Updated Society for Vascular Surgery guidelines for management of extracranial carotid disease

Management of carotid bifurcation stenosis is a cornerstone of stroke prevention and has been the subject of extensive clinical investigation, including multiple controlled randomized trials. The appropriate treatment of patients with carotid bifurcation disease is of major interest to the community of vascular surgeons. In 2008, the Society for Vascular Surgery published guidelines for treatment of carotid artery disease. At the time, only one randomized trial, comparing carotid endarterectomy (CEA) and carotid stenting (CAS), had been published. Since that publication, four major randomized trials comparing CEA and CAS have been published, and the role of medical management has been re-emphasized. The current publication updates and expands the 2008 guidelines with specific emphasis on six areas: imaging in identification and characterization of carotid stenosis, medical therapy (as stand-alone management and also in conjunction with intervention in patients with carotid bifurcation stenosis), risk stratification to select patients for appropriate interventional management (CEA or CAS), technical standards for performing CEA and CAS, the relative roles of CEA and CAS, and management of unusual conditions associated with extracranial carotid pathology. Recommendations are made using the GRADE (Grades of Recommendation Assessment, Development and Evaluation) system, as has been done with other Society for Vascular Surgery guideline documents.[corrected] The perioperative risk of stroke and death in asymptomatic patients must be <3% to ensure benefit for the patient. CAS should be reserved for symptomatic patients with stenosis of 50% to 99% at high risk for CEA for anatomic or medical reasons. CAS is not recommended for asymptomatic patients at this time. Asymptomatic patients at high risk for intervention or with <3 years life expectancy should be considered for medical management as the first-line therapy.     

Relationship of Psychosocial Risk Factors, Certain Personality Traits and Myocardial Infarction in Indians: A Case�Ccontrol Study

Objective:

To investigate the relationship of psychosocial factors (lack of social support, stress and subjective well-being) and personality traits with myocardial infarction (MI).

Materials and Methods:

A case–control study involving 100 cases and 100 matched controls was conducted in Lok Nayak Hospital, New Delhi.

Results:

Stress over 1 year was significantly higher in cases (P < 0.001). However, difference was not significant when scores of social support (P = 0.2), Presumptive Stressful Life Event (PSLE) over lifetime (P = 0.058) and subjective well-being (P = 0.987) were compared. MI was significantly associated with hyperactive (P < 0.001), dominant (P = 0.03), egoistic (P < 0.001) and introvert (P < 0.001) personalities.

Conclusion:

Certain personality traits and recent stress may be important risk factors of MI, especially in Indians. The finding may have implications on the preventive strategies planned for MI patients.     

Body Mass Index and obesity: Tailoring “cut-off” for an Asian Indian male population

Background: Obesity/overweight is a recognized risk factor for a host of disorders. The disease risk stratification is commonly based on the Quetelets Index (Body Mass Index-BMI), a surrogate measure of fatness. The currently used BMI cut-offs to classify people as overweight or obese in Armed Forces have been defined in studies on Caucasian populations. However, because of differences in body structure and composition in different ethnic, socioeconomic, cultural and regional groups the correspondence between BMI and body fat content varies between populations. We conducted this pilot study in the Indian Navy to define BMI cut-offs for overweight and obesity using body fat content derived from Skin Fold Thickness as the standard.     

Toxicity of thallium on isolated rat liver mitochondria: The role of oxidative stress and MPT pore opening

Thallium(I) is a highly toxic heavy metal; however, up to now, its mechanisms are poorly understood. The authors' previous studies showed that this compound could induce reactive oxygen species (ROS) formation, reduced glutathione (GSH) oxidation, membrane lipid peroxidation, and mitochondrial membrane potential (MMP) collapse in isolated rat hepatocyte. Because the liver is the storage site of thallium, it seems that the liver mitochondria are one of the important targets for hepatotoxicity. In this investigation, the effects of thallium on mitochondria were studied to investigate its mechanisms of toxicity. Mitochondria were isolated from rat liver and incubated with different concentrations of thallium (25–200 µM). Thallium(I)‐treated mitochondria showed a marked elevation in oxidative stress parameters accompanied by MMP collapse when compared with the control group. These results showed that different concentrations of thallium (25–200 µM) induced a significant (P < 0.05) increase in mitochondrial ROS formation, ATP depletion, GSH oxidation, mitochondrial outer membrane rupture, mitochondrial swelling, MMP collapse, and cytochrome c release. In general, these data strongly supported that the thallium(I)‐induced liver toxicity is a result of the disruptive effect of this metal on the mitochondrial respiratory complexes (I, II, and IV), which are the obvious causes of metal‐induced ROS formation and ATP depletion. The latter two events, in turn, trigger cell death signaling via opening of mitochondrial permeability transition pore and cytochrome c expulsion. © 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 232–241, 2015.