Evidence map›Paper›PMID 42172265›Full record

ArticlePloS one2026

Hemodynamic effects of prophylactic amiodarone assessed by pressure-volume analysis in anesthetized female pigs in sinus rhythm-An exploratory study.

Laura Svanekjær, Emma Illum, Peter H Frederiksen, Louise Linde, Anika Klein, Karoline Korsholm Jeppesen, Ann Banke, Sarah Holle, Lisette O Jensen, Henrik Schmidt and 3 more

Abstract read
In one paragraph

Article in PloS one, 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
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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

13 authors.

Laura SvanekjærDepartment of Cardiothoracic Anaesthesiology, Odense University Hospital, Odense, Denmark.ORCID https://orcid.org/0009-0000-1235-6969
Emma IllumDepartment of Cardiology, Odense University Hospital, Odense, Denmark.
Peter H FrederiksenDepartment of Cardiology, Odense University Hospital, Odense, Denmark.
Louise LindeDepartment of Cardiology, Odense University Hospital, Odense, Denmark.
Anika KleinDepartment of Cardiology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Karoline Korsholm JeppesenDepartment of Cardiology, Odense University Hospital, Odense, Denmark.
Ann BankeDepartment of Cardiology, Odense University Hospital, Odense, Denmark.ORCID https://orcid.org/0000-0002-1036-580X
Sarah HolleDepartment of Cardiology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.ORCID https://orcid.org/0000-0001-8426-617X
Lisette O JensenDepartment of Cardiology, Odense University Hospital, Odense, Denmark.ORCID https://orcid.org/0000-0002-4838-2429
Henrik SchmidtDepartment of Cardiothoracic Anaesthesiology, Odense University Hospital, Odense, Denmark.
Jens F LassenDepartment of Cardiology, Odense University Hospital, Odense, Denmark.
Jacob E MøllerDepartment of Cardiology, Odense University Hospital, Odense, Denmark.ORCID https://orcid.org/0000-0003-2873-5845
Hanne B RavnDepartment of Cardiothoracic Anaesthesiology, Odense University Hospital, Odense, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIntravenous amiodarone is used for acute management of severe arrhythmias and can cause hypotension. However, amiodarone's direct hemodynamic and myocardial effects during sinus rhythm are not well characterized.

methodsTwenty-five anesthetized female pigs (75-80 kg) received a 300 mg intravenous bolus amiodarone over 30 minutes. To assess hemodynamic effects, animals were instrumented with a left ventricular conductance catheter, a pulmonary artery catheter, a carotid artery Doppler flow probe, and a renal vein catheter. Data were recorded at baseline, after 15 and 30 minutes and presented as median with interquartile ranges.

resultsAmiodarone reduced systolic and mean arterial blood pressure by 12% (p < 0.001) after 30 minutes infusion, primarily driven by 24% reduction in cardiac output due to combined deceased heart rate (87 (79; 99) beats per minute (bpm) to 72 (62; 81) bpm, p < 0.001) and stroke volume (69 (64; 79) mL to 64 (48; 73) mL, p = 0.004). End-systolic elastance (EES) decreased (0.54 (0.33; 0.63) mmHg/mL to 0.43 (0.29; 0.51) mmHg/mL, p < 0.001), while systemic vascular resistance and arterial elastance (EA) remained unchanged, resulting in an increased EA/EES ratio from 2.45 (2.01;3.53) to 3.26 (2.55; 4.30) (p < 0.001). This impaired cardiac function led to reduced carotid artery blood flow and renal perfusion pressure.

conclusionInfusion of 300 mg amiodarone intravenously in anesthetized pigs in sinus rhythm impaired left ventricular contractility and caused ventriculo-arterial decoupling with increased EA/EES ratio. This led to reduced cardiac output, blood pressure, and reduced carotid- and renal blood flow.

Indexed as

AmiodaroneAnti-Arrhythmia AgentsHemodynamicsAnesthesiaAnimalsBlood PressureCardiac OutputFemaleHeart RateStroke VolumeSwineAmiodaroneAnti-Arrhythmia Agents

Identifiers

PMID42172265
PMCPMC13196969

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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.