Beeta-adrenoblokaatorid arteriaalse hüpertensiooni ravis

Beeta-adrenoblokaatorid on kroonilise südamepuudulikkuse, ägeda müokardiinfarkti ja kodade virvendusarütmia ravi nurgakivid (1). Ehkki arteriaalse hüpertensiooni ravis on neid kasutatud üle poole sajandi, vaieldakse jätkuvalt selle üle, kas nad peaksid tüsistumata primaarse hüpertensiooni esmavaliku ravimite arsenali kuuluma või mitte. Viimase aja teadusuuringutes on näidatud, et BBd ei hoia kardiovaskulaarsündmusi, eeskätt insulti ära niisama hästi nagu teised hüpertensiooniravimite klassid (2, 3). Need uuringud on valdavalt tehtud atenolooliga, kuid kuna BBd on farmakoloogiliselt heterogeenne ravimiklass, ei pruugi tegemist olla klassiefektiga (4). Artiklis on antud ülevaade BBde farmakodünaamikast ja -kineetikast ning selgitatud uuematele uuringutele toetudes, miks hüpertensiooni käsitlusjuhendites BBde kasutamissoovitused erinevad. BBde esindajatest ja kõrvaltoimetest saab täpsemalt lugeda Eesti Arstis varem ilmunud artiklist (5). Artikli eesmärk on hõlbustada teadmistepõhist BBde kasutamist arteriaalse hüpertensiooni ohjamiseks. Eesti Arst 2018; 97(4):204–212 &nbsp

Tööalaste õiguste laiendamine iseseisvale lepingupartnerile

https://www.ester.ee/record=b5360991*es

Vastupidavustreening – kas rohkem on parem?

Arvestades vastupidavustreeningu kasvavat populaarsust ning treeningukoormuste suurenemist harrastajate seas, muutub üha aktuaalsemaks küsimus treeningu mõjust tervisele. Viimase kümne aasta teadusuuringutes on viidatud suuremahulise vastupidavustreeningu (näiteks pikamaajooksu, ­suusatamise ja ­jalgrattaspordi) võimalikule ebasoodsale mõjule südame­veresoonkonnale, mistõttu on selle kasulikkus tervisele küsimärgi alla sattunud. Artiklis on antud ülevaade suuremahulise vastupidavustreeningu mõjust südame­veresoonkonna tervisele eeskätt tervetel täiskasvanud harrastussportlastel

Three families with mild PMM2-CDG and normal cognitive development

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Three families with mild PMM2-CDG and normal cognitive development

Congenital disorders of glycosylation (CDG) are caused by defective glycosylation of proteins and lipids. PMM2-CDG is the most common subtype among the CDG. The severity of PMM2-CDG is variable. Patients often have a recognizable phenotype with neurological and multisystem symptoms that might cause early death. We report six patients from three families who are diagnosed with a clinically mild PMM2-CDG and have normal cognitive development. All these patients had delayed gross motor skills with mild-to-moderate neurological findings. Cerebellar hypoplasia was detected in all siblings for whom brain MRI was performed. In 5/6 children the Wechsler Intelligence Scale for Children (WISC) showed normal cognitive development with full scale IQ scores ranging from borderline to average. Four patients were diagnosed with PMM2-CDG at the age of 8 years or later as their neurological symptoms were quite mild and they had been able to participate in regular school programs. We report patients with p.Val231Met/p.Arg239Trp and p.Ile120Thr/p.Gly228Cys genotypes which may cause milder variants of PMM2-CDG.status: publishe

Atenolol’s Inferior Ability to Reduce Central vs Peripheral Blood Pressure Can Be Explained by the Combination of Its Heart Rate-Dependent and Heart Rate-Independent Effects

Objective. Whether the inferior ability of atenolol to reduce central (aortic) compared to peripheral (brachial) blood pressure (BP) is related to its heart rate (HR)-dependent or -independent effects, or their combination, remains unclear. To provide further mechanistic insight into this topic, we studied the acute effects of atenolol versus nebivolol and ivabradine on systolic blood pressure amplification (SBPA; peripheral systolic BP minus central systolic BP) in a model of sick sinus syndrome patients with a permanent dual-chamber cardiac pacemaker in a nonrandomized single-blind single-group clinical trial. Methods. We determined hemodynamic indices noninvasively (Sphygmocor XCEL) before and at least 3 h after administration of oral atenolol 50 or 100 mg, nebivolol 5 mg, or ivabradine 5 or 7.5 mg during atrial pacing at a low (40 bpm), middle (60 bpm), and high (90 bpm) HR level in 25 participants (mean age 65.5 years, 12 men). Results. At the low HR level, i.e., when the drugs could exert their HR-dependent and HR-independent effects on central BP, only atenolol produced a significant decrease in SBPA (mean change 0.74 ± 1.58 mmHg (95% CI, 0.09–1.40; P=0.028)), indicating inferior central vs peripheral systolic BP change. However, we observed no significant change in SBPA with atenolol at the middle and high HR levels, i.e., when HR-dependent mechanisms had been eliminated by pacing. Conclusion. The findings of our trial with a mechanistic approach to the topic imply that the inferior ability of atenolol to reduce central vs peripheral BP can be explained by the combination of its heart rate-dependent and -independent effects. This trial is registered with NCT03245996