RESUMEN
Tsunamis are triggered by sudden seafloor displacements, and usually originate from seismic activity at faults. Nevertheless, strike-slip faults are usually disregarded as major triggers, as they are thought to be capable of generating only moderate seafloor deformation; accordingly, the tsunamigenic potential of the vertical throw at the tips of strike-slip faults is not thought to be significant. We found the active dextral NW-SE Averroes Fault in the central Alboran Sea (westernmost Mediterranean) has a historical vertical throw of up to 5.4 m at its northwestern tip corresponding to an earthquake of Mw 7.0. We modelled the tsunamigenic potential of this seafloor deformation by Tsunami-HySEA software using the Coulomb 3.3 code. Waves propagating on two main branches reach highly populated sectors of the Iberian coast with maximum arrival heights of 6 m within 21 and 35 min, which is too quick for current early-warning systems to operate successfully. These findings suggest that the tsunamigenic potential of strike-slip faults is more important than previously thought, and should be taken into account for the re-evaluation of tsunami early-warning systems.
RESUMEN
BACKGROUND AND AIM: Calcidiol (vitamin D metabolite) plasma levels vary with sun exposure (SE). However, it is not known if SE influences its prognostic ability. We have studied the effect of SE on plasma levels of the components of mineral metabolism (calcidiol, fibroblast growth factor-23 [FGF-23], parathormone [PTH], and phosphate [P]) and on their prognostic value in patients with coronary artery disease (CAD). METHODS AND RESULTS: We studied prospectively 704 patients with stable CAD. Clinical variables and baseline calcidiol, FGF-23, PTH, and P plasma levels were assessed. We divided the population in two subgroups, according to the period of plasma extraction: High SE (HSE) (April-September) and low SE (LSE) (October-March). The outcome was the development of acute ischemic events (acute coronary syndrome, stroke, or transient ischemic attack), heart failure, or death. Mean follow-up was 2.15 ± 0.99 years. Calcidiol and P levels were higher in HSE group. In the whole population, calcidiol (HR = 0.84 for each 5 ng/ml increase, 95% CI = 0.71-0.99; p = 0.038) and FGF-23 (HR = 1.14 for each 100 RU/ml increase, 95% CI = 1.05-1.23; p = 0.009) were predictors of the outcome, along with age, hypertension, body-mass index, peripheral artery disease, and P levels. In the LSE subgroup, calcidiol (HR = 0.75; 95% CI = 0.57-0.99; p = 0.034) and FGF-23 (HR = 1.34; 95% CI = 1.13-1.58; p = 0.003) remained as predictors of the outcome. In the HSE group calcidiol and FGF-23 had not independent prognostic value. CONCLUSIONS: In patients with stable CAD, low calcidiol and high FGF-23 plasma levels predict an adverse prognosis only when the sample is obtained during the months with LSE. SE should be taken into account in the clinical practice.