Artery Dissection Research Articles

Endovascular treatment for posterior inferior cerebellar artery aneurysm with vertebral artery stenosis: The critical role of diagnosing osteophyte compression

Background: Vertebral artery (VA) stenosis can be caused by several factors, including arteriosclerosis, arterial dissection, and mechanical compression. Symptomatic vertebrobasilar insufficiency caused by VA stenosis due to mechanical compression associated with head rotation is well-known as Bow Hunter’s syndrome. However, an accurate diagnosis of asymptomatic osteophyte compression-induced nonrotational VA stenosis is difficult. We report a case of left posterior inferior cerebellar artery aneurysm with severe left VA stenosis, treated with stent-assisted coil embolization following appropriate diagnosis. Case Description: A 72-year-old female patient was found to have severe asymptomatic VA stenosis at the V2 segment (C4–5 level of the cervical spine) on cerebral angiography. Osteophyte compression-induced VA stenosis was suspected, which was confirmed by cone-beam computed tomography. The VA stenosis improved by flexing the neck and fixing the head position, following which the endovascular treatment was successfully completed. Conclusion: The site of the VA stenosis is critical in determining the etiology. Atherosclerotic VA stenosis often occurs at the origin of the artery or V4 segment, whereas bony compression-induced stenosis is more likely to occur at the V2 segment. Diagnosis and appropriate management of VA stenosis is based on determining the site.

Coeliac artery dissection in neuroendocrine neoplasms: coincidence or cause?

Coeliac artery dissection in neuroendocrine neoplasms: coincidence or cause?

Abstract 4145821: Serial Vascular Responses of Balloon-expandable Stent with Biodegradable Film-type Graft in a Rabbit Iliac Artery Dissection Model (BioGard Study)

Introduction and Background: Arterial dissection during endovascular therapy rarely occurs but can be lethal. A significant blood volume extravasation during coronary artery interventions is related to the very high mortality (20-30%). In this hyperacute emergent clinical situation, covered stents have been considered as a primary measure to prevent further serious arterial events. A fabric-based covered graft stents yield poor clinical outcomes. To overcome these challenges, the balloon-expandable stent with biodegradable film-type graft for treating arterial dissection was invented. Research Questions and Objectives: A novel balloon-expandable stent with biodegradable film graft for overcoming these issues would be valid for efficacy and safety in a rabbit iliac artery dissection model. Method and Approach: Eighteen iliac artery dissections were induced by balloon over-inflation on angiography (Ellis type 2 or 3) and treated using the test device (3.0 x 24 mm). Subsequently, twelve animals underwent histologic examinations and micro-computed tomography (CT) at 0, 2, 4, and 8 weeks and 3, 6, 9, and 12 months and angiography at one-year. Results and Data: There were no adverse cardiovascular events during the one-year. Early-stage histologic examination revealed complete sealing of disrupted vessels by the device, exhibiting mural hematoma, peri-stent red thrombi, and dense infiltration of inflammatory cells. Mid- and long-term histologic examination showed patent stents with neointimal hyperplasia over the stents (% area stenosis: 11.8 at 2weeks, 26.1 at 1month, 29.7 at 3months, 49.2 at 9months, and 51.0 at 1year), along with mild peri-strut inflammatory response (Grade: 1-2 at mid-term and 0-1 at long-term). The graft film became scarcely visible after six months. Both CT and angiography revealed no instances of thrombotic occlusion or in-stent restenosis (% diameter stenosis: 5.7 at 2weeks, 12.3 at 1month, 14.2 at 3months, 25.1 at 9months, and 26.6 at 1 year). Conclusion: The novel balloon-expandable stent with a biodegradable film graft demonstrates feasibility in managing severe artery dissection and preventing lethal vascular events in animal model. Future human studies are warranted to validate these findings and elucidate the clinical outcomes of the study.

Laparoscopic total pancreatectomy with total mesopancreas dissection using counterclockwise technique and tail-first approach.

Laparoscopic total pancreatectomy (LTP) is technically challenging and infrequently documented in the literature. In this paper, we present a new approach for performing fully LTP, a pancreatic tail-first approach with a counterclockwise technique, to accomplish total mesopancreas dissection and standard lymphadenectomy en bloc. Firstly, the tail and body of the pancreas without the spleen were dissected retrogradely, starting from the lower border of the body of pancreas and then from left to right. After that, a counterclockwise dissection of the tail and body of the pancreas was performed. The splenic artery and vein were divided at the terminal end of the pancreatic tail. The spleen was preserved. The entire body and tail of the pancreas were then pulled to the right side. This maneuver facilitated the isolation and dissection of arteries in the retropancreatic region more easily via laparoscopy, including the splenic artery, gastroduodenal artery, and supporting superior mesenteric artery first-approach. It also enabled total mesopancreas dissection. The inferior pancreaticoduodenal artery was resected last during this phase. The remainder of the dissection was like that of a laparoscopic pancreaticoduodenectomy with total mesopancreas dissection, involving two laparoscopic manual anastomoses. The operative time was 490 minutes and the total blood loss was 100 mL. Pathology revealed a low-grade intraductal papillary mucinous neoplasm extending from the head to the tail of the pancreas.

Abstract 4138583: Incidence and Outcomes of Heparin-Induced Thrombocytopenia Among Patients Undergoing Left Ventricular Assist Device Implantation

Background: Left Ventricular Assist Devices (LVAD) are being increasingly used as a bridge to transplant and destination therapy for advanced (stage D) heart failure. Heparin-induced thrombocytopenia (HIT) increases the risk of thromboembolic and bleeding events. HIT is also a well-known complication in patients undergoing LVAD implantation. This study examines the incidence and impact of HIT on outcomes in LVAD implants using a nationwide database from 2016 to 2020. Methods: We queried the National Inpatient Sample database for 2016-2020 to identify all adults ≥ 18 who underwent LVAD insertion using ICD 10 codes. LVAD recipients were dichotomized into two cohorts by the presence of HIT. Our primary outcome was in-hospital mortality. Secondary outcomes included vascular complications, acute kidney injury (AKI), length of stay, and total cost. Outcomes were adjusted for demographic variables, hospital-level characteristics, and comorbidities using regression analysis. Results: A total of 19975 (95% CI: 18328 - 21622) hospitalization records for LVAD insertion were identified, out of which HIT occurred in 1.8%. There were significant differences in AKI requiring dialysis, (p < 0.03) cardiogenic shock, (p<0.01), mechanical ventilation (p<0.01), pulmonary embolism (PE) (p< 0.001) and acute deep vein thrombosis (DVT) (p< 0.001) which occurred more in HIT. In-hospital mortality was not significantly associated with HIT (adjusted odds ratio [aOR] 1.49, 95% CI :0.73-3.04, p value 0.28). Older age (aOR 1.02; 95% CI: 1.01-1.02) was associated with mortality after LVAD insertion. AKI, ischemic stroke, hemorrhagic stroke, acute coronary syndrome, arterial dissection, cardiogenic shock, and mechanical ventilation were significantly associated with in-hospital mortality. Our analysis did not show any differences in the incidence of vascular complications, stroke, intraoperative bleeding, blood transfusions and AKI between the HIT and non-HIT group. The HIT group stayed longer in the hospital 39 days (95% CI: 36- 38) vs 37 days (95% CI: 35- 44) and incurred higher total hospital cost of $1,101,638 vs. $1,245,616) although this was not statistically significant. Conclusion: Among US hospitalized patients undergoing LVAD implants, HIT was significantly associated with a higher risk of AKI requiring dialysis, PE, acute DVT, cardiogenic shock and need for mechanical ventilation. It was however not associated with a higher risk of in-hospital mortality.

Abstract 4136274: A Case of Myocardial Infarction with Non-obstructive Coronary Arteries (MINOCA) Complicated by a Ventricular Septal Defect (VSD)

Case: A 69-year-old woman with a history of hypertension and tobacco use disorder presented with acute chest pain. The patient was found to have classic anterior ST elevation myocardial infarction (STEMI) pattern on electrocardiogram (ECG) with high-sensitivity troponin of 12,772 ng/L and was taken emergently to the catheterization laboratory. Coronary angiography showed tortuous coronary vessels though without evidence of obstructive coronary artery disease, plaque rupture, ulceration, dissection, or vasospasm. Transthoracic echocardiogram showed an apical ventricular septal defect (VSD) with normal left ventricular systolic function of 60%. Cardiac computed tomography (CT), confirmed a discrete apical VSD that was 7.93 mm in diameter and multiple small VSDs distally in the septum. Right heart catheterization revealed severe left-to-right shunting with a ratio of pulmonary blood flow to systemic blood flow (Qp:Qs) of 2.8. Early surgical repair of the apical VSD was pursued despite known high operative risk given the hemodynamic significance of the shunt. The patient developed ongoing hemodynamic instability from cardiogenic shock with inability to ween from intra-aortic balloon pump (IABP). Unfortunately, because of the location of the residual VSDs and elevated panel-reactive antibody testing of 98%, the patient was deemed to not be a candidate for percutaneous closure or heart transplantation, respectively. Discussion: An acquired ventricular septal defect (VSD) is a rare and catastrophic complication of myocardial infarction, typically with a culprit obstructive coronary artery lesion identified on coronary angiography. Acquired VSDs in myocardial infarction with nonobstructive coronary arteries (MINOCA) is an even more rare phenomenon. Possible causes include low flow, inflammation, intimal disruption, or vasospasm of coronary arteries. Our case highlights that MINOCA can present with life-threatening complications similar to obstructive STEMI. The timing of intervention and treatment approach of acquired VSDs remains an area of debate. The life-threatening effects of VSDs make it critical to manage in a multidisciplinary manner involving advanced imagers, interventional cardiologists, cardiothoracic surgeons, and heart failure specialists. This case emphasizes the importance of maintaining a high index of suspicion for abnormal coronary anatomy, even in patients with MINOCA, and prompt interdisciplinary decision making to reduce mortality.

Abstract 4114597: Spontaneous coronary artery dissection: Case series and review of associated cardiovascular risks

Background: Spontaneous coronary artery dissection (SCAD) has emerged as an important cause of ACS, myocardial infarction, and sudden death particularly among young women and individuals with few conventional atherosclerotic risk factors. We reveiwed possible risk factors that could predispose to SCAD. Methods: We reviewed 13 consecutive patients presenting with SCAD across three different institutions over a period of 5 yrs and determined risk fatcors associated with this disase entity. Results: 13 patients presented with SCAD represented % 0.5 of the total number of patients who underwent cardiac cathaterizations for chest pain requiring admissions. 11/13 (84%) were female. 5/13 (38%) were Caucasian or Hispanic, and 3/13 (23%) were African-American. Mean age age was 49.3 + years. 8/13 (61%) had associated hyperlipidemia with LDL levels > than 110 mg/dL, 9/13 (64%) had an A1c < 5.6% and only 1/13 (0.07%) had A1c of 6.4%. HTN was present in 6/13 (46%) of patients, and family history of SCD or heart disease were only seen in 2/13 (15%). None of the patients had features suggestive of associated fibromuscular dysplasia or connecive tissue disease. D-dimer was elevated in 5/13 (38%) with average value of 1578 ng/dL. Inflammatory markers were reviewed, only 3 patient has had ESR and CRP ordered, and only 1/3 had a mildly elevated CRP 3.9 mg/dL. Only 1/13 (0.07%) required intervention which was due to further drop in her ejection fraction requiring PCI, with improvement in her symptoms. All patients were treated with dual anti-platelet therapy for 1 year, 1 was discontinued due to persitent chest pain and decision was made to treat with only aspirin. Traditionally, risks for SCAD were thought to be due to non-atheresclerotic factors, however our case series shows that more then 60% of patients had elevated LDL's and 46% with hypertension, implying that traditional atheresclerotic risk factors should not be ignored and may play a crucial role. Autoimmune diseases were not found in any of our patients. Conclusion and implications: In this series patients who had SCAD had conventional risk factors of CAD including HLD and hypertension. The variability of co morbidities makes the identification of specific risk factors very difficult and none of the patients had Fibromuscular dysplasia or any signs of inflammation. Elevated D Dimer was also seen in a majority of patients, and all but one was managed medically with a favorable outcome

Abstract 4138217: A Machine Learning-Based Novel Risk Score Model for Spontaneous Coronary Artery Dissection

Background: Spontaneous coronary artery dissection (SCAD) remains a poorly understood differential diagnosis of acute coronary syndrome (ACS). We aimed to develop a machine learning-based risk score model to predict in-hospital mortality in patients with SCAD. Methods: The National Inpatient Sample (NIS) 2016-2020 database was used to identify all adult patients (≥18 years of age) with SCAD, identified using ICD-10 code I25.42. Relevant clinical characteristics and outcomes were extracted. The primary endpoint was in-hospital all-cause mortality. The dataset was randomly split into 3 subsets: training, validation, and testing, with a ratio of 0.7, 0.2, and 0.1, respectively. The risk score was generated using R software’s Autoscore package, which is a machine learning-based automatic clinical score generator, and performance was evaluated using the area under receiver-operative characteristics curve (AUC) with 95% confidence intervals (95%CI). Results: Among the 8,260 SCAD patients identified [age 60.9±14.4 years, female 4,708 (57%)], there were 480 (5.8%) primary outcome events. Out of the top 20 covariates seen in the Parsimony plot, we used six for our risk score (0–100): age, comorbidity burden, cardiogenic shock, balloon pump, extracorporeal membrane oxygenation, and race (Figure 1A). The AUC for the derivation and validation cohorts was 0.862 (0.817–0.907) and 0.833 (0.788–0.879), respectively (Figures 1B and 1C). Conclusion: We developed and internally validated a machine learning-based risk score model to predict outcomes in patients with SCAD with a high AUC of 0.833 (0.788–0.879). Risk score models guide decision-making, and future studies are needed for external validation of our findings.

Gene Commonality in Arterial Circuits Throughout the Body.

The common genetic underpinnings of thoracic aortic aneurysms and aneurysms and dissections of several other major arterial circuits have been described in the literature. These include thoracic and abdominal aortic aneurysms, thoracic and intracranial aneurysms, thoracic aortic aneurysms, and spontaneous coronary artery dissections. In this study, we provide a unified report of these observations and investigate any genetic commonality between the above four arterial circulations.

Abstract 4138024: Identifying the Medications with the Greatest Reduction in Mortality in Coronary Artery Dissection

Introduction: Coronary artery dissection (CD) is a potentially fatal complication, usually arising either spontaneously or iatrogenically. Therefore, identifying treatment methods that reduce mortality is of great importance. The American College of Cardiology recommendations stipulate that patients who have experienced CD may benefit from beta-blocker therapy, as beta-blockers have been shown to reduce the incidence of recurrent CD. Currently, there is little published data in support of beta-blockers providing mortality reduction for CD. Given the significant risk of mortality from CD, we aimed to test the veracity of these recommendations using a retrospective multicenter study as well as having a main objective of exploring means to lower mortality in CD. Methods: We conducted a retrospective, multicenter cohort that identified 2,104 patients diagnosed with CD. We extracted the data from across 16 West Florida hospitals in between the years of 2017-2022. Our patients were identified and stratified based on common lab values and cardioprotective medications they were taking. Chi-square and binary logistic regression was used to calculate odds ratios for mortality. The odds ratio estimate for mortality was our primary outcome with attention given to factors that were associated with an increased or decreased likelihood of mortality in patients with CD. Results: Patients on beta-blockers, angiotensin converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB) were the only variables that were statistically significant. Out of 2,104 patients, 1,562 patients were on beta-blockers (74.2%), and 921 were on an ACEi/ARB (43.8%). Our data revealed that the odds ratio for mortality in patients with CD while on beta blockers was 0.375 (p-value 0.0009, confidence interval 0.210-0.669), and while on ACEi/ARBs was 0.447 (p-value 0.0077, confidence interval 0.247-0.808). These results indicate a significant reduction in mortality in patients who are taking beta-blockers and/or ACEi/ARB medications after being diagnosed with CD. Conclusion: Our data can be viewed as supportive of the current recommendation for the primary use of beta-blockers in patients with spontaneous CD, as well as suggesting angiotensin receptor blockers and angiotensin-converting enzyme inhibitors as possible additional therapies

Abstract 4142798: Differences in Clinical presentation in Spontaneous Coronary Artery Dissection vs. Type 1 Myocardial Infarction

Background: Spontaneous coronary artery dissection (SCAD) refers to the nontraumatic, non-iatrogenic, and nonatherosclerotic separation of the coronary artery wall leading to acute coronary syndrome. This condition predominantly affects women with minimal or no traditional cardiac risk factors. We aimed to determine the differences in clinical presentation between SCAD and Type 1 myocardial infarction (MI) in the Aurora Health Care community. Methods: A retrospective, matched cohort, multicenter community study was carried out on adult patients aged >18 years admitted to all Aurora Hospitals from January 2012 to December 2022. A total of 57 patients were diagnosed with SCAD during that period. SCAD group and Type 1 MI group were matched by age and gender at a 1:5 ratio using a propensity score-based matching. Outcomes between the SCAD and the Type 1 MI groups were compared using chi-squared tests or Fisher’s exact tests, and t-tests or nonparametric equivalents (Wilcoxon). Results: A higher percentage of Type 1 MI patients presented as NSTEMI compared to SCAD patients (70% vs. 59.6%, p=0.028). Although not statistically significant, SCAD patients had a higher occurrence of STEMI than Type 1 MI patients (42.1% vs. 32.6%, p=0.169). On admission, SCAD patients had a higher maximum troponin (12,000 vs. 3,550, p=0.012). Type 1 MI patients had higher HgbA1C (6 vs. 5.4, p=0.0008). Both patients had similar LDL levels, but Type 1 MI had lower HDL levels (44 vs. 48, p=0.024). ESR, CRP, and D-dimer levels showed no significant difference. LV ejection fraction was 53% in both groups, and the LV global longitudinal strain was similar. The Type 1 MI group exhibited higher grades of diastolic dysfunction (Grade 2 and Grade 3) and mitral valve disease. E/e was higher in Type 1 MI compared to SCAD (11.5 vs 8.8, p <0.0001). Type 2 SCAD was most prevalent at presentation, with the most frequently affected artery being LAD (47.4%) and the most frequently affected branch vessel being obtuse marginal (36.4%). The most common location was distal (59.6%), followed by mid (22.8%), with the diameter of the vessel involved mostly between 2-3.5 mm. Conclusion: This study observed that although more SCAD patients presented as STEMI with higher troponins, Type 1 MI patients were sicker overall. These differences in clinical findings can aid in diagnosis as the management of these two populations differ.

Diagnosing Monogenic Stroke at Younger Age.

An increasing number of monogenic conditions underlying stroke are being identified. We explored the possibilities of increasing the diagnostic yield of monogenic stroke in a population under 56 years of age. Fifty probands ≤55 years at their first stroke episode were characterized clinically and investigated by whole genome sequencing. Probands had one or more of: (1) one or more first to second degree relatives with stroke under 60 years or same stroke-causing condition/disease; (2) no hypertension, hypercholesterolemia, diabetes, heart disease, or smoking; or (3) either multiple stroke episodes or multiple arterial dissections. Variants with minor allele frequency under 0.01, identified by using our stroke gene panels, were assessed. The stroke subtypes, including large artery atherosclerotic, large artery nonatherosclerotic (tortuosity, dolichoectasia, aneurysm, nonatherosclerotic dissection, or occlusion), cerebral small vessel disease, cardioembolic (arrhythmia, heart defect, or cardiomyopathy), coagulation dysfunctions (venous thrombosis, arterial thrombosis, or bleeding tendency), intracerebral hemorrhage, vascular malformations (cavernoma or arteriovenous malformations), metabolic disorders, or cryptogenic embolic, were used for genotype-phenotype correlation. In a final step, we combined genetic and clinical information to determine if the genetic variant likely was the cause of stroke in the patients. Whole genome sequencing of younger patients with stroke identified 17 clinically matching genetic variants in 15 of 50 (30%) patients, while a stronger clinical correlation with stroke was established in only 6 (12%) of them. Stroke-related genetic variants were identified in 4 of 5 (80%) patients with cardioembolic stroke subtype, 3 of 4 (75%) with intracerebral hemorrhage, 7 of 18 (39%) with cryptogenic embolic stroke, 1 of 6 (17%) with small vessel disease, and 3 of 15 (20%) of patients with nonatherosclerotic large artery stroke, including 1 of 11 (9%) with cervical dissection stroke. Careful clinical interpretation of whole genome data using stroke gene panels can detect monogenic causes of early stroke, allowing individualized follow-up and opening new possibilities for potential treatment.

Duodenal Obstruction Caused by an Isolated Spontaneous Celiac Artery Dissection.

Duodenal Obstruction Caused by an Isolated Spontaneous Celiac Artery Dissection.

Validation of a diagnostic support tool for early recognition of cervical arterial dissection in primary care

BackgroundCervical arterial dissection (CeAD) is a leading cause of stroke in young adults with an early presentation often mimicking musculoskeletal pain. Currently, no validated tests exist and CAD may be missed. A diagnostic support tool could help guide urgent referral for imaging, when to monitor, or when safe to proceed with treatment, and ultimately help stroke prevention. ObjectivesTo validate a 4-criteria diagnostic support tool for early recognition of CeAD in primary care, to refine tool descriptors as needed, and propose optimal cut-offs for clinical application. DesignProspective observational study MethodParticipants with radiologically confirmed CeAD and controls without CeAD were identified from adults >18 years presenting to a tertiary metropolitan hospital with initial diagnosis of headache or neck pain. All were scored with criteria out of7 (acute onset pain [2], recent trauma/infection [1], neurological features [2], age <55 years [2]). Diagnostic values were calculated to determine cut offs and the tool was refined based on the analysis. ResultsThirty participants with CeAD and 261 controls with non-CeAD causes of headache and neck pain were included. The diagnostic support tool was an ‘excellent’ predictor of CeAD (AUC 0.83) but demonstrated poor specificity. Refining the tool to ‘acute/sudden onset’ [1], ‘unusual/unfamiliar headache/neck pain’ [1], recent trauma/infection [1] and neurological features ≥2 [1], scored out of 4, showed 100 % sensitivity and 74 % specificity to detect CeAD at a cut-off of 3/4 (AUC 0.87). ConclusionsThe refined tool shows acceptable clinical utility at a cut-off ≥3, where referral for vascular imaging is recommended. Further validation in Emergency and primary care is needed.

A Case of Subarachnoid Hemorrhage Due to Vertebral Artery Dissection Following Spontaneous Coronary Artery Dissection on the Same Day: A Clinical Image

A woman in her 60s with well-controlled dyslipidemia presented with anterior chest pain. The electrocardiogram, chest radiograph, and echocardiogram were unremarkable; however, cardiac enzymes levels were elevated. Coronary angiography performed after dual antiplatelet therapy revealed spontaneous coronary artery dissection (SCAD). On the same day, the patient complained of mild headache that was initially treated as migraine. Hours later, the patient reported severe headache, followed by a decline in consciousness. Computed tomography of the head showed subarachnoid hemorrhage, while the angiography revealed bilateral vertebral artery dissection. The ruptured right vertebral artery dissecting aneurysm was treated with coil embolization. Despite treatment, the patient died seven days later. Autopsy confirmed dissections of the coronary and vertebral arteries. Although SCAD is rare, it often coexists with extracoronary vascular abnormalities due to systemic arterial fragility. Therefore, consider cerebrovascular disorders and promptly implementing diagnostic and management strategies in patients with SCAD and headaches is necessary.

Bifurcation analysis of pressure-induced detachment of a rod adhered to a plate

We study the lift of an elastica adhering to a flat rigid surface induced by a pressure difference. Adhesion is modelled by a cohesive force that decreases linearly with separation. Using a nonlinear local analysis, we determine the bifurcation diagram that governs the peeling process under quasi-static conditions. We show that the delamination emerges through a discontinuous transition: a normal form of the bifurcation diagram allows us to draw in a simple way the main physical mechanism, elucidating the local validity of the theory at the transition. We predict that the pressure, as a function of the detachment length, undergoes an initial drop followed by an approximately constant behaviour, while the detachment length at the transition is always finite and is roughly proportional to the elasto-adhesion length. This analysis can be the starting point to understand more complex-related problems that arise in fracture mechanics or in biology, such as testing of adhesives in a flowfield and the arterial dissection.

Coronary Artery Vasculitis and Encasement: Multimodality Imaging Findings and Mimics.

Coronary artery vasculitis (CAV) and coronary artery encasement are rarely diagnosed conditions that are important diagnostic considerations, particularly in patients with acute coronary syndrome without traditional cardiovascular risk factors or systemic illness. Vasculitis refers to inflammation of the blood vessel walls, which can be primary or secondary. This process should be distinguished from neoplastic involvement of the coronary arteries, termed coronary artery encasement. Prospective diagnosis of these diseases is challenging, often requiring multidisciplinary workup with careful attention to clinical presentation and multiorgan findings. While CAV and coronary artery encasement can be indistinguishable at coronary CT angiography, certain imaging features help order the differential diagnosis. CAV should be considered when there is smooth wall thickening that is circumferential and/or continuous. A diagnosis of coronary artery encasement is favored when there is irregular or nodular wall thickening that is eccentric to the vessel lumen. Epicardial fat stranding may also appear more extensive compared with CAV. Potential mimics of CAV include atherosclerosis, acute plaque rupture, coronary artery aneurysm, and spontaneous coronary artery dissection. Detection and diagnosis of CAV may help avoid complications related to accelerated atherosclerosis and infarction. Radiologists should be familiar with the range of pathologic conditions that can affect the coronary arteries beyond atherosclerosis as they may be the first to raise such diagnostic possibilities, guiding next steps in patient workup and management. ©RSNA, 2024 Supplemental material is available for this article.

Recurrent Posterior Circulation Infarction Caused by Vertebral Artery Dissection Secondary to Atlas Hypoplasia.

Recurrent Posterior Circulation Infarction Caused by Vertebral Artery Dissection Secondary to Atlas Hypoplasia.

ST-elevation myocardial infarction from spontaneous coronary artery dissection with high thrombus burden

ST-elevation myocardial infarction from spontaneous coronary artery dissection with high thrombus burden

Clinical characteristics and predictors of recurrence from the Australia-New Zealand Spontaneous Coronary Artery Dissection (ANZ-SCAD) registry

Abstract Background Spontaneous coronary artery dissection (SCAD) is an increasingly recognised cause of acute coronary syndrome (ACS), particularly in young women. Our understanding of SCAD remains incomplete with limited prospective data on determinants of SCAD recurrence. Purpose We aimed to describe the clinical characteristics, incidence and predictors of SCAD recurrence and major adverse cardiovascular events (MACE) in patients with SCAD from a large, multicentre registry. Methods Observational, multi-centre prospective and retrospective cohort study recruiting patients with SCAD from 23 hospitals in Australia and New Zealand. Patients aged=&amp;gt;18 years with SCAD and an ACS were eligible for inclusion. Prospectively recruited patients gave their informed consent while a waiver of consent was granted for retrospectively recruited patients. An independent core laboratory adjudicated invasive coronary angiography images to confirm the diagnosis of SCAD. The primary outcome was SCAD recurrence, defined as de novo spontaneous dissection with new ACS symptoms and cardiac enzyme elevation, not due to extension of the index lesion. Cox proportional hazard models were used to evaluate the association between SCAD recurrence and predefined clinical variables. Results From a total 487 patients recruited, 423 (132 prospective and 291 retrospective) patients with SCAD confirmed on core laboratory review were included for analysis. Mean age was 52.4±10.7 years, 89.7% were female and 73.1% were Caucasian. At discharge, 75.2% were on beta-blockers, 27.9% single antiplatelet and 61.9% dual antiplatelet (DAPT). At 15 (interquartile range 5-36) months median follow-up, SCAD recurrence occurred in 3.3%, with an overall MACE of 6.6%. On multivariate analysis, the presence of fibromuscular dysplasia (FMD) or other extra-cardiac vascular abnormalities [adjusted hazard ratio (HR) 5.63, 95% confidence interval (CI), 2.09-15.3, p&amp;lt;0.001], and past history of stroke (adjusted HR 7.99, 95% CI, 1.51-42.4, p=0.015) were associated with higher SCAD recurrence. Discharge beta-blockers was not independently associated with SCAD recurrence, while dual antiplatelet therapy that combined ticagrelor with aspirin was associated with a higher risk of recurrence (adjusted HR 2.47, 95% CI, 1.9-15.6, p=0.048). Conclusion SCAD recurrence comprised half of overall MACE in people with SCAD. The risk of SCAD recurrence was more than 5-fold higher in patients with FMD or other extra-cardiac vascular abnormalities. Dual-antiplatelet therapy that comprised ticagrelor and aspirin was associated with a higher risk of SCAD recurrence.