Intramural Hemorrhage Research Articles

Imaging Findings in Cardiovascular Involvements of IgG4 Related Disease: A Systematic Review Study.

Immunoglobulin G4-related disease (IgG4-RD) is a fibroinflammatory condition characterized by IgG4-positive plasma cell infiltration that can affect multiple organs, including the cardiovascular system. The diagnosis of IgG4-RD relies on a combination of clinical, serological, radiological, and pathological findings. However, due to the varied and insidious clinical presentations, normal IgG4 levels in a significant percentage of patients, and frequent multi-organ involvement, imaging plays a crucial role in the diagnosis of IgG4-RD. The aim of study is to comprehensively examine the imaging findings in IgG4-related cardiovascular disease for accurate diagnosis and appropriate treatment. A systematic search was conducted across electronic databases, PubMed, Scopus, and Web of Sciences, until 1 September 2023, following PRISMA guidelines by searching major databases for studies reporting detailed cardiovascular imaging findings in IgG4-RD. The search yielded 68 studies (60 case reports, 5 case series, 2 cross-sectional, 1 case-control) with 120 cases of cardiovascular IgG4-RD. Most of the cases were male, averaging 62.8 years. The common initial symptoms were dyspnea and chest pain. The most common imaging finding was vasculopathy, including vessel wall thickening, periarteritits, periaortitis, aortitis, stenosis, ectasia, aneurysm formation, intramural hemorrhage, fistula formation, and dissection, followed by pericardial involvement and mediastinal masses. Case series and cross-sectional studies also showed vasculopathy being the most common finding on various imaging modalities, including angiography and PET/CT, highlighting the complex pathology of IgG4-RD. This study evaluated current IgG4-RD articles, revealing a higher prevalence in men and vasculopathy as the most common cardiovascular complication.

Evaluation of an Antithrombotic Surface-Coated Flow Diverter in a Rabbit Model without Dual Antiplatelet Drugs

OBJECTIVEFlow diverters (FDs) carry the risk of thromboembolic complications associated with the device and bleeding complications associated with dual antiplatelet therapy. We hypothesize that an antithrombotic surface coated flow diverter(BSCFD) would have less acute thrombus formation and better endothelialization on the device surface compared to uncoated flow diverter. METHODSAn antithrombotic surface coated FD(BSCFD) was developed. Acute clot formation and chronic endothelialization over the device were assessed in 8 rabbit models comparing to its prototype FD(PFD) at 2 hours and 1 month by Scanning Electron Microscopy(SEM) and Histologic images. Nonparametric score data, including thrombus, injury, endothelialization, adventitial inflammation, intramural bleeding and intimal hyperplasia were compared between BSCFD and PFD using Kendall coefficient of rank correlation. RESULTSParent artery and branch artery were patent on DSA in 8 BSCFDs and 6 PFDs. There was 1 intra-stent thrombosis in PFDs at 2 hours and 1 intra-stent stenosis in PFD at 1 month. SEM at 2 hours showed that large amount of blood cells adhered to the surface of all 4 PFDs, and no blood cells were found on the surface of all 4 BSCFDs. At SEM and histological analysis of 1 month, there were less inflammation(Kendall’s Tau-B=-0.818, p＝0.022), less vessel wall injury（Kendall’s Tau-B=-0.764, p＝0.032）and better endothelialization(Kendall’s Tau-B=0.818, p＝0.022) in BSCFDs. CONCLUSIONIn the rabbit model, the BSCFD is associated with less thrombus formation at acute stage, less inflammation, less vessel injury and better endothelialization on the device surface compared to the PFD.

Cardiovascular magnetic resonance 3D LGE imaging for atrial fibrillation ablation

Abstract Objective To assess feasibility and reliability of cardiac magnetic resonance (CMR) imaging in visualizing left atrial (LA) structural changes that patients with paroxysmal atrial fibrillation (PAF) undergo acutely and long-term post ablation. Two different ablation methods i.e pulsed filed ablation (PFA) and cryoablation were studied. Background Pulmonary vein (PV) isolation has become the cornerstone technique for catheter ablation in patients with drug-refractory atrial fibrillation (AF). At present, almost all ablation technologies are mediated by a thermal effect. Recently, pulsed field ablation (PFA) has been introduced as a new energy source. PFA is a non-thermal ablative modality in which high voltage ultra-short pulses are applied to target tissue, while preserving the extracellular matrix architecture, nerves, and microvascular structures. Few data exist showing different structural LA changes between the two methods using Three-Dimensional (3D) Late Gadolinium Enhancement (LGE) Imaging. Methods CMR imaging was performed pre-ablation, acutely (<24 h), and 3 months post-ablation in 10 patients with paroxysmal atrial fibrillation (AF) undergoing pulmonary vein (PV) isolation with PFA (n = 5) or cryoablation (n = 5). 3D LGE and T2-weighted images were analysed. We obtained two data sets of 3D whole heart LGE imaging with high resolution, 20minutes post gadolinium injection. Patients underwent two acquisitions: the conventional respiratory navigated, electrocardiographically-gated 3D fast gradient echo (1.3slice thickness, 256x256 matrix acquisition) and the image-navigated isotropic high resolution 3D LGE with Dixon water-fat separation. 3D LGE data were analysed using a dedicated (ADAS LA) software in order to produce a 3D-LA model visualization of LGE areas. Results In the acute stage, LGE volume was 50% larger after PFA vs. cryoablation (P < 0.001), and oedema on T2 imaging was significantly smaller (visual estimation) on PFA cases. LGE rings surrounding PV ostia were more homogeneous after PFA, with no sign of microvascular damage or intramural hemorrhage as compared to cryoablation cases. In the chronic stage, the majority of acute LGE had disappeared after PFA, whereas most LGE persisted after cryo-ablation. The two 3D LGE sequences used for analysis showed complete agreement in the visualization of atrial scar with superior image quality of the novel sequence. The mean acquisition time for 3D LGE imaging was 11±4minutes for the conventional fast gradient echo sequence, and 5±2minutes for the novel 3D self-image navigated LGE sequence. Conclusions CMR imaging may help in visualization and understanding of LA structural remodeling post different ablation techniques.

Enhanced expression of miR-20a driven by nanog exacerbated the degradation of extracellular matrix in thoracic aortic dissection

Thoracic aortic dissection (TAD) is a life-threatening vascular disease manifested as intramural bleeding in the medial layers of the thoracic aorta. The key histopathologic feature of TAD is medial degeneration, characterized by depletion of vascular smooth muscle cells (VSMCs) and degradation of extracellular matrix (ECM). MicroRNA, as essential epigenetic regulators, can inhibit the protein expression of target genes without modifying the sequences. This study aimed to elucidate the role and underlying mechanism of miR-20a, a member of the miR-17-92 cluster, in regulating ECM degradation during the pathogenesis of TAD. The expression of the miR-17-92 cluster was significantly increased in synthetic VSMCs derived from TAD lesions compared to contractile VSMCs isolated from normal thoracic aortas. Notably, the expression of miR-20a was increased in VSMCs in response to serum exposure and various stimuli. In TAD lesions, the expression of miR-20a was significantly negatively correlated with that of elastin. Elevated expression of miR-20a was also observed in thoracic aortas of TAD mice induced by β-aminopropionitrile fumarate and angiotensin II. Overexpression of miR-20a via mimic transfection enhanced the growth and invasive capabilities of VSMCs, with no significant impact on their migratory activity or the expression of phenotypic markers (α-SMA, SM22, and OPN). Silencing of miR-20a with inhibitor transfection mitigated the hyperactivation of MMP2 in VSMCs stimulated by PDGF-bb, as evidenced by reduced levels of active-MMP2 and increased levels of pro-MMP2. Subsequently, TIMP2 was identified as a novel target gene of miR-20a. The role of miR-20a in promoting the activation of MMP2 was mediated by the suppression of TIMP2 expression in VSMCs. In addition, the elevated expression of miR-20a was found to be directly driven by Nanog in VSMCs. Collectively, these findings indicate that miR-20a plays a crucial role in maintaining the homeostasis of the thoracic aortic wall during TAD pathogenesis and may represent a potential therapeutic target for TAD.

Inherited Stanford A DeBakey I Aortic Dissection: Unveiling Genetic Predispositions and Surgical Management

BACKGROUND: Aortic dissection refers to the disruption of the medial layer of the aorta caused by intramural hemorrhage. This leads to the separation of the layers of the aortic wall, resulting in the establishment of a true lumen and a false lumen, which may or may not be connected. The prevalence of aortic dissection ranges from 0.2% to 0.8%. Additionally, a notable percentage, surpassing 20%, of individuals exhibit a familial inclination towards thoracic aorta dissection. CASE PRESENTATION: A male patient in his middle age, 41 years old, with risk factors of uncontrolled hypertension, obesity, and a familial propensity to aortic dissection, presented to the emergency department exhibiting symptoms of chest pain. It characterized the sensation as having a tearing quality and indicated that it extended towards the abdomen region. The results of the test revealed several notable findings. A blood pressure reading of 235/133, a wider mediastinum and cardiomegaly on the chest X-ray, a slight increase in Hs-Troponin levels, and an electrocardiogram showed sinus rhythm with left ventricular hypertrophy. He underwent a computed tomography scan, which revealed the existence of an aortic dissection that extended from the ascending to the descending aorta without any aortic valve involvement. He was assessed with a Stanford A. DeBakey I aortic dissection, and underwent successful therapy for aortic arch replacement with the elephant trunk procedure, and plans to undertake an endovascular procedure for the descending aorta in the upcoming period. CONCLUSION: Aortic dissection is a pathological disorder that may exhibit hereditary inheritance, and the choice of surgical technique is dependent on the specific underlying disease.

Spontaneous coronary artery dissection and fibromuscular dysplasia: insights into recent developments.

Spontaneous coronary artery dissection (SCAD), an uncommon cause of acute coronary syndrome, continues to be a poorly understood disease predominantly affecting females. It is characterized by an abrupt separation in the coronary arterial wall due to intramural bleeding. Fibromuscular dysplasia (FMD) is a non-atherosclerotic arteriopathy manifesting in medium and small-sized arteries. It is a concomitant disease found among SCAD patients. In some studies, FMD prevalence in SCAD patients ranges between 25%-86%, which can be explained through varying screening techniques or modalities. The potential association has been elucidated in some studies; notably, not only has a genetic link been recently delineated between SCAD and FMD, but there is data to suggest that FMD not only can predispose to SCAD but can also be a potential predictor of its recurrence. However, a clear-cut correlation between the two has still not been established due to conflicting reports in the literature. To further dive into its pathology, it is crucial to highlight the importance of systematic screening in SCAD in order to identify associated risk factors and to be used as a method of FMD detection in such patients. Together, the two pathologies pose unique challenges in understanding its pathophysiology, diagnosis and management, as there is no clear evidence of a definitive treatment plan for patients with SCAD and FMD. A potentially beneficial modality of management is physical exercise, which is currently understudied in the long-term approach to treatment for patients with concomitant SCAD and FMD. Limited research in this field brings disadvantages to the understanding of the association between these two diseases, in order to give rise to better management recommendations. This mini-review aims to highlight the recent developments in the association between SCAD and FMD, its potential genetic association and some insights in screening, diagnosis, and management.

In Situ Saphenous Vein Bypass Grafting in Peripheral Arterial Disease of the Lower Extremities

Objective: To evaluate the efficacy and safety of the valvulotome device used to cut venous valves and in situ bypass in the treatment of peripheral arterial disease (PAD) of the lower extremities. Methods: In this study, the basic principles of in situ saphenous vein bypass are mentioned, specifically for a novel valvulotome device (NODⓇ Valvulotome device, Invamed/ Ankara/Turkey). In this context, the effectiveness of the method was evaluated by interpreting the results of some studies on in situ saphenous vein bypass. Results: In situ bypass has an effective rate for long-term outcomes with approximately 80%, 90% and 95% for primary patency (no evidence of restenosis with a maximum systolic rate >2.5 or sonography-based occlusion), secondary patency (patency maintained by repeated intervention after complete bypass occlusion), and limb salvage (absence of major amputations), respectively. The side effects, including vessel perforation and intramural bleeding, are very low. The technical success rate is very high. Valvulotomes are easy to use by the surgeons and provide comfort for the patients. Conclusions: In situ bypass is effective and safe in PAD treatment. Valvulotome provides ease of use for surgeons and comfort for patients.

Cholesterol Crystals in Odontogenic Cysts: An In-Depth Narrative of Pathogenesis

Cholesterol crystals (CCs) are a relatively common finding in infected odontogenic cysts occurring in about 60% of the cases. Histopathologically, these appear as longitudinal cleft-like spaces or may appear as a collection in cholesterol granulomata. The occurrence of CCs in odontogenic cysts is closely associated with the pathophysiology of the lesions. Despite being fairly common, not much is known about the sources of cholesterol, the mechanism of formation of these clefts, their pathogenesis, and their clinical implications. The present article focuses on describing CCs with respect to their contents, pathogenesis, and clinical implications. Our review describes the mechanism of the formation of CCs in a detailed manner along with a pictorial depiction of the cascade of events involved in the process. The formation of cholesterol granulomata is a cumulative effect of the breakdown of erythrocytes and leukocytes, intramural hemorrhage, decreased blood supply and lymphatic drainage, hypoxic conditions, increased vascular permeability, accumulation and rupture of lipid-laden macrophages, and foreign body reaction. It would be of great interest to pathologists to have an in-depth understanding of the pathogenesis, nature, and implications of CCs, which are very common yet enigmatic entities.

Ultrasound features of an unusual intramural gastric haemorrhage secondary to rodenticide intoxication in a dog

AbstractA 3‐year‐old, neutered, female, mix‐breed dog was presented with a history of acute haemorrhagic vomiting, diarrhoea, anorexia and lethargy. The patient had a hyperkinetic pulse, pale mucous membranes, bilateral hyphema and the capillary refill time was increased. Coagulation testing showed increased values. Abdominal ultrasound revealed diffuse thickening of the submucosal layer with hyperechoic peritoneum and enlargement of the gastric lymph node. The presumptive diagnosis was gastric wall haemorrhage secondary to rodenticide intoxication. The dog responded to treatment and was discharged after 48 hours. Fifteen days later, the thickness and layering of the stomach wall was normal. Gastric wall haemorrhage is a rare condition in dogs with rodenticide intoxication, which requires a biopsy for confirmation. However, the risk of haemorrhage does not make this feasible. In this case, the authors suspect that submucosal gastric thickening was secondary to anticoagulant rodenticide intoxication based on history, clinical examination, haematological analysis and coagulation testing.

Morphoimmunohistochemical changes in the coronary arteries early after stenting

Introduction: Modern methods of surgical treatment for coronary heart disease include stenting and bypass surgery. In this regard, a morphoimmunohistochemical study of the state of the coronary arteries in the early stages after stenting will make it possible to predict postoperative complications. Materials and methods: The protocols of autopsies of 20 deceased were studied (10 men, mean age 64.7 years, 10 women, mean age 76.9 years). In 85 %, progressive stenosing atherosclerosis of the mouth of the left coronary artery (CA) and the anterior interventricular branch was noted. Taking into account the development of complications after stenting, three chronological groups were identified: 1) up to 3 days; 2) 37 days; 3) 715 days. The computer program ImageJ (US National Institutes of Health, USA) was used for CA morphometry. Statistical processing of the obtained results was carried out on a personal computer using the statistical tools of the Statistica 10 program. Result : It was shown that during the first 3 days after stenting of coronary arteries, acute damage to endothelial cells in the form of desquamation, dystrophic and necrobiotic processes, intramural hemorrhages in the areas of atheromas localization are observed in their walls. After 37 days and later, 715 days after stenting of the coronary artery, parietal mixed (fibrin-leukocytic), fibrin thrombi with signs of organization are observed in the lumens of the coronary artery, which is combined with the phenomena of neoangiogenesis of the artery wall. Conclusions: Damage to endothelial cells and related disturbances in the rheological properties of blood due to the expression of von Willebrand factor can initiate endothelial dysfunction with the development of thrombosis, thromboembolism of small coronary branches, which can cause myocardial perfusion disorders with the development of acute infarction.

A Case of Spontaneous Coronary Artery Dissection in the Setting of Exogenous Testosterone.

Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome, occurring when there is separation of the coronary artery walls by intramural hemorrhage creating a false lumen. This compresses the arterial lumen, compromising the ability of the coronary artery to perfuse the myocardial tissue. Spontaneous coronary artery dissection is usually fatal, with risk factors including pregnancy, young age, and female sex, birth control, and other hormonal therapies.In this case report, we describe the case of a 31-year-old biological female transitioning to male with exogenous testosterone who experienced a SCAD. Given the known risk factors for SCAD, such as pregnancy and exogenous hormone therapy, this case raises additional considerations regarding rare unintended consequences of testosterone therapy.

Severe Preeclampsia Complicated by Placental Abruption Leads to Fetal Distress

Placental abruption is a common complication of preeclampsia. It is an obstetric emergency that occurs when the placenta partially or completely separates from the uterine wall. The diagnosis is usually made clinically or objectively. It is relatively rare but put a serious risk for both the fetus and the mother. We reported a case of a 32-year-old multigravid patient at 35-36 weeks gestation who presented with moderate vaginal bleeding and lower abdominal pain. Her obstetric history included one premature vaginal delivery. Her blood pressure started to rise in the second trimester of pregnancy. The examination revealed that her blood pressure was 190/120 mmHg, and she had pitting edema on her extremities and tender uterine fundus. The fetal heart rate was bradycardia at 100 beats per minute. Placental abruption and fetal distress were suspected. An emergency cesarean section was performed. Intraoperatively, the uterus showed intramural bleeding and was livid, with the beginning of Couvelaire-uterus. The uterus was left in situ. In conclusion, placental abruption interrupts the vital function of the placentae which leads to fetal hypoxia and even fetal death. It is an obstetric emergency that requires immediate intervention to save the fetus and reduce the risk of complications in the mother.

Multimodality Imaging Approach to Spontaneous Coronary Artery Dissection

Spontaneous Coronary Artery Dissection (SCAD) refers to the spontaneous separation of the layers of the vessel wall caused by intramural hemorrhage, with or without an intimal tear. The "typical" SCAD patient is a middle-aged woman with few traditional cardiovascular risk factors, and it's frequently associated with pregnancy. Because of its low incidence, its pathophysiology is not fully understood. SCAD presents as an acute coronary syndrome, with chest pain, dyspnea, syncope, or heartbeat, even if diagnosis and clinical handling are different: coronary angiography is currently the main tool to diagnose SCAD; however, in doubtful cases, the use of both invasive and noninvasive cardiovascular imaging methods such as intravascular ultrasound or optical coherence tomography may be necessary. This paper aims to review the current state of knowledge on SCAD to address its demographic features, clinical characteristics, management, and outcomes, focusing on diagnostic algorithms and main multimodality imaging techniques.

Arterial dissections: Common features and new perspectives.

Arterial dissections, which involve an abrupt tear in the wall of a major artery resulting in the intramural accumulation of blood, are a family of catastrophic disorders causing major, potentially fatal sequelae. Involving diverse vascular beds, including the aorta or coronary, cervical, pulmonary, and visceral arteries, each type of dissection is devastating in its own way. Traditionally they have been studied in isolation, rather than collectively, owing largely to the distinct clinical consequences of dissections in different anatomical locations - such as stroke, myocardial infarction, and renal failure. Here, we review the shared and unique features of these arteriopathies to provide a better understanding of this family of disorders. Arterial dissections occur commonly in the young to middle-aged, and often in conjunction with hypertension and/or migraine; the latter suggesting they are part of a generalized vasculopathy. Genetic studies as well as cellular and molecular investigations of arterial dissections reveal striking similarities between dissection types, particularly their pathophysiology, which includes the presence or absence of an intimal tear and vasa vasorum dysfunction as a cause of intramural hemorrhage. Pathway perturbations common to all types of dissections include disruption of TGF-β signaling, the extracellular matrix, the cytoskeleton or metabolism, as evidenced by the finding of mutations in critical genes regulating these processes, including LRP1, collagen genes, fibrillin and TGF-β receptors, or their coupled pathways. Perturbances in these connected signaling pathways contribute to phenotype switching in endothelial and vascular smooth muscle cells of the affected artery, in which their physiological quiescent state is lost and replaced by a proliferative activated phenotype. Of interest, dissections in various anatomical locations are associated with distinct sex and age predilections, suggesting involvement of gene and environment interactions in disease pathogenesis. Importantly, these cellular mechanisms are potentially therapeutically targetable. Consideration of arterial dissections as a collective pathology allows insight from the better characterized dissection types, such as that involving the thoracic aorta, to be leveraged to inform the less common forms of dissections, including the potential to apply known therapeutic interventions already clinically available for the former.

Placental Abruption as a Complication of Preeclampsia that Causes Fetal Distress

Background
 Placental abruption is a common complication of preeclampsia. It is an obstetric emergency which occurs when the placenta partially or completely separates from the uterine wall. The diagnosis is usually made clinically or objectively. It is relatively rare but put a serious risk for both the fetus and the mother.
 Case presentation 
 We reported a case of a 32-year-old multigravida patient at 35-36 weeks gestation presented with moderate vaginal bleeding and lower abdominal pain. Her obstetric history included one premature vaginal delivery. Her blood pressure started to rise in the second trimester of pregnancy. The examination revealed that her blood pressure was 190/120 mmHg, she had pitting edema on her extremities and tender uterine fundus. The fetal heart rate was bradycardia at 100 beats per minute. Placental abruption and fetal distress were diagnosed. An emergency cesarean section was performed. Intraoperatively, the uterus showed intramural bleeding and was livid, with the beginning of Couvelaire-uterus. The uterus was left in situ.
 Conclusion
 As a conclusion, placental abruption interrupts the vital function of the placentae which leads to fetal hypoxia and even fetal death. It is an obstetric emergency that requires immediate intervention to save the fetus and reduce the risk of complications in the mother.

Life-threatening gastrointestinal bleeding caused by jejunal heterotopic gastric mucosa in an adult dog: a rare case report

BackgroundHeterotopic gastric mucosa has been scarcely reported in the veterinary literature. Its presence can be asymptomatic or associated with various clinical signs ranging from apathy, vomiting, to abdominal pain. This report illustrates the presence of heterotopic gastric mucosa in the jejunum of an adult dog. It is the first to describe severe anemia, requiring acute blood transfusion, following intestinal hemorrhage caused by heterotopic gastric mucosa.Case presentationA twelve-year-old, intact male Maltese dog was presented with a history of apathy, vomiting and anemia. The dog was on a strict diet for recurrent diarrhea, food intolerance and skin allergy. Clinical examination revealed severe anemic mucous membranes and painful abdominal palpation. Blood examination confirmed severe regenerative anemia. Ultrasonography showed an intestinal neoplasm, gall bladder sludge and non-homogeneous liver parenchyma. Three-view thoracic radiographs failed to show any metastatic lesions or enlarged lymph nodes. After initial stabilization and blood transfusion, a midline exploratory laparotomy was performed. Three different masses were found in the jejunum. Resection and anastomosis of approximately 40 cm of jejunum was performed, followed by liver and lymph node biopsy and placement of an esophagostomy tube. Two days after surgery the dog started to clinically improve and was discharged from the hospital on the sixth day after surgery. Histopathology revealed the intestinal masses to be heterotopic gastric mucosa associated with intramural cystic distensions, multifocal ulceration and bleeding into the intestinal lumen. Two years after surgery, the dog did not have a recurrence of anemia or gastrointestinal signs.ConclusionsThis case demonstrates that heterotopic gastric mucosa can be considered one of the differential diagnoses in case of severe anemia due to gastrointestinal hemorrhage and suspected intestinal tumors. Although in most described cases in literature the finding seems to be incidental on necropsy, our report shows that heterotopic gastric mucosa can be the etiology of life-threatening signs. In addition, because no recurrent diarrhea episodes occurred after surgical resection of the ectopic tissue, it is likely that the heterotopic gastric mucosa was the cause of the food intolerance signs in this dog.

Abstract 301: Inhibition Of Tlr-7 Signaling Attenuates TAAD Formation

The critical role for chronic inflammation in the development of thoracic aortic aneurysms and dissections (TAADs) has been recognized in both experimental and clinical settings. However, challenges remain on translating this knowledge to clinical applications. In this study, we tested the hypothesis that TLR-7 signaling triggered by self-RNAs substantiates chronic inflammation, promoting TAAD formation. A mouse TAAD model induced by SMC-specific deletion of Tgfbr1 ( Tgfbr1 iko ) was used. In this model, the expression of TLR-7 was progressively upregulated during the early stages, resulting in a two-fold differential at two weeks compared to control aortas ( P =0.003). RNAScope assays showed that cells located in the media and adventitia were responsible for the upregulation. Additionally, immunofluorescence (IF) staining showed that TLR-7 is induced in human TAADs. Treatment with hydroxychloroquine, which inhibits TLR-7 receptor function, significantly reduced the number of intimal/medial tears ( P =0.026) and mitigated intramural hemorrhage ( P =0.007) compared with vehicle controls (n=7/group). Further assays with bone marrow derived dendritic cells demonstrated that RNAs, particularly small RNAs, extracted from TAADs induced significantly higher IFNα/β levels compared with normal aortas ( P =0.025). Similarly, RNAs extracted from Tgfbr1 iko SMCs induced higher levels of IFNα, IP-10, and MCP1 compared with those harvested from wild type SMCs. Necroptosis (labeled with RIPK3 and pMLKL) and RNA-oxidation (labeled with 8-OHG) were evident in the media of TAADs, and might serve as the source for the endogenous TLR-7 ligand. Finally, treatment with the TLR-7 specific inhibitor, M5049, at a dose of 1.0 or 5.0 mg/kg/day via oral gavage prevented dilation of TAADs at four weeks compared with vehicle controls (9% vs. 8% vs. 23%, P<0.001). In conclusion, self-RNAs released from stressed and dying cells is associated with chronically inflamed aortic tissue and promotes TAAD development via triggering TLR-7 signaling. Blocking TLR-7 signaling may represent a novel strategy to treat human TAADs.

Reperfusion Injury-Related Intramyocardial Hemorrhage

Myocardial reperfusion injury is defined as the death of cardiomyocytes as a direct result of one or more events initiated by reperfusion. These events could be inflammation, oxidative stress, calcium overload, neurohumoral activation, cytotoxicity of anaerobic metabolites, etc. Intramyocardial hemorrhage as a consequence of ischemia–reperfusion injury during acute myocardial infarction and subsequently is frequent and portends worse prognosis. Animal studies have demonstrated that intramyocardial hemorrhage does not occur with ST-elevation myocardial infarction unless myocardium is reperfused with blood. Magnetic resonance imaging is the technique of choice for its detection but has limited availability in emergencies and is expensive. Echocardiography can be used for indirect myocardial tissue characterization. Echocardiography coupled with myocardial contrast imaging is increasingly being used for detecting hemorrhage in infarcted segments. In the presence of wall motion abnormality, increased segmental echogenicity, significantly increased wall thickness underlying hypermobile endocardium, and neocavitations within the myocardium are the characteristic features. Occasionally, extensive wall splitting and formation of pseudotumor due to large hematoma are the striking features of intramyocardial hemorrhage. Intramyocardial hemorrhage in acute myocardial infarction can occur during early phase, following reperfusion and during remodeling process. There is no definite echocardiographic imaging method to assess reperfusion hemorrhage in vivo, but signal-void cavity-like or cystic appearance within the myocardium in the setting of myocardial infarction is highly suggestive. Detecting hypointense area of hemorrhage could be complicated by low-intensity echoes emanating from the normal myocardium. Echocardiography should be performed in every patient before and after reperfusion therapy and serially till discharge. There are no studies comparing the diagnostic yield of echocardiography compared to magnetic resonance imaging. Those with obvious myocardial hematoma need special attention with regard to antiremodeling agents, dual antiplatelet therapy, and possibly surgery. A majority of patients with significant intramural hemorrhage end up having reduced left ventricular function, adverse remodeling, true or pseudo-aneurysms, and even heart failure although spontaneous resorption has also been reported.

When COVID-19 delays the management of an urgent heart condition: A rare case of a spontaneous dissection of two coronary arteries.

Some severe life‐threatening conditions could be misdiagnosed during the current COVID‐19 pandemic.

Pulsed field ablation prevents chronic atrial fibrotic changes and restrictive mechanics after catheter ablation for atrial fibrillation.

AimsPulsed field ablation (PFA), a non-thermal ablative modality, may show different effects on the myocardial tissue compared to thermal ablation. Thus, this study aimed to compare the left atrial (LA) structural and mechanical characteristics after PFA vs. thermal ablation.Methods and resultsCardiac magnetic resonance was performed pre-ablation, acutely (<3 h), and 3 months post-ablation in 41 patients with paroxysmal atrial fibrillation (AF) undergoing pulmonary vein (PV) isolation with PFA (n = 18) or thermal ablation (n = 23, 16 radiofrequency ablations, 7 cryoablations). Late gadolinium enhancement (LGE), T2-weighted, and cine images were analysed. In the acute stage, LGE volume was 60% larger after PFA vs. thermal ablation (P < 0.001), and oedema on T2 imaging was 20% smaller (P = 0.002). Tissue changes were more homogeneous after PFA than after thermal ablation, with no sign of microvascular damage or intramural haemorrhage. In the chronic stage, the majority of acute LGE had disappeared after PFA, whereas most LGE persisted after thermal ablation. The maximum strain on PV antra, the LA expansion index, and LA active emptying fraction declined acutely after both PFA and thermal ablation but recovered at the chronic stage only with PFA.ConclusionPulsed field ablation induces large acute LGE without microvascular damage or intramural haemorrhage. Most LGE lesions disappear in the chronic stage, suggesting a specific reparative process involving less chronic fibrosis. This process may contribute to a preserved tissue compliance and LA reservoir and booster pump functions.