Background:The anterior cruciate ligament (ACL) is the most frequently injured ligament in the knee for which surgery is performed. United States national estimates of ACL reconstruction vary widely.Purpose:This study sought to use the most recently available Centers for Disease Control and Prevention data to investigate changes in the utilization of inpatient and ambulatory surgery for ACL tears in the United States.Study Design:Descriptive epidemiology study.Methods:The National Survey of Ambulatory Surgery, conducted in 1994, 1995, 1996, and 2006 (data from 1994, 1996, and 2006 were used in the study), and the National Hospital Discharge Survey, conducted between 1990 and 2007, were used to identify cases of ACL reconstruction. The data were analyzed for trends in demographics, treatment, and utilization.Results:Between 1994 and 2006, the population-adjusted estimate of the rate of ACL reconstructions increased by 37% (33.0/100,000 capita or 86,837 total procedures to 45.1/100,000 capita or 134,421 total procedures). There was an increase in the proportion of females undergoing reconstruction in both the ambulatory (30% to 40%) and inpatient (29% to 47%) settings over the study period, with a 304% increase in the sex-adjusted estimate of the rate of female ambulatory procedures between 1994 and 2006. Age-adjusted estimates of the rates of ambulatory ACL reconstruction increased among all age groups, with a 924% increase in patients less than 15 years of age. Concurrent meniscectomy remained relatively constant in the ambulatory (37% to 40%) and inpatient (37% to 33%) settings between 1994 and 2007. Private insurance was the largest compensator, representing 77% of cases in 2006. Between 1994 and 2006, the use of peripheral nerve blocks during ambulatory surgery increased from 0.7% to 30.8%.Conclusion:The rate of ACL reconstruction increased dramatically between 1990 and 2007 based on the National Survey of Ambulatory Surgery and National Hospital Discharge Survey databases, which represents the most up-to-date publicly available data. Knowledge of this increase and national practice patterns may aid policy makers and surgeons in appropriately allocating health care resources to ensure quality patient care.

We examined vascular function in an inactive muscle bed, the forearm, during lower limb exercise and determined the contribution of endothelium-derived nitric oxide (NO) to the hyperemic response. Eight young males were randomized to participate in two studies, each consisting of two bouts of lower limb exercise, separated by a 30-min recovery. Peak forearm blood flow (PFBF) and mean blood flow (MFBF) were continuously recorded at baseline and during exercise using continuous high-resolution vascular ultrasound and Doppler flow velocity measurement. During one session, the brachial artery was cannulated to allow continuous infusion of saline or N(G)-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase. The alternate session was performed to control for possible effects of repeated exercise. At 60, 100, and 160 W, L-NMMA significantly decreased both PFBF and MFBF compared with the saline infusion. These results suggest that systemic production of NO occurs during exercise in resting vessel beds, which do not feed metabolically active tissue. This finding provides a plausible explanation for the antiatherogenic benefits of exercise.

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It is well established that endothelial dysfunction is present in coronary artery disease (CAD), although few studies have determined the effect of training on peripheral conduit vessel function in patients with CAD. A randomized, crossover design determined the effect of 8 wk of predominantly lower limb, combined aerobic and resistance training, in 10 patients with treated CAD. Endothelium-dependent dilation of the brachial artery was determined, by using high-resolution vascular ultrasonography, from flow-mediated vasodilation (FMD) after ischemia. Endothelium-independent vasodilation was measured after administration of glyceryl trinitrate (GTN). Baseline function was compared with that of 10 control subjects. Compared with matched healthy control subjects, FMD and GTN responses were significantly impaired in the untrained CAD patients [3.0 +/- 0.8 (SE) vs. 5.8 +/- 0.8% and 14.5 +/- 1.9 vs. 20.4 +/- 1.5%, respectively; both P < 0.05]. Training significantly improved FMD in the CAD patients (from 3.0 +/- 0.8 to 5.7 +/- 1.1%; P < 0.05) but not responsiveness to GTN (14.5 +/- 1.9 vs. 12.1 +/- 1.4%; P = not significant). Exercise training improves endothelium-dependent conduit vessel dilation in subjects with CAD, and the effect, evident in the brachial artery, appears to be generalized rather than limited to vessels of exercising muscle beds. These results provide evidence for the benefit of exercise training, as an adjunct to routine therapy, in patients with a history of CAD.