Transarterial embolization followed by staged hepatectomy versus emergency hepatectomy for ruptured HCC: a meta-analysis

Background To compare the efficacy and safety between emergency hepatectomy (EH) and emergency transarterial embolization (TAE) followed by staged hepatectomy (SH) in the treatment of spontaneous ruptured hepatocellular carcinoma (rHCC). Methods Databases (PubMed, EMBASE, Web of science, Cochrane Library, ClinicalTrial.gov, CNKI, Wanfang and VIP) were searched for all relevant comparative studies from January 2000 to October 2020. Odds ratio (OR) and mean difference (MD) with 95% confidence interval (CI) were pooled for dichotomous and continuous variables, respectively. Subgroup analyses based on the kind of embolization were conducted. RevMan 5.3 software was adopted for meta-analysis. Results Eighteen studies with 871 patients were finally included in this meta-analysis, 448 in EH group and 423 in TAE + SH group. No significant difference was observed in successful hemostasis (P = 0.42), postoperative hospital stay (P = 0.12), complication rate (P = 0.08) between EH and TAE + SH group. However, TAE + SH group was associated with shorter operating time (P < 0.00001), fewer perioperative blood loss (P = 0.007), fewer blood transfusion (P = 0.003), lower in-hospital mortality (P < 0.00001) and higher 1-year survival as well as 3-year survival (P < 0.0001; P = 0.003) compared with EH group. Conclusion Compared with EH, TAE + SH could reduce perioperative operating time, blood loss, blood transfusion, mortality rate and increase the long-term survival rate of the rHCC patients, which may be a better treatment for resectable rHCC (AU)

Short-term air pollution exposure and mechanisms of plaque instability in acute coronary syndromes: An optical coherence tomography study.

BACKGROUND AND AIMS: Air pollution is emerging as an important risk factor for acute coronary syndrome (ACS). In this study, we investigated the association between short-term air pollution exposure and mechanisms of coronary plaque instability evaluated by optical coherence tomography (OCT) imaging in ACS patients. METHODS: Patients with ACS undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT. Based on each case's home address, the mean daily exposures to several pollutants, including particulate matter 2.5 (PM2.5), on the same day of ACS and in the immediate days (up to 6 days) prior to the index ACS, were collected. RESULTS: 139 ACS patients were included [69 (49.6%) had PR and 70 (50.4%) IFC]. Patients with PR, compared to those with IFC, had higher PM2.5 exposure levels on the same day of ACS, without differences in the immediate 6 days before index ACS. At multivariate analysis, PM2.5 exposure on the same day of ACS was the only independent predictor of PR [OR = 1.912 per SD (8.6 µg/m3), CI95 % (1.087-3.364), p = 0.025]. Patients with PR presented a steady increase in PM2.5 daily exposure levels in the days preceding the occurrence of ACS, with a peak the day of ACS (p for trend = 0.042) CONCLUSIONS: This study demonstrates for the first time that a higher short-term PM2.5 exposure, on the same day of ACS, is associated with an increased risk of PR as a pathobiological mechanism of coronary plaque instability.

[The 502nd case: thrombocytopenia, splenomegaly, disseminated intravascular coagulation, and spontaneous rupture of the spleen].

A young man with a history of thrombocytopenia for seven years presented with splenomegaly and fever and rapidly evolved to disseminated intravascular coagulation (DIC) and hemorrhagic shock. Spontaneous rupture of the spleen was diagnosed. The critical patient underwent an emergency splenectomy. Pathological examination revealed splenic peliosis, an extremely rare disease with unknown etiology and pathogenesis. Despite the high mortality rate due to spontaneous splenic rupture with DIC, the patient was successfully treated and the details of the case are presented in this report.

Utility of optical coherence tomography in acute coronary syndromes.

Studies utilizing intravascular imaging have replicated the findings of histopathological studies, identifying the most common substrates for acute coronary syndromes (ACS) as plaque rupture, erosion, and calcified nodule, with spontaneous coronary artery dissection, coronary artery spasm, and coronary embolism constituting the less common etiologies. The purpose of this review is to summarize the data from clinical studies that have used high-resolution intravascular optical coherence tomography (OCT) to assess culprit plaque morphology in ACS. In addition, we discuss the utility of intravascular OCT for effective treatment of patients presenting with ACS, including the possibility of culprit lesion-based treatment by percutaneous coronary intervention.

Coronary artery plaque rupture and erosion: Role of wall shear stress profiling and biological patterns in acute coronary syndromes.

AIMS: Wall shear stress (WSS) is involved in coronary artery plaque pathological mechanisms and modulation of gene expression. This study aims to provide a comprehensive haemodynamic and biological description of unstable (intact-fibrous-cap, IFC, and ruptured-fibrous-cap, RFC) and stable (chronic coronary syndrome, CCS) plaques and investigate any correlation between WSS and molecular pathways. METHODS AND RESULTS: We enrolled 24 CCS and 25 Non-ST Elevation Myocardial Infarction-ACS patients with IFC (n = 11) and RFC (n = 14) culprit lesions according to optical coherence tomography analysis. A real-time PCR primer array was performed on peripheral blood mononuclear cells for 17 different molecules whose expression is linked to WSS. Computational fluid dynamics simulations were performed in high-fidelity 3D-coronary artery anatomical models for three patients per group. A total of nine genes were significantly overexpressed in the unstable patients as compared to CCS patients, with no differences between IFC and RFC groups (GPX1, MMP1, MMP9, NOS3, PLA2G7, PI16, SOD1, TIMP1, and TFRC) while four displayed different levels between IFC and RFC groups (TNFα, ADAMTS13, EDN1, and LGALS8). A significantly higher WSS was observed in the RFC group (p < 0.001) compared to the two other groups. A significant correlation was observed between TNFα (p < 0.001), EDN1 (p = 0.036), and MMP9 (p = 0.005) and WSS values in the RFC group. CONCLUSIONS: Our data demonstrate that IFC and RFC plaques are subject to different WSS conditions and gene expressions, suggesting that WSS profiling may play an essential role in the plaque instability characterization with relevant diagnostic and therapeutic implications in the era of precision medicine.

New insights into fibrous cap thickness of vulnerable plaques assessed by optical coherence tomography.

OBJECTIVE: Vulnerable plaques with fibrous cap thickness (FCT) of ≤65 µm are prone to rupture and/or thrombosis. However, plaques with FCT > 65 µm cause acute myocardial infarction and even sudden death. We aimed to investigate the relationship between 65 < FCT ≤ 80 µm and plaque rupture and/or thrombosis using optical coherence tomography (OCT). METHODS: OCT was performed on culprit lesions in 502 consecutively enrolled patients to identify FCT. Patients were classified into three groups according to FCT: Group A (FCT ≤ 65 µm, n = 147), Group B (65 < FCT ≤ 80 µm, n = 84) and Group C (FCT > 80 µm, n = 271). Clinical and laboratory data was collected from the inpatient medical record system. RESULTS: Plaques with thinner FCT, especially < 65 µm, were more susceptible to rupture and/or thrombosis (P < 0.001). Plaques with FCT between 65 and 80 µm had a higher probability of rupture and/or thrombosis than those with FCT > 80 µm (P < 0.001). In multivariable analysis, FCT ≤ 65 µm and 65 < FCT ≤ 80 µm were independent predictors for plaque rupture ([FCT ≤ 65 µm vs. FCT > 80 µm]: OR = 8.082, 95% CI = 4.861 to 13.435, P < 0.001; [65 < FCT ≤ 80 µm vs. FCT > 80 µm]: OR = 2.463, 95% CI = 1.370 to 4.430, P = 0.003), thrombosis ([FCT ≤ 65 µm vs. FCT > 80 µm]: OR = 25.224, 95% CI = 13.768 to 46.212, P < 0.001; [65 < FCT ≤ 80 µm vs. FCT > 80 µm]: OR = 3.675, 95% CI = 2.065 to 6.542, P < 0.001) and plaque rupture with thrombosis ([FCT ≤ 65 µm vs. FCT > 80 µm]: OR = 22.593, 95% CI = 11.426 to 44.674, P < 0.001; [65 < FCT ≤ 80 µm vs. FCT > 80 µm]: OR = 4.143, 95% CI = 1.869 to 9.184, P < 0.001). CONCLUSIONS: OCT-assessed 65 < FCT ≤ 80 µm was independently associated with increased risk of plaque rupture and/or thrombosis compared with FCT > 80 µm.

Spontaneous rupture of a large splenic artery aneurysm in a 59-year-old male patient with pemphigus vulgaris: a case report.

BACKGROUND: There is currently no information on the anatomical risk factors for splenic artery aneurysm rupture, specifically the location or size of the lesion; therefore, reporting this entity to obtain data and ultimately reduce morbidity and mortality is essential. Here we report a case of a male patient with spontaneous rupture of a large splenic artery aneurysm presenting with abdominal pain. CASE PRESENTATION: A 59-year middle-eastern male, with known pemphigus vulgaris presented with a chief complaint of headache and syncope, followed by abdominal pain along with severe metabolic acidosis. A contrast-enhanced computed tomography scan of the abdomen and pelvic showed a splenic artery aneurysm of 33 × 30 mm with a 150 × 90 mm hematoma formation around the aneurysm site. The patient underwent an operation and splenectomy, with confirmation of the diagnosis of ruptured splenic artery aneurysm. CONCLUSION: It is essential to consider splenic aneurysm rupture as a second-line differential diagnosis, especially among patients with comorbid diseases, as this can lead to timely and appropriate lifesaving intervention.

Clinical features and lipid profiles of plaque erosion over lipid-rich plaque versus fibrous plaque in patients with acute coronary syndrome.

BACKGROUND AND AIMS: Pathological reports have shown that plaque erosion (PE), a common cause of acute coronary syndrome (ACS), can form in both fibrous plaque and lipid-rich plaque (LRP). In plaque rupture (PR), which is the main cause of ACS, the underlying plaque is LRP with a thin fibrous cap. In this study, we aimed to investigate the clinical features and lipid profiles of PE with or without LRP in comparison with those of PR. METHODS: A total of 166 patients with ACS, who underwent percutaneous coronary intervention using optical coherence tomography (OCT) and met the criteria for PR or PE, were included. LRP was defined as plaque with a maximal lipid arc (>180°). Culprit lesions were categorized into PR and PE with/without LRP [PE(Lipid) or PE(Fibrous)]. RESULTS: The prevalence of PR, PE(Lipid), and PE(Fibrous) was 104 (62.7%), 43 (25.9%), and 19(11.4%), respectively. The patients with PR and PE(Lipid) had a significantly higher peak creatine kinase level (1338 and 1584U/L, respectively, p < 0.01) and prevalence of ST-elevation myocardial infarction (71.2% and 79.1%, respectively, p < 0.01) than those with PE(Fibrous) (214U/L and 21.1%, respectively). The various lipid profiles were mostly comparable between the patients with PE(Lipid) and PR, but different in those with PE(Fibrous). The levels of small dense low-density lipoprotein cholesterol were significantly higher in the patients with PR and PE(Lipid) than in those with PE(Fibrous) (39.0, 35.3, and 25.7 mg/dL, respectively, p = 0.02). CONCLUSIONS: The clinical features and lipid profiles are substantially different between PE(Lipid) and PE(Fibrous), but are somewhat similar between PE(Lipid) and PR.

Arthroscopic Caudal Cruciate Ligament Damage in Canine Stifles with Cranial Cruciate Ligament Disease.

OBJECTIVE: The aim of this study was to describe the arthroscopic changes to the caudal cruciate ligament (CdCL) in dogs with cranial cruciate ligament disease. STUDY DESIGN: Arthroscopic video recordings (n = 117) of the stifle with cranial cruciate ligament disease were reviewed. The extent of CdCL tearing was described. Signalment, palpable stifle stability and the presence of a meniscal tear were recorded. Pathology of the synovial joint and the synovium overlying the CdCL were scored at two time points.Two-way interactions were investigated (p < 0.05). Univariate analysis and a Wald test (p < 0.20) were performed. Factors were retained with a Wald test p < 0.05 or if a confounder, then a changing model coefficient >15%. A weighted kappa statistic was used to evaluate intraobserver agreement. RESULTS: Caudal cruciate ligament tearing was identified in 94% of stifles. Longitudinal tearing (76%) was the most common type of damage (45% partial, 31% full thickness). Synovitis was present in all joints and changes to the synovium overlying the CdCL were less frequently identified (67%).Synovitis was associated with the degree to CdCL tearing. Synovitis overlying the CdCL was associated with lower body weight and lower CdCL damage. CONCLUSION: Caudal cruciate ligament damage is common in dogs with cranial cruciate ligament disease and longitudinal tearing was the most common injury identified. Severity of joint pouch synovitis was positively correlated with the degree of CdCL damage and the portion of the CdCL not exposed to the synovium was unaffected. These findings suggest synovitis is likely a contributor to CdCL injury.

Plaque erosion masquerading as spontaneous coronary artery dissection: A case of sudden coronary death.

The three most common mechanisms of thrombosis in acute coronary syndrome (ACS) are plaque rupture, plaque erosion and calcified nodule. Plaque erosion occurs over an intact fibrous cap, commonly over pathological intimal thickening (PIT) rather than thin cap fibroatheroma (TCFA), and is more common among younger and female patients.1 A very rare mechanism of ACS is spontaneous coronary artery dissection (SCAD), resulting from the formation of an intramural hematoma and/or intimal disruption.2 We present a case of sudden coronary death with the appearance of SCAD on coronary computed tomography angiography (CCTA).

The Importance of Nodule Size in the Management of Ruptured Thyroid Nodule After Radiofrequency Ablation: A Retrospective Study and Literature Review.

Background: Nodule rupture is a relatively uncommon yet severe complication of radiofrequency ablation (RFA). When nodule rupture occurs, determining suitable therapeutic management is a critical issue. A study herein aimed to identify the predictive factors affecting the management of post-RFA nodule rupture. Methods: Post-RFA nodule rupture data of 9 patients were enrolled from 2 medical centers. A literature investigation was performed, uncovering nodule rupture data of 17 patients. A total of 26 patients were analyzed and divided into two groups, categorized as patients requiring either invasive or conservative therapeutic management. Data including initial symptoms, imaging, therapeutic management, and prognosis were reviewed and compared between the two groups. Results: Significant differences in nodule diameter, and the ablation time of the course prior to rupture (RUP time) were noted between the two groups (p = 0.045 and 0.008, respectively). Logistic regression analysis indicated the initial nodule diameter and RUP time significantly affected the requirement of invasive treatment (OR 1.99 and 1.11, respectively). Considering practicality, when a nodule with an initial maximum diameter of >4.5cm ruptured, invasive management was suggested (sensitivity 69% and specificity 79%). Conclusion: Though nodule ruptures can be managed conservatively, a ruptured nodule with an initial maximum diameter of >4.5cm may require invasive management. Understanding the significant clinical and imaging features will help physicians make an appropriate risk assessment to determine the correct treatment in a timely manner.

Sudden unexpected death due to spontaneous pneumothorax caused by ruptured bilateral pulmonary bullae.

Sudden unexpected death due to pneumothoraces caused by spontaneous rupture of bilateral pulmonary bullae is rare. This article reports the case of a 16-year-old girl who experienced this rare phenomenon without any precipitating factors. The patient did not have a history of chest pains or smoking but experienced chest tightness in the early morning and collapsed and died 4 h later. Autopsy identified the cause of death to be bilateral pneumothoraces and massive bilateral pulmonary collapse (atelectasis) due to ruptured apical bullae of the bilateral lungs. No injuries or other significant pathological findings were identified. A low body mass index (16.5) may have been a risk factor for the spontaneous tension pneumothoraces. In some situations, genetic counseling and testing may be helpful in identifying a heritable process associated with spontaneous pneumothoraces.

Internal modulation of proteolysis in vascular extracellular matrix remodeling: role of ADAM metallopeptidase with thrombospondin type 1 motif 5 in the development of intracranial aneurysm rupture.

Intracranial aneurysms (IAs) are common cerebrovascular diseases that carry a high mortality rate, and the mechanisms that contribute to IA formation and rupture have not been elucidated. ADAMTS-5 (ADAM Metallopeptidase with Thrombospondin Type 1 Motif 5) is a secreted proteinase involved in matrix degradation and ECM (extracellular matrix) remodeling processes, and we hypothesized that the dysregulation of ADAMTS-5 could play a role in the pathophysiology of IA. Immunofluorescence revealed that the ADAMTS-5 levels were decreased in human and murine IA samples. The administration of recombinant protein ADAMTS-5 significantly reduced the incidence of aneurysm rupture in the experimental model of IA. IA artery tissue was collected and utilized for histology, immunostaining, and specific gene expression analysis. Additionally, the IA arteries in ADAMTS-5-administered mice showed reduced elastic fiber destruction, proteoglycan accumulation, macrophage infiltration, inflammatory response, and apoptosis. To further verify the role of ADAMTS-5 in cerebral vessels, a specific ADAMTS-5 inhibitor was used on another model animal, zebrafish, and intracranial hemorrhage was observed in zebrafish embryos. In conclusion, our findings indicate that ADAMTS-5 is downregulated in human IA, and compensatory ADAMTS-5 administration inhibits IA development and rupture with potentially important implications for treating this cerebrovascular disease.

Cirsoid aneurysm rupture of the splenic artery as a rare cause of fatal hemoperitoneum.

Cirsoid aneurysms are rare arteriovenous malformations without any capillaries interposed and almost always observed in the scalp region. These types of aneurysms are so-called "cirsoid" because of their serpiginous appearance. In this report, the authors present the first case of a lethal spontaneous rupture of a cirsoid aneurysm of the splenic artery, which could be diagnosed only by post-mortem histologic examination. The victim was a 70-year-old man who was suddenly found dead in bed while he was hospitalized and waiting for a scheduled cardiac surgery. A forensic autopsy was ordered due to the suspicion that the man's death could have been related to medical malpractice. An accurate autopsy and a complete forensic histologic examination could clarify the cause of death, which was identified in the spontaneous rupture of a cirsoid aneurysm of the splenic artery. The case is intended to be used as source data for similar forensic cases, where the cause of a massive hemoperitoneum is difficult to be identified.

Sudden and unexpected death in childhood due to an undiagnosed hepatoblastoma: Case report and review of literature.

The sudden and unexpected death of an infant or child due to cancer is a particularly rare event. Most of the cases concern primary growths located in vital organs such as the heart or the brain. Only in an extremely small number of cases does it occur in infants or children affected by liver cancer. Herein we report the sudden and unexpected death of a 3-and-a-half-year-old infant, who due to an undiagnosed tumor of the liver, namely hepatoblastoma, suffered a major intra-abdominal (hemoperitoneum) bleed, leading to a fatal hemorrhagic trauma. In cases like these, it is of utmost importance to carry out both an autopsy as well as complete histological tests in order to determine if the hepatic tumor is the real cause of death or if it was a mere chance finding. In the case of sudden and unexplained deaths in infancy and childhood, the forensic pathologist should always consider that other complications, for example, those correlated with hepatoblastoma could, in fact, cause sudden death given that this particular tumor is often scarcely symptomatic and can remain undiscovered for a long period of time.

RNA-seq identifies circulating miRNAs as potential biomarkers for plaque rupture in patients with ST-segment elevation myocardial infarction.

BACKGROUND: Plaque rupture (PR) and plaque erosion (PE) are the two major pathological phenotypes in acute coronary syndrome. Since microRNAs have been found to be involved in the mechanisms of PR and PE, we investigated the diagnostic utility of microRNAs in differentiating between patients with PR and patients with PE. METHODS: MicroRNA sequencing was performed on plasma from 21 patients with PR, 20 patients with PE and 17 healthy control subjects (HCs). 24 miRNAs were selected for validation in 20 PR patients and 20 PE patients and 8 miRNAs were further validated in an independent replication cohort (82 patients with PR, 84 patients with PE and 59 HCs) by applying quantitative real-time polymerase chain reaction. Then we analyzed pathways associated with significant miRNAs in PR. RESULTS: MiR-744-3p, miR-324-3p and miR-330-3p were significantly upregulated in the PR group compared with the PE group (Log10miR-744-3p: 0.26[--0.28-1.57] versus -0.41[-0.83--0.03], padj < 0.001; Log10miR-324-3p: 0.40[-0.09-0.84] versus -0.12[-0.53-0.29], padj < 0.001; Log10miR-330-3p: 0.34[0.08-0.93] versus -0.07[-0.65-0.22], padj < 0.001), The area under the receiver operating characteristic curve for the combination of these three miRNAs in distinguishing between PR from PE in training and test set was 0.764 (0.679-0.850, sensitivity = 86.2%, specificity = 54.4%, P < 0.001) and 0.768 (0.637-0.898, sensitivity,65.4%, specificity:80.0%, P = 0.001), respectively. CONCLUSION: A set of circulating microRNAs (miR-744-3p, miR-330-3p, and miR-324-3p) is associated with PR and has clinical utility as a diagnostic marker for distinguishing the plaque phenotype in STEMI patients.