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7%) by Thomson Grading System of Micromedex. All of them have been proved by literature evidence of level 1 to 4, in which 19 (82.6%) by Level 1 evidence, 21 (91.3%) by Level 1 to 2 evidence and 2 (8.7%) only by level 3 to 4 evidence. This can provide a theoretical basis to clinicians in prescribing. Our next work is to perfect some details about evidence assessment to improve the reliability.

Implant rates for cardiac implantable electronic devices (CIED), including permanent pacemakers (PPM) and implantable cardioverter defibrillators (ICD), have increased globally in recent decades. This is the first national study providing a contemporary analysis of national CIED implant trends by sex-specific age groups over an extended period.

Patient characteristics and device type were identified for ten years (2009 to 2018) using procedure coding in the National Minimum Datasets, which collects all New Zealand (NZ) public hospital admissions. CIED implant rates represent implants/million population.

New PPM implant rates increased by 4.6%/year (p<0.001), increasing in all age groups except patients <40 years. Males received 60.1% of new PPM implants, with higher implant rates across all age groups compared to females. The annual increase in age-standardised implant rates was similar for males and females (3.4% vs 3.0%, p=0.4). By 2018 the overall PPM implant rate was 538/million. New ICD implant rates increased by 4.2%/year (p<0.001), increasing in all age groups except patients <40 and ≥80 years. Males received 78.1% of new ICD implants, with higher implant rates across all age groups compared to females. The annual increase in age-standardised implant rates was higher in males compared to females (3.5% vs 0.7%, p<0.001). By 2018 the overall ICD implant rate was 144/million.

CIED implant rates have increased steadily in NZ over the past decade but remain low compared to international benchmarks. Males had substantially higher CIED implant rates compared to females, with a growing gender disparity in ICD implant rates. This article is protected by copyright. All rights reserved.

CIED implant rates have increased steadily in NZ over the past decade but remain low compared to international benchmarks. Males had substantially higher CIED implant rates compared to females, with a growing gender disparity in ICD implant rates. This article is protected by copyright. All rights reserved.

The so-called "thunderstorm asthma" (TA) is an uncommon but dramatic outbreak of asthma attacks occurring during a thunderstorm in the pollen and moulds season. Mechanisms which make the pollen able to enter the deeper airways and provoke severe asthma symptoms are still unclear.

To test the hypothesis that sub-pollen particles (SPPs) originated from the rupture by an osmotic shock of pollen associated with TA contain allergens.

After hydration, SPPs released from pollen grains of grass, pellitory, olive, cypress, ragweed and birch were isolated and determined by microscopy. Allergens were determined by in vitro ELISA inhibition tests indirectly using the sera from 10 polyreactive patients. An inhibition <50% was considered as negative, 50%-75% moderate and>75% complete.

The inhibition experiments showed that the SPPs from birch and cypress were unable to inhibit serum IgE reactivity to Bet v 1 and Cup a 1, respectively. Ragweed SPPs inhibited ragweed pollen extract and Amb a 1 by 75.8±0.11% and 81.2±0.15%, respectively. Olive and pellitory SPPs retained almost the whole IgE-binding capability in all cases tested. Grass SPPs inhibited 32±0.06% of Lolium perenne Lol p 1 and 65% of Phleum pratense extracts, but results were highly variable for individual allergens (97.5%-0.03% for Phl p 2, 45.3±0.12% for Phl p 5, 24.7±0.22% for Phl p 6, and 38.3±0.2% for Phl p 1).

Inhibition experiments confirm the hypothesis that SSPs obtained after the osmotic shock of pollen involved in TA, namely grass, pellitory and olive tree pollen, contain allergens and therefore they can induce severe asthma attacks during thunderstorms.

Inhibition experiments confirm the hypothesis that SSPs obtained after the osmotic shock of pollen involved in TA, namely grass, pellitory and olive tree pollen, contain allergens and therefore they can induce severe asthma attacks during thunderstorms.

Tafamidis is an effective treatment for transthyretin amyloid cardiomyopathy (ATTR-CM) in the Tafamidis in Transthyretin Cardiomyopathy Clinical Trial (ATTR-ACT). While ATTR-ACT was not designed for a dose-specific assessment, further analysis from ATTR-ACT and its long-term extension study (LTE) can guide determination of the optimal dose.

In ATTR-ACT, patients were randomized (212) to tafamidis 80 mg, 20 mg, or placebo for 30 months. Patients completing ATTR-ACT could enrol in the LTE (with placebo-treated patients randomized to tafamidis 80 or 20 mg; 21) and all patients were subsequently switched to high-dose tafamidis. All-cause mortality was assessed in ATTR-ACT combined with the LTE (median follow-up 51 months). In ATTR-ACT, the combination of all-cause mortality and cardiovascular-related hospitalizations over 30 months was significantly reduced with tafamidis 80 mg (P=0.0030) and 20 mg (P=0.0048) vs. placebo. All-cause mortality vs. placebo was reduced with tafamidis 80 mg [Cox hazards model (95% confidence interval) 0.690 (0.487-0.979), P=0.0378] and 20 mg [0.715 (0.450-1.137), P=0.1564]. The mean (standard error) change in N-terminal pro-B-type natriuretic peptide from baseline to Month 30 was -1170.51 (587.31) (P=0.0468) with tafamidis 80 vs. 20 mg. see more In ATTR-ACT combined with the LTE there was a significantly greater survival benefit with tafamidis 80 vs. 20 mg [0.700 (0.501-0.979), P=0.0374]. Incidence of adverse events in both tafamidis doses were comparable to placebo.

Tafamidis, both 80 and 20 mg, effectively reduced mortality and cardiovascular-related hospitalizations in patients with ATTR-CM. The longer-term survival data and the lack of dose-related safety concerns support tafamidis 80 mg as the optimal dose.

ClinicalTrials.gov NCT01994889; NCT02791230.

ClinicalTrials.gov NCT01994889; NCT02791230.