The relative nature of a "normal" myocardial perfusion SPECT.

With an array of non-invasive imaging modalities available to diagnose and risk stratify individuals with suspected coronary artery disease (CAD), myocardial perfusion SPECT (MPS) has distinguished itself from others owing to its wealth of prognostic data. This is not only true for patients with greater extent, severity, and reversibility of MPS abnormalities, but also for those with normal MPS findings. The salutatory prognosis of those with a normal MPS test has lead to the implication of a ‘‘warranty period’’ following a normal SPECT stress test. While tempting to generalize this ‘‘warranty period’’ to all patients undergoing MPS, rates of freedom from adverse cardiac events differ significantly for patients with normal exercise MPS as compared to patients with normal pharmacological MPS. The reasons for these observed differences based on the method of hyperemia induction may seem intuitive; patients who undergo pharmacological MPS tend toward older age, greater numbers of CAD risk factors, increased non-cardiac co-morbidities and reduced functional status, a known powerful predictor of mortality. Nevertheless, because prior studies comparing those undergoing exercise vs pharmacological MPS have not accounted for these clinical differences, it remains unknown whether the prognostic ability of a normal MPS also differs for individuals who can against cannot exercise. To address this question, Rozanski et al undertook an important study evaluating the prognostic differences between normal exercise and normal pharmacological MPS—as defined by a summed stress score B3—among patients with similar clinical profiles. The authors followed 6,069 patients without known CAD for 10.2 ± 1.7 years for rates of all-cause mortality. By propensity score analysis accounting for age, gender, angina typicality, CAD risk factors, medications, and baseline findings at the time of MPS testing (including heart rate, blood pressure, and presence of left ventricular hypertrophy), the authors further compared 1,125 patients with normal exercise MPS (defined by summed stress score B 3) matched to 1,125 patients with normal pharmacological MPS for long-term all-cause mortality, as well as short-term 2.6 ± 2.1 years cardiac death and non-fatal myocardial infarction. Within propensity-matched groups manifesting normal MPS findings, individuals undergoing pharmacological MPS still experienced an annualized mortality rate that was almost twofold that of their exercising counterparts (3.9% vs 1.6%, P \ .0001), a relationship consistently observed across all age groups and independent of smoking status, diabetic state, body mass index, presence of left ventricular hypertrophy, or history of peripheral vascular disease. Even more divergent differences were observed for short-term cardiac outcomes between propensity-matched patients manifesting normal exercise vs normal pharmacological MPS, with a nearly sixfold higher annualized rate of cardiac events (1.1% vs 0.2%, P \ .0001) and a sevenfold higher annualized rate of cardiac death (0.7% vs 0.1%, P = .0002). After partitioning individuals undergoing exercise MPS by Bruce treadmill protocol duration, rates of all-cause mortality for individuals undergoing pharmacological MPS were found to be similar to those in the lowest functioning exercise category, that is, exercising \3 min (3.9% vs 3.4%, P = .65). This study represents the latest in an important series of studies published by this group examining the essential clinical and test characteristics that influence the prognostic features of MPS findings. In this study, examining matched patients with normal exercise vs normal pharmacological MPS, the study cohort was large, the follow-up period long, and the study analytics appropriate. A particularly illustrative finding was that From the Division of Cardiology, Department of Medicine, and Department of Radiology, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY. Reprint requests: James K. Min, MD, Division of Cardiology, Department of Medicine, Weill Cornell Medical College, New York Presbyterian Hospital, 520 E 70th Street, K415, New York, NY 10021; jkm2001@med.cornell.edu, runone123@gmail.com. J Nucl Cardiol 2010;17:983–4. 1071-3581/$34.00 Copyright 2010 American Society of Nuclear Cardiology. doi:10.1007/s12350-010-9301-8