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Radial artery occlusion (RAO) can result from transradial catheterization. We compared the incidence of RAO with 2 heparin dosage regimens after transradial coronary angiography, and we evaluated the efficacy and safety of transient homolateral ulnar artery compression to achieve acute radial artery recanalization. Patients referred for coronary angiography were randomized to very-low-dose heparin (2,000 IU) or low-dose heparin (5,000 IU). On sheath removal, hemostasis was obtained using the TR band with a plethysmography-guided patent hemostasis technique. In the case of RAO as assessed by duplex ultrasonography 3 to 4 hours after hemostasis, immediate 1-hour ulnar artery compression was applied. Hematomas >15 cm(2) were also assessed. We randomized 465 patients, 222 in the 2,000-IU group and 243 in the 5,000-IU group. The baseline and procedural characteristics were comparable in both groups. The incidence of initial RAO was 5.9% in the 2,000-IU group and 2.9% in the 5,000-IU group (p = 0.17), with a compression time of 2.10 ± 0.78 hours and 2.25 ± 0.82 hours, respectively (p = 0.051). After ulnar artery compression, the final incidence of RAO was 4.1% in the 2,000-IU group and 0.8% in the 5,000-IU group (p = 0.03). The incidence of local hematoma was 2.3% and 3.7% in the 2,000- and 5,000-IU groups, respectively (p = 0.42). In conclusion, acute RAO after transradial catheterization can be recanalized by early 1-hour homolateral ulnar artery compression. This simple nonpharmacologic method was effective and safe in patients with very-low- and low-dose heparin. Nevertheless, the incidence of final RAO remained significantly lower after a higher anticoagulation level.

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OBJECTIVES: An association between aortic valve calcification and osteoporosis has been observed. The aim of this study was to assess the association between bisphosphonate treatment for osteoporosis and the progression of calcific aortic stenosis (AS). METHODS: A retrospective study of patients with AS (mean gradient ≥10 mm Hg), preserved renal function and two echocardiographies >8 months apart was performed. The patients were divided into those treated with bisphosphonates for osteoporosis and those not treated and then subdivided into mild (mean gradient <30 mm Hg) and moderate-to-severe AS groups. We compared the annualized gradient change between the groups and identified predictors of AS progression. RESULTS: We analyzed the outcomes of 103 patients (51% females, age 68 ± 10 years, follow-up 29 ± 13 months), of whom 57 had mild and 46 moderate-to-severe AS. Bisphosphonates were taken by 28 patients, of whom 22 had mild and 6 moderate-to-severe AS. In the patients with mild AS, the annualized mean gradient change was lower in the bisphosphonate-treated than in the untreated patients (0.1 ± 3.3 vs. 2.8 ± 3.3 mm Hg/year; p = 0.002) and was negatively associated with bisphosphonate treatment (ß coefficient -2.36%, 95% confidence interval -4.47 to -0.26; p = 0.028) independent of age, gender and baseline gradient. CONCLUSION: Bisphosphonate treatment was independently associated with slower progression of mild AS in patients with preserved renal function.

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BACKGROUND: Calcific aortic stenosis (AS) is an atherosclerosis-related process and the most common cause of valve disease requiring surgery. OBJECTIVE: To assess the association of inflammatory markers with AS in advanced atherosclerosis. METHODS: Consecutive patients with coronary artery disease (CAD) associated with AS were prospectively identified (mean transvalvular aortic gradient of 30 mmHg or greater). Subjects with aortic sclerosis (mean transvalvular aortic gradient of 10 mmHg or less) served as controls. All patients underwent clinical evaluation, echocardiography and coronary angiography. RESULTS: One hundred twenty-two patients with AS (85 men) and 101 with aortic sclerosis (76 men) of similar CAD severity were enrolled. The AS patients were older (mean [+/- SD] 71+/-7 years versus 66+/-7 years; P<0.001), had higher soluble vascular adhesion molecule-1 (s-VCAM-1) levels (1533+/-650 mug/L versus 1157+/-507 mug/L; P<0.001), but lower soluble intercellular adhesion molecule-1 (s-ICAM-1) (254+/-81 mug/L versus 293+/-84 mug/L; P<0.01) and soluble E-selectin (53+/-28 mug/L versus 62+/-29 mug/L; P<0.05) levels. The two groups did not differ with respect to C-reactive protein level (3+/-2.9 mg/L versus 3.4+/-2.6 mg/L; P not significant). Higher s-VCAM-1 (OR 1.09, 95% CI 1.04 to 1.14; P<0.001) and lower s-ICAM-1 (OR 0.82, 95% CI 0.72 to 0.94; P<0.001) levels were associated with AS after adjustment for age. CONCLUSION: Increased s-VCAM-1 levels were associated with calcific AS in patients with significant CAD.

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BACKGROUND: In calcific aortic valve disease, the early lesion is similar to atherosclerotic plaque, but later calcification prevails. Parathyroid hormone (PTH) and vitamin D are the principal calcium pool regulators, so the present study was designed to assess their association with aortic stenosis (AS) in patients with significant coronary artery disease (CAD), and preserved renal function. METHODS AND RESULTS: The 122 consecutive patients with AS (mean gradient > or =30 mmHg) plus CAD, and 101 patients with nonobstructive aortic sclerosis (mean gradient < or =10 mmHg) plus CAD, as controls, were prospectively enrolled. The AS patients were older (71+/-7 vs 66+/-7 years; p<0.001), had higher serum intact (i)PTH (51.4 [39-70] vs 37.4 [27-50] pg/ml; p<0.001), and lower plasma vitamin D (32.0 [25-40] vs 35.8 [27-55] nmol/L; p=0.003) levels than those with aortic sclerosis. The groups did not differ significantly in creatinine level (93 [82-105] vs 96 [85-107] micromol/L, p=0.19), calcium - phosphate product, occurrence of hypertension, smoking, diabetes, dyslipidemia, or body mass index. The iPTH (odds ratio (OR) 1.04, 95% confidence interval (CI) 1.02-1.05; p<0.001) and vitamin D levels (OR 0.97, 95% CI 0.95-0.99; p=0.003) were independently associated with AS. CONCLUSION: Higher serum iPTH with lower vitamin D levels were independently associated with calcific AS in CAD patients.

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BACKGROUND/AIMS: Aortic stenosis (AS) and hypertension are associated with cardiac hypertrophy and aortic dilatation. The effect of their coincidence on the ascending aortic dimensions has not yet been evaluated, and therefore was the aim of our study. METHODS: We performed cross-sectional analysis of history, clinical, angiographic and echocardiographic data of consecutive patients evaluated before surgery for non-rheumatic AS. RESULTS: The study sample included 225 patients (age 68+/-9 years, 60% males), with mean transaortic gradient of 55+/-17 mmHg. Hypertension was present in 153 (68%) patients. The hypertensives had more severe dyspnea (NYHA class 2.2+/-0.9 vs 1.9+/-0.9, p = 0.05) and higher prevalence of coronary artery disease (57% vs 33%, p = 0.001), but did not differ from the normotensives in the ascending aortic dimensions, the left ventricular mass, ejection fraction and remodeling patterns. Wider ascending aortic dimensions were independently associated with bicuspid aortic valve (p<0.001), and with maximal gradient in those with tricuspid aortic valve. Vasodilators were used in 84 (54%) hypertensives. CONCLUSION: We found hypertension in 68% of patients with severe AS. Bicuspid aortic valve and stenosis severity were independent predictors of ascending aortic dimensions, but not the history of hypertension and blood pressure.

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BACKGROUND: Dilatation of the ascending aorta in aortic stenosis may be partly explained by intrinsic wall structure changes, but the relative contribution of altered hemodynamics is unclear. The aim of this study was to assess the association between ascending aortic dimensions and valve stenosis severity. METHODS AND RESULTS: An analysis of echocardiographic examinations was conducted in 296 patients with aortic stenosis (179 males, mean age 71 years), 57 with bicuspid and 239 with tricuspid aortic valve, mean transaortic gradient 43+/-20 mmHg, and not more than moderate aortic regurgitation. Aortic dimensions at the level of annulus, sinuses of Valsalva, sinotubular junction and proximal ascending aorta were measured. Only height (p<0.001), degree of aortic regurgitation (p<0.01) and presence of bicuspid aortic valve (p<0.001) were independent predictors of ascending aortic dimensions. CONCLUSIONS: An independent association between aortic pressure gradients and proximal ascending aortic dimensions was not observed in patients with bicuspid or tricuspid aortic valve stenosis. Therefore, the poststenotic dilatation of the ascending aorta is not explained by aortic stenosis severity itself. Possible nonhemodynamic causes deserve detailed study at the time of diagnosis.

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