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ACC/AHA 2008 Performance Measures for Adults With ST-Elevation and Non-ST-Elevation Myocardial Infarction

ACC/AHA 2008 Guidelines for the Management of Adults With Congenital Heart Disease
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J Am Coll Cardiol, 2004; 43:592-598, doi:10.1016/j.jacc.2003.07.052
© 2004 by the American College of Cardiology Foundation
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CLINICAL RESEARCH

Ischemic and viable myocardium in patients with Non–Q-Wave or Q-Wave myocardial infarction and left ventricular dysfunction

A clinical study using positron emission tomography, echocardiography, and electrocardiography

Hua Yang, MD*, Min Pu, MD, FACC*,*, David Rodriguez, MD*, Donald Underwood, MD, FACC*, Brian P. Griffin, MD, FACC*, Vidyasagar Kalahasti, MD*, James D. Thomas, MD, FACC* and Richard C. Brunken, MD, FACC{dagger}

* Department of Cardiology, Cleveland, Ohio, USA
{dagger} Department of Nuclear Medicine, Cleveland Clinic Foundation, Cleveland, Ohio, USA

Manuscript received May 21, 2003; revised manuscript received July 17, 2003, accepted July 28, 2003.

* Reprint requests and correspondence: Dr. Min Pu, Division of Cardiology, H047, Milton S. Hershey Medical Center, Penn State University, 500 University Avenue Drive, P.O. Box 850, Hershey, Pennsylvania 17033-0850, USA.
minpu{at}psu.edu

This study was partially presented at the 2001 Scientific Sessions of the American Heart Association, November 11 to 14, 2001, Anaheim, California.


   Abstract
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Methods
 Results
 Discussion
 References
 
OBJECTIVES: We investigated whether patients with non–Q-wave myocardial infarction (NQMI) have more ischemic viable myocardium (IVM) than patients with Q-wave myocardial infarction (QMI).

BACKGROUND: Non–Q-wave myocardial infarction is associated with higher incidences of cardiac events than QMI, suggesting more myocardium at risk in NQMI.

METHODS: To identify myocardial ischemia, hibernation, and scar, the resting and stress 82rubidium perfusion and F-18 fluorodeoxyglucose metabolic positron emission tomographic imaging (PET) was performed in 64 consecutive patients with NQMI (n = 21) or QMI (n = 43). Echocardiography was performed for assessment of left ventricular function and wall motion index (WMI). The relationships between PET, echocardiographic, and electrocardiographic findings were analyzed.

RESULTS: There were no significant differences in left ventricular ejection fraction (LVEF) between NQMI and QMI groups (28 ± 10% vs. 25 ± 11%, p > 0.05). Ischemic and viable myocardium was more common in NQMI than in QMI (91% vs. 61%, p < 0.05). The total amount of IVM was significantly higher in NQMI than in QMI (6.5 ± 5.2 vs. 2.9 ± 2.8 segments, p < 0.001). Neither the number of Q waves, residual ST-segment depression of ≥0.5 mm or elevation of ≥1 mm, nor LVEF and WMI were significant predictors for IVM. Wall motion index correlated with scar segments (r = 0.54, p < 0.001) and LVEF (r = –0.67, p < 0.001).

CONCLUSIONS: Ischemic and viable myocardium is common in patients with NQMI and left ventricular dysfunction, suggesting that aggressive approaches should be taken to salvage the myocardium at risk in such patients.

Abbreviations and Acronyms
  IVM = ischemic viable myocardium
  LVEF = left ventricular ejection fraction
  MI = myocardial infarction
  NQMI = non–Q-wave myocardial infarction
  PET = positron emission tomography
  QMI = Q-wave myocardial infarction
  WMI = wall motion score index
  18FDG = fluorodeoxyglucose-18
  82Rb = rubidium-82

Traditionally, myocardial infarction (MI) may be categorized as Q-wave MI (QMI) or non–Q-wave MI (NQMI) based on the electrocardiogram (ECG). Although QMI is frequently associated with transmural MI, and NQMI with nontransmurality, pathological studies have demonstrated that the presence of Q waves on the ECG does not reliably differentiate transmural from nontransmural scar (1,2). There are both pathophysiological and clinical differences between NQMI and QMI (2,3). Q-wave MI is almost always associated with ST elevation, and thrombolytic therapy decreases mortality. Non–Q-wave MI often presents with non–ST-elevation MI, and thrombolysis is not beneficial (4,5) or even harmful (6,7).

Although NQMI may have infarct size smaller than QMI as measured by peak creatine kinase levels (3,8), it is often associated with higher incidence of late cardiac events including recurrent ischemia, angina, or MI than QMI (9,10). Despite a favorable early prognosis, a long-term survival in patients with NQMI is similar to that in patients with QMI (11). Postinfarction ischemia, angina, and reinfarction presage increased late mortality in patients recovering from NQMI (12–14), suggesting that patients with NQMI might have more myocardium at risk (stress-induced ischemia and/or hibernating myocardium) than individuals with QMI. These clinical characteristics of NQMI have led to a speculation that an invasive strategy with early revascularization would improve outcome in patients with NQMI. However, two large clinical trials had contradictory results (15,16). The objective of this study was to investigate whether patients with NQMI had more stress-induced ischemia and/or hibernating myocardium identified by positron emission tomography perfusion (PET) with metabolic imaging than those with QMI. The study also evaluated whether resting electrocardiography and echocardiography can be used to predict myocardium at risk in patients with NQMI or QMI and left ventricular dysfunction. In this study, we specifically investigated patients with left ventricular dysfunction after NQMI or QMI because left ventricular dysfunction is strongly associated with prognosis, and left ventricular function may significantly improve after revascularization of ischemic viable myocardium (IVM) (17–19).


   Methods
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Results
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Patient population.   Seventy-three consecutive patients with clinical history of MI (more than one month after acute MI) were studied. A 12-lead ECG, echocardiography, and PET were performed as clinically indicated. Mean left ventricular ejection fraction (LVEF) was 26 ± 11% by echocardiography. Patients were divided into NQMI and QMI groups according to the presence or absence of the pathological Q-wave in at least two contiguous leads on a resting 12-lead ECG. Q-wave MI was defined by two criteria: 1) documented MI by clinical history and cardiac enzymes, 2) pathological Q waves were present in two contiguous leads in a 12-lead ECG. Non–Q-wave MI was defined by the following criteria: 1) documented MI by clinical history and/or cardiac enzymes, 2) no Q-wave in a 12-lead ECG. There were 21 patients meeting NQMI criteria and 43 patients meeting QMI criteria. Nine patients with nondiagnostic ECG (seven patients with left bundle branch block and two patients with pacing rhythm) were excluded from the study because we were unable to determine whether the patients had Q-wave or non–Q-wave MI. Clinical characteristics of these 64 patients are listed in Table 1.


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  		Table 1 Clinical Characteristics in the Patients With NQMI or QMI

 
ECG.   Patients were divided into the QMI or NQMI groups depending on the presence (QMI) or absence (NQMI) of pathological Q waves on 12-lead resting ECG. Pathological Q-wave was considered present if Q-wave was equal to, or greater than, 0.04 seconds in duration and deeper than one-fourth of the following R wave in voltage. Four major infarct regions (septal, anterior, lateral, and inferior) were defined in this study according to the location of Q waves. Septal infarction was defined as the presence of pathologic Q waves in precordial leads V1 to V3. Anterior infarction was defined as the preservation of the R-wave in V1 with pathological Q-wave in at least two leads from V2 to V5. If Q waves were present in both septal V1 to V3 and anterior leads V4 to V5, infarction was considered as two regions (septal plus anterior regional infarction). Lateral infarction was defined by pathologic Q waves in at least two of leads I, aVL, or V6. Inferior infarction was identified by the presence of pathological Q waves in at least two of leads II, III, or aVF. A multiregional infarction determined by ECG was defined when more than one region was involved. The number of ECG leads with ST-segment elevation of ≥1 mm or ST depression of ≥0.5 mm and the sum of ST-segment elevation of ≥1 mm or ST depression of ≥0.5 mm was also analyzed.

PET study.   Positron emission tomography was performed using a Posicam scanner (Positron Corp., Houston, Texas). After transmission images of the thorax were obtained (minimum 60 M counts), 60 mCi of rubidium-82 (82Rb) was given intravenously, and 4-min resting perfusion images were obtained. Following isotope decay, 0.56 ml/kg of dipyridamole was infused intravenously over a 4-min interval. A second dose of 60 mCi was given, and 82Rb stress perfusion images were acquired for 4 min. Positron emission tomography metabolic imaging was performed following oral glucose loading (25 to 50 g) 40 min after 3 to 10 mCi of fluorodeoxyglucose-18 (18FDG) was given intravenously. Twenty-one transaxial images were reconstructed and corrected for soft tissue attenuation using the transmission images. Images were resliced into standard horizontal long-axis, vertical long-axis, and short-axis views. The resliced PET images were displayed on a VAX workstation (Digital Equipment, Hewlett-Packard, Palo Alto, California), utilizing 5%, 10%, or continuous display color bars. A perfusion defect was defined as a relative tracer concentration of <70% of maximal myocardial activity. Reversible perfusion defect (ischemia) was determined as a perfusion defect detected on 82Rb dipyridamole-stress perfusion images with no perfusion defect detected on resting images in the same segments with improvement in relative tracer concentration from the stress to the resting images of 15% or greater. Fixed perfusion defect was determined when perfusion defect was detected on both resting and 82Rb dipyridamole-stress perfusion images in the same segments. Because myocardial scar and hibernating myocardium might present as fixed defects on the 82Rb dipyridamole perfusion images, the resting 18FDG imaging was further performed to differentiate scar (concordantly decreased 18FDG uptake in the segments with perfusion defects on resting 82Rb perfusion images) from hibernation (increased 18FDG uptake of 15% or more in the segments with perfusion defects on resting 82Rb perfusion images). The left ventricle was divided into 24 segments (20) with four principal regions: septal, anterior, lateral, and inferior regions (Fig. 1). Because of significant variation and overlaps of coronary artery blood supply, a scar detected by PET in two or more principal regions were considered as multiregional infarction. For example, if scars were identified in the anterior, anterior lateral, and lateral regions, we considered two regional infarctions (PET criteria). If scars were identified in anterior and anterior lateral regions, we considered them as one region because only one principal region was involved (anterior region). Total IVM was defined as the reversal defect segments (ischemia) plus mismatched defect segments (hibernation). The localizing sensitivity of the ECG was given by the percentage of patients with PET scar in a particular distribution who also had a pathologic Q-wave in that region; specificity was defined by the percentage of patients without a scar in a distribution who did not have a corresponding pathologic Q-wave there.



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  		Figure 1 Illustration of the 24-segment model in the positron emission tomographic study. Left ventricle was divided into 24 segments with four principal regions: septal (S), anterior (A), lateral (L), and inferior (I) regions. Each principal region was sliced into basal, mid-, distal, and apical layers in the vertical and horizontal views. The segments between the principal regions were anterior septum (as), anterior lateral (al), inferior lateral (il), and inferior septum (is) as shown in the short-axis view. The basal septum (horizontal axis) was not accounted as a myocardial segment because of nonmyocardial membrane. Instead, the apical segment was accounted as the 24th segment.

 
Left ventricular function.   Left ventricular dimension, wall motion, and LVEF were assessed using two-dimensional echocardiography as routine clinical practice. Standard parasternal long-, short-, four-, and two-chamber views were obtained. The left ventricle was divided into 16 segments as described by the American Society of Echocardiography (21), and segmental wall motion was scored as 1 = normal, 2 = hypokinesis, 3 = akinesis, 4 = dyskinesis, 5 = aneurysm. Wall motion index (WMI) was calculated as the total scores divided by the number of segments.

Statistical analysis.   Values are expressed as the mean ± SD. Student unpaired t test was used to compare the means of continuous variables for the two independent groups. The chi-square testing was used to examine the difference in discrete variables. Linear regression analysis was used to explore the relationship between the number of Q waves on ECG and the number of scars on PET, and the relationship between LVEF and WMI. All values were expressed as mean values ± SD. A p value <0.05 was considered statistically significant.


   Results
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Discussion
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Clinical characteristics.   No significant differences in age, gender, heart rate, history of coronary artery bypass grafting, left ventricular dimension and LVEF, severity of mitral regurgitation, or mean wall motion index were noted between the NQMI and the QMI groups (Table 1, p > 0.05). Multivessel coronary artery disease was more common in the QMI group (72 % vs. 38 %, p < 0.05) than the NQMI group in this study.

IVM.   Ischemic and hibernating myocardium were more common in the patients with NQMI (91%) than QMI (61%, p < 0.05). The segments with ischemia were 3.2 ± 3.7 in the NQMI group and 1.7 ± 2.6 in the QMI group (p = 0.06). The segments with hibernation were 3.3 ± 4.5 in the NQMI group and 1.2 ± 1.7 in the QMI group (p < 0.01). The total number of IVM (combination of ischemia and hibernation) was significantly higher in the NQMI group than in the QMI group (Fig. 2). The number of segments with scar appeared to be more common in QMI (7.6 ± 3.8) than in NQMI (6.5 ± 4.2), but it did not reach statistical significance (p = 0.33). Patients with a larger amount of myocardium at high risk (>3 segments with IVM) were twofold higher in the NQMI group than the QMI group (71% vs. 35%, p < 0.01). Although LVEF tended to be slightly lower in the QMI group than in the NQMI group (28 ± 10 vs. 25 ± 11%), it did not reach statistical significance (p = 0.39). There were weak, but significant, negative correlations between the number of scar segments and the number of ischemic segments (r = –0.34, p = 0.006) and hibernation segments (r = –0.35, p = 0.005) in the combined NQMI and QMI groups, suggesting that patients with a larger amount of scar (a large infarction) had less IVM. There was no significant correlation between the number of ischemic segments and the number of hibernation segments (r = 0.08, p = 0.52).



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  		Figure 2 Comparison of ischemic viable myocardium and myocardial scar between the patients with non–Q-wave myocardial infarction (NQMI) and those with Q-wave myocardial infarction (QMI).

 
Relationship between PET and ECG.   Table 2 lists the sensitivity and specificity of ECG Q-wave for the diagnosis of MI in the different regions using PET image as a reference standard in 43 patients with QMI. Anterior Q waves had the highest specificity of the four regions. Although the diagnosis of lateral regional infarction by ECG Q-wave had high specificity (93%), the sensitivity (25%) was lower than the diagnosis of septal (67%, p < 0.05), inferior (62%, p < 0.05), and anterior (53%, p = 0.06) regional infarctions. There was no significant relationship between the number of Q waves and the number of the scar segments on PET (r = 0.31, p = 0.08) in the QMI group. However, a single regional infarction identified by PET was more common in the NQMI group than the QMI group (62% vs. 28%, p < 0.05), and multiple regional infarctions on PET were more common in the QMI group than in the NQMI group (72% vs. 38%, p < 0.05). Table 3 lists clinical and echocardiographic characteristics in the patients with single and multiregional infarctions determined by PET. Patients with one regional infarction had fewer Q waves, fewer diseased coronary vessels (p < 0.01), lower mean WMI (p < 0.01), and higher LVEF (p < 0.01) than those with multiregional infarctions. Patients with one regional infarction had more segments with IVM (p < 0.01) and a fewer segments with myocardial scar (p < 0.001) than those with multiregional infarctions.


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  		Table 2 Sensitivity and Specificity of Q-Wave of ECG for Diagnosis of Myocardial Scars Identified by a Positron Emission Tomography in Different Infarct Location in the QMI Group (n = 43)

 

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  		Table 3 Comparison of a Signal Region With and Multiple Regional Infarctions (Scar) Identified by a Positron Emission Tomography

 
Prediction of IVM by echocardiography and ECG.   In the QMI group, the average number of Q waves was 4.2 ± 2.0 in the patients with IVM and 4.7 ± 2.2 in the patients without IVM (p > 0.05). As indicated in Table 4, there were no significant differences in the number of leads with ST segment elevation of ≥1 mm or with ST segment depression of ≥0.5 mm, in the sum of ST segment elevation or depression in millimeter, LVEF, WMI, or left ventricular dimension between the patients with and without IVM. There was no significant relationship between the number of Q waves and LVEF, or between the total number of segments with IVM and LVEF. Wall motion indexes were significantly correlated with the number of scar segments (r = 0.54, p < 0.001) and LVEF (r = –0.67, p < 0.001) in the combined QMI and NQMI groups. There were no significant correlations between WMI and the number of ischemic segments (r = 0.25, p > 0.05).


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  		Table 4 Prediction of Ischemic Viable Myocardium by Echocardiography and Electrocardiography

 

   Discussion
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 Discussion
References
 
The prevalence of NQMI has increased over the past two decades. This may be related to more accurate identification of MI by use of specific cardiac enzyme markers (troponin, creatine kinase-MB). Early reperfusion with thrombolytic therapy and acute percutaneous coronary artery intervention may reduce QMI and increase NQMI. However, a long-term prognosis of NQMI is not significantly different from that of QMI. Because of frequent postinfarction cardiac events, the 1987 American College of Cardiology/American Heart Association Joint Task Force Report on Guidelines for Coronary Arteriography recommended that NQMI was the class I indication for coronary angiography (22).

Frequent cardiac events (postinfarction angina, MI) in patients with NQMI strongly suggest that myocardium may be at high risk due to incomplete reperfusion. Incompletely perfused myocardium may manifest as stress-induced ischemia and/or hibernation (severe resting ischemia). The current study confirms the clinical concern that patients with NQMI have more myocardium in jeopardy than patients with QMI. Early studies with a small number of patients reported that viable myocardium detected by PET was more common in patients with NQMI than in those with QMI (23). Hashimoto and colleagues (24) reported that viable myocardium was observed in 10 (91%) of 11 patients with NQMI, but in only 4 (36%) of 11 patients with QMI. The present study not only showed that IVM was more common in NQMI than in QMI (91% vs. 61%, p < 0.05), but the amount of IVM was significantly greater in NQMI than in QMI. Although one trial (15) did not demonstrate clinical benefit of an invasive strategy with early coronary angiographically directed revascularization after NQMI, a recent study showed that patients who were managed with such an invasive strategy had less cardiac events (postinfarction angina and rehospitalization) than those managed conservatively (16). Our study shows a high prevalence of IVM in the patients with NQMI, further supporting the use of the aggressive invasive approach.

When left ventricular dysfunction is present after MI, assessment of myocardial viability is critically important. In patients with substantial myocardial viability, left ventricular function may significantly improve after revascularization. Patients with little viability preoperatively have a high rate of early and late cardiac death and the need for heart transplantation after coronary bypass surgery as compared with patients with extensive viability (25,26). Patients with viable myocardium had substantially better event-free survival with revascularization in comparison with medical therapy (27,28). In this study, resting echocardiography and electrocardiography were not shown to be very useful for identifying IVM in patients with left ventricular dysfunction in either QMI or NQMI. There was no significant correlation between IVM and the number of ECG Q waves, WMI, or LVEF. However, WMI significantly correlated with scar segments and LVEF. The current study showed a high prevalence of IVM in patients with NQMI and left ventricular dysfunction. Patients with NQMI and one regional infarction were most likely to have IVM in other regions. This suggests that a complete assessment of myocardial perfusion, residual myocardial ischemia, and hibernation are necessary after NQMI, particularly in patients with left ventricular dysfunction. Early coronary angiogram with necessary revascularization may be considered in patients with NQMI. Our study showed the sensitivity of ECG for detecting lateral infarction was poor. Routine ECG was neither sensitive nor specific for identification of IVM, which was consistent with the recent report that ST-segment elevation during stress test might indicate myocardial scar rather than viable myocardium after MI (29).

In the current study, we combined resting and stress 82Rb perfusion imaging with resting 18FDG imaging. The resting and stress 82Rb perfusion imaging identified ischemic myocardium (reversible perfusion defect) through the detection of reduced coronary artery flow. However, 82Rb perfusion imaging was unable to differentiate hibernating myocardium from myocardial scar in the segments with perfusion defects on both resting and stress 82Rb perfusion images (fixed defects); 18FDG metabolic PET imaging identified hibernating myocardium in the segments with fixed defects. The advantage of the combination was to maximally identify IVM at high risk (both ischemia and hibernation). This is particularly important in a patient with left ventricular dysfunction because both stress-induced ischemia and hibernating myocardium could exist in a patient, and IVM is strongly associated with ischemic events (25,26,30). Without this combination, one might have potentially missed either hibernating myocardium if resting, and stress 82Rb perfusion imaging was performed only, or stressed-induced ischemia if resting 18FDG image was performed only.

Although PET used in this study is considered as a gold standard with a high sensitivity for the detection of hibernating myocardium, it is relatively expensive, and not widely available. A single photon emission computed tomography with resting thallium later redistribution or reinjection 18 to 24 h after an initial thallium injection has been shown to be useful for identifying IVM (31–33). Further standardization of the thallium redistribution technique and imaging protocol will enhance this technique. Exercise echocardiography has been widely used for the detection of myocardial ischemia. It is less expensive, with sensitivity and specificity approximately equivalent to single photon emission computed tomography. Dobutamine echocardiography has been used for the identification of IVM (34–36) with a high specificity for predicting recovery of systolic function after revascularization, although the sensitivity for the detection of myocardial viability is slightly lower than the nuclear techniques (37,38). Both thallium redistribution imaging and dobutamine echocardiography can be used to identify IVM in QMI and NQMI. Recently, cardiac magnetic resonance has been shown to be useful for identifying myocardial viability (39).

Study limitations.   Previous coronary artery bypass grafting may alter blood supply to myocardium, and we did not have detailed information regarding coronary collateral circulation, making it difficult to determine culprit lesions in a few patients. The number of the patients in this study is relatively small, and we did not have long-term follow-up data. Therefore, we are unable to assess the prognostic value of IVM in QMI and NQMI after revascularization. However, previous studies have clearly demonstrated the clinical importance of IVM for prognosis and beneficial effect of coronary revascularization (19,25–28,34–36,40). In this study, we did not have uniform cardiac enzyme data because patients had old MI, and measurements of cardiac enzymes were performed in different laboratories with different normal references. Therefore, we are unable to determine a relationship between cardiac enzymes and myocardial scar, hibernation, and ischemia identified by PET.


   References
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