wave Infarct Groups
In TIMI II, approximately half of the patients who evolved a postlytic non–Q-wave and Q-wave infarction were randomly assigned to an invasive or a conservative postinfarct strategy. Within 42 days of study entry, the occurrence of fatal and nonfatal reinfarction, death, and combined death and reinfarction were similar for patients assigned to the invasive or conservative strategy, regardless of the infarct type (ie, Q wave or non–Q wave).
The non–Q-wave and Q-wave patients in the conservative strategy group who experienced spontaneous or exercise-induced ischemia received coronary angiography and underwent coronary revascularization if technically feasible by study design, potentially reducing event rates in these TIMI II patients. The findings from this secondary analysis are consistent with the overall results of the TIMI II trial13 and demonstrate that patients with a first acute myocardial infarction who evolve either a non–Q-wave or a Q-wave myocardial infarction after early (ie, ≤4 hours) intravenous thrombolysis experience a comparable clinical outcome and suggest satisfactory clinical outcomes whether managed by either an invasive or a conservative postlytic strategy.
The TIMI II data are further supported by the recently completed TIMI IIIB study,26 which reported similar 42-day rates of reinfarction and combined death and reinfarction in patients with unstable angina or non–Q-wave myocardial infarction regardless of whether an invasive or a conservative strategy was used. In TIMI IIIB, most patients presented with ST-segment depression or T-wave inversion; in TIMI II, all enrolled patients were required to exhibit ST-segment elevation on the qualifying ECG. Additional studies that assess postlytic revascularization strategies in larger series of non–Q-wave patients who present with ST-segment elevation would be important to confirm our observations.
The exclusion of very elderly patients (>76 years), patients with prior myocardial infarction, and patients dying or developing reinfarction within the initial 24 hours after thrombolysis limits this secondary analysis to a relatively low-risk patient population. In the overall TIMI II study of 3339 patients, the mortality rate was 1.9% within the initial 18 hours of study enrollment.27 Thus, high-risk patients who died before the acquisition of the day-2 ECG were not included for comparison in this analysis.
The ECG criteria for diagnosis of non–Q-wave and Q-wave myocardial infarction are not standardized. The prognostically established Minnesota code criteria were used in TIMI II, in contrast to some of the earlier studies of non–Q-wave and Q-wave infarction.3 19 23 24 25 28 The time of ECG classification of non–Q-wave and Q-wave myocardial infarction has also varied in previous studies, with most classifications performed at hospital discharge.29 In the present report, categorization of infarct type was based on the day-2 ECG since this is the time frame physicians use most frequently to make clinical decisions concerning cardiac catheterization in stable patients. Eisenberg et al30 report progression of non–Q-wave to Q-wave infarction in only 1.5% of patients treated with thrombolytic therapy from 24 hours to hospital discharge. Thus, the potential for overestimating the percentage of non–Q-wave myocardial infarctions in the present study is small.
The findings from this secondary TIMI II analysis indicate ECG, angiographic, and clinical outcome differences among patients with a first acute myocardial infarction evolving early non–Q-wave or Q-wave myocardial infarction. However, early (ie, 21-day) and 1-year mortality and reinfarction rates were similar for the two infarct groups. The occurrence of combined death and reinfarction by 42 days was similar in both infarct groups receiving an invasive or a conservative postlytic treatment strategy as used in the TIMI II trial. A longer-term follow-up will be necessary to confirm these early observations between the two infarct groups given the differences in left ventricular function and congestive heart failure.
Minnesota Q-Wave Code Criteria
Anterolateral Site (Leads I, aVL, and V6)
1-1-1 Q/R amplitude ratio ≥1/3, plus Q duration ≥0.03 second in lead I or V6.
1-1-2 Q duration ≥0.04 second in lead I or V6.
1-1-3 Q duration ≥0.04 second, plus R amplitude ≥3 mm in lead aVL.
1-2-1 Q/R amplitude ratio ≥1/3, plus Q-wave duration ≥0.02 second and <0.03 second in lead I or V6.
1-2-2 Q duration ≥0.03 second and <0.04 second in lead I or V6.
1-2-3 QS pattern in lead I.
1-2-8 Initial R amplitude decreasing to 2 mm or less in every beat between V5 and V6. (All beats in lead V5 must have an initial R >2 mm.)
1-3-1 Q/R amplitude ratio ≥1/5 and <1/3, plus Q duration ≥0.02 second and <0.03 second in lead I or V6.
1-3-3 Q duration ≥0.03 second and <0.04 second, plus R amplitude ≥3 mm in lead aVL.
Inferior Site (Leads II, III, and aVF)
1-1-1 Q/R amplitude ratio ≥1/3, plus Q duration ≥0.03 second in lead II.
1-1-2 Q duration ≥0.04 second in lead II.
1-1-4 Q duration ≥0.05 second in lead III, plus a Q-wave amplitude ≥1.0 mm in the majority of beats in lead aVF.
1-1-5 Q duration ≥0.05 second in lead aVF.
1-2-1 Q/R amplitude ratio ≥1/3, plus Q duration ≥0.02 second and <0.03 second in lead II.
1-2-2 Q duration ≥0.03 second and <0.04 second in lead II.
1-2-3 QS pattern in lead II.
1-2-4 Q duration ≥0.04 second and <0.05 second in lead III, plus a Q-wave ≥1.0 mm amplitude in the majority of beats in aVF.
1-2-5 Q duration ≥0.04 second and <0.03 second in lead aVF.
1-2-6 Q amplitude ≥5.0 mm in lead III or aVF.
1-3-1 Q/R amplitude ratio ≥1/5 and <1/3, plus Q duration ≥0.02 second and <0.03 second in lead II.
1-3-4 Q duration ≥0.03 second and <0.04 second in lead III, plus a Q-wave ≥1.0 mm amplitude in the majority of beats in lead aVF.
1-3-5 Q duration ≥0.03 second and <0.04 second in lead aVF.
1-3-6 QS pattern in each of leads III and aVF.
Anterior Site (Leads V1, V2, V3, V4, and V5)
1-1-1 Q/R amplitude ratio ≥1/3 plus Q duration ≥0.03 second in any of leads V2, V3, V4, V5.
1-1-2 Q duration ≥0.04 second in any of leads V1, V2, V3, V4, V5.
1-1-6 QS pattern when initial R-wave is present in adjacent lead to the right on the chest, in any of leads V2, V3, V4, V5, V6.
1-1-7 QS pattern in all of leads V1-V4 or V1-V5.
1-2-1 Q/R amplitude ratio ≥1/3, plus Q duration ≥0.02 second and <0.03 second, in any of leads V2, V3, V4, V5.
1-2-2 Q duration ≥0.03 second and <0.04 second in any of leads V2, V3, V4, V5.
1-2-7 QS pattern in all of leads V1, V2, and V3.
1-2-8 Initial R amplitude decreasing to 2.0 mm or less in every beat between any of leads V2 and V3, V3 and V4, or V4 and V5. (All beats in the lead immediately to the right on the chest must have an initial R >2 mm.)
1-3-1 Q/R amplitude ratio ≥1/5 and <1/3 plus Q duration ≥0.02 second and <0.03 second in any of leads V2, V3, V4, V5.
1-3-2 QS pattern in lead V1 and V2.
We express our appreciation to Marilyn J. Utt and Sally Peebles for their assistance in preparation of the manuscript.
Reprint requests to TIMI Coordinating Center, Maryland Medical Research Institute, Inc, 600 Wyndhurst Ave, Baltimore, MD 21210.
Guest editor for this article was J. David Bristow, MD, Oregon Health Sciences University, Portland.
↵1 Investigators and participating centers are listed in N Engl J Med. 1989;320:618-627.
- Received June 13, 1994.
- Revision received November 22, 1994.
- Accepted December 3, 1994.
- Copyright © 1995 by American Heart Association
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