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Dr. Ling is a member of the Diagnostic Radiology Department National Institutes of Health Clinical Center.
Correspondence to: Alexander Ling, MD, NIH Clinical Center, Building 10, Room 1C-660, Bethesda, MD 20892; e-mail: al52x{at}nih.gov
Despite the best efforts of clinicians to limit coronary angiography to symptomatic patients likely to have ischemic heart disease (coronary artery disease [CAD]), a significant minority will be discovered to have no significant vascular stenosis, occlusion, or spasm.1 2 3 Accordingly, there has been continued interest in understanding the pathophysiology of these patients and in distinguishing them from patients with CAD. The term syndrome X has been variously applied but commonly is understood to refer to patients with chest pain and ECG changes during exercise stress testing consistent with myocardial ischemia, but neither spasm nor CAD by angiography. Observed features include female predominance, pain atypical of classic angina, inconsistent response to medical therapy, and, in a subset, various hemodynamic and metabolic correlates of cardiac ischemia.
In the nearly 3 decades since this term has come into use, syndrome X has resisted facile explanation. It is thought by many to be heterogeneous and multifactorial, in that most investigators4 have been able to suggest a pathophysiologic mechanism for only a fraction of their affected study populations; some appear to have abnormal myocardial flow reserve, some have hypersensitivity to visceral pain, some have additional markers of myocardial ischemia, or subangiographic atherosclerosis. Differences among investigations have been compounded by differences in study focus and methods of characterization of the studied patient population.
While the underlying pathophysiology has remained uncertain, the excellent prognosis of patients with syndrome X has enjoyed near universal acceptance.3 5 6 7 8 That some of these patients continue to have chest pain, occasionally with attendant hospitalization and catheterization, suggests the difficulty of management, as well as the human and economic costs involved. If it were possible to reliably recognize these patients prior to angiography, the costs and occasional morbidity of this procedure might be avoided. However, if such an implied new diagnostic test were imperfect, it would be better to err in the direction of detecting all patients with CAD rather than all patients with syndrome X, because effective treatments for CAD are available, and delay making the diagnosis of CAD can have serious consequences.
In this issue of CHEST (see page 1525), Chen and colleagues report on the use of electron beam CT (EBCT) to quantitate coronary artery calcification in three groups of patients: those with syndrome X, those with CAD, and those without either (who served as control subjects). EBCT has been shown to noninvasively and sensitively detect and quantify calcification in the epicardial coronary arteries. The CT coronary artery calcification score provides a measure of overall atherosclerotic plaque burden, an index of risk of future coronary events, and is predictive of obstructive CAD.9 10 11 12 In the current study, all three groups had members with calcification. The distribution of scores for syndrome X overlapped with the distributions of both other groups, but the median score for syndrome X was much lower than for CAD (1 vs 202). In the large range of scores where the groups overlapped, hypertension, hypercholesterolemia, and coronary artery calcification score > 5 were found to be independent, though presumably imperfect, predictors of membership in the CAD group. The authors also demonstrated an effect of patient age, with older patients tending to higher scores in both the CAD and syndrome X groups. This same trend has previously been observed among asymptomatic subjects.13
Does this mean patients with chest pain and a positive stress test result should have EBCT prior to coronary angiography? It seems hard to justify this position on the basis of either the current study or the earlier work of Shemesh et al.14 Both studies found that the coronary artery calcification score partially distinguishes patients with syndrome X from normal subjects and patients with angiographic CAD. Both studies found that scores above a threshold value (117 units for Chen et al and 602 units for Shemesh et al14 ) guaranteed the patient had CAD. However, because the calcification score is known not to be predictive of location or severity of obstruction, such patients still need angiography to define these factors prior to possible revascularization. Moreover, patients with lower scores are in the region of greatest overlap between syndrome X and CAD. In this range, the calcification score cannot confidently distinguish CAD from syndrome X, yet by definition angiography does so completely. This is demonstrated by Table 6 (see page 1530), which shows limited negative predictive value for patients < 60 years old, the group pertinent to most North American and European patients with syndrome X. However, because the studied CAD group included 10 of 53 patients with insignificant CAD, and further characterization of subjects’ ischemia, such as by stress thallium imaging, is unavailable, it would be interesting to know if those CAD patients with the lowest calcification scores also had the least worrisome ischemia. Were this the case, the performance of CT as a triage method might be improved.
Before EBCT can be adopted as a routine diagnostic test in the clinical evaluation of syndrome X, it must provide better segregation of patients with obstructive CAD from syndrome X (segregation of syndrome X from normal subjects is evident based on clinical presentation). Specifically, it must provide better negative predictive value in order to reliably identify patients without CAD. How might this occur? It might be accomplished by further technologic development, perhaps by using thinner CT images, faster image acquisition, or contrast media injection (ie, CT coronary angiography). Further analysis of clinical data might show existence of a lower threshold of coronary calcification below which a patient presenting with chest pain and abnormal exercise tolerance test results could safely be managed without conventional coronary angiography. Also, combining the EBCT results with other noninvasive test results might improve overall diagnostic segregation. Finally, construction and validation of an algorithm, such as selectively performing CT on patients with equivocal treadmill exercise tests (excluded from the current study), or performing stress thallium studies on patients with lower calcification scores, may yet establish a niche for EBCT in this condition.
References
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