734 Have I lost my large rupture cavity? The fingerprint of atherosclerotic plaque healing detected by serial optical coherence tomography imaging

A 64-year-old man, prior smoker, with a history of paroxysmal atrial fibrillation was referred to our hospital due to worsening dyspnoea, progressively worsening angina, and a positive stress EKG testing. Coronary angiography (CAG) showed an angiographically intermediate stenosis of the mid left anterior descending (LAD) artery and a focal, complex lesion of the distal right coronary artery (RCA) (Figure 1A and B, red arrow). Treatment of the LAD stenosis was deferred based on a negative fractional flow reserve value (i.e. 0.85). Optical coherence tomography (OCT) imaging (ILUMIEN OPTIS, Abbott Vascular, Santa Clara, CA) was performed to better characterize the RCA lesion, which disclosed a ruptured thin-cap fibroatheroma (TCFA) with a large ‘empty’ cavity (Figure 1C–G, red arrows) and overlying ‘layered’ tissue (Figure 1H, white arrowheads). Based on these OCT findings, suggestive of initial plaque healing, and on a large residual lumen dimension (i.e. minimum lumen area, MLA, at the rupture site: 7.7 mm2), this lesion was not treated with percutaneous coronary intervention. The patient was discharged on aspirin, edoxaban, metoprolol, rosuvastatin, and ezetimibe, and remained clinically stable for more than 1 year. Due to angina recurrence, a new CAG was performed 18 months after the first admission, revealing a progression of the mid LAD stenosis that was treated with a 2.5/28 mm drug-eluting stent, and an improvement of the RCA lesion angiographic appearance (smooth contour) (Figure 1A′–B′). RCA OCT imaging was repeated demonstrating a complete healing of the large rupture cavity with all the hallmarks of the reparative process (Figure 1C′–H′): (1) re-established fibrous cap integrity and smooth vessel lumen profile; (2) thickening of the fibrous cap and reduction of lipid burden (i.e., transformation of TCFA into thick-cap fibroatheroma, ThCFA); (3) replacement of the ‘empty’ cavity with new ‘granulation tissue’; (4) initial calcification of the plaque; (5) heterogeneous signal-rich layers with distinct optical-signal intensity (layered, ‘onion-like’ pattern); and (6) mild lumen narrowing (MLA at the rupture site: 6.9 mm2).

Application value of preoperative dual-source computed tomography in assessing the rupture site of thoracic aortic dissection

Objective To investigate the application value of dual-source computed tomography (DSCT) in preoperative assessment the rupture site of an thoracic aortic dissection (TAD). Methods A retrospective analysis of preoperative DSCT, multislice computed tomography (MSCT), and transthoracic echocardiography (TTE) results of 150 patients with suspected TAD in our hospital was conducted, and the intraoperative findings or interventional treatment results were used as the diagnostic gold standard. Results Of all 150 suspected TAD patients, 123 patients were confirmed to have TAD. The rupture site of TAD was in the ascending aorta in 46 patients, in the aortic arch in 13 patients, and in the descending aorta in 64 patients. The sensitivity of DSCT, MSCT, and TTE for locating the rupture site of the TAD was 100%, 93.5%, and 89.5%, respectively, and the specificity was 100%, 88.9%, and 81.5%. The differences were statistically significant. The distance between the actual rupture site and the one diagnosed by DSCT, MSCT, and TTE was 1.9 ± 1.2 mm, 5.1 ± 2.7 mm, and 7.8 ± 3.5 mm, respectively; the latter two were significantly worse than DSCT. The size of the rupture site diagnosed by DSCT, MSCT, and TTE was 1.5 ± 0.8 cm, 1.7 ± 0.9 cm, and 1.9 ± 1.0 cm, respectively. The size of the rupture site diagnosed by DSCT was not significantly different from the actual size of 1.4 ± 0.7 cm, while those by MSCT and TTE were. Conclusion DSCT has high sensitivity and specificity in diagnosing the rupture site of TAD and can clearly locate the rupture site. It can be a preferred imaging method for TAD.

Selective YAP activation in Procr cells is essential for ovarian stem/progenitor expansion and epithelium repair

Ovarian surface epithelium (OSE) undergoes recurring ovulatory rupture and OSE stem cells rapidly generate new cells for the repair. How the stem cell senses the rupture and promptly turns on proliferation is unclear. Our previous study has identified that Protein C Receptor (Procr) marks OSE progenitors. In this study, we observed decreased adherent junction and selective activation of YAP signaling in Procr progenitors at OSE rupture site. OSE repair is impeded upon deletion of Yap in these progenitors. Interestingly, Procr+ progenitors show lower expression of Vgll4, an antagonist of YAP signaling. Overexpression of Vgll4 in Procr+ cells hampers OSE repair and progenitor proliferation, indicating that selective low Vgll4 expression in Procr+ progenitors is critical for OSE repair. In addition, YAP activation promotes transcription of the OSE stemness gene Procr. The combination of increased cell division and Procr expression leads to expansion of Procr+ progenitors surrounding the rupture site. These results illustrate a YAP-dependent mechanism by which the stem/progenitor cells recognize the ovulatory rupture, and rapidly multiply their numbers, highlighting a YAP-induced stem cell expansion strategy.

Role of magnetic resonance vessel wall imaging in detecting and managing ruptured aneurysms among multiple intracranial aneurysms

Background: Wall enhancement of intracranial saccular aneurysms in high-resolution magnetic resonance vessel wall imaging (MR-VWI) might indicate a ruptured aneurysm. Therefore, this study aimed to determine the diagnostic ability of wall enhancement to detect the ruptured aneurysms among multiple aneurysms. Methods: Patients with subarachnoid hemorrhage (SAH) and multiple intracranial aneurysms who underwent MR-VWI before craniotomy and clipping were included in the study. Three-dimensional T1-weighted fast spin-echo sequences were obtained before and after gadolinium injection. Aneurysm rupture was estimated based on the subarachnoid clot distribution, aneurysmal contours, and MR-VWI findings. We selectively performed surgical clipping and confirmed the rupture site intraoperatively. Results: Thirteen patients with SAH with 13 ruptured and 17 unruptured aneurysms were treated at out facility. The accuracy rate of rupture site diagnosis using MR-VWI was 69.2% (9/13 cases). Each unruptured aneurysm was equally or more strongly enhanced in the other four cases than the ruptured aneurysms. In three of the four unruptured aneurysms with positive MR-VWI findings, atherosclerosis of the aneurysmal wall was observed during simultaneous or elective clipping surgery. Further, clipping surgery was performed without intraoperative rupture in two cases with the help of MR-VWI findings. Conclusion: Correct diagnosis of the rupture site using MR-VWI alone was unreliable due to false positives caused by the wall enhancement of unruptured aneurysms with atherosclerosis. Therefore, ruptured aneurysms should be detected using more information in addition to MR-VWI images. MR-VWI may be advantageous to determine surgical strategies when managing patients with SAH and multiple aneurysms.

Left ventricular free wall rupture -- a real nightmare

Left ventricular free wall rupture (LVFWR) is a most rare but often lethal mechanical complication of acute myocardial infarction (AMI). The mortality rate for LVFWR is described from 75% to 90% and it is the cause for 20% of in-hospital deaths after AMI. Death results essentially from the limited time available for emergent intervention after onset of symptoms. Emergency surgery is indicated and normally the rupture site is easily identified, but it may not be apparent macroscopically, corresponding to transmyocardial or subepicardial dissection with an external rupture far from the infarction site, or already thrombosed and contained. Repair of the ventricular wall is usually achieved either by suturing the edges of the tear or closing it with patches of artificial material or biological tissues, usually using some kind of biological glue. However, several cases of successful conservative management have been described. In this Editorial, I comment on the metanalysis conducted by Matteucci et al, published in this issue of the Journal, including 11 non-randomized studies and enrolling a total of 363 patients, which brings a great deal of new knowledge that can help not only in the prevention but also in the management of this dreadful complication of AMI.

Hemodynamic features of an intracranial aneurysm rupture predicted by perianeurysmal edema: A case report

Background: Perianeurysmal edema (PAE) has been suggested as an indicator of potential aneurysm rupture; however, the hemodynamic features of these aneurysms are still unknown. A computational fluid dynamic (CFD) analysis was performed to evaluate the hemodynamic features of a very rare case of a ruptured middle cerebral artery (MCA) aneurysm with PAE. Case Description: A 65-year-old woman presented with disturbed consciousness. A subarachnoid hemorrhage due to an azygos anterior cerebral artery (ACA) aneurysm rupture was suspected. An unruptured MCA aneurysm with PAE was identified in the left temporal lobe. Although the ACA aneurysm was clipped to prevent re-bleeding, the MCA aneurysm subsequently ruptured 6 days later. Clipping of the MCA aneurysm was performed, and hemosiderin deposits suggestive of sentinel bleeding were found on the surface of the aneurysm dome. CFD analysis revealed unstable hemodynamic stress at the expanded bleb area after rupture, localized to the rupture site. Moreover, this analysis revealed flow impingement with pressure elevation and low wall shear stress, which indicated increased inflammation and aneurysm wall thinning that likely led to rupture. Conclusion: Hemosiderin deposits at the aneurysm wall and PAE indicates leakage from a cerebral aneurysm. Hemodynamic stress at the aneurysm may promote an inflammatory response and lead to wall weakening accompanied by PAE. Based on our findings, we recommend that surgical intervention should be considered as the first line of treatment for such aneurysms to prevent rupture.

Influence of Achilles tendon rupture site on surgical repair outcomes

Purpose: This study aims to measure the distance between the common site of Achilles tendon rupture and calcaneal insertion through ultrasound and to compare the outcomes between proximal and distal rupture groups. Methods: We investigated the electronic medical records of 117 patients and preoperative ultrasound describing the rupture site. Among 88 patients, we compared the patient-reported outcome and re-rupture rate of proximal and distal rupture groups. Results: The mean rupture site of the 117 included subjects was 4.5 ± 1.3 cm. The rupture site had a weak negative correlation with body mass index ( ρ = −0.230, P = 0.013). Furthermore, 77% of the patients with distal rupture reported good outcome (Achilles Tendon Rupture Score > 80) compared to 56% of the patients with proximal rupture ( P = 0.041). Conclusion: Patients with proximal rupture had less satisfactory postoperative outcomes than those with distal rupture.

Prevalence, Features, and Prognosis of Artery‐to‐Artery Embolic ST‐Segment–Elevation Myocardial Infarction: An Optical Coherence Tomography Study

Background The major underlying mechanisms contributing to acute coronary syndrome are plaque rupture, plaque erosion, and calcified nodule. Artery‐to‐artery embolic myocardial infarction (AAEMI) was defined as ST‐segment–elevation myocardial infarction caused by migrating thrombus formed at the proximal ruptured plaque. The aim of this study was to investigate the prevalence and clinical features of AAEMI by using optical coherence tomography. Methods and Results This study retrospectively enrolled 297 patients with ST‐segment–elevation myocardial infarction who underwent optical coherence tomography before percutaneous coronary intervention. Patients were divided into 4 groups consisting of plaque rupture, plaque erosion, calcified nodule, and AAEMI according to optical coherence tomography findings. The prevalence of AAEMI was 3.4%. The culprit vessel in 60% of patients with AAEMI was right coronary artery. Minimum lumen area at the culprit site was larger in AAEMI compared with plaque rupture, plaque erosion, and calcified nodule (4.0 mm 2 [interquartile range (IQR), 2.2–4.9] versus 1.0 mm 2 [IQR, 0.8–1.3] versus 1.0 mm 2 [IQR, 0.8–1.2] versus 1.1 mm 2 [IQR, 0.7–1.6], P <0.001). Lumen area at the rupture site was larger in patients with AAEMI compared with patients with plaque rupture (4.4 mm 2 [IQR, 2.5–6.7] versus 1.5 mm 2 [IQR, 1.0–2.4], P <0.001). In patients with AAEMI, the median minimum lumen area at the occlusion site was 1.2 mm 2 (IQR, 1.0–2.1), 40% of them had nonstent strategy, and the 3‐year major adverse cardiac event rate was 0%. Conclusions AAEMI is a rare cause for ST‐segment–elevation myocardial infarction and has unique morphological features of plaque including larger lumen area at rupture site and smaller lumen area at the occlusion site.

Validation of diagnostic criteria and histopathological characterization of cardiac rupture in the mouse model of nonreperfused myocardial infarction

We show that cardiac rupture accounts for 50% of deaths in C57BL/6J mice undergoing nonreperfused myocardial infarction protocols. Overestimation of rupture events in published studies likely reflects the low specificity of hemothorax as a criterion for documentation of rupture. In contrast, identification of a gross rupture site has high specificity and low sensitivity. We also show that mice dying of rupture have increased macrophage influx and attenuated myofibroblast infiltration in the infarct. These findings are consistent with a role for perturbations in the balance between inflammatory and reparative responses in the pathogenesis of postinfarction cardiac rupture. We also report that the male predilection for rupture in infarcted mice is not associated with increased inflammatory activation of myeloid cells.