ArticleHerz2015
[New therapy concepts for heart failure with preserved ejection fraction].
Article in Herz, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 2 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The management of patients with heart failure and preserved ejection fraction (HFpEF) remains challenging and requires an accurate diagnosis. Although currently no convincing therapy that can prolong survival in patients with HFpEF has been established, treatment of fluid retention, heart rate and control of comorbidities are important cornerstones to improve the quality of life and symptoms. In recent years many new therapy targets have been tested for development of successful interventional strategies for HFpEF. Insights into new mechanisms of HFpEF have shown that heart failure is associated with dysregulation of the nitric oxide-cyclic guanosine monophosphate-protein kinase (NO-cGMP-PK) pathway. Two new drugs are currently under investigation to test whether this pathway can be significantly improved by either the neprilysin inhibitor LCZ 696 due to an increase in natriuretic peptides or by the soluble guanylate cyclase stimulator vericiguat, which is also able to increase cGMP. In addition, several preclinical or early phase studies which are currently investigating new mechanisms for matrix, intracellular calcium and energy regulation including the role of microRNAs and new devices are presented and discussed.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.