Evidence map›Paper›PMID 28439851›Full record

ReviewCurrent cardiology reports2017

Exploring the Pathophysiology of Takotsubo Cardiomyopathy.

Wengen Chen, Vasken Dilsizian

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current cardiology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Coronavirus Disease 2019 and Takotsubo Syndrome.Reviews in cardiovascular medicine · 2022
    Review
  3. Review
  4. The role of adrenergic and muscarinic receptors in stress-induced cardiac injury.Pflugers Archiv : European journal of physiology · 2021
    Article
  5. Article
  6. Stress cardiomyopathy associated with vasodilator stress testing.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2020
    Article
  7. Stunned and Hibernating Myocardium: Where Are We Nearly 4 Decades Later?Journal of the American Heart Association · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
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

2 authors at 1 institution in 1 country.

Wengen ChenDepartment of Diagnostic Radiology and Nuclear Medicine, University of Maryland School of Medicine, 22 S. Greene street, Baltimore, MD, 21201, USA. wchen5@umm.edu.
Vasken DilsizianDepartment of Diagnostic Radiology and Nuclear Medicine, University of Maryland School of Medicine, 22 S. Greene street, Baltimore, MD, 21201, USA.
University of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThe purpose of this review is to explore the pathophysiology of Takotsubo cardiomyopathy by appraising the interplay between myocardial perfusion, function, metabolism, and, particularly, sympathetic innervation. RECENT

findingsA number of hypotheses have been proposed to explain the pathogenesis of Takotsubo cardiomyopathy, which include (1) catecholamine cardiac toxicity, (2) myocardial sympathetic innervation disruption, (3) coronary vasospasm, (4) myocardial microvascular dysfunction, and (5) aborted myocardial infarction. These proposals are primarily derived from findings of nuclear myocardial perfusion, metabolism, and cardiac sympathetic innervation imaging. Although data in the literature are not necessarily uniform, the two most plausible working postulates for explaining the phenomenon are (1) regional myocardial stunning (due to coronary vasospasm, microvascular dysfunction, or aborted myocardial infarction) and (2) cardiac sympathetic innervation disruption or toxicity. Current data suggest that disturbances of both coronary circulation and neural innervation are associated with the Takotsubo cardiomyopathy: myocardial stunning from transient ischemic attack and sympathetic innervation disruption. It remains to be determined, however, whether the observed leading mechanistic explanations that have gained momentum are merely the sequelae of the disease rather than its primary etiology.

Indexed as

Coronary CirculationCoronary VasospasmHeartHumansMicrovesselsMyocardial InfarctionMyocardial StunningSympathetic Nervous SystemTakotsubo Cardiomyopathy123I-metaiodobenzylguanidineCardiac sympathetic imagingMyocardial metabolic imagingStunned myocardiumTakotsubo cardiomyopathy

Identifiers

PMID28439851
OpenAlexW2608456820

What OpenQuestion 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 OpenQuestion graph.