ABSTRACT
Detecting vulnerable plaque is complicated for several reasons. Imaging and physiologically based detection modalities are under extensive evaluation and described elsewhere in this book. As we learn to reliably detect early vulnerable plaque, clinicians will soon confront problems arising from imperfect test performance and low prevalence populations. Imperfect diagnostic tests for fixed CAD include treadmill, nuclear, and echocardiographically based evaluation.20,21
Diagnostic test performance improves proportionally to disease prevalence.21,22
Sensitivity (true positive tests/subjects with disease) and specificity (true negatives/subjects without disease) are prevalence independent, while positive and negative predictive values (PPV, true positive tests/all positive tests; NPV, true negative tests/all negative tests) are prevalence dependent.23 Detecting vulnerable plaque is initially complicated.The low disease prevalence of high-risk subjects in the general population amplifies the diagnostic problems for vulnerable plaque. No test as yet has high sensitivity or specificity (prevalence independent parameters), so diagnostic errors are high, with many false positives and negatives (prevalence dependent parameters).Thus identification of markers permitting highly sensitive and specific detection is needed. Such a marker is the pathophysiologic equivalent of troponin -T, troponin-I, and CK-MB (creatine kinase-myocardial band), all highly sensitive and specific for myocardial infarction (MI).
