Response to Letters Regarding Article, “Mechanisms of Myocardial Infarction in Women Without Angiographically Obstructive Coronary Artery Disease”

Abstract

Dr Ward suggests that plaque ruptures identified by the core laboratory in our study 1 were not responsible for troponin elevation and instead had a nonischemic cause, and that these plaque ruptures may have been caused by intravascular ultrasound. We respectfully disagree. We believe that the observed ruptured plaques were responsible for troponin elevation in patients in this study for several reasons. First, all patients presented with acute onset of ischemic symptoms, and we find it very unlikely that plaque rupture is incidental in this setting. We acknowledge that it is impossible to exclude plaque rupture caused by the intravascular ultrasound procedure in this or any study using intravascular ultrasound. Though we did not include stable control patients, we reference in the manuscript 2 previous publications that reported no plaque rupture in a total of 155 stable patients without myocardial infarction, most of whom had atherosclerotic disease on intravascular ultrasound. 2,3 Furthermore, 75% of participants in our study who were found to have plaque disruption had T2 signal hyperintensity, which indicates acute myocardial edema. As shown in the representative image in the published article (Figures 4Aiv and 4Av), T2 hyperintensity in those patients with plaque disruption generally involved a large territory. We believe, therefore, that the culprit artery may have been transiently occluded, causing early myocardial injury. This hypothesized occlusion was relieved by the time of angiography, and the duration of decreased flow must have been sufficiently short to avoid the development of myocardial changes consistent with late gadolinium enhancement (LGE). Moreover, the presence of LGE does not equate with "definite MI": Note that only 10 of 17 participants who manifested LGE on the cardiac magnetic resonance had an ischemic pattern of LGE on the cardiac magnetic resonance, whereas others suggested a nonischemic cause or had a mixed pattern. Further studies are needed to definitively link cause and effect in this patient population.We agree with Drs Chen and Zhang that some patients with a nonischemic cause of chest pain, as evidenced by a nonischemic pattern of myocardial injury, do meet the universal criteria for diagnosis of myocardial infarction, as in our study, the referenced study by Assomull et al, 4 and several other prior publications. [5][6][7][8] All patients enrolled in this study had a clinical diagnosis of myocardial infarction and were referred for angiography on the basis of this diagnosis, which may explain our lower observed prevalence of LGE suggestive of myocarditis compared with prior publications. We did not think it appropriate to exclude these patients from the study retrospectively. In our study, as in prior reports, not all participants had T2 signal hyperintensity and/or LGE on cardiac magnetic resonance. This finding highlights the somewhat insensitive nature of cardiac magnetic resonance for localization of myocardial injury in patients who have been proven to have myocardial ...