ArticleEuropean heart journal2023
Takotsubo syndrome is a coronary microvascular disease: experimental evidence.
Article in European heart journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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.
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Who cites it
35 citing papers in PubMed, 67 citations in OpenAlex.
- Spontaneous Coronary Artery Dissection and Takotsubo Syndrome: Converging Mechanisms, Diagnostic Pitfalls, and a Unified Clinical Algorithm.Journal of clinical medicine · 2026Review
- Metformin as a potential therapeutic agent in broken heart syndrome: Targeting AMPK-dependent cardio-protection and microvascular function.Molecular biology reports · 2026Review
- Takotsubo syndrome: pathophysiological insights and innovations in patient care.Nature reviews. Cardiology · 2026Review
- Coronary Microvascular Dysfunction in Cardiomyopathies: Insights on Clinical and Prognostic Roles.Reviews in cardiovascular medicine · 2026Review
- [Rare cases of stress cardiomyopathy triggered by pulmonary embolism and reverse Takotsubo].Revista medica del Instituto Mexicano del Seguro Social · 2026Article
- Redox Regulation of Microvascular Physiology and Pathophysiology: Insights into Therapeutic Strategies and Limitations.Antioxidants & redox signaling · 2025Review
- Heart-Brain axis: is microvascular dysfunction the link between stroke and Takotsubo syndrome?The international journal of cardiovascular imaging · 2025Review
- Impaired Coronary Microcirculation and Myocardial Systolic Function: A Narrative Review on Non-Invasive Assessment in Cardiovascular Diseases.Life (Basel, Switzerland) · 2025Review
- NR3C1/GLMN-Mediated FKBP12.6 Ubiquitination Disrupts Calcium Homeostasis and Impairs Mitochondrial Quality Control in Stress-Induced Myocardial Damage.International journal of molecular sciences · 2025Article
- Transcriptome High-Throughput Sequencing Analysis of lncRNA and mRNA Expression in Patients with Coronary Slow Flow.Arquivos brasileiros de cardiologia · 2025Article
- Exploring sex-specific clinical features in Chinese patients with Takotsubo syndrome.BMC cardiovascular disorders · 2025Article
- Myocardial microvascular function assessed by cardiovascular magnetic resonance first-pass perfusion in patients with Takotsubo syndrome.European radiology · 2025Article
- The Genetic Puzzle of the Stress-Induced Cardiomyopathy (Takotsubo Syndrome): State of Art and Future Perspectives.Biomolecules · 2025Review
- Trends and outcomes of different mechanical circulatory support modalities for refractory cardiogenic shock in Takotsubo cardiomyopathy.American heart journal plus : cardiology research and practice · 2025Article
- Takotsubo is an acute myocardial ischaemic syndrome.European heart journal · 2025Article
- A case report of Kounis syndrome presenting with coronary angina pectoris and coronary microcirculatory disturbance, resulting in takotsubo cardiomyopathy-like changes.European heart journal. Case reports · 2025Article
- The Evolving Features of Takotsubo Syndrome.Current cardiology reports · 2025Review
- The Evolving Features of Takotsubo Syndrome.Current cardiology reports · 2025Review
- Case Report: Onset of Takotsubo syndrome during a heart rehabilitation session.Frontiers in cardiovascular medicine · 2025Article
- Prognostic Value of Frailty in Patients With Takotsubo Cardiomyopathy.Clinical cardiology · 2025Article
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Authors and funding
22 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsTakotsubo syndrome (TTS) is a conundrum without consensus about the cause. In a murine model of coronary microvascular dysfunction (CMD), abnormalities in myocardial perfusion played a key role in the development of TTS. METHODS AND
resultsVascular Kv1.5 channels connect coronary blood flow to myocardial metabolism and their deletion mimics the phenotype of CMD. To determine if TTS is related to CMD, wild-type (WT), Kv1.5-/-, and TgKv1.5-/- (Kv1.5-/- with smooth muscle-specific expression Kv1.5 channels) mice were studied following transaortic constriction (TAC). Measurements of left ventricular (LV) fractional shortening (FS) in base and apex, and myocardial blood flow (MBF) were completed with standard and contrast echocardiography. Ribonucleic Acid deep sequencing was performed on LV apex and base from WT and Kv1.5-/- (control and TAC). Changes in gene expression were confirmed by real-time-polymerase chain reaction. MBF was increased with chromonar or by smooth muscle expression of Kv1.5 channels in the TgKv1.5-/-. TAC-induced systolic apical ballooning in Kv1.5-/-, shown as negative FS (P < 0.05 vs. base), which was not observed in WT, Kv1.5-/- with chromonar, or TgKv1.5-/-. Following TAC in Kv1.5-/-, MBF was lower in LV apex than in base. Increasing MBF with either chromonar or in TgKv1.5-/- normalized perfusion and function between LV apex and base (P = NS). Some genetic changes during TTS were reversed by chromonar, suggesting these were independent of TAC and more related to TTS.
conclusionAbnormalities in flow regulation between the LV apex and base cause TTS. When perfusion is normalized between the two regions, normal ventricular function is restored.
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Registered trials
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.