Aim: Research shows that subclinical hypothyroidism (SCH) is related to an increased carotid intima –media thickness (CIMT), a surrogate marker of subclinical cardiovascular disease (CVD). It is controversial whether or not SCH should be treated to reduce CVD morbidity and mortality. This meta-analysis aimed to determine whether SCH is associated with an increase in CIMT as compared to Euthyroidism (EU) and whether thyroxin (T4) treatment in SCH can reverse the change in CIMT.Methods: Two independent reviewers conducted an extensive database research up to December 2016. A total of 12 clinical trials discussed the effect of Thyroxin on CIMT values at pre- and post-treatment in subjects with SCH.Results: CIMT was significantly higher among SCH (n = 280) as compared to EU controls (n = 263) at baseline; the pooled weighted mean difference (WMD) of CIMT was 0.44 mm [95% confidence interval (CI) 0.14, 0.74], p = 0.004; I2 = 65%. After treatment with thyroxin in subjects with SCH (n = 314), there was a statistically significant decrease in CIMT from pre- to post-treatment; the pooled WMD of CIMT decrease was [WMD −0.32; 95% CI (−0.47, −0.16), p = < 0.0001; I2 = 2%], and it was no longer different from EU controls [WMD 0.13 mm; 95% CI (−0.04, 0.30); p = 0.14; I2 = 27%]. The total cholesterol (TC), triglycerides (TG), and low-density lipoprotein (LDL) were higher in SCH as compared to EU controls and decreased significantly after treatment with thyroxin.Conclusion: This meta-analysis shows that thyroxin therapy in subjects with SCH significantly decreases CIMT and improves lipid profile, modifiable CVD risk factors. Thyroid hormone replacement in subjects with SCH may play a role in slowing down or preventing the progression of atherosclerosis.

In patients with lower GI bleeding, both full GBS and modified GBS can predict the need for hospital-based interventions and mortality.

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Objective: Carotid intima media thickness (CIMT) is well-known marker of cerebrovascular & CVD outcomes. Recent literature has discussed association of sleep duration with stroke &CVD, but still limited evidence exists regarding the true relationship of sleep duration with CIMT. The aim of this study is to determine association of short& long sleep duration with CIMT. Method: Baptist Health South Florida, a not for profit organization, conducted a randomized, non-blinded controlled trial in 2014.This study examined effect of web based interventions on reducing CVD risk in employees. The inclusion criteria were physician diagnosed T2DM and/or Metabolic Syndrome. We used cross sectional data for analysis. Per CDC.gov guidelines, we categorized self-reported sleep duration (hrs) as short (<7), reference (≥7-<9) and long sleep (≥9). CIMT was measured via carotid US screening device by Panasonic CardioHealth Station. Result: Study population (n=183; 74% female, 49% Hispanic) with mean age 51±10 years. Mean CIMT(mm) in females [0.879±0.15] and males [0.911±0.19] was not different (p>0.05). Atherosclerotic plaque was defined as any obvious focal luminal encroachment > 1.2 mm. In multivariate logistic regression model, per hour increase in sleep duration was associated with twice the odds of increase in CIMT >1.2mm [OR 2.15;95% CI (1.15-4.02)]. However, once we compared the reference sleep with short and long sleep duration categories, we determined, as compared to 7-9 hrs (ref) of sleep, the odds of CIMT >1.2 in those sleeping <7 hrs [OR 1.23; 95% CI (0.27-5.53)] and those sleeping ≥9 hrs [OR 2.91; 95% CI (0.33-25.42)] were not significant in adjusted model. Conclusion: Although we observed that per hour increase in sleep was related to increase in CIMT >1.2mm (risk of plaque), but we did not find any significant increased risk of plaque in either short or long sleep duration. Longitudinal studies with larger sample size are needed to clarify this association.