In patients with acute coronary syndromes, atherosclerotic plaque rupture with subsequent vessel occlusion causes irreversible myocardial damage. Milder forms of plaque rupture with subsequent microembolization of atherothrombotic burden into the coronary circulation, however, may occur in patients with stable CAD or even in presumably healthy subjects. Thus, more than a decade ago, healed plaque destruction was observed in postmortem studies (3), whereas angioscopy studies demonstrated that silent plaque rupture is present in ∼20% of patients with stable CAD (4). Especially in diabetic patients, plaque rupture is expected to remain subclinical, so that the presence of increased plaque burden and troponin leakage in the absence of unstable angina is not surprising. Furthermore, such plaque microembolization and subsequent micronecrosis may subsequently result in the release of alarmin cytokines by stressed cardiomyocytes (5). This may then elicit systemic proinflammatory responses, again contributing to vascular remodeling processes and microvascular dysfunction, thus possibly being part of a vicious circle that encompasses silent plaque rupture, systemic inflammation, and myocardial injury. To confirm this hypothesis, the detection by gadolinium-positive myocardial fibrosis within the perfusion bead of coronary vessels with increased noncalcified plaque burden will be decisive in future biomarker and multimodality imaging studies. Rubin et al. (1) should be commended for their comprehensive analysis because their study represents an important contribution in the area of ischemic heart disease, considering hs-cTnT as a phenotype for increased cardiovascular risk in those with asymptomatic diabetes. Now, future studies are warranted to test whether hs-cTnT and other biomarkers can be used as therapeutic targets in stable CAD.