Evidence map›Paper›PMID 35972638›Full record

ReviewCurrent cardiology reports2022

Ischemic Cardiomyopathy and Heart Failure After Acute Myocardial Infarction.

Marco Giuseppe Del Buono, Francesco Moroni, Rocco Antonio Montone, Lorenzo Azzalini, Tommaso Sanna, Antonio Abbate

Open access · hybridAbstract readReview
In one paragraph

Review in Current cardiology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 2 pooled it
23.3field-weighted citation impact, top 1% of its field
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

106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 157 citations in OpenAlex.

  1. Pooled it
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  3. Effect of Nicotinamide Adenine Dinucleotide on Heart Failure Caused by Ischemic Cardiomyopathy: A Randomized, Placebo-Controlled Trial.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2026
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46 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 3 countries.

Marco Giuseppe Del BuonoDepartment of Cardiovascular Medicine, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo Agostino Gemelli, 1, 00168, Rome, Italy. marcodelbuono@hotmail.it.ORCID 0000-0002-7483-6164
Francesco MoroniBerne Cardiovascular Research Center, University of Virginia, Charlottesville, VA, USA.
Rocco Antonio MontoneDepartment of Cardiovascular Medicine, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo Agostino Gemelli, 1, 00168, Rome, Italy.
Lorenzo AzzaliniDivision of Cardiology, Department of Medicine, University of Washington, Seattle, WA, USA.
Tommaso SannaDepartment of Cardiovascular Medicine, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo Agostino Gemelli, 1, 00168, Rome, Italy.
Antonio AbbateBerne Cardiovascular Research Center, University of Virginia, Charlottesville, VA, USA.
Agostino Gemelli University Polyclinic · ITUniversity of Virginia · USUniversità Cattolica del Sacro Cuore · ITUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewIschemic cardiomyopathy refers to systolic left ventricular dysfunction in the setting of obstructive coronary artery disease and represents the most common cause of heart failure worldwide. It is often the combination of an irreversible loss of viable mass following an acute myocardial infarction (AMI) with a dysfunctional, but still viable, myocardium in the context of a chronically reduced myocardial blood flow and reduced coronary reserve. Medical treatments aiming at modulating neurohumoral response and restoring blood flow to the ischemic cardiomyocytes were shown to dramatically abate the occurrence of ventricular dysfunction and adverse remodeling in ischemic cardiomyopathy. RECENT

findingsNovel therapeutic approaches, such as mechanical unloading and modulation of the inflammatory response, appear to be promising. Furthermore, the understanding of the mechanisms by which, despite optimal treatment, heart failure ensues after AMI, with or without adverse remodeling and systolic dysfunction, is a critical step in the search for novel ways to tackle heart failure risk beyond preservation of left ventricular volumes and systolic function. In this review article, we explore the principal pathophysiological mechanisms and pathways of heart failure in ischemic cardiomyopathy, therapeutic opportunities, and knowledge gaps in this area.

Indexed as

CardiomyopathiesHeart FailureMyocardial InfarctionMyocardial IschemiaVentricular Dysfunction, LeftHumansCoronary artery diseaseHeart failureHFrEFIschemic cardiomyopathyMyocardial infarctionRemodeling

Identifiers

PMID35972638
PMCPMC9556362
OpenAlexW4291972524

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.