Intraobserver Reliability and Interobserver Agreement in Radiographic Classification of Heterotopic Ossification.

The most widely used radiologic classification system for heterotopic ossification after total hip arthroplasty (THA) is the Brooker scale. In 2002, Della Valle et al proposed a modified rating system for heterotopic ossification to increase intraobserver reliability and interobserver agreement. To date, no study comparing these 2 classification systems has been conducted. Moreover, these studies were grossly underpowered. In the current study, 3 clinicians reviewed the charts of 236 patients with documented radiographic heterotopic ossification at least 2 months after THA and independently graded the amount of heterotopic ossification according to the Brooker and Della Valle classification systems. Then the intraobserver reliability and the interobserver agreement of each classification system were calculated with Cohen's kappa (κ) coefficient of agreement. The Brooker scale showed moderate to substantial intraobserver reliability (0.43≤κ<0.71), and the Della Valle classification system showed substantial intraobserver reliability (0.65≤κ<0.77). Both classification systems showed moderate interobserver agreement (0.40≤κ<0.60). Della Valle grade C (ie, presence of bone spurs from the pelvis or femur leaving less than 1 cm between opposing surfaces and apparent bone ankylosis) and Brooker grade IV had the best interobserver agreement. The best interobserver agreement for any grade was seen with grade C of the Della Valle classification system, which showed substantial interobserver reliability (0.60≤κ<0.80). The Della Valle classification system may be slightly better in patients with large amounts of heterotopic ossification, but both classification systems lack sufficient clarity and are open to significant subjective interpretation. [Orthopedics. 2017; 40(1):e54-e58.].

Modest visceral fat gain causes endothelial dysfunction in healthy humans.

OBJECTIVES: The aim of this study was to determine the impact of fat gain and its distribution on endothelial function in lean healthy humans. BACKGROUND: Endothelial dysfunction has been identified as an independent predictor of cardiovascular events. Whether fat gain impairs endothelial function is unknown. METHODS: A randomized controlled study was conducted to assess the effects of fat gain on endothelial function. Forty-three normal-weight healthy volunteers were recruited (mean age 29 years; 18 women). Subjects were assigned to gain weight (approximately 4 kg) (n=35) or to maintain weight (n=8). Endothelial function (brachial artery flow-mediated dilation [FMD]) was measured at baseline, after fat gain (8 weeks), and after weight loss (16 weeks) for fat gainers and at baseline and follow-up (8 weeks) for weight maintainers. Body composition was measured by dual-energy X-ray absorptiometry and abdominal computed tomographic scans. RESULTS: After an average weight gain of 4.1 kg, fat gainers significantly increased their total, visceral, and subcutaneous fat. Blood pressure and overnight polysomnography did not change after fat gain or loss. FMD remained unchanged in weight maintainers. FMD decreased in fat gainers (9.1+/-3% vs. 7.8+/-3.2%, p=0.003) but recovered to baseline when subjects shed the gained weight. There was a significant correlation between the decrease in FMD and the increase in visceral fat gain (rho=-0.42, p=0.004), but not with subcutaneous fat gain (rho=-0.22, p=0.15). CONCLUSIONS: In normal-weight healthy young subjects, modest fat gain results in impaired endothelial function, even in the absence of changes in blood pressure. Endothelial function recovers after weight loss. Increased visceral rather than subcutaneous fat predicts endothelial dysfunction. (Fat Gain and Cardiovascular Disease Mechanisms; NCT00589498).

Familial premature coronary artery disease mortality and obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) is linked to both coronary artery disease (CAD) and sudden death, but any causal role remains unclear. A family history of premature CAD and related mortality is an independent risk factor for the development of CAD. We hypothesized that OSA is associated with a family history of premature mortality from ischemic heart disease. METHODS: We prospectively studied 588 subjects who underwent polysomnography from May 2000 to June 2004. Demographics, comorbidities, family history of cardiovascular disease, and the ages and causes of death for 10 strata of family members were recorded for all subjects. We excluded those subjects with known causes of premature cardiac death, such as hypertrophic cardiomyopathy and long-QT syndrome. OSA was defined by American Academy of Sleep Medicine criteria (ie, apnea-hypopnea index >or= 5). Premature CAD mortality was defined as death due to ischemic heart disease or sudden cardiac death before 55 years of age (men) or 65 years of age (women). RESULTS: Polysomnography confirmed OSA in 316 subjects and excluded it in 202 subjects. The unadjusted odds ratio (OR) for OSA and a family history of premature CAD mortality was 2.11 (95% confidence interval [CI], 1.10 to 4.31; p = 0.031). After adjusting for each subject's sex, body mass index, and history of CAD, there was a significant and independent association between OSA and family history of premature CAD mortality (OR, 2.13; 95% CI, 1.04 to 4.66; p = 0.046). CONCLUSIONS: Regardless of their own CAD status, people with OSA are more likely than those without OSA to have a family history of premature CAD mortality.

Hemodynamic and autonomic effects of smokeless tobacco in healthy young men.

OBJECTIVES: The aim of this study was to investigate the acute hemodynamic and autonomic effects of smokeless tobacco. BACKGROUND: Smokeless tobacco use is increasing. Its cardiovascular effects are not well understood. METHODS: Sixteen healthy, male, habitual snuff tobacco users (aged 22 +/- 1 year) were studied, using a randomized, double-blind, placebo-controlled, crossover design with two separate experimental sessions: placebo and tobacco. Muscle sympathetic nerve activity (MSNA), electrocardiogram, blood pressure, calf blood flow, nicotine, and catecholamines were measured. RESULTS: Snuff tobacco increased plasma nicotine from 2.8 +/- 0.5 ng/ml to 10.4 +/- 1.1 ng/ml. Mean blood pressure increased by 10 +/- 1 mm Hg, and heart rate increased by 16 +/- 2 beats/min. Peripheral vascular resistance, MSNA, and norepinephrine concentration did not change with tobacco, but epinephrine increased by approximately 50%. CONCLUSIONS: Oral snuff tobacco increases heart rate, blood pressure, and epinephrine. Despite the increase in blood pressure, there is no decrease in either MSNA or peripheral vascular resistance. Smokeless tobacco is a powerful autonomic and hemodynamic stimulus. Catecholamine release from the adrenal medulla likely contributes to this response.