A Randomized Trial Comparing Short versus Prolonged Hemostasis with Rescue Recanalization by Ipsilateral Ulnar Artery Compression: Impact on Radial Artery Occlusion-The RESCUE-RAO Trial.

BACKGROUND: Despite the enormous benefits of radial access, this route is associated with a risk of radial artery occlusion (RAO). OBJECTIVE: We compared the incidence of RAO in patients undergoing transradial coronary angiography and intervention after short versus prolonged hemostasis protocol. Also we assessed the efficacy of rescue 1-hour ipsilateral ulnar artery compression if RAO was observed after hemostasis. Material and Methods. Patients referred for elective transradial coronary procedures were eligible. After 6 F radial sheath removal, patients were randomized to short (3 hours) (n = 495) or prolonged (8 hours) (n = 503) hemostasis and a simple bandage was placed over the puncture site. After hemostasis was completed, oximetry plethysmography was used to assess the patency of the radial artery. RESULTS: One thousand patients were randomized. Baseline characteristics were similar between both groups with average age 61.4 ± 9.4 years (71% male) and PCI performed on half of the patients. The RAO rate immediately after hemostasis was 3.2% in the short hemostasis group and 10.1% in the prolonged group (p < 0.001). Rescue recanalization was successful only in the short group in 56.2% (11/19); at hospital discharge, RAO rates were 1.4% in the short group and 10.1% in the prolonged group (p < 0.001). CONCLUSION: Shorter hemostasis was associated with significantly less RAO compared to prolonged hemostasis. Rescue radial artery recanalization was effective in > 50%, but only in the short hemostasis group.

Carotid and Aortic Stiffness in Patients with Heterozygous Familial Hypercholesterolemia.

BACKGROUND: The role of plasma cholesterol in impairing arterial function and elasticity remains unclear. We evaluated arterial stiffness, measured locally in the common carotid artery by high-resolution echo-tracking, and aortic stiffness, using carotid-femoral pulse wave velocity (PWV) (the "gold-standard" measurement of arterial stiffness), in treatment-naive patients with heterozygous familial hypercholesterolemia (FH). METHODS: The study included 66 patients with FH (10-66 years old) and 57 first-degree relatives without FH (11-61 years old). Carotid-femoral PWV was determined by SphygmoCor (AtCor, Australia). The parameters of carotid stiffness ß-index, Peterson elastic modulus and local PWV were assessed with regard to the common carotid artery at a distance of 1cm from the bifurcation (AlokaProsound Alpha7, Japan). RESULTS: FH patients showed significantly higher ß-index (6.3(4.8-8.2) vs. 5.2(4.2-6.4), p = 0.005), Ep (78(53-111) kPa vs. 62(48-79) kPa, p = 0.006), local PWV (5.4(4.5-6.4) m/c vs. 4.7(4.2-5.4) m/c, p = 0.005), but comparable values of carotid-femoral PWV (6.76(7.0-7.92) m/c vs. 6.48(6.16-7.12) m/c, p = 0.138). Carotid arteries and the aorta stiffened with age in patients with FH, but after 30 years, carotid arteries stiffened more significantly than the aorta. CONCLUSIONS: Our study demonstrated that treatment-naive patients with FH had stiffer carotid arteries than their relatives, but showed no difference in aortic stiffness. We also found out that the rate of reduction of elasticity of the aorta and carotid arteries in FH patients varies: it is observed earlier in carotid arteries than in the aorta.

Ultrasound markers that describe plaques are more sensitive than mean intima-media thickness in patients with familial hypercholesterolemia.

A widely adopted ultrasound surrogate marker for predicting cardiovascular risk is mean intima-medial thickness (mean-IMT). There are, however, certain limitations to this methodology. We compared the severity of carotid atherosclerosis in adult patients with high cardiovascular risk (patients with familial hypercholesterolemia [FH] and without previous statin treatment) and in their adult FH-free first-degree relatives using not only mean-IMT, but also maximum-IMT, plaque number, plaque score and percent area stenosis. Mean-IMT has not differed in both groups (0.64 ± 0.18 mm vs. 0.58 ± 0.13 mm in the control group, p = 0.349). Maximum-IMT (0.99 ± 0.35 vs. 0.76 ± 0.19, p = 0.0057), plaque number (3 ± 3 vs. 1 ± 2, p = 0.0009), plaque score (5.14 ± 4.97 mm vs. 1.58 ± 3.09 mm, p = 0.0009) and percent area stenosis (38% ± 22% vs. 12% ± 20%, p = 0.0004) were significantly higher for FH patients than for their relatives. We have demonstrated that plaque number, plaque score and percent area stenosis markers were more sensitive than mean-IMT for cardiovascular risk estimation in patients with familial hypercholesterolemia.