Vascular Causes Research Articles

Prévalence et caractéristiques de la dysfonction érectile chez les patients coronariens à l'Institut de cardiologie d'Abidjan en Côte d'Ivoire

IntroductionErectile dysfunction (ED) represents an independent and/or predictive risk factor for coronary heart disease according to many studies. The aim of our study is to determine the prevalence and risk factors associated with erectile dysfunction in coronary patients confirmed by coronary angiography. Material and methodWe conducted a descriptive and analytical cross-sectional study. A total of 60 patients were included with proven atheromatous coronary lesions after coronary angiography. The study period was from June 1, 2020 to February 29, 2021. After assessment of erectile status based on the short version of the International Index of Erectile Function (IIEF-5). Measures of association were adjusted odds ratios and odd ratios with their confidence intervals. Multivariate analysis was conducted using logistic regression. Only patients with erectile insufficiency underwent penile pharmocodoppler. ResultsThe mean age was 56 ± 8.4 years with extremes of 28 and 65 years. Erectile status was classified according to the IIEF-5 score as follows: severe ED (32%), moderate (13%), mild (15%) and normal erectile function (40%). The time to onset of ED was> 2 years in 69.4% of cases before the onset of coronary artery disease with a mean time of 2.37 years ± 1.29.In 20% of the cases, the patients were already on treatment before the erectile disorder, 65% undergoing treatment after the erectile disorder and 15% had no undergoing treatment. The main factors associated with ED were: high blood pressure (OR = 7; p = 0.0007), dyslipidemia (OR = 4.86; p = 0.004), diabetes (OR = 3.8; p = 0.02), obesity (OR = 4, 45; p = 0.02) as well as beta blockers (OR = 5.3; p = 0.004), calcium channel blockers (OR = 4.5; p = 0.004) and angiotensin-converting enzyme inhibitors (OR = 4.3; p = 0.008). The vascular cause clearly dominates (95%) of which 61% arterial mechanism, 17% mixed and 17% venous mechanism. The factor associated with a decrease PSVpi was the diabetes (OR = 28; p = 0.01). In multivariate analysis, no factor was statistically associated with ED or decrease in PSVpi. ConclusionIsolated ED appears as an early marker of generalized endothelial dysfunction. Hence the advantage of systematic screening, especially in subjects at risk of cardiovascular disease.

Kesiapsiagaan Keluarga Pasien Yang Keluarganya Menderita Stroke Dalam Menghadapi Situasi Bencana Di Kota Ternate

Background: The World Health Organization (WHO, 2016) states that there are several groups that are vulnerable when a disaster occurs, including children, pregnant women, the elderly, people with malnutrition and people with chronic diseases or immune disorders. Stroke as one of the groups affected by the disaster conditions that occurred. Stroke is a medical condition characterized by changes or neurological deficits caused by impaired blood supply to the brain, can be due to acute injury of the central nervous system (CNS) by vascular causes, including cerebral infarction, intracerebral hemorrhage and subarachnoid hemorrhage. in. Methods: This type of research is analytical descriptive with a cross sectional study approach. Result : There is still a lack of understanding of families, especially regarding aspects of actions that must be taken to anticipate disasters, not following the formulation of policies, emergency plans, disaster early warning systems, so that they do not support community preparedness.

CORRELATION OF NIHSS WITH SHORT TERM COMPLICATIONS OF ACUTE ISCHEMIC CVA PATIENT RECEIVING THROMBOLYSIS

Stroke is characterized as a neurological decit attributed to an acute focal injury of the central nervous system (CNS) by a vascular cause, including cerebral infarction, intracerebral haemorrhage (ICH) and subarachnoid hemorrhage. Thrombolysis is associated with its own complication and side effects and also have its own contraindication which should be kept in mind when thrombolysis is planned for the patient. Of all thrombolysis- related complications, intracerebral haemorrhage causes the most signicant morbidity and mortality. A prospective, longitudinal observational study was done, in which 47 consecutive cases of ischemic CVA, were included from march 2020 to October 2021. The demographics, risk factors, biochemical parameters and outcomes (mortality and complications) were assessed, until discharge or in-hospital death. After 24 hours of thrombolysis, 7 patients had NIHSS between 0-4 (1 patient on arrival),19 patient had NIHSS of 5-15 (15 patients on arrival), 6 patients had NIHSS of 16-20 (11 patients on arrival) and 15 patients had NIHSS of 21-42 (20 patients on arrival). Intra cranial bleed was signicantly more among subjects with NIHSS score (after 24 hours) of 21-42 with 4 out of 7 patients in that group followed by 2 patients with NIHSS of 16-20. Deterioration of power was seen in 3 patients with 2patients of NIHSS of 21-42. Seizure occurred in 2 patients with single patient in NIHSS of 16-20 and 21-42 group respectively. NIHSS at admission and 24hrs after admission is clinical score which could be assessed bedside and helps in assessing prognosis for the patients.

Abstract 15104: Diverse Associations Between Long-Term Body Mass Index Variability and Midlife Cognitive Function: The Bogalusa Heart Study

Introduction: Evidence shows that individual variation of body weight over time may have a role in explaining cognitive decline later in life independent from obesity status. Yet, the effect of long-term variability from childhood on midlife cognitive function (CF), as well as race differences remains unclear. This study examines this association among Black and White middle-aged individuals from a community cohort in Bogalusa, Louisiana. Methods: A total of 1,268 participants (59.5% women, 34.4% Black) from the Bogalusa Heart Study who had > 4 BMI measurements from childhood (mean age: 9.5 ± 3.5), and complete neuropsychological (NP) tests assessment to evaluate CF at midlife (48.2 ± 5.2) were studied. CF was measured with a global cognitive score (GCS). Long-term BMI variability was computed as standard deviation (SD), coefficient of variation (CV), deviation from age-predicted values (DEV), and residual SD (RSD). Regression models were used to evaluate the associations between BMI variability and GCS. Covariates included age, sex, race, cardiovascular risk factors, depression, class II obesity (BMI ≥ 35kg/m 2 ) at midlife, alcohol use, education and employment status. Race, sex and BMI variability interactions were evaluated. Results: Overall, higher DEV and RSD [Beta (SE): -0.30 (0.10); p = 0.003, and – 0.17 (0.08); p = 0.025, respectively] was associated with lower GCS. Interactions between SD, CV, DEV, and RSD with race were significant, but not with sex. Stratified analyses of the relationship between BMI variability measures and GCS showed the following result among White participants [DEV Beta (SE): -0.25 (0.10); p = 0.01] and Black participants [DEV Beta (SE): -0.03 (0.13); p = 0.81], respectively. Conclusion: We identified diverse associations between BMI variability from childhood and cognitive function in midlife. Although Black participants appear more resilient to the influence of BMI variability on CF in midlife, further studies are needed to identify the nature of this complex phenomenon and its potential to contribute to vascular causes of cognitive decline and dementia.

Abstract 12536: Type A Aortic Dissection in a Young Marfanoid Filipino Male Eventually Developing Fungal Mediastinitis: A Case Report

Introduction: Aortic Dissection (AD) results from a tear between the layers of the aorta. This is often seen among older males or those with heritable connective tissue disorders, and it mostly presents as chest pain. Management involves surgical repair wherein post procedure complications are to be expected. Mediastinitis, or deep sternal wound infection, however, is likewise unusual. Case Presentation: We present a case of a 29-year-old Filipino male presenting with sudden diffuse abdominal pain; he had no comorbidities and had no significant history suggestive of connective tissue disorders. Physical examination was mostly unremarkable. CT Aortogram revealed presence of dissection from the proximal ascending aorta up to the common iliac arteries, with the entry tear measuring 8.5mm at the level of T5, with extension to the proximal branches of the aortic arch, both common carotid arteries, right renal, right internal and external iliac arteries. Echocardiogram also showed a normal aortic valve but with dilated sinus of Valsalva(4.5cm, z-score 5.13). The patient underwent a Modified Bentall Procedure with Cabrol Shunt, with delayed closure of operative site due to extensive bleeding. Cystic medial necrosis was not seen on biopsy. After developing persistent post-operative fever, repeat chest CT showed a fluid collection in the mediastinum encasing the ascending aorta and main pulmonary trunk; culture of abscess fluid was positive for Candida tropicalis . He was then given prolonged parenteral followed by oral antifungal therapy and subsequently discharged improved. Discussion: Vascular causes of abdominal pain should be considered in patients with scant history and physical findings. Major vascular surgery has expected complications such as bleeding and infection; the management of such complications should incorporate a multidisciplinary approach as in such cases, a trial of medical management may be safer than repeat surgery.

Abstract 11587: Intriguing Genetic Overlap Between SCAD and TAD

Importance: Thoracic aortic dissections (TAD) are a well-known vascular cause of sudden death. Spontaneous coronary artery dissections (SCAD) are emerging as an important cause of early-onset myocardial infarction and sudden death. Genetic variants in multiple connective tissue genes have been recognized to underlie TAD; other genetic variants have similarly been recognized to underlie SCAD. Little data is available regarding any genetic commonality between TAD and SCAD. Objective: To determine any genetic overlap between genes coding for TAD and SCAD. Methods: Extensive review of 17 various retrospective and prospective clinical studies published between 2016 and 2022 exploring genetic studies of TAD and SCAD was performed using PubMed and Orbis. Articles highlighting the significant plausible triggers for TAD or SCAD were analyzed. Separate lists of causative genes were constructed for TAD and SCAD—and then commonalities sought. A Venn diagram was constructed to display the genetic overlap and common physiological pathways involved. Results: We identified a definite, meaningful overlap of fourteen independent genes based on GWAS or other genetic methods. Associated genetic pathways involved various biological processes including: Elastin degradation, smooth muscle cell function and the TGF-pathway. Overlapping genes included the following: COL3A1, TGFB2, SMAD3, MYLK, TGFBR2, TGFBR1, LOX, FBN1, NOTCH1, ELN, COL5A1, COL5A2, COL1A2, MYH11. Corresponding molecular pathways were investigated and correlated for both diseases. Conclusions and relevance: We are not aware of other studies searching for genetic commonalities between TAD and SCAD. We have successfully identified overlapping genes—and their corresponding molecular pathways—for TAD and SCAD. We hope these insights will lead to further clinical and scientific understanding of each disease via study of their fundamental commonalities.

ODP529 Update on the Prevalence and Pathogenesis of Central Hypothyroidism

Abstract Background Central hypothyroidism (CH) is a rare form of hypothyroidism characterized by insufficient stimulation of a normal thyroid gland by the thyroid-stimulating hormone (TSH). It can be of pituitary origin (secondary hypothyroidism) or hypothalamic origin (tertiary hypothyroidism). The diagnosis is suspected by the finding of low serum free thyroxine associated with low, normal, or slightly elevated serum TSH, in the absence of goiter. This review presents an update on the prevalence and pathogenesis of different types of CH. Methods A systematic search of literature was conducted using the search terms hypothyroidism, central hypothyroidism, congenital central hypothyroidism, acquired central hypothyroidism, TSH deficiency, prevalence, and pathogenesis. Results The prevalence of overt hypothyroidism in the US population is at least 0.3% and the prevalence of subclinical hypothyroidism ranges from 4% to 10%. Primary hypothyroidism is more prevalent in females. The prevalence of CH ranges from 1: 13,000 to 1: 120,000. CH is observed in less than 1% of hypothyroid subjects, with no evidence of sex predominance. Itcan occur prenatally (congenital CH) or after birth (acquired CH). Congenital CH, which is a rare cause of CH (prevalence around 1: 13,000), may result from genetic/malformative causes [e. g., pituitary-specific transcription factor defects, TSH-beta subunit gene mutations, isolated TSH-releasing hormone (TRH) deficiency, TRH receptor gene mutation, immunoglobulin superfamily member 1 deficiency, De Morsier syndrome, Prader Willi syndrome]. In 60% of the cases, congenital CH is associated with other pituitary hormone deficiencies and in 40% of the cases, congenital CH is due to isolated TSH deficiency. Acquired CH, which is the most common cause of CH andusually associated with other pituitary hormone deficiencies, results from the destruction or inhibition of the pituitary and/or hypothalamus. In decreasing order of frequency, acquired CH can be secondary to invasive and/or compressive lesions (e. g., pituitary macroadenomas, craniopharyngiomas, pituitary metastases, carotid aneurysm), iatrogenic factors (e. g., surgery or irradiation, glucocorticoids, dopaminergic drugs, somatostatin analogs, immune checkpoint inhibitors), trauma (e. g., brain injury), vascular causes (e. g., pituitary apoplexy, postpartum pituitary necrosis, hemorrhage), autoimmunity (e. g., lymphocytic hypophysitis), infiltrative lesions (e. g., hemochromatosis, sarcoidosis), and infections (e. g., tuberculosis, syphilis). Conclusion CH is a rare cause of hypothyroidism resulting from a variety of congenital or acquired causes. Acquired CH is the most common cause of CH. In many cases, both congenital and acquired CH are associated with multiple pituitary hormone deficiencies. Isolated TSH deficiency is rare and usually of congenital origin. Presentation: No date and time listed

Vascular disease and apathy symptoms in the very old: A cross-sectional and longitudinal meta-analysis of individual participant data.

Previous findings suggest a vascular foundation underlying apathy, but transdiagnostic and prospective evidence on vascular apathy is scarce. This study examines the association between vascular disease and the presence and development of apathy symptoms in the very old. Four cohorts of the Towards Understanding Longitudinal International older People Studies (TULIPS)-consortium were included in a two-staged, individual participant data meta-analysis using generalized linear mixed models. Vascular disease was defined as a history of any clinical atherosclerotic pathology (angina pectoris, myocardial infarction, intermittent claudication, transient ischemic attack, stroke or related surgeries) and was related to apathy symptoms as repeatedly measured by the Geriatric Depression Scale (GDS-3A ≥2) over a maximum of 5years. Of all 1868 participants (median age 85years old), 53.9% had vascular disease and 44.3% experienced apathy symptoms. Participants with vascular disease had a 76% higher risk of apathy symptoms at baseline (odds ratio (OR) 1.76, 95% confidence interval (CI) 1.32-2.35), irrespective of depressive symptoms and only partially explained by stroke. Conversely, there was no association of vascular disease with the occurrence of apathy symptoms longitudinally, both in those with apathy at baseline (OR 1.00, 95% CI 0.84-1.20) and without (OR 0.96, 95% CI 0.84-1.09). Vascular disease in the very old is associated with apathy symptoms cross-sectionally, but not proven longitudinally, independent of depressive symptoms. These findings query a vascular cause underlying apathy symptoms. However, the consistency of our cross-sectional findings in direction and magnitude across the TULIPS-consortium do emphasize international relevance of the interplay of vascular factors and apathy in advanced age, which meaning needs further unravelling.

HEMOLYTIC ANEMIA IN ALCOHOL USE DISORDER: A CASE OF ZIEVE SYNDROME

HEMOLYTIC ANEMIA IN ALCOHOL USE DISORDER: A CASE OF ZIEVE SYNDROME

S2939 Ashwagandha Toxicity: A Rare Case of Drug Induced Liver Injury (DILI)

Introduction: The pursuance of natural and herbal remedies by many has brought with it further knowledge of the many causes of Drug Induced Liver Injury (DILI). Many of these "natural" over-the-counter (OTC) supplements may not be benign due to the lack of scientific analysis and unregulated production. Ashwagandha is a supplement used for memory enhancement, management of anxiety, and general increase in vitality. We present a case of Ashwagandha DILI in a healthy 36-year-old man. Case Description/Methods: A 36-year-old male presented to our institution with 1 week of fatigue, jaundice, nausea and subjective fevers. Upon presentation he was hemodynamically stable and afebrile. Physical exam was notable for jaundice without other stigmata of liver disease or mental status changes. He was found to have acute liver injury with lab chemistries remarkable for AST= 1482 U/L, ALT= 1375 U/L, Tbili= 22.3 mg/dL, alkaline phosphatase= 202 U/L and an INR of 1.6. He denied alcohol and drug use, recent travel or sick contacts. Medications list was notable for cetirizine, diphenhydramine (both taken as needed), OTC testosterone supplements, OTC apple cider vinegar gummies BID and OTC ashwagandha gummies BID. Workup was negative for autoimmune, infectious, metabolic, obstructive and vascular causes of liver injury. Acetaminophen level and urine drug screen were negative. Trans-jugular liver biopsy revealed evidence of acute portal and lobular hepatitis and cholestasis, suggestive of DILI. Patient's liver enzymes continued to downtrend (AST=929, ALT=765, Tbili=22.5) after withdrawal of his supplements and was discharged (Figure). Discussion: Ashwagandha causing DILI has been infrequently reported in the literature. One case series of 5 patients in Iceland and a single case in Japan reported that ashwagandha is an uncommon culprit linked to acute liver injury. None of the reported cases necessitated liver transplant. Average time to resolution and normalization of LFTs was 3.5 months and R values usually ranged in the mixed range (R value 2-5). The case series also revealed that ashwagandha's toxicity could be dose dependent, as higher peaks in LFT's were tied to recent increases in ashwagandha dosing. Although ashwagandha has been a rarely reported cause of DILI, a thorough history of medication and OTC supplements in patients with undifferentiated acute liver injury may yield more cases. Further study and reporting of DILI in the ever-growing supplement market appears to be required to minimize potential injury.Figure 1.: Tranjugular Liver Biopsy Findings.

S2686 A Rare but Potentially Fatal Cause of Abdominal Pain: Segmental Arterial Mediolysis

Introduction: Segmental arterial mediolysis (SAM) is a rare disease, defined as a nonatherosclerotic, noninflammatory disruption of the arterial medial layer of a medium- to large-sized artery. We describe a case of a healthy woman with acute onset abdominal pain subsequently found to have spontaneous peritoneal hemorrhage from SAM. Case Description/Methods: A 52-year-old former professional female athlete developed abrupt onset lower abdominal pain with nausea and vomiting. Pain was 10/10 in severity with a sharp and crampy quality. She denied fevers, diarrhea, melena, bloody stool, ill contacts, recent travel, or prior episodes. Past medical history was significant for endometrial polyp, menopause, and iron deficiency. She had no prior surgeries. Family history included colon cancer in her father and ovarian cancer in her mother. Her abdomen was soft with tenderness in the lower quadrants with the remainder of the exam unremarkable. Labs including CBC, BMP, LFT, lipase, beta hCG, troponin, ESR, CRP, serum acetone, urinalysis, and lactic acid were reassuring. CT abdomen and pelvis with and without contrast demonstrated hyperenhancing hepatic lesions suggestive of hemangiomas. Ultrasound of the pelvis with duplex was normal with arterial and venous duplex waveforms to both ovaries. On the second day of hospitalization, she had another episode of abdominal pain with labs demonstrating a hemoglobin drop from 13.7 g/dL to 10.2 g/dL. Repeat CT abdomen pelvis with contrast demonstrated large volume hemorrhagic ascites up to 16 cm in size with concerns for active hemorrhage in the left upper quadrant. Diagnostic angiography was performed by Interventional radiology which did not show active arterial hemorrhage although demonstrated fusiform dilatation of the distal middle colic artery and short segment focal fusiform dilatation of the left colic artery at the splenic flexure suggestive of SAM. She subsequently underwent diagnostic laparoscopy and evacuation of hemoperitoneum with over 1L of unclotted blood evacuated with a mesenteric hematoma noted in the distal transverse and proximal descending mesocolon. The spontaneous peritoneal hemorrhage was thought to be secondary to underlying arterial abnormalities triggered by minor trauma. (Figure) Discussion: Vascular causes of abdominal pain such as segmental arterial mediolysis are uncommon. Awareness of noninflammatory and nonatherosclerotic artery diseases such as SAM need to be recognized since they can be fatal if not treated promptly.Figure 1.: Fig 1 demonstrates a bleeding artery as seen on CT abdomen and pelvis with intravenous contrast. Fig 2 demonstrates the large hemoperitoneum in the left upper quadrant seen on CT abdomen and pelvis.

Approach to persistent ascites after liver transplantation.

Persistent ascites (PA) after liver transplantation (LT), commonly defined as ascites lasting more than 4 wk after LT, can be expected in up to 7% of patients. Despite being relatively rare, it is associated with worse clinical outcomes, including higher 1-year mortality. The cause of PA can be divided into vascular, hepatic, or extrahepatic. Vascular causes of PA include hepatic outflow and inflow obstructions, which are usually successfully treated. Regarding modifiable hepatic causes, recurrent hepatitis C and acute cellular rejection are the leading ones. Considering predictors for PA, the presence of ascites, refractory ascites, hepato-renal syndrome type 1, spontaneous bacterial peritonitis, hepatic encephalopathy, and prolonged ischemic time significantly influence the development of PA after LT. The initial approach to patients with PA should be to diagnose the treatable cause of PA. The stepwise approach in evaluating PA includes diagnostic paracentesis, ultrasound with Doppler, and an echocardiogram when a cardiac cause is suspected. Finally, a percutaneous or transjugular liver biopsy should be performed in cases where the diagnosis is unclear. PA of unknown cause should be treated with diuretics and paracentesis, while transjugular intrahepatic portosystemic shunt and splenic artery embolization are treatment methods in patients with refractory ascites after LT.

Positive horizontal-canal head impulse test is not a benign sign for acute vestibular syndrome with hearing loss.

BackgroundDiagnosis of acute vestibular syndrome (AVS) with hearing loss is challenging because the leading vascular cause—AICA territory stroke—can appear benign on head impulse testing. We evaluated the diagnostic utility of various bedside oculomotor tests to discriminate imaging-positive and imaging-negative cases of AVS plus hearing loss.MethodWe reviewed 13 consecutive inpatients with AVS and acute unilateral hearing loss. We compared neurologic findings, bedside and video head impulse testing (bHIT, vHIT), and other vestibular signs (including nystagmus, skew deviation, and positional testing) between MRI+ and MRI– cases.ResultsFive of thirteen patients had a lateral pontine lesion (i.e., MRI+); eight did not (i.e., MRI–). Horizontal-canal head impulse test showed ipsilateral vestibular loss in all five MRI+ patients but only in three MRI– patients. The ipsilesional VOR gains of horizontal-canal vHIT were significantly lower in the MRI+ than the MRI– group (0.56 ± 0.11 vs. 0.87 ± 0.24, p = 0.03). All 5 MRI+ patients had horizontal spontaneous nystagmus beating away from the lesion (5/5). One patient (1/5) had direction-changing nystagmus with gaze. Two had skew deviation (2/5). Among the 8 MRI– patients, one (1/8) presented as unilateral vestibulopathy, four (4/8) had positional nystagmus and three (3/8) had isolated posterior canal hypofunction.ConclusionThe horizontal-canal head impulse test poorly discriminates central and peripheral lesions when hearing loss accompanies AVS. Paradoxically, a lateral pontine lesion usually mimics unilateral peripheral vestibulopathy. By contrast, patients with peripheral lesions usually present with positional nystagmus or isolated posterior canal impairment, risking misdiagnosis as central vestibulopathy.

Rivaroxaban in Rheumatic Heart Disease–Associated Atrial Fibrillation

BackgroundTesting of factor Xa inhibitors for the prevention of cardiovascular events in patients with rheumatic heart disease–associated atrial fibrillation has been limited.MethodsWe enrolled patients with atrial fibrillation and echocardiographically documented rheumatic heart disease who had any of the following: a CHA2DS2VASc score of at least 2 (on a scale from 0 to 9, with higher scores indicating a higher risk of stroke), a mitral-valve area of no more than 2 cm2, left atrial spontaneous echo contrast, or left atrial thrombus. Patients were randomly assigned to receive standard doses of rivaroxaban or dose-adjusted vitamin K antagonist. The primary efficacy outcome was a composite of stroke, systemic embolism, myocardial infarction, or death from vascular (cardiac or noncardiac) or unknown causes. We hypothesized that rivaroxaban therapy would be noninferior to vitamin K antagonist therapy. The primary safety outcome was major bleeding according to the International Society of Thrombosis and Hemostasis.ResultsOf 4565 enrolled patients, 4531 were included in the final analysis. The mean age of the patients was 50.5 years, and 72.3% were women. Permanent discontinuation of trial medication was more common with rivaroxaban than with vitamin K antagonist therapy at all visits. In the intention-to-treat analysis, 560 patients in the rivaroxaban group and 446 in the vitamin K antagonist group had a primary-outcome event. Survival curves were nonproportional. The restricted mean survival time was 1599 days in the rivaroxaban group and 1675 days in the vitamin K antagonist group (difference, −76 days; 95% confidence interval [CI], −121 to −31; P<0.001). A higher incidence of death occurred in the rivaroxaban group than in the vitamin K antagonist group (restricted mean survival time, 1608 days vs. 1680 days; difference, −72 days; 95% CI, −117 to −28). No significant between-group difference in the rate of major bleeding was noted.ConclusionsAmong patients with rheumatic heart disease–associated atrial fibrillation, vitamin K antagonist therapy led to a lower rate of a composite of cardiovascular events or death than rivaroxaban therapy, without a higher rate of bleeding. (Funded by Bayer; INVICTUS ClinicalTrials.gov number, NCT02832544.)

Cerebrovascular pulsatile tinnitus: causes, treatments, and outcomes in 164 patients with neuroangiographic correlation

BackgroundPulsatile tinnitus (PT) can cause significant detriment to quality of life and may herald a life-threatening condition. Endovascular evaluation is the gold standard for the definitive diagnosis of PT and...

Efficacy and safety evaluation of rivaroxaban vs. warfarin among non-valvular atrial fibrillation patients undergoing lower extremity revascularization.

IntroductionThe efficacy and safety of antithrombotic strategies remain uncertain in patients with atrial fibrillation undergoing lower-extremity revascularisation.Materials and methodsBetween January 2011 and November 2021, 319 patients with atrial fibrillation after lower-extremity revascularisation received rivaroxaban or warfarin treatment as anticoagulation regimens with different antiplatelet therapy strategies. The primary efficacy outcome was the composite of acute limb ischaemia, major amputation for vascular causes, myocardial infarction, ischaemic stroke, clinically driven target lesion revascularisation, and death from vascular causes. The safety outcomes were major bleeding events according to the International Society on Thrombosis and Haemostasis classification criteria.ResultsA total of 178 and 141 patients received rivaroxaban and warfarin treatments, respectively, after revascularisation with or without antiplatelet regimens. The incidence of the primary efficacy outcome at 36 months in the rivaroxaban group (44 patients, 24.7%) tended to be lower than that in the warfarin group (43 patients, 30.5%) (hazard ratio, 0.870; 95% confidence interval, 0.565–1.339; P = 0.527). The incidence of the secondary efficacy outcomes decreased in the rivaroxaban group (56 patients, 31.6%) compared with that in the warfarin group (61 patients, 43.2%). Major bleeding events occurred in three patients (1.7%) in the rivaroxaban group and five patients (3.5%) in the warfarin group; no significant difference in fatal or intracranial bleeding was observed between the groups.ConclusionThis study describes practical experience regarding the use of rivaroxaban and warfarin in patients with peripheral arterial disease complicated by non-valvular atrial fibrillation following endovascular intervention. The efficacy and safety outcomes do not differ significantly between rivaroxaban and warfarin.

Treatable Ataxias: How to Find the Needle in the Haystack?

Treatable ataxias are a group of ataxic disorders with specific treatments. These disorders include genetic and metabolic disorders, immune-mediated ataxic disorders, and ataxic disorders associated with infectious and parainfectious etiology, vascular causes, toxins and chemicals, and endocrinopathies. This review provides a comprehensive overview of different treatable ataxias. The major metabolic and genetic treatable ataxic disorders include ataxia with vitamin E deficiency, abetalipoproteinemia, cerebrotendinous xanthomatosis, Niemann-Pick disease type C, autosomal recessive cerebellar ataxia due to coenzyme Q10 deficiency, glucose transporter type 1 deficiency, and episodic ataxia type 2. The treatment of these disorders includes the replacement of deficient cofactors and vitamins, dietary modifications, and other specific treatments. Treatable ataxias with immune-mediated etiologies include gluten ataxia, anti-glutamic acid decarboxylase antibody-associated ataxia, steroid-responsive encephalopathy associated with autoimmune thyroiditis, Miller-Fisher syndrome, multiple sclerosis, and paraneoplastic cerebellar degeneration. Although dietary modification with a gluten-free diet is adequate in gluten ataxia, other autoimmune ataxias are managed by short-course steroids, plasma exchange, or immunomodulation. For autoimmune ataxias secondary to malignancy, treatment of tumor can reduce ataxic symptoms. Chronic alcohol consumption, antiepileptics, anticancer drugs, exposure to insecticides, heavy metals, and recreational drugs are potentially avoidable and treatable causes of ataxia. Infective and parainfectious causes of cerebellar ataxias include acute cerebellitis, postinfectious ataxia, Whipple’s disease, meningoencephalitis, and progressive multifocal leukoencephalopathy. These disorders are treated with steroids and antibiotics. Recognizing treatable disorders is of paramount importance when dealing with ataxias given that early treatment can prevent permanent neurological sequelae.

Imaging in Uterine Artery Pseudoaneurysm: A Rare, Potentially Fatal Cause of Secondary Post-partum Hemorrhage

Secondary postpartum hemorrhage is one of the important cause of postpartum morbidity and mortality. Uterine artery pseudoaneurysm is a rare, potentially fatal but treatable cause of secondary post-partum hemorrhage. If not diagnosed timely, it can lead to life-threatening hemorrhage. We report the case of a 41-year-old woman who presented with profuse vaginal bleeding on 32nd day of cesarean section. On imaging a left uterine artery pseudoaneurysm was found in the uterine wall with blood clots in the uterine cavity. Patient was managed with aggressive fluid resuscitation and immediate interventional radiology procedure of selective embolization of pseudoaneurysm. High index of suspicion is needed to search for rare vascular causes like pseudoaneurysm.

A Study on the Pathogenesis of Vascular Cognitive Impairment and Dementia: The Chronic Cerebral Hypoperfusion Hypothesis.

The pathogenic mechanisms underlying vascular cognitive impairment and dementia (VCID) remain controversial due to the heterogeneity of vascular causes and complexity of disease neuropathology. However, one common feature shared among all these vascular causes is cerebral blood flow (CBF) dysregulation, and chronic cerebral hypoperfusion (CCH) is the universal consequence of CBF dysregulation, which subsequently results in an insufficient blood supply to the brain, ultimately contributing to VCID. The purpose of this comprehensive review is to emphasize the important contributions of CCH to VCID and illustrate the current findings about the mechanisms involved in CCH-induced VCID pathological changes. Specifically, evidence is mainly provided to support the molecular mechanisms, including Aβ accumulation, inflammation, oxidative stress, blood-brain barrier (BBB) disruption, trophic uncoupling and white matter lesions (WMLs). Notably, there are close interactions among these multiple mechanisms, and further research is necessary to elucidate the hitherto unsolved questions regarding these interactions. An enhanced understanding of the pathological features in preclinical models could provide a theoretical basis, ultimately achieving the shift from treatment to prevention.

Cross-sectional Imaging of the Duodenum: Spectrum of Disease.

Cross-sectional Imaging of the Duodenum: Spectrum of Disease.