Global longitudinal LA epsilon/SR parameters determined by 2D speckle tracking echocardiography are feasible and reproducible indices for the evaluation of LA function.

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The purpose of this study was to evaluate the effects of aroma massage applied to middle-aged women with hypertension. The research study had a nonequivalent control group, nonsynchronized design to investigate the effect on home blood pressure (BP), ambulatory BP, and sleep. The hypertensive patients were allocated into the aroma massage group (n = 28), the placebo group (n = 28), and the no-treatment control group (n = 27). To evaluate the effects of aroma massage, the experimental group received a massage with essential oils prescribed by an aromatherapist once a week and body cream once a day. The placebo group received a massage using artificial fragrance oil once a week and body cream once a day. BP, pulse rate, sleep conditions, and 24-hour ambulatory BP were monitored before and after the experiment. There was a significant difference in home systolic blood pressure (SBP) (F = 6.71, P = 0.002) between groups after intervention. There was also a significant difference in SBP (F = 13.34, P = 0.001) and diastolic blood pressure (DBP) (F = 8.46, P = 0.005) in the laboratory between aroma massage and placebo groups. In sleep quality, there was a significant difference between groups (F = 6.75, P = 0.002). In conclusion, aroma massage may help improve patient quality of life and maintain health as a nursing intervention in daily life.

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In vascular smooth muscle cells, reactive oxygen species (ROS) were known to mediate platelet-derived growth factor (PDGF)-induced cell proliferation and NADH/NADPH oxidase is the major source of ROS. NADH/NADPH oxidase is controlled by rac1 in non-phagocytic cells. In this study, we examined whether the inhibition of rac1 by adenoviral-mediated gene transfer of a dominant negative rac1 gene product (Ad.N17rac1) could reduce the proliferation of rat aortic vascular smooth muscle cells (RASMC) stimulated by PDGF via decreasing intracellular ROS. RASMC were stimulated by PDGF (80 ng/mL) with or without N-acetylcysteine 1 mM or infected with 100 mutiplicity of infection of Ad.N17rac1. Intracellular ROS levels were measured at 12 hr using carboxyl-2', 7'-dichlorodihydrofluorescein diacetate confocal microscopy. At 72 hr, cellular proliferation was evaluated by cell number counting and XTT assay. Compared with control, ROS levels were increased by 2-folds by PDGF. NAC and Ad.N17rac1 inhibited PDGF-induced increase of ROS by 77% and 65%, respectively. Cell number was increased by PDGF by 1.6-folds compared with control. NAC and Ad.N17rac1 inhibited PDGF-induced cellular growth by 45% and 87%, respectively. XTT assay also showed similar results. We concluded that inhibition of rac1 in RASMCs could reduce intracellular ROS levels and cellular proliferation induced by PDGF.

Morphologic changes of small-sized post-stent malapposition have not been sufficiently evaluated. We investigated serial changes of minimal post-stent malapposition with a follow-up optical coherence tomography (OCT) study. Post-stent OCT and intravascular ultrasound (IVUS) and follow-up OCT were performed in 26 patients with minimal post-stent malapposition. Serial changes of number and percent of malapposition struts, and mean extra-stent malapposition area were measured in OCT analysis. Zotarolimus-eluting stent (ZES), sirolimus-eluting stent (SES), and paclitaxel-eluting stent (PES) were deployed in 17, 7 and 2 patients, respectively. Mean durations of the follow-up OCT study were 5.7 ± 3.0 months. The minimal post-stent malapposition cannot be detected by the IVUS, but be visualized with an OCT examination. According to different drug-eluting stents, malapposed stent struts were defined as the struts with detachment from the vessel wall ≥160 μm for SES, ≥130 μm for PES, and ≥110 μm for ZES. The percent of malapposition struts significantly decreased from 12.2 ± 11.0% post-stent to 1.0 ± 2.2% follow-up (P < 0.001). There was a significant decrease in the mean extra-stent malapposition area from 0.35 ± 0.16 mm(2) post-stent to 0.04 ± 0.11 mm(2) follow-up (P < 0.001). Complete disappearance of stent malapposition was also observed in 22 (85%) patients. In conclusion, minimal stent malapposition which is not detectable by IVUS may disappear or decrease in follow-up OCT evaluation.

Renin-angiotensin system (RAS) blockers have shown clinical outcomes superior to those of the beta (β)-blocker atenolol, despite similar reductions in the peripheral blood pressure (BP), perhaps because of different impacts on central hemodynamics. However, few comparative studies of RAS blockers and newer vasodilating β-blockers have been performed. We compared the central hemodynamic effects of losartan and carvedilol in a prospective, randomized, open, blinded end point study. Of the 201 hypertensive patients enrolled, 182 (49.6±9.9 years, losartan group=88 and carvedilol group=94) were analyzed. Carotid-femoral pulse wave velocity (cfPWV), aortic augmentation index (AIx), AIx corrected for a heart rate (HR) of 75 beats per minute (AIx@HR75) and central BP were measured noninvasively at baseline and after a 24-week treatment regimen with losartan or carvedilol. After 24 weeks, there were no between-group differences in the brachial BP, cfPWV, AIx@HR75 or central BP changes, except for a more favorable AIx effect with losartan. The changes in all measured metabolic and inflammatory parameters were also not significantly different between the two groups, except for uric acid. Losartan and carvedilol showed generally comparable effects on central hemodynamic indices, metabolic profile, inflammatory parameters and peripheral arterial pressure with a 24-week treatment.

Background and ObjectivesWhen monotherapy is inadequate for blood pressure control, the next step is either to continue monotherapy in increased doses or to add another antihypertensive agent. However, direct comparison of double-dose monotherapy versus combination therapy has rarely been done. The objective of this study is to compare 10 mg of amlodipine with an amlodipine/valsartan 5/160 mg combination in patients whose blood pressure control is inadequate with amlodipine 5 mg.Subjects and MethodsThis study was conducted as a multicenter, open-label, randomized controlled trial. Men and women aged 20-80 who were diagnosed as having hypertension, who had been on amlodipine 5 mg monotherapy for at least 4 weeks, and whose daytime mean systolic blood pressure (SBP) ≥135 mmHg or diastolic blood pressure (DBP) ≥85 mmHg on 24-hour ambulatory blood pressure monitoring (ABPM) were randomized to amlodipine (A) 10 mg or amlodipine/valsartan (AV) 5/160 mg group. Follow-up 24-hour ABPM was done at 8 weeks after randomization.ResultsBaseline clinical characteristics did not differ between the 2 groups. Ambulatory blood pressure reduction was significantly greater in the AV group compared with the A group (daytime mean SBP change: -14±11 vs. -9±9 mmHg, p<0.001, 24-hour mean SBP change: -13±10 vs. -8±8 mmHg, p<0.0001). Drug-related adverse events also did not differ significantly (A:AV, 6.5 vs. 4.5 %, p=0.56).ConclusionAmlodipine/valsartan 5/160 mg combination was more efficacious than amlodipine 10 mg in hypertensive patients in whom monotherapy of amlodipine 5 mg had failed.