• Users Online: 116
  • Print this page
  • Email this page
Export selected to
Endnote
Reference Manager
Procite
Medlars Format
RefWorks Format
BibTex Format
   Table of Contents - Current issue
Coverpage
April-June 2019
Volume 2 | Issue 2
Page Nos. 25-53

Online since Wednesday, October 9, 2019

Accessed 361 times.

PDF access policy
Journal allows immediate open access to content in HTML + PDF
View as eBookView issue as eBook
Access StatisticsIssue statistics
RSS FeedRSS
Hide all abstracts  Show selected abstracts  Export selected to  Add to my list
ORIGINAL ARTICLE  

Mortality risk stratification in patients with asymptomatic carotid stenosis p. 25
A Giannopoulos, S Kakkos, MB Griffin, G Geroulakos, D Tsalikakis, Andrew Nicolaides
DOI:10.4103/VIT.VIT_10_19  
AIMS: The aim of this analysis was to (a) determine the long-term 5-year all-cause and cardiovascular (CV) mortality in patients with asymptomatic internal carotid artery stenosis (ACS), (b) identify risk factors that could be used in mortality risk stratification, and (c) develop a model for predicting a patient's risk of CV death within 5 years. METHODS: This was a multicenter natural history study involving 1121 patients with ACS undergoing medical intervention alone. Proportional-hazards models were used to calculate all-cause and CV mortality using clinical and plaque texture features. RESULTS: Totally 1121 patients with 50%–99% ICA stenosis (European Carotid Surgery Trial criteria) from the Asymptomatic Carotid Stenosis and Risk of Stroke study were included in this analysis for mortality. Mean follow-up was 48 months (range, 6–96 months). There were 213 (19%) deaths during follow-up. Average annual all-cause mortality was 4.6%. About 68.1% of all deaths were due to CV causes. Independent predictors of all-cause mortality were age, male gender, carotid stenosis >80% (NASCET criteria), diabetes, cardiac failure, left ventricular hypertrophy (LVH) on electrocardiogram (ECG), smoking, absence of antiplatelet therapy, and history of vertebrobasilar symptoms. It was also shown that age, male gender, diabetes, fibrinogen >3.6 g/L, carotid stenosis >80% (NASCET criteria), cardiac failure, absence of antiplatelet therapy, and LVH on ECG were independent risk factors for CV mortality. Receiver operating characteristic curves for the above models were 0.709 (95% confidence interval [CI], 0.659–0.754) and 0.701 (95% CI, 0.656–0.746), respectively. The CV mortality prediction model could identify several subgroups of asymptomatic patients with different risk. The highest 90%–100% predicted 5-year CV mortality carried 25 times the risk of the low-risk subgroup in which the 5-year predicted CV mortality was 4%. CONCLUSION: Mortality risk can be taken into consideration in clinical practice, in order to identify patients with ACS who are unlikely to benefit from carotid endarterectomy. The majority of patients with ACS have a very high risk of myocardial infarction and should not be denied aggressive risk factor modification or a full cardiac investigation according to the current guidelines.
[ABSTRACT]  [HTML Full text]  [PDF]  [Mobile Full text]  [EPub]  [Sword Plugin for Repository]Beta
REVIEW ARTICLES Top

Molecular targets for improving arteriovenous fistula maturation and patency p. 33
Jolanta Gorecka, Arash Fereydooni, Luis Gonzalez, Shin Rong Lee, Shirley Liu, Shun Ono, Jianbiao Xu, Jia Liu, Ryosuke Taniguchi, Yutaka Matsubara, Xixiang Gao, Mingjie Gao, John T Langford, Bogdan Yatsula, Alan Dardik
DOI:10.4103/VIT.VIT_9_19  
The increasing prevalence of chronic and end-stage renal disease creates an increased need for reliable vascular access; although arteriovenous fistulae (AVF) are the preferred mode of hemodialysis access, 60% fail to mature and only 50% remain patent at 1 year. Fistulae mature by diameter expansion and wall thickening; this outward remodeling of the venous wall in the fistula environment relies on a delicate balance of extracellular matrix remodeling, inflammation, growth factor secretion, and cell adhesion molecule upregulation in the venous wall. AVF failure occurs via two distinct mechanisms with early failure secondary to lack of outward remodeling, that is, insufficient diameter expansion or wall thickening, whereas late failure occurs with excessive wall thickening due to neointimal hyperplasia and insufficient diameter expansion in a previously functional fistula. In recent years, the molecular basis of AVF maturation and failure are becoming understood to develop potential therapeutic targets to aid maturation and prevent access loss. Erythropoietin-producing hepatocellular (Eph) carcinoma receptors, along with their ligands and ephrins, determine vascular identity and are critical for vascular remodeling in the embryo. Manipulation of Eph receptor signaling in adults, as well as downstream pathways, is a potential treatment strategy to improve the rates of AVF maturation and patency. This review examines our current understanding of molecular changes occurring following fistula creation, factors predictive of fistula success, and potential areas of intervention to decrease AVF failure.
[ABSTRACT]  [HTML Full text]  [PDF]  [Mobile Full text]  [EPub]  [Sword Plugin for Repository]Beta

Venous circulation and William Harvey: A historical review p. 42
Kenneth Myers
DOI:10.4103/VIT.VIT_11_19  
Greco–Roman concepts regarding the circulation persisted until the 1600s even though many were incorrect. It was held that blood flows in veins from the liver to the periphery where it is consumed. It was not until the 1500s that anatomists identified venous valves and explored their function. This, in part, allowed William Harvey to describe the circulation as we know it today. This study included review of the literature and translations of William Harvey's books including De Motu Co]rdis which were published in 1628. Harvey's description of the venous circulation started the intense exploration of venous physiology that continues today. The resultant concepts of venous reflux associated with varicose disease have allowed practitioners to develop contemporary management.
[ABSTRACT]  [HTML Full text]  [PDF]  [Mobile Full text]  [EPub]  [Sword Plugin for Repository]Beta
CASE REPORT Top

Anterior spinal cord infarction as a complication of bronchial artery embolization in the management of recurrent hemoptysis p. 51
Ramandeep Singh, Siddharth Prakash, Paramdeep Singh, Rupinderjeet Kaur, Rubal Rai
DOI:10.4103/VIT.VIT_12_19  
Bronchial artery embolization (BAE) is an established minimally invasive approach for the treatment of massive or recurrent hemoptysis. There are several minor complications associated with the procedure. A rare complication of the procedure is spinal cord infarction due to embolization of anterior spinal artery. A 48-year-old male patient of old pulmonary tuberculosis presented with fibrocalcified lesions in the right upper lobe on chest X-ray and recurrent hemoptysis. Angiography revealed bleeding from a branch of single right intercostobranchial trunk. The day following the procedure, the patient complained of weakness and pain in lower limbs. Magnetic resonance imaging dorsolumbar spine revealed acute spinal cord infarct from D2 to D5 vertebral levels. This case demonstrates that spinal cord ischemia may occur during BAE, despite all the precautionary measures.
[ABSTRACT]  [HTML Full text]  [PDF]  [Mobile Full text]  [EPub]  [Sword Plugin for Repository]Beta