Evidence map›Paper›PMID 42758371›Full record

ReviewThe Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology2026

An integrated overview of acute heart failure: a narrative review of pathophysiological mechanisms and contributing factors.

Mohammadjavad Sotoudeheian, Mohammad Moradi, Mohammad Pirhayati, Seyed-Mohamad-Sadegh Mirahmadi, Reza Azarbad, Mohammad Sedigh Dakkali, Mehdi Taghizadeh, Hamidreza Pazoki Toroudi

Abstract readReview
In one paragraph

Review in The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Mohammadjavad SotoudeheianPhysiology Research Center, Iran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0001-7181-2944
Mohammad MoradiSchool of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Mohammad PirhayatiSchool of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0002-2619-3731
Seyed-Mohamad-Sadegh MirahmadiSchool of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Reza AzarbadCellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.
Mohammad Sedigh DakkaliSchool of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Mehdi TaghizadehShahid Madani Hospital, Tabriz University of Medical Sciences, Tabriz, Iran.
Hamidreza Pazoki ToroudiPhysiology Research Center, Iran University of Medical Sciences, Tehran, Iran. pazoki1970@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute heart failure (AHF) is a significant cardiovascular syndrome characterized by either new-onset heart failure (HF) or acutely decompensated heart failure (ADHF), typically presenting with systemic and pulmonary congestion. The European Society of Cardiology has reinforced the importance of early guideline-directed medical therapy (GDMT) initiation and individualized decongestive strategies. This article explores current knowledge of AHF pathophysiology. The simplified hemodynamic paradigm previously used to explain AHF has been replaced over the past few decades by a more complex network of interacting mechanisms. MAIN TEXT: The clinical presentation of AHF reflects a heterogeneous combination of cardiac abnormalities and systemic pathophysiological processes rather than a single disease entity. Despite overlapping clinical presentations, AHF arises from diverse underlying conditions and pathophysiological mechanisms. Left ventricular systolic or diastolic dysfunction elevates filling pressures, contributing to increased preload and afterload, which in turn promotes pulmonary congestion. End-organ dysfunction may result from the combined effects of venous congestion, impaired perfusion, and neurohormonal and inflammatory activation. Despite advances, limited progress in acute management may contribute to persistently poor outcomes in AHF patients.

conclusionInitial management of AHF commonly includes intravenous diuretics for patients with congestion, while vasodilators and other therapies are selected according to congestion status, perfusion, blood pressure, hemodynamic profile, clinical phenotype, and the predominant underlying pathophysiological mechanism. This review examines pathophysiological processes contributing to AHF onset and progression, highlighting clinical implications and therapeutic targets.

Indexed as

Fluid shiftsHeart failureNeurohormonesPrimary hypertension

Identifiers

PMID42758371
PMCPMC13589015

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.