Atorvastatin Treatment Is Associated With Less Augmentation of the Carotid Pressure Waveform in Hypertension A Substudy of the Anglo- Scandinavian Cardiac Outcome Trial (ASCOT)

Imperial College Healthcare NHS Trust, Londinium, England, United Kingdom
Hypertension (Impact Factor: 6.48). 08/2009; 54(5):1009-13. DOI: 10.1161/HYPERTENSIONAHA.109.130914
Source: PubMed


Hydroxymethylglutaryl-CoA reductase inhibitors (statins) reduce cardiovascular events in hypertensive subjects, but their effect on carotid BP, pressure augmentation, and wave reflection is unknown. We compared the effect of atorvastatin with placebo in a substudy of the lipid-lowering arm of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT-LLA). Hypertensive patients (n=142; age=43 to 79 years; 127 male) with total cholesterol < or = 6.5 mmol/L were randomized to atorvastatin 10 mg or placebo. Carotid BP and flow velocity were measured by tonometry and Doppler ultrasound. Augmentation index (carotid AI(x)) was calculated, and waveforms were separated into backward and forward components by wave intensity analysis. Brachial BP was similar in atorvastatin and placebo groups. Carotid AI(x) and augmentation pressure were significantly less in patients randomized to atorvastatin (mean [SD]: 21.7 [12.1] versus 25.9 [10.3] %; P=0.027 and 10.2 [6.5] versus 13.1 [6.6] mm Hg; P=0.016, respectively), and atorvastatin treatment was associated with significantly less wave reflection from the body. Carotid systolic BP was slightly lower in the atorvastatin group, but there was a statistically significant interaction between lipid-lowering and antihypertensive regimen with lower carotid systolic BP in patients randomized to amlodipine-based therapy and atorvastatin. Carotid wave velocity, timings of waves, and wave intensities did not differ significantly between atorvastatin and placebo groups. Atorvastatin treatment is associated with less augmentation of the carotid BP waveform and less wave reflection from the body. This could contribute to the reduction in risk of cardiovascular events by statins.

Full-text preview

Available from:
  • Source
    • ". Publication bias indicators for the outcome of ΔSBP (3A), ΔDBP (3B), and ΔDBP after excluding one large study (3C) in the studies considering statins compared to placebo therapy in normotensive patients. [23] [24]), and single gender studies [21], as well as trials with diabetic [24] [27] [29] and non-diabetic patients [21] [23] [32] [34] [36] were excluded from the analysis (p = 0.40, p = 0.34, p = 0.39, p = 0.52, and p = 0.75, respectively) (Table 2). The lack of efficacy of statins was also observed when analyzing only trials with the duration of therapy longer than 2 years [23] [24] (the weighted mean difference was −0.11 with 95% CI = −1.27 to 1.05; p = 0.86). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective: The aim of this meta-analysis was to investigate whether statin therapy is associated with blood pressure (BP)-lowering in patients with or without hypertension. Background: The beneficial effects of statins on the cardiovascular system may in part be related to effects beyond lipid-lowering. It has been suggested that statins may reduce BP; however the available data are still ambiguous and often conflicting. Methods: Data from Scopus, PubMed, Web of Science, and the Cochrane Central Register of Controlled Trials for the years 1966-January 2012 were searched for studies that investigated the effect of statins on BP in normotensive or in hypertensive subjects. We included all randomized controlled clinical trials that investigated this effect. Changes in systolic and diastolic BP were the key outcomes of interest. Results: The final analysis included 18 trials and 5628 subjects (4692 normotensive and 936 hypertensive patients) randomized to receive either statins or placebo. The weighted mean difference of systolic (Delta SBP) and diastolic blood pressure (Delta DBP) in normotensive patients for the 11 statin trials included were 0.03 (95% CI: -0.95-1.02; p = 0.95) and -0.28 (95% CI: -0.80-0.24; p = 0.29), respectively. For hypertensive patients treated with statins (8 trials) the weighted mean difference of Delta SBP and Delta DBP were 1.45 (95% CI: -0.49-3.39; p = 0.14) and -1.32 (95% CI: -3.93-1.28; p = 0.32) respectively. Conclusions: Despite previous suggestions statin therapy in normotensive or hypertensive patients does not lead to significant reductions in systolic or diastolic BP.
    International Journal of Cardiology 10/2013; 168(3):2816-2824. DOI:10.1016/j.ijcard.2013.03.068 · 4.04 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: A conventional p^{+}-n (or n^{+}-p ) planar avalanche photodiode with a 10<sup>-4</sup>cm<sup>2</sup>active area has ∼2.5 × 10<sup>-4</sup>cm<sup>2</sup>total area because of its protecting guard ring and has a series resistance of ∼50 to 100 ohms. For narrow-band applications, multiplications greater than 10 are necessary to equal the available output power of a conventional nonavalanching p-i-n photodiode. In broad-band applications, significant multiplications are necessary to compete favorably with the p-i-n when the active area is less than 10<sup>-4</sup>cm<sup>2</sup>or when the signal frequency is > 1 GHz. A p-n^{+} planar structure is discussed that eliminates the need for a guard ring because positive junction curvature occurs on the high-resistivity side. The p-n^{+} diodes can be designed to have resistances (R s ∼2 ohms), capacitances (C < 1 pf), and RC cutoff frequencies (f co >100 GHz) equivalent to those of the p-i-n and to have uniform multiplication as well. Closer array spacings can be achieved than with the guard ring structure, as well as higher effective quantum efficiencies in the avalanche mode. Practical realization of the p-n^{+} structure has been achieved in silicon by a combination of epitaxial and doped-oxide processing. Seven-mil-diameter junctions with high breakdown voltage (110 V) and uniform avalanche properties have been constructed.
    IEEE Transactions on Electron Devices 11/1968; 15(10-15):735 - 741. DOI:10.1109/T-ED.1968.16507 · 2.47 Impact Factor
  • Source

    Hypertension 09/2009; 54(5):958-9. DOI:10.1161/HYPERTENSIONAHA.109.137638 · 6.48 Impact Factor
Show more