Predictors and Implications of Q-Waves in ST-Elevation Acute Coronary Syndromes

Article Outline

• Abstract
• Methods
  • Statistical Methods
  • Funding Source
• Results
• Discussion
  • Incidence of Q-Waves
  • Factors Associated with Development of Q-Waves
  • Implications of Q-Waves
  • Study Strengths and Limitations
  • Conclusions
• Acknowledgments
• References
• Copyright

Abstract 

Background

Q-waves in ST-elevation acute coronary syndromes carry adverse implications. We sought to determine the frequency, predictors, and implications of Q-waves in the current era that includes primary percutaneous coronary interventions.

Methods

There were 14,916 patients evaluated in a multicenter observational study. They presented with ST-elevation acute coronary syndromes between 1999 and 2006. Clinical variables were compared between patients with versus without presenting Q-waves, with an additional comparison in the latter group between those with versus without subsequent development of Q-waves.

Results

ST-elevation myocardial infarction occurred in 88.6% of patients. Q-waves were present on the initial electrocardiogram in 3929 patients and developed later in an additional 3085 patients. The incidence of Q-waves at presentation or during hospitalization decreased from 61% to 39% between 1999 and 2006 (linear trend P<.001). Both presenting and subsequent Q-waves were associated with greater likelihood of coronary occlusions and higher cardiac marker elevations (P <.001). Multivariate analysis showed that presenting Q-waves were associated with male sex (odds ratio [OR] 1.28), increased age (OR 1.06 per 5 years), diabetes (OR 1.26), smoking (OR 1.11), chronic aspirin (OR 0.79), acute aspirin (OR 0.87), other chronic cardiac medications (OR 0.80), prior heart failure (OR 0.67), and prior coronary artery disease (OR 0.61). Presenting Q-waves were independently associated with increased in-hospital mortality (OR 1.46), but Q-waves at presentation or during hospitalization did not impact 6-month mortality.

Conclusions

Q-waves in ST-elevation acute coronary syndromes are decreasing in incidence. Q-waves are a major determinant of in-hospital mortality, and targeted interventions should be directed to these high-risk patients.

Keywords: Acute coronary syndrome, Electrocardiography, Myocardial infarction, Myocardial ischemia

As the definition of acute myocardial infarction continues to evolve, Q-waves remain important in the diagnosis of acute or chronic myocardial infarction. Q-waves can localize the culprit artery, allow dating of the event, and approximate the size of the affected myocardium.¹ Typically, acute myocardial infarctions are divided into those with or without ST-elevation, having largely replaced prior stratification by the presence or absence of Q-waves. Although historically, Q-waves have been associated with transmural infarcts, recent studies contradict this,² and report that infarct size might be the strongest predictor of Q-wave development.³, ⁴

The Q-wave carries significant prognostic implications,⁵ and serial electrocardiograms (ECGs) are recommended following an acute myocardial infarction, in part to monitor for Q-waves that may help assess the extent of infarction and success of reperfusion therapy.⁶ Furthermore, the majority of ST-elevation acute coronary syndromes are reported to develop Q-waves.⁷

The treatment of myocardial infarction has significantly evolved over the past decade, with the development of improved medical and reperfusion strategies. The objectives of this large multinational observational sudy were to determine the frequency, predictors, and prognostic implications of Q-waves in contemporary patients hospitalized with ST-elevation acute coronary syndromes. Data from the Global Registry of Acute Coronary Events project were utilized for the present investigation.

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Methods 

Analysis for this project was performed using the Global Registry of Acute Coronary Events database. This worldwide registry (111 study sites in 14 countries) was used to assess major clinical variables in acute coronary syndrome patients between 1999 and 2006. Descriptions of the data collection methods have been previously published.⁸, ⁹, ¹⁰ The registry was designed to provide data on an unbiased, representative population of acute coronary syndrome patients. Patients were excluded if the event was precipitated by significant noncardiovascular co-morbidities, including acute anemia or hyperthyroidism. Study investigators at each hospital obtained appropriate approval for data collection from their ethics or institutional review boards. To obtain an unselected population, the initial 10 to 20 consecutive eligible patients were recruited at each site per month. Trained coordinators used standardized case report forms to collect data. Demographic characteristics, past medical history, presenting symptoms, biochemical and ECG findings, treatments, and outcome data were collected. Standardized definitions for all diagnoses and variables were used.⁹, ¹⁰ Audits were regularly performed at all hospitals. Written reports were provided quarterly to each site to provide hospital-specific feedback about patient characteristics, presentation, management, and outcomes. The study protocol is consistent with the principles of the Declaration of Helsinki.

Inclusion criteria for this cohort required new or presumptively new ST-elevations of ≥1 mm in 2 or more consecutive leads or new or presumptively new left bundle branch block. Patients were not required to have elevated cardiac enzymes for inclusion. Exclusion criteria included transfer patients (because of the impact of delay on the development of Q-waves), those with prior myocardial infarction (because of the anticipated high prevalence of existing Q-waves), or patients treated with reperfusion by coronary artery bypass grafting only (because accurate time to reperfusion therapy was not available). To meet criteria, Q-waves were required to be present in 2 consecutive leads and to be at least 40 ms in duration or 1/3 of the R-wave height. The study cohort comprised 14,916 patients, of whom 6-month follow-up data were available in 11,208 patients.

Statistical Methods 

Two sets of comparisons were performed, with the first between patients with or without Q-waves on the initial hospital ECG. The second considered patients without Q-waves on the initial ECG, and compared those with versus those without subsequent development of Q-waves during hospitalization. The Fisher's exact test and the Wilcoxon rank sum test were used for univariate comparisons of discrete and continuous variables, respectively, between the respective comparison groups. The Cochran-Armitage Trend Test was used to evaluate potentially changing trends over time in the frequency of Q-waves.

We developed separate multivariable regression models to identify variables associated with the occurrence of Q-waves on the presentation ECG and the development of first-onset Q-waves after presentation. Variables with a potential impact on the development of Q-waves were selected. For Q-waves on presentation, a stepwise logistic regression model was used with the following candidate variables: age, sex, chronic aspirin therapy, other chronic evidence-based medications (beta-blocker, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, or statin), prehospital acute aspirin, prehospital acute thienopyridine, prehospital acute heparin, prehospital acute glycoprotein IIB/IIIA inhibitor, patient delay (symptom onset to hospital arrival), history of coronary artery disease, diabetes, smoking, heart failure, dyslipidemia, angina, percutaneous coronary intervention, coronary artery bypass graft surgery, hypertension, peripheral arterial disease, transient ischemic attack or stroke, or renal insufficiency.

To determine variables associated with Q-waves only after admission, they needed to precede Q-wave development. As a result, patients with first-onset Q-waves after 24 hours were compared with patients with no Q-waves at any time, and candidate variables were considered if they ocurred within 24 hours of presentation. The following candidate variables were used: age, sex, chronic aspirin, other chronic evidence-based medications (beta-blocker, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, or statin), other acute evidence-based medications (beta-blocker, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, or statin), acute aspirin, acute thienopyridine/heparin/glycoprotein IIB/IIIA inhibitor, chronic heparin/thienopyridine, patient delay (symptom onset to hospital arrival), history of coronary artery disease, diabetes, smoking, heart failure, dyslipidemia, angina, percutaneous coronary intervention, coronary artery bypass graft surgery, hypertension, peripheral arterial disease, transient ischemic attack or stroke, renal insufficiency, systolic blood pressure, Killip class, initial creatinine, pulse, elevated initial cardiac markers, presenting cardiac arrest, percutaneous coronary interventions versus no reperfusion in the initial 24 hours, fibrinolytics versus no reperfusion in the initial 24 hours, and both percutaneous coronary interventions and fibrinolytics versus no reperfusion in the initial 24 hours.

We also assessed the independent predictive value of Q-waves on in-hospital and 6-month mortality, after adjusting for the respective risk model variables. To examine the impact of Q-waves on in-hospital mortality, the stepwise logistic regression model controlled for published risk score variables: age, systolic blood pressure, Killip class, pulse, positive initial cardiac markers, cardiac arrest, and ST-segment depression.⁹

To assess the effect of Q-waves on 6-month mortality (among patients surviving hospitalization), the stepwise logistic regression model included the published risk score variables from 2 separate studies: age, history of heart failure, history of peripheral artery disease, systolic blood pressure, Killip class, initial creatinine, pulse, positive initial cardiac markers, presenting cardiac arrest, ST-segment depression, and percutaneous coronary interventions during hospitalization.¹⁰, ¹¹ History of myocardial infarction was not considered a candidate variable given the exclusion criteria of this study. Additional variables included treatment with fibrinolytics in the initial 24 hours versus no reperfusion, and combined percutaneous coronary interventions during hospitalization and fibrinolytics within the initial 24 hours versus no reperfusion.

All tests of statistical significance were done at alpha=0.05. Statistical analysis was performed with SAS software version 9.1 (SAS Institute Inc., Cary, NC).

Funding Source 

This research was supported by an unrestricted grant from Sanofi-Aventis, Paris, France.

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Results 

This study sample consisted of 14,916 patients from 111 sites in 14 countries. On the initial ECG, Q-waves were present in 3929 (26.3%) patients, and developed later during hospitalization in an additional 3085 (20.7%) patients. A total of 7681 (51.5%) patients did not have Q-waves at presentation or during hospitalization; the presence or absence of Q-waves after presentation was unknown in 221 patients (1.5%). The incidence of Q-waves at any time (at presentation or during hospitalization) decreased from approximately 61% to 39% between 1999 and 2006 (P <.001 for trend). Elevated cardiac markers occurred in 88.6% of the total study population.

Patients with prior coronary artery disease or coronary revascularization were less likely to develop Q-waves, while those taking chronic evidence-based medications also were less likely to develop Q-waves (Table 1). Patients with Q-waves on the initial ECG were more likely to present with heart failure at the time of hospitalization.

Table 1. Patient Characteristics

	Initial ECG			Subsequent ECG (No Q-Waves on Initial ECG)
	No Q-Waves n=10,987	Q-Waves n=3929	P-Value	No Q-Waves n=7681	Q-Waves n=3085	P-value
Demographics
Age, median in years (25th, 75th percentile)	64(53,74)	66(55,76)	<.001	64(53,75)	61(52,71)	<.001
Male sex (%)	69	71	.089	67	75	<.001
Prehospital delay, median in minutes (25th, 75th percentile)	140(78,275)	212(105,553)	<.001	145(78,302)	130(76,232)	<.001
Past medical history
Coronary artery disease (%)	7.8	5.1	<.001	9.4	3.9	<.001
Hypertension (%)	50.4	49.7	.434	52.7	45.0	<.001
Diabetes (%)	18.0	21.0	<.001	18.9	15.8	<.001
Smoking (%)	59.0	58.2	.359	56.2	66.2	<.001
Dyslipidemia (%)	34.3	31.2	<.001	34.8	33.7	.301
Heart failure (%)	4.0	3.3	.052	4.8	1.7	<.001
Percutaneous coronary intervention (%)	4.1	2.7	<.001	4.9	2.3	<.001
Coronary artery bypass graft surgery (%)	2.7	1.8	.002	3.4	1.0	<.001
Chronic medications
Aspirin (%)	16.0	13.3	<.001	18.2	10.7	<.001
Beta-blocker (%)	14.2	10.1	<.001	15.7	10.7	<.001
Angiotensin converting enzyme inhibitor or receptor blocker (%)	18.8	16.6	.002	20.7	14.5	<.001
Statin (%)	10.3	8.5	.001	11.5	7.6	<.001
Presenting features
Heart failure (%)	15.5	20.7	<.001	16.5	13.4	<.001
Pulse, median in beats per minute (25th, 75th percentile)	76(64,90)	80(68,95)	<.001	77(65,90)	75(62,87)	<.001
Systolic blood pressure, median in mm Hg (25th, 75th percentile)	139(120,159)	137(120,155)	.027	140(120,160)	136(118,155)	<.001

ECG=electrocardiogram. The n for each column represents the total number of observations; observations for individual variables may be less due to missing values. P-values for binomial variables from Fisher's Exact test, and for continuous variables from Wilcoxon rank-sum test.

Anterior ST-elevations or a culprit lesion in the left anterior descending artery were more likely to be associated with presenting Q-waves, in contrast to lateral or inferior ST-elevations or culprit lesions in other arteries on cardiac catheterization (Table 2). The presence of Q-waves at any time was associated with higher cardiac marker elevations, and a greater incidence of coronary artery occlusion on cardiac catheterization.

Table 2. Studies and Management

	Initial ECG			Subsequent ECG (No Q-Waves on Initial ECG)
	No Q-Waves n=10,987	Q-Waves n=3929	P-Value	No Q-Waves n=7681	Q-Waves n=3085	P-Value
Presenting ECG
Anterior ST-elevations (%)	39.6	52.7	<.001	41.5	35.3	<.001
Inferior ST-elevations (%)	48.8	46.5	.013	43.0	63.2	<.001
Lateral ST-elevations (%)	25.9	26.3	.672	24.2	30.2	<.001
Left bundle branch block (%)	9.2	2.3	<.001	12.2	1.5	<.001
Culprit lesion
Left main artery (%)	1.1	1.1	1.000	1.4	0.5	<.001
Left anterior descending artery (%)	41.9	54.4	<.001	44.7	35.8	<.001
Left circumflex artery (%)	14.7	7.7	<.001	15.5	12.9	.008
Right coronary artery (%)	37.8	33.5	<.001	33.0	48.4	<.001
Unknown/other (%)	4.5	3.4	.016	5.5	2.5	<.001
Culprit artery flow
Occluded (%)	43.5	53.9	<.001	40.2	51.2	<.001
Slow (%)	17.1	15.3	.074	16.4	18.7	.039
Normal (%)	19.3	14.9	<.001	20.4	16.6	<.001
Unknown (%)	20.1	15.8	<.001	23.0	13.6	<.001
Acute medication (≤24 hours)
Aspirin (%)	94.2	95.2	.023	93.4	96.3	<.001
Thienopyridine (%)	54.5	51.2	.003	54.3	58.1	.002
Heparin (%)	80.8	80.3	.494	80.9	81.8	.299
Glycoprotein IIb/IIIa (%)	26.3	25.5	.370	25.4	28.7	.001
Beta-blocker (%)	70.5	68.7	.040	70.6	71.0	.707
Angiotensin-converting enzyme inhibitor or receptor blocker (%)	45.8	49.5	<.001	46.9	44.0	.007
Statin (%)	44.4	42.5	.039	43.9	48.2	<.001
Reperfusion (≤24 hours)
No intervention (%)	38.4	43.2	<.001	47.0	17.1	<.001
Percutaneous coronary interventions only (%)	27.9	28.0	.948	27.0	30.7	<.001
Fibrinolytics only (%)	28.2	24.6	<.001	22.3	42.3	<.001
Both percutaneous coronary interventions and fibrinolytics (%)	5.5	4.3	.005	3.7	9.9	<.001
Time arrival to reperfusion
Percutaneous coronary interventions only, median in minutes (25th, 75th percentile)	88(52,143)	90(50,155)	.824	95(60,168)	65(40,110)	<.001
Any fibrinolytics, median in minutes (25th, 75th percentile)	30.0(15,55)	31.0(15,61)	.033	30.0(16,59)	29.0(14,53)	.001
Cardiac markers (peak during initial 24 hours)	n=4971	n=1503		n=3684	n=1287
Troponin, median of ratio to upper limits of normal (25th, 75th percentile)	75(14,285)	103(29,370)	<.001	50(8.9,189)	203(51,556)	<.001
Creatine kinase, median of ratio to upper limits of normal (25th, 75th percentile)	5.2(1.7,11)	6.7(2.6,14)	<.001	3.9(1.3,9.3)	9.3(4.6,16)	<.001
Creatine kinase-MB, median of ratio to upper limits of normal (25th, 75th percentile)	8.4(3.0,21)	9.8(3.6,28)	<.001	6.7(2.3,17)	13.8(6.2,31)	<.001

ECG=electrocardiogram.

The n for each column represents the total number of observations; observations for individual variables may be less due to missing values. P-values for binomial variables from Fisher's Exact test, and for continuous variables from Wilcoxon rank-sum test.

Variables independently related to Q-waves on the initial ECG are shown in Figure 1, while those for Q-waves that develop after presentation are shown in Figure 2.

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• Figure 1. 

  Variables associated with Q-waves on the initial ECG (n=10,939). ECG=electrocardiogram; OR=odds ratio; CI = confidence interval; other meds=beta-blocker, angiotensin-converting enzyme inhibitor or receptor blocker, or statin versus none. OR for increased age per 5 years.

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• Figure 2. 

  Variables associated with new-onset Q-waves after initial 24 hours (n=7404). OR=odds ratio; CI=confidence interval.

Univariate results suggest increased in-hospital mortality in patients with presenting Q-waves. In patients with no Q-waves on presentation, later Q-waves were associated with lower in-hospital mortality (Table 3). To evaluate the impact of Q-waves on in-hospital mortality, a logistic regression model added presenting Q-waves to established mortality risk factors, which found that presenting Q-waves were associated with increased in-hospital mortality independent of previous risk factors (Figure 3).

Table 3. Outcomes

	Initial ECG			Subsequent ECG (No Q-Waves on Initial ECG)
	No Q-Waves	Q-Waves	P-Value	No Q-Waves	Q-Waves	P-Value
In-hospital outcomes	n=10,987	n=3929		n=7681	n=3085
Heart failure or pulmonary edema (%)	14.0	20.3	<.001	13.4	15.3	.013
Cardiogenic shock (%)	5.5	8.7	<.001	5.6	5.6	.963
Cardiac arrest or malignant arrhythmia (%)	9.8	12.3	<.001	9.5	10.4	.138
Renal failure (%)	3.4	5.8	<.001	3.5	3.4	.726
Death (%)	6.0	10.0	<.001	6.7	4.2	<.001
6-month outcomes	n=8317	n=2892		n=5736	n=2403
Post-discharge death (%)	3.8	5.2	<.001	4.4	2.4	<.001
Reinfarction (%)	2.5	2.8	.411	2.6	2.1	.235
Unscheduled cardiac catheterization (%)	8.2	6.8	<.001	8.2	8.4	.819
Rehospitalization for cardiac disease (%)	15.5	15.3	.804	15.9	15.0	.333

ECG=electrocardiogram.

The n for each column represents the total number of observations; observations for individual variables might be less due to missing values.

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• Figure 3. 

  Presenting variables associated with in-hospital mortality (n=13,160). Presenting Q-waves were independently associated with increased in-hospital mortality. OR=odds ratio; CI=confidence interval. OR for increased age per 5 years, for systolic blood pressure per 5 mm Hg, for pulse per 5 beats per minute, and for creatinine per 1 mg/dL.

Univariate results noted increased 6-month mortality in patients presenting with Q-waves. In patients with no Q-waves on presentation, subsequent Q-waves were associated with lower 6-month mortality. A logistic regression model added Q-waves at any time to established mortality risk factors, and found that Q-waves were not associated with a difference in 6-month mortality after adjusting for a variety of potentially confounding prognostic factors (OR 1.15, 95% confidence interval, 0.93-1.43).

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Discussion 

The incidence of Q-waves in ST-elevation acute coronary syndrome patients has decreased over the time of this study, and Q-waves now develop in a minority of such patients. A large majority of patients had elevated cardiac enzymes and therefore had ST-elevation myocardial infarctions, while a small proportion of patients did not have these, suggesting spontaneous or rapid reperfusion that did not result in an acute myocardial infarction, false-positive ST-elevations, left bundle branch block without myocardial infarction, or other causes. In the contemporary era, presenting Q-waves continue to have important prognostic implications during hospitalization, but do not appear to impact 6-month survival after discharge.

These findings may reflect significant changes in the management and outcomes of acute coronary syndrome patients recently reported in the Global Registry of Acute Coronary Events cohort. Between 1999 and 2006, there was increased use of evidence-based medications, cardiac catheterizations and percutaneous coronary interventions (including primary percutaneous coronary interventions), and a corresponding decrease in the use of fibrinolytics. These temporal changes were associated with a significantly lower in-hospital morbidity and mortality over the study period.¹²

Incidence of Q-Waves 

Development of Q-waves has been reported in the majority of ST-elevation myocardial infarction patients,¹³ typically within 9 hours following a myocardial infarction.¹⁴ Studies with fibrinolytics noted Q-waves on the presenting ECG in 33%-39% of ST-elevation myocardial infarction patients,¹⁵, ¹⁶ while a randomized trial of 15,222 ST-elevation myocardial infarction patients treated with fibrinolytics noted Q-waves on the presenting ECG in 67% of patients.¹⁷ During hospitalization, Q-waves have been reported in 80% of patients treated with fibrinolytics,¹⁸ while pooled data from 5 randomized controlled trials that included fibrinolytic therapy reported that Q-waves developed in 86% of patients.¹⁹

Randomized controlled trials typically have a selection bias toward the inclusion of healthier patients, and Q-waves would be expected to be less common in these patients. However, in this contemporary cohort, Q-waves occur in a minority of patients following ST-elevation acute coronary syndromes, with the incidence of Q-waves decreasing between 1999 and 2006. A likely explanation for these findings is that there has been a significant improvement over time in expediting the diagnosis and transfer of ST-elevation acute coronary syndrome patients, with improved medical and reperfusion management.

Factors Associated with Development of Q-Waves 

Our study corroborates earlier data suggesting a protective effect of certain variables on the development of presenting Q-waves. Prior coronary artery disease appears protective against Q-waves, and it is plausible that this is mediated via ischemic preconditioning,²⁰ which could limit infarct size and therefore Q-wave development. Chronic medications may decrease the incidence of Q-waves through alterations in platelet and endothelial function or decreased myocardial oxygen demand. The incidence of previously established coronary artery disease is small in this cohort that excluded patients with prior myocardial infarction, so the majority of patients on these medications were presumptively being treated for primary prevention of coronary artery disease or for risk factors. The association of these medications with fewer Q-waves and hence smaller infarcts affirms the importance of optimal risk factor modification for primary prevention of coronary artery disease.

The strong influence of diabetes and smoking on the development of presenting Q-waves is not surprising. Diabetes is known to increase endovascular inflammation²¹ and thrombogenicity,²² while cigarette smoking has been associated with coronary vasoconstriction, decreased coronary flow, and increased myocardial oxygen demand.²³ In addition, decreased myocardial reperfusion has been reported in patients with diabetes receiving primary percutaneous coronary intervention for ST-elevation myocardial infarction.²⁴ These factors may contribute to the increased incidence of Q-waves and larger infarcts in patients with these modifiable risk factors.

The use of fibrinolytics has been associated with fewer Q-waves during hospitalization.¹⁹ In this study, reperfusion was associated with increased new-onset Q-waves after 24 hours, although Q-waves that develop only 24 hours or later after admission would be expected to represent reinfarction or postprocedural infarction, rather than represent the initial ST-elevation acute coronary syndromes.

Implications of Q-Waves 

Several studies evaluating fibrinolytics in ST-elevation myocardial infarction patients have reported an increased mortality associated with Q-waves.¹⁵, ¹⁶, ¹⁷, ¹⁸, ¹⁹ The relevance of these findings in the setting of contemporary treatment that includes primary percutaneous coronary interventions is less clear.

In this study, patients with Q-waves on the initial ECG were more likely to present with heart failure, have larger infarcts based on peak cardiac enzymes, have an occluded culprit artery on cardiac catheterization, and have increased in-hospital morbidity and mortality. After controlling for a variety of prognostic factors, presenting Q-waves were associated with increased in-hospital mortality, suggesting that presenting Q-waves are important in the risk-stratification and prognosis of these patients.

Patients with presenting Q-waves had increased 6-month mortality, while in patients without presenting Q-waves, subsequent Q-waves were associated with lower 6-month mortality. After controlling for prognostic factors, there was no significant association between Q-waves at any time (at admission or during hospitalization) and 6-month mortality. These findings suggest that Q-waves do not impact 6-month survival, and may reflect the beneficial impact of current medical and reperfusion strategies.

Nearly 40% of ST-elevation acute coronary syndrome patients did not receive reperfusion therapy within the initial 24 hours, despite guidelines and clear evidence of a substantial mortality benefit when eligible patients are treated with early percutaneous coronary interventions or fibrinolytics.⁶ This suggests that continued improvement in the proportion of ST-elevation acute coronary intervention patients receiving reperfusion therapy is needed worldwide.

Study Strengths and Limitations 

This study represents a large multinational registry of patients that reflects a global contemporary perspective of the evaluation and management of ST-elevation acute coronary syndromes. Limitations include the obervational nature of the study. Some patients with silent infarcts and preexisting Q-waves would be expected in the study population, although to minimize this number, patients with prior myocardial infarction were excluded, and Q-waves were required to be new or presumedly new. A small proportion of patients were treated with both percutaneous coronary interventions and fibrinolytics, and clearly separating these patients into those with facilitated versus rescue percutaneous coronary interventions was not possible.

Conclusions 

The incidence of Q-waves in the setting of ST-elevation acute coronary syndromes has significantly decreased over recent years and now occurs in a minority of patients worldwide. They are associated with larger infarcts and more occlusive lesions. Presenting Q-waves are associated with increased in-hospital mortality, although Q-waves on presentation or later do not impact 6-month mortality. Given the prognostic importance of presenting Q-waves on hospital survival, these findings suggest that more aggressive surveillance and management of these patients may be needed.

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Acknowledgments 

We would like to acknowledge the assistance of Robert J. Goldberg, PhD, Department of Medicine, University of Massachusetts Medical School, for critical review of the manuscript.

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