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Although most studies were performed with sestamibi, comparable results have been obtained with tetrofosmin. In a multicenter study, Heller and colleagues [16] found a sensitivity of 90% in 357 patients who underwent acute MPI. Negative predictive value (NPV) was equally high at 99%, with only two patients who had small non-Q-wave MIs having negative acute MPI. In our study in which 319 patients had TnI elevations, sensitivity of those who had acute MPI with sesta-mibi (75%) and tetrofosmin (80%) were similar, as was the proportion who had CK-MB MI (84% versus 87%) [16].

2 15

VS 12

17.9

C+SPECT

Fig. 4. Incremental prognostic value of rest tetrofosmin SPECT imaging over clinical variables. Model A: clinical variables; Model B: A plus three or more risk factors (RF); Model C: B plus admission ECG and chest pain (CP) at the time of tetrofosmin injection. (Modified from Heller GV, Stowers SA, Hendel RC, et al. Clinical value of acute rest techne-tium-99m tetrofosmin tomographic myocardial perfusion imaging in patients with acute chest pain and nondiagnostic electrocardiograms. J Am Coll Cardiol 1998;31:1011-17; with permission.)

Comparison with troponin

Although markers of necrosis, such as troponin, are considered the gold standard for identifying MI, rest MPI does have some important advantages over using markers alone. First, myocardial markers are by definition abnormal only in patients who have necrosis, and therefore are negative in patients who have ischemia alone. Also, given the time required for imaging and processing, acute MPI results can be available within 1 to 2 hours after injection. In contrast, markers of necrosis are not detectable in the blood until several hours after the damage has occurred. To achieve a high sensitivity, sampling must be performed over an 8- to 9-hour period [40]. Thus, the sensitivity of MPI is significantly higher than that of the initial troponin (Fig. 5).

A second advantage of acute MPI is that it can identify risk area, and therefore better quantitate overall cardiac risk. For example, two patients who have similar low-peak TnI values—one secondary to occlusion of a small branch vessel and the other resulting from a brief occlusion of the proximal portion of a major vessel—have markedly different areas at risk and the potential for markedly different outcomes, which can be readily determined using MPI.

Acute MPI has some limitations when used to assess patients who have chest pain. Acute MI, acute ischemia, and prior MI all cause perfusion defects, and differentiation is not possible based on the images alone. However, patients who have prior MI are at higher risk for acute events and are usually not candidates for primary triage to a subsequent outpatient evaluation. Sensitivity for identifying necrosis is imperfect for MPI, as at least 3% to 5% of the left ventricle must be ischemic for a defect to be detected. However, the many patients who have negative rest MPI despite marker elevations have nonsignificant disease on coronary angiography [25], and therefore are at low risk for short-term adverse outcomes, although aggressive risk factor modification would still be indicated. Therefore, rather than being seen as competitive diagnostic tools for evaluating patients presenting to the ED with chest pain, markers and MPI should be considered complementary.

Timing of tracer injection

Although it appears that sensitivity of acute MPI decreases as the symptom-free interval increases, the reduction is highly variable. In the case of thallium, Wackers and colleagues [3] performed thallium-201 scintigraphy in 98 patients admitted with chest pain who had MI excluded. When imaged within 6 hours of the last anginal symptoms, 57% of the patients had abnormal studies; however, when imaged after 12 hours, only 8% had abnormal studies. Similar results have been reported by Van der Wieken and colleagues [4].

Studies using technetium agents also demonstrate higher sensitivity when injection is

MI+Sig

Fig. 5. Sensitivity of MPI (dark bars), the initial troponin I (open bars), and troponin I (light bars) for identifying end points. Asterisk denotes P < .001 compared with perfusion imaging; # denotes P < .001 compared with serial troponin. Rev, revascularization; Sig, significant disease (>70% stenosis). (Data from Kontos MC, Jesse RL, Anderson FP, et al. Comparison of myocardial perfusion imaging and cardiac troponin I in patients admitted to the emergency department with chest pain. Circulation 1999;99:2073-8.)

performed during or soon after pain. Bilodeau and colleagues [9] found that the sensitivity of MPI for detection of coronary artery disease was 96% in 45 patients injected with tracer during chest pain. When the same patients were rein-jected later while pain-free, the sensitivity had decreased to 65%. However, in both cases the sensitivity was significantly higher than that of the initial ECG. In contrast, we found that when patients were injected within 6 hours of symptoms, sensitivity was similar for identifying patients who had MI, revascularization, or significant coronary disease between those who were injected with and without symptoms [15]. Others have also reported high sensitivity despite the absence of symptoms during injection [12].

One explanation relates to the difference in the underlying mechanisms causing perfusion defects in patients who have ACS as compared with those undergoing stress testing. Rather than causing true ischemia, stress perfusion defects result from flow heterogeneity between areas supplied by coronary arteries with and without significant stenoses. The perfusion tracer is injected at the time of maximal flow imbalance, with a rapid return of coronary flow to baseline once the patient stops exercising. In contrast, in patients who have ACS, perfusion defects result from the combination of intermittent thrombotic occlusion and vasoconstriction in the setting of complex coronary morphology [41], resulting in marked decreased coronary blood flow [42] and persistently decreased regional myocardial perfusion [41]. Because regional hypoperfusion is one of the first steps in the ischemic cascade, symptoms of chest discomfort are often a late clinical manifestation, so that regional hypoperfusion will frequently be present even in the absence of symptoms. Suboptimal flow frequently persists despite prolonged treatment with newer pharmacologic treatments, such as glycoprotein IIb/IIIa antagonists [43,44].

Perfusion defects may also result from distal embolization of a proximal thrombus leading to downstream microvascular obstruction [45]. In a study of 75 patients who underwent sestamibi injection during rotational atherectomy, a procedure in which distal embolization of micropar-ticles is frequent, perfusion defects were present in 65% of patients [45].

Finally, a third potential mechanism was reported in an interesting study of 40 patients who had a percutaneous intervention. Fram and colleagues [46] found that perfusion abnormalities persisted in patients injected with Tc-99m sestamibi at varying intervals after balloon inflation, although the size of the perfusion defect decreased as the interval after the procedure increased. One explanation is that the pharmaco-dynamics of sestamibi are dependent on membrane and mitochondrial functional integrity, which may be depressed as a result of lingering metabolic alterations, especially in high-energy metabolites that occur after transient ischemia.

All of these findings strongly support the conclusion that the sensitivity of acute MPI will be dependent on the extent, duration, severity, and reperfusion status of the ischemic insult. It must be kept in mind that chest pain is not the gold standard for myocardial ischemia and that silent ischemia is common. In patients who have been pain-free for prolonged periods, acute MPI will have a lower sensitivity for detection of the presence of coronary disease, but persistent abnormality suggests a more complex and possibly unstable condition associated with higher risk.

Special populations

Although not normally considered candidates for acute MPI because of their higher pretest likelihood of ischemia, rest MPIs can provide useful additional diagnostic information in selected subgroups of patients who have known coronary artery disease. This group includes patients who have a nonischemic ECG and atypical symptoms (particularly if they are different from their typical angina), those who have had a recent negative cardiac evaluation, or those in whom the risk for coronary angiography is increased, such as patients who have significant renal disease. In patients who have multivessel disease, such as those who have had prior bypass surgery, the ability to determine risk area can be used to delineate the culprit lesion.

It should be recognized that patients who have prior MI, especially those who have Q waves, are likely to have perfusion defects, and that subsequent repeat rest-imaging after a pain-free period is required to differentiate new ischemia from old infarction. Alternatively, if prior images are available, they can be used for comparison to determine the significance of perfusion defects. When deciding whether to pursue further invasive or noninvasive treatment, it has been our experience that minor differences in images when compared with prior studies are unlikely to be of clinical significance.

Another group of patients in whom ED rest MPI can be useful are those presenting with cocaine-associated chest pain. In the absence of ischemic ECG changes or known coronary disease, the risk for ACS is low [47]. Rather than admitting the patient, an alternative evaluation process is to perform rest MPI, with discharge if images are negative. We found that in 216 consecutive patients who had chest pain after recent cocaine use who underwent ED MPI, only five (2.3%) patients had abnormal studies, including two who had acute MI [48]. None of the 38 patients who had normal MPI had subsequently acute MI by biomarkers after admission to the CCU, and only 7% of the 67 patients undergoing subsequent stress MPI had reversible myocardial perfusion defects. At 30-day follow-up there were no cardiac events in patients who had normal rest MPI. This finding indicates that hospital admission can be avoided in this subgroup of patients who have a history of cocaine use if rest MPI is negative.

Cost-effectiveness

The ability to discharge patients directly from the ED has obvious cost implications. Despite the application of complex and expensive technology, ED MPI can be cost-effective if the number of patients admitted is decreased [16,49-51]. Several observational studies have confirmed that cost reductions occur when rest MPI is used as an integral part of patient management. Costs are reduced in two ways. One obvious mechanism is by discharging more patients directly from the ED, with an increase in the admission of more appropriate patients. A second mechanism is by more appropriate selection of diagnostic procedures, as the rate of coronary angiography in low-risk patients is reduced [39,49]. A preliminary analysis from the ERASE study confirms that using ED MPI as a key part of the initial diagnostic strategy was cost-effective, with costs reduced to an average of $70 per patient [52].

Incorporation into chest pain evaluation

Recent updated guidelines for the clinical use of cardiac radionuclide imaging indicate that acute ED MPI has a Class IA indication for assessing myocardial risk in patients who have possible ACS and have nondiagnostic ECGs and negative initial serum markers and enzymes, if available [53].

In addition, recommendations for using MPI in the ED have been published [54]. The recommended patient selection criteria are similar to those used for admission to a chest pain evaluation unit. Patients should be low risk (no ischemic ECG changes or history of coronary disease) and hemodynamically stable. The optimal use of MPI as a triage tool is in patients who will be discharged home and have stress testing as an outpatient if imaging is negative.

One of the first programs to incorporate rest MPI as a strategy was at Virginia Commonwealth University Medical Center (formerly Medical College of Virginia). In contrast to most chest pain programs, the systematic chest pain protocol developed and implemented is designed for all chest pain patients, with MPI used for evaluation of lower-risk patients (Table 2) [14]. All patients presenting to the ED with chest pain or other symptoms consistent with myocardial ischemia undergo rapid evaluation with assignment to a triage level, which is based on the probability of having MI or myocardial ischemia derived from clinical and ECG variables. After the initial evaluation, patients thought to be at high risk (those who have ischemic ECG changes and those who have known coronary disease experiencing typical symptoms) and characterized as levels 1 and 2 are admitted directly to the CCU. Patients considered low to moderate risk for ACS (eg, absence of is-chemic ECG changes or history of coronary disease) undergo further risk stratification using acute rest MPI [14]. Level 3 patients are admitted as observation patients and undergo a rapid rule-in protocol. Level 4 patients are evaluated in the ED. If images are either negative or unchanged from previous studies, patients are discharged home and scheduled for outpatient stress testing. If MPI is positive, they are admitted and advanced to the level 2 treatment protocol.

It is important to appreciate the difference in the role of acute rest MPI between level 3 and level 4 patients. In level 3 patients, the presence of a significant perfusion defect identifies a high-risk patient in whom early initiation of aggressive treatment is indicated, with the potential for early intervention. Negative MPI and negative markers, on the other hand, identify patients who can safely undergo early stress testing and discharge. Although the identification of higher-risk patients is the focus of much interest, the ability to better risk-stratify intermediate-risk patients into low-risk who can be stressed safely is an important advantage. In contrast, the role of MPI in patients

Acute chest pain diagnostic treatment pathways at Medical College of Virginia/Virginia Commonwealth University Medical Center

Primary risk assignment

Probability of AMI

Probability of ischemia

Diagnostic criteria

Disposition

Secondary risk stratification

Treatment strategy

Level 1: AMI

Level 2: Definite or highly probable ACS

Level 3: Probable ACS

Level 4: Possible UA

Level 5: Very low suspicion for AMI or UA

Ischemic ST elevation Acute posterior MI

Ischemic ECG Acute CHF Known CAD with typical symptoms

Nonischemic ECG and either:

Typical symptoms >30 min, no CAD, or Atypical symptoms >30 min, known CAD, Nonischemic ECG and either:

Typical symptoms

<30 min, or Atypical symptoms, Evaluation must clearly document a noncardiac etiology for the symptoms

Admit CCU

Admit CCU Fast track rule-in protocol

Observation Fast track rule-in protocol

ED evaluation

ED evaluation as deemed necessary

Serial ECGs Cardiac markers every

6-8 h until peak Serial ECGs Cardiac Markers at 0, 3, 6, and 8 h If rule-in for AMI (markers positive) continue every 6-8 h until peak

Cardiac Markers at 0, 3, 6, and 8 h Serial ECGs

As appropriate for the clinical condition

Fibrinolytics within 30 min Primary PCI within 90 min

IV UFH or SC LMWH IV and/or topical NTG IV and/or PO Beta Blocker Clopidogrel

GP IIb/IIIa inhibitor if TnI positive Cath/PCI ASA

If cardiac markers or MPI positive: treat per level 2 protocol If negative: stress

MPI positive: admit to level 2 treatment protocol MPI negative: discharge; schedule out patient stress

As appropriate for the clinical condition

Abbreviations: ACS, acute coronary syndrome; AMI, acute myocardial infarction; ASA, aspirin; CAD, coronary artery disease; CCU, coronary care unit; CHF, congestive heart failure; ED, emergency department; GP, glycoprotein; IV, intravenous; LMWH, low molecular weight heparin; MPI, myocardial perfusion imaging; NTG, nitro-glycerin; PCI, percutaneous intervention; TnI, troponin I; UA, unstable angina; UFH, unfractionated heparin.

5 20

H Level 2 m Level 3 0 Level 4 ■ (+) MPI S (-) MPI

MI or Revasc

Fig. 6. Cardiac outcomes compared with the initial triage level assignment and the MPI results. The incidence of MI or MI or revascularization was significantly different among level 2 (hatched bars), level 3 (vertical bars), and level 4 (diagonal bars) patients. Patients who had positive imaging (dark bars) had an incidence of MI or MI or revascularization similar to the level 2 patients. (Adapted from Tatum JL, Jesse RL, Kontos MC, et al. Comprehensive strategy for the evaluation and triage of the chest pain patient. Ann Emerg Med 1997; 29:116-23; with permission.)

H Level 2 m Level 3 0 Level 4 ■ (+) MPI S (-) MPI

MI or Revasc

Fig. 6. Cardiac outcomes compared with the initial triage level assignment and the MPI results. The incidence of MI or MI or revascularization was significantly different among level 2 (hatched bars), level 3 (vertical bars), and level 4 (diagonal bars) patients. Patients who had positive imaging (dark bars) had an incidence of MI or MI or revascularization similar to the level 2 patients. (Adapted from Tatum JL, Jesse RL, Kontos MC, et al. Comprehensive strategy for the evaluation and triage of the chest pain patient. Ann Emerg Med 1997; 29:116-23; with permission.)

who are considered level 4 is to diagnose unsuspected ACS and prevent the inadvertent discharge of these patients from the ED. Follow-up stress testing is used to exclude significant coronary disease.

This simple risk stratification scheme accurately separates patients into high-, intermediate-, and low-risk groups. The ability of MPI to further risk stratify lower-risk patients is also obvious, as outcomes in patients who have positive MPI are similar to those in the patients considered high-risk level 2 (Fig. 6) [14]. Close collaboration of the CCU and nuclear medicine staff has resulted in the ability to successfully triage patients who do not have known coronary disease and have large perfusion defects at the time of imaging directly to coronary angiography and revascularization.

Patients presenting with chest pain are evaluated similarly to the Medical College of Virginia protocol. Patients who present without chest pain undergo rest SPECT thallium imaging. If images are negative, subsequent stress SPECT Tc-99m sestamibi imaging is immediately performed. If rest images are abnormal, the patient is re-evaluated for possible ACS before stress testing.

Summary

The rapid triage of the patient who has suspected ACS continues to be a challenge. Chest pain and other symptoms suggestive of ischemia remain nonspecific and frequent presentations to the ED. The ECG appropriately remains the first triage tool and is essential for identifying the patient who requires admission; however, numerous studies have demonstrated that it is inadequate for triaging most of the remaining patients. Acute MPI has been shown to have a high NPV and is a powerful risk stratification tool. When MPI is used in conjunction with the newer biomarkers such as troponin, the combination provides an impressive risk profile.

The inherent success of acute MPI in the ACS population is not serendipitous but rather based on the knowledge of the pathophysiology of ACS and the ischemic cascade that has been elucidated through the work of many investigators. The fact that one of the earliest events in the cascade is a marked reduction in absolute blood flow, leading to metabolic ischemia and its functional consequences, led researchers decades ago to attempt to noninvasively detect this early signature of ACS. However, as is often the case, these early investigators were limited by available technology. With the development of technological advances such as SPECT imaging and the introduction of Tc-99m-labeled MPI agents, it became possible to translate basic science observations into meeting a recognized patient need. Importantly, the ability to noninvasively assess perfusion acutely in combination with a quantitative measurement of function has important prognostic power. The studies that followed have confirmed that when this information is applied to the appropriate population in a timely manner it has significant clinical impact. A key aspect of the clinical success of nuclear cardiology techniques in this and other settings has been the ability to standardize all aspects of this process, from image acquisition to computerassisted diagnosis. As new techniques are applied to the ACS population, the same questions posed earlier will need to be answered for each new technique.

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