Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (800 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A transient left ventricular apical dysfunction or ballooning accompanied by electrocardiographic (ECG) T wave inversions. This abnormality is associated with high levels of catecholamines, either administered or endogenously secreted from a tumor or during extreme stress.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Cardiomyopathy, Takotsubo; Tako-Tsubo Cardiomyopathy; Cardiomyopathy, Tako-Tsubo; Tako-Tsubo Cardiomyopathies; Tako Tsubo Cardiomyopathy; Tako-Tsubo Syndrome; Syndrome, Tako-Tsubo; Tako Tsubo Syndrome.
Where it fits in the MeSH classification
- Broader topics
- Cardiomyopathies; Ventricular Dysfunction, Left
Related concepts
- Catecholamines
Research landscape
PubMed indexes 5,079 records tagged with the MeSH heading “Takotsubo Cardiomyopathy” (counts retrieved 2026-10-29). 1,522 of them (30.0%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 3,119 records.
Reviews account for 672 records (13.2%) and meta-analyses for 46. Randomized controlled trials number 9 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 581 |
| 2010-2019 | 3,119 |
| 2020 onward | 1,522 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 672 | 13.2% |
| Meta-analyses | 46 | 0.9% |
| Randomized controlled trials | 9 | 0.2% |
Method: PubMed query "Takotsubo Cardiomyopathy"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Takotsubo Syndrome: Pathophysiology, Emerging Concepts, and Clinical Implications | 2022 | Review article Design not recorded in structured metadata | 305 | cc by PMID 35344411 · DOI · PMC7612566 |
| Cardiac macrophages regulate isoproterenol-induced Takotsubo-like cardiomyopathy | 2022 | Research article Design not recorded in structured metadata | 47 | cc by PMID 35132957 · DOI · PMC8855841 |
| Circulating microRNAs predispose to takotsubo syndrome following high-dose adrenaline exposure | 2022 | Research article Design not recorded in structured metadata | 46 | cc by PMID 34155498 · DOI · PMC9214785 |
| Takotsubo syndrome in the setting of cardiac pacing: A review of mechanistic and clinical perspectives | 2026 | Review article Design not recorded in structured metadata | 3 | cc by PMID 41857469 · DOI · PMC13002712 |
Takotsubo Syndrome: Pathophysiology, Emerging Concepts, and Clinical Implications [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Takotsubo syndrome is a condition characterized by acute transient left ventricular systolic dysfunction, which at presentation can be challenging to distinguish from acute myocardial infarction.
- Closing excerpt
- Only then can evidence-based management strategies be established to improve clinical outcomes of this potentially lethal condition.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (227 words)
Takotsubo syndrome is a condition characterized by acute transient left ventricular systolic dysfunction, which at presentation can be challenging to distinguish from acute myocardial infarction. Although previously thought to be a benign, self-limiting condition, recent studies have confirmed that patients with takotsubo syndrome have persistent subtle ongoing cardiac dysfunction, and many continue to have limiting symptoms despite restoration of left ventricular ejection fraction. Moreover, these patients have a substantial burden of morbidity and mortality, as well, with high rates of subsequent major adverse cardiovascular events that approach those of patients with acute coronary syndrome. The mechanisms behind this condition remain elusive. Despite substantial research, the medical community continues to have an incomplete understanding of its underlying pathogenesis and pathophysiology. Catecholamine-induced myocardial injury is the most established and well-known theory, but this does not explain all the clinical features and presentations of the condition, and numerous other pathways and abnormalities are emerging. Because of the poor understanding of its underlying pathophysiology, there is a lack of evidence-based interventions to treat the acute episode, to avoid recurrences, and to prevent major adverse cardiovascular events. This highlights the need for further research to gain a better understanding of the underlying pathophysiology to inform appropriate randomized controlled trials of interventions targeting the causative pathways. Only then can evidence-based management strategies be established to improve clinical outcomes of this potentially lethal condition.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35344411 · DOI · PMC7612566
Cardiac macrophages regulate isoproterenol-induced Takotsubo-like cardiomyopathy [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Takotsubo syndrome (TTS) is an acute, stress-induced cardiomyopathy that occurs predominantly in women after extreme physical and/or emotional stress.
- Closing excerpt
- Collectively, our findings identify macrophages as a critical regulator of TTS pathogenesis that can be targeted for therapeutic gain.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (194 words)
Takotsubo syndrome (TTS) is an acute, stress-induced cardiomyopathy that occurs predominantly in women after extreme physical and/or emotional stress. To date, our understanding of the molecular basis for TTS remains unknown and, consequently, specific therapies are lacking. Myocardial infiltration of monocytes and macrophages in TTS has been documented in clinical studies. However, the functional importance of these findings remains poorly understood. Here, we show that a single high dose of isoproterenol (ISO) in mice induced a TTS-like cardiomyopathy phenotype characterized by female predominance, severe cardiac dysfunction, and robust myocardial infiltration of macrophages. Single-cell RNA-Seq studies of myocardial immune cells revealed that TTS-like cardiomyopathy is associated with complex activation of innate and adaptive immune cells in the heart, and macrophages were identified as the dominant immune cells. Global macrophage depletion (via clodronate liposome administration) or blockade of macrophage infiltration (via a CCR2 antagonist or in CCR2-KO mice) resulted in recovery of cardiac dysfunction in ISO-challenged mice. In addition, damping myeloid cell activation by HIF1α deficiency or exposure to the immunomodulatory agent bortezomib ameliorated ISO-induced cardiac dysfunction. Collectively, our findings identify macrophages as a critical regulator of TTS pathogenesis that can be targeted for therapeutic gain.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35132957 · DOI · PMC8855841
Circulating microRNAs predispose to takotsubo syndrome following high-dose adrenaline exposure [3]
Abstract reading summary — source excerpts
- Opening excerpt
- AimsTakotsubo syndrome (TTS) is an acute heart failure, typically triggered by high adrenaline during physical or emotional stress.
- Closing excerpt
- Since these miRs have been associated with anxiety and depression, they could provide a mechanism whereby priming of the heart by previous stress causes an increased likelihood of TTS in the future.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (242 words)
AimsTakotsubo syndrome (TTS) is an acute heart failure, typically triggered by high adrenaline during physical or emotional stress. It is distinguished from myocardial infarction (MI) by a characteristic pattern of ventricular basal hypercontractility with hypokinesis of apical segments, and in the absence of culprit coronary occlusion. We aimed to understand whether recently discovered circulating biomarkers miR-16 and miR-26a, which differentiate TTS from MI at presentation, were mechanistically involved in the pathophysiology of TTS.Methods and resultsmiR-16 and miR-26a were co-overexpressed in rats with AAV and TTS induced with an adrenaline bolus. Untreated isolated rat cardiomyocytes were transfected with pre-/anti-miRs and functionally assessed. Ventricular basal hypercontraction and apical depression were accentuated in miR-transfected animals after induction of TTS. In vitro miR-16 and/or miR-26a overexpression in isolated apical (but not basal), cardiomyocytes produced strong depression of contraction, with loss of adrenaline sensitivity. They also enhanced the initial positive inotropic effect of adrenaline in basal cells. Decreased contractility after TTS-miRs was reproduced in non-failing human apical cardiomyocytes. Bioinformatic profiling of miR targets, followed by expression assays and functional experiments, identified reductions of CACNB1 (L-type calcium channel Cavβ subunit), RGS4 (regulator of G-protein signalling 4), and G-protein subunit Gβ (GNB1) as underlying these effects.ConclusionmiR-16 and miR-26a sensitize the heart to TTS-like changes produced by adrenaline. Since these miRs have been associated with anxiety and depression, they could provide a mechanism whereby priming of the heart by previous stress causes an increased likelihood of TTS in the future.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34155498 · DOI · PMC9214785
Takotsubo syndrome in the setting of cardiac pacing: A review of mechanistic and clinical perspectives [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Takotsubo syndrome (TTS) is a reversible form of acute cardiac syndrome usually arising in response to various emotional and physical stressors.
- Closing excerpt
- The present paper aims to focus on mechanistic and clinical implications of TTS due to cardiac pacing procedures including conventional permanent pacemaker implantation (PPI) and conduction system pacing (CSP) along with a particular emphasis on intraventricular mechanical factors as potential TTS triggers in this context.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (137 words)
Takotsubo syndrome (TTS) is a reversible form of acute cardiac syndrome usually arising in response to various emotional and physical stressors. TTS due to cardiac pacing has been an uncommon phenomenon mostly attributable to a variety of periprocedural conventional stressors including anxiety, pain and low cardiac output. Interestingly, intraventricular mechanical factors might also play a pivotal role in TTS evolution due to cardiac pacing. Notably, this phenomenon may be potentially underdiagnosed due to a variety of factors including atypical symptoms and masked electrocardiographic (ECG) changes potentially suggesting its higher incidence in clinical practice.The present paper aims to focus on mechanistic and clinical implications of TTS due to cardiac pacing procedures including conventional permanent pacemaker implantation (PPI) and conduction system pacing (CSP) along with a particular emphasis on intraventricular mechanical factors as potential TTS triggers in this context.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41857469 · DOI · PMC13002712
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article International Expert Consensus Document on Takotsubo Syndrome (Part I): Clinical Characteristics, Diagnostic Criteria, and Pathophysiology [5]
- Research article Current state of knowledge on Takotsubo syndrome: a Position Statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology [6]
- Research article International Expert Consensus Document on Takotsubo Syndrome (Part II): Diagnostic Workup, Outcome, and Management [7]
- Research article Pathophysiology of Takotsubo Syndrome [8]
- Research article Stress Cardiomyopathy Diagnosis and Treatment: JACC State-of-the-Art Review [9]
- Research article Pathophysiology of Takotsubo Syndrome: JACC State-of-the-Art Review [10]
References
- Singh T, Khan H, Gamble DT, Scally C, Newby DE, Dawson D. Takotsubo Syndrome: Pathophysiology, Emerging Concepts, and Clinical Implications. . 2022. PMID 35344411 · DOI · PMC7612566
- Liao X, Chang E, Tang X, Watanabe I, Zhang R, Jeong HW, et al.. Cardiac macrophages regulate isoproterenol-induced Takotsubo-like cardiomyopathy. . 2022. PMID 35132957 · DOI · PMC8855841
- Couch LS, Fiedler J, Chick G, Clayton R, Dries E, Wienecke LM, et al.. Circulating microRNAs predispose to takotsubo syndrome following high-dose adrenaline exposure. . 2022. PMID 34155498 · DOI · PMC9214785
- Yalta K, Ozkan U, Yetkin E. Takotsubo syndrome in the setting of cardiac pacing: A review of mechanistic and clinical perspectives. . 2026. PMID 41857469 · DOI · PMC13002712
- Ghadri JR, Wittstein IS, Prasad A, Sharkey S, Dote K, Akashi YJ, et al.. International Expert Consensus Document on Takotsubo Syndrome (Part I): Clinical Characteristics, Diagnostic Criteria, and Pathophysiology. Eur Heart J. 2018. PMID 29850871 · DOI · PMC5991216
- Lyon AR, Bossone E, Schneider B, Sechtem U, Citro R, Underwood SR, et al.. Current state of knowledge on Takotsubo syndrome: a Position Statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2016. PMID 26548803 · DOI
- Ghadri JR, Wittstein IS, Prasad A, Sharkey S, Dote K, Akashi YJ, et al.. International Expert Consensus Document on Takotsubo Syndrome (Part II): Diagnostic Workup, Outcome, and Management. Eur Heart J. 2018. PMID 29850820 · DOI · PMC5991205
- Pelliccia F, Kaski JC, Crea F, Camici PG. Pathophysiology of Takotsubo Syndrome. Circulation. 2017. PMID 28606950 · DOI
- Medina de Chazal H, Del Buono MG, Keyser-Marcus L, Ma L, Moeller FG, Berrocal D, et al.. Stress Cardiomyopathy Diagnosis and Treatment: JACC State-of-the-Art Review. J Am Coll Cardiol. 2018. PMID 30309474 · DOI · PMC7058348
- Lyon AR, Citro R, Schneider B, Morel O, Ghadri JR, Templin C, et al.. Pathophysiology of Takotsubo Syndrome: JACC State-of-the-Art Review. J Am Coll Cardiol. 2021. PMID 33602474 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.