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Objectives To assess the impact of the Centers for Medicare and Medicaid Services (CMS) national coverage determination (NCD) on access for patients with aortic stenosis (AS) with transcatheter aortic valve replacement (TAVR) in a tertiary care center. Background TAVR has given hope to patients with AS who are deemed inoperable. The effects of the NCD on access to patients with AS has not been evaluated. Materials and Methods A total of 94 inoperable AS patients were evaluated and treated from December 2011 through June of 2012 with TAVR. Patients who underwent transfemoral (TF) vs. non-TF access were compared. The CMS NCD was released on May 1, 2012 and on July 1, 2012, the nontransfemoral access program was put on hold due to lack of reimbursement. Results Patients in the TF (n = 33) and non-TF access (n = 61) groups were similar in age (85.2 ± 6.3 vs. 84.8 ± 6.6 P = 0.74) and STS mortality (9.38 ± 5.33 vs. 7.91 ± 3.69, P = 0.074). The iliofemoral arteries were larger diameter in the TF group (7.72 ± 1.49 vs. 6.21 ± 1.78, P < 0.001) and males (7.39 ± 1.81 vs. 6.1 ± 1.61 P < 0.001). More women underwent valve implantation via non-TF access (73 vs. 23%, P = 0.03). After the NCD, 21 patients who previously qualified for non-TF TAVR would not be reimbursed by CMS. Four died soon after. Conclusions After the NCD, the proportion of inoperable patients with severe AS that can be treated with TAVR was greatly reduced due the lack of reimbursement for TAVR via non-TF access. This effect is particularly pronounced in women. © 2014 Wiley Periodicals, Inc.

This study was designed to determine whether sex differences in platelet function exist in families with premature atherosclerosis. Compared with men, women have a greater risk of death and recurrent events following myocardial infarction and coronary artery bypass graft surgery. The reasons for this sex discrepancy are unknown. Because blood platelets play a central role in the formation of pathologic thrombi at sites of ruptured atheromatous plaques, we postulated that sex differences in platelet function exist that may be partly responsible for the sex difference in coronary artery disease (CAD) outcomes.We compared platelet reactivity in 400 asymptomatic men and women with family histories of premature CAD. Subjects were participants in the Johns Hopkins Sibling Study, a prospective investigation of coronary risk factors in asymptomatic, apparently healthy siblings of people with documented CAD.The platelets from women bound more fibrinogen in response to low and high concentrations of adenosine diphosphate. This sex difference was greater in whites than in African Americans. Age did not have an impact on these findings, although platelets from women 48 to 59 years old tended to bind less fibrinogen than those younger than 48 years. Female platelets also demonstrated greater spontaneous aggregation compared with male platelets, and women had higher levels of plasma thromboxane than men did. These differences were independent of smoking, hypertension, diabetes, hypercholesterolemia, or aspirin use.In asymptomatic individuals with family histories of premature CAD, platelets from women are more reactive than platelets from men. This observation cannot be explained by differences in cardiac risk factors.

Transcatheter aortic valve replacement (TAVR) has become the standard of care for inoperable patients with aortic stenosis (AS). Prior to release of the Centers for Medicare and Medicaid Services (CMS) national coverage determination (NCD), the TAVR access route was at the discretion of the treating

46 A novel transgenic mice has been generated which overexpresses the constitutively activated mutant form of human Rac 1 (Rac-CA), a small GTP-binding protein of the Rho family, in smooth muscle cells. Experiments were conducted to determine whether chronic activation of Rac-1 affects blood pressure (BP) and heart rate (HR). Male Rac-CA and control mice were prepared for chronic cardiovascular monitoring using carotid arterial catheters infused with heparinized saline. BP and HR were measured continuously for more than 4 days. Results show an increased BP in Rac-CA with no change in HR or water intake. BP was consistently higher in Rac-CA mice (Figure), averaging 122±4 vs 109±4 mm Hg during the dark phase (Rac-CA vs Control). HR showed a night/day rhythm with no differences between the Rac-CA and Controls, respectively, 640±15 vs 610±11 bpm (dark) and 572 ±39 vs 578 ±18 (light). These results illustrate that alteration in intracellular signaling (reactive oxygen species) in vascular smooth muscle produces changes in blood pressure. The mild to moderate hypertension observed in this animal model is similar to the human condition.