The next generation of prognostic series: Where we can improve on risk stratification?

A large portion of the evidence base on the utility of nuclear cardiology examines the ability to prognosticate varying subsets of patients based on the extent and severity stress myocardial perfusion abnormalities, left ventricular function, and other ancillary markers at rest and stress imaging. An extensive evidence base reports that we can clearly define low to high risk strata of patients and the importance of this information is to guide the intensity of post-imaging therapeutic management strategies. Under the principle of guiding the intensity of therapeutic intervention based on risk or hazard estimates, patient management strategies can be tailored to the expected event rates. Applying this approach, patients at the very highest risk should receive the most intensive care with consideration of surgical care coupled with guideline-directed medical therapy. The concept of intensive care matching the expected hazard in a patient is based on the strategy of initiating effective care that reduces risk and thereby alters the expected hazard for events. There is an expected gradation in risk reduction whereby higher risk patients receive a greater proportional risk reduction as compared to lower risk patients who receive minimal risk reduction. In this manner, secondary prevention strategies largely result in a greater proportional risk reduction as compared to primary prevention approaches. By targeting the highest risk, we alter the natural history of these patients with prevalent myocardial perfusion abnormalities and thereby improve patient outcomes. There are exceptions to this (e.g., risk altering ischemia-guided intervention is frequently less effective in patients with severe left ventricular dysfunction) 4,5 but this is an overall premise that guides both individualized patient management as well as the design of varying clinical research projects. All of these prior approaches to clinical management of the patient with stable ischemic heart disease have been applied for several decades, and it seems difficult to imagine that this successful approach has limitations. For the field of nuclear cardiology, there is a wealth of evidence on risk stratification but do we always apply uniform methodology and where are areas of improvement or those where we can further our knowledge base on the adverse sequelae of atherosclerotic or other diseases following the index examination. It is important to note that we rarely have uniformity in the definitions for many of the components of any given prognostic series; with exception death from all-causes. In some cases, a report may use cardiovascular and in another ischemic death which may differentially include all forms of death including heart failure or fatal stroke. In the case of cardiac death, often the series do not define or enumerate the admixture of reported outcomes based on end-stage ischemic heart disease, fatal myocardial infarction, or sudden cardiac death. Attribution of causality is fundamental to discerning prognostic groups and has been rarely applied in cardiovascular imaging. The inclusion of resuscitated cardiac arrest may also be considered as part of the endpoint combination. Nonfatal events are even more challenging as the type of infarct (ST or non-ST elevation) or its size clearly matters in terms of treatment strategies but within the nuclear cardiology literature are uniformly lumped into one category for prognostic purposes. The details of the specific cardiac biomarkers, upper limits of normal, and related electrocardiographic signs and symptoms are uniformly excluded from methods sections in prognostic series. This is particularly important for the documentation of periprocedural events where varying definitions for acute myocardial infarction have been employed. Clearly, the details and differences across endpoints Reprint requests: Leslee J. Shaw, PhD, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Room 529, 1462 Clifton Road NE, Atlanta, GA 30324; lshaw3@emory.edu J Nucl Cardiol 2015;22:1145–7. 1071-3581/$34.00 Copyright 2015 American Society of Nuclear Cardiology.