Response to the Letter by Opolski et al Regarding Article, “Computed Tomography Coronary Angiography in Patients With Acute Myocardial Infarction Without Significant Coronary Stenosis”

Abstract

We thank Opolski et al for their comments and appreciate their interest in our study.1 They raise several points, which we address below. As the authors note, coronary atherosclerosis is a common finding also in asymptomatic patients; indeed, we think that, in the special setting of patients with acute myocardial infarction proven by cardiac magnetic resonance imaging and without significant coronary stenosis, coronary atherosclerosis is often underestimated because of an apparently normal coronary angiogram. As a consequence, the diagnosis may be challenged, and patients may not receive an adequate secondary prevention therapy.The mechanisms of myocardial infarction in this setting are certainly multiple and are not related exclusively to atherosclerosis, but we think that the different distributions of coronary plaque patterns between infarct-related arteries (IRAs) and non-IRAs support that coronary atherosclerosis may be the most likely mechanism in a number of patients.As the authors suggest, a control group could be useful to support the data, but we do not think that patients excluded from the study could represent an appropriate control group; they cannot be classified clearly, because they are symptomatic patients with high troponin but unclear diagnosis.The 64-slice computed tomography technology has a limited spatial resolution compared with intravascular ultrasound or optical coherence tomography, but several studies have shown that plaque area measurements are accurate compared with intravascular ultrasound.2 As the authors correctly note, in our study, coronary plaques were located more frequently in the left anterior descending coronary artery, but we do not think that this finding is responsible for the larger plaque areas in IRAs. In fact, it is well known that coronary plaques cluster in the proximal segments, 3 but coronary arteries caliper in the proximal segments do not differ significantly, except for the left main vessel. Therefore, the higher plaque area and remodeling index are not related exclusively to location. In our analysis, we took into account only coronary arteries with coronary plaques.Previous studies have shown that coronary computed tomography is a reliable noninvasive method to analyze coronary plaque composition, but it is not able to visualize plaque disruption. Therefore, it cannot identify culprit plaques in acute coronary syndrome. Taking into account this limitation, our aim was to investigate whether coronary plaques located on IRAs showed a different morphological pattern compared with non-IRA plaques. We think that this type of analysis can provide some important clues. In fact, our data highlight an increased burden of plaques with vulnerable features in IRAs. Of course, the analysis includes both culprit and nonculprit plaques located on IRAs, but in our opinion, this fact reinforces the results because the presence of nonculprit plaques probably mitigates the differences between IRA and non-IRA plaques.