Takotsubo Syndrome: Clinical Manifestations, Etiology and Pathogenesis.
Etiology
endothelin-1
microRNAs.
pathogenesis
stress cardiomyopathy
takotsubo syndrome
Journal
Current cardiology reviews
ISSN: 1875-6557
Titre abrégé: Curr Cardiol Rev
Pays: United Arab Emirates
ID NLM: 101261935
Informations de publication
Date de publication:
2021
2021
Historique:
received:
06
09
2019
revised:
02
12
2019
accepted:
12
12
2019
pubmed:
30
1
2020
medline:
23
6
2021
entrez:
30
1
2020
Statut:
ppublish
Résumé
The purpose of the review is the analysis of clinical and experimental data on the etiology and pathogenesis of takotsubo syndrome (TS). TS is characterized by contractile dysfunction, which usually affects the apical region of the heart without obstruction of coronary artery, moderate increase in myocardial necrosis markers, prolonged QTc interval (in 50% of patients), sometimes elevation of ST segment (in 19% of patients), increase N-Terminal Pro-B-Type Natriuretic Peptide level, microvascular dysfunction, sometimes spasm of the epicardial coronary arteries (in 10% of patients), myocardial edema, and life-threatening ventricular arrhythmias (in 11% of patients). Stress cardiomyopathy is a rare disease, it is observed in 0.6 - 2.5% of patients with acute coronary syndrome. The occurrence of takotsubo syndrome is 9 times higher in women, who are aged 60-70 years old, than in men. The hospital mortality among patients with TS corresponds to 3.5% - 12%. Physical or emotional stress do not precede disease in all patients with TS. Most of patients with TS have neurological or mental illnesses. The level of catecholamines is increased in patients with TS, therefore, the occurrence of TS is associated with excessive activation of the adrenergic system. The negative inotropic effect of catecholamines is associated with the activation of β2 adrenergic receptors. An important role of the adrenergic system in the pathogenesis of TS is confirmed by studies which were performed using 125I-metaiodobenzylguanidine (125I -MIBG). TS causes edema and inflammation of the myocardium. The inflammatory response in TS is systemic. TS causes impaired coronary microcirculation and reduces coronary reserve. There is a reason to believe that an increase in blood viscosity may play an important role in the pathogenesis of microcirculatory dysfunction in patients with TS. Epicardial coronary artery spasm is not obligatory for the occurrence of TS. Cortisol, endothelin-1 and microRNAs are challengers for the role of TS triggers. A decrease in estrogen levels is a factor contributing to the onset of TS. The central nervous system appears to play an important role in the pathogenesis of TS.
Identifiants
pubmed: 31995013
pii: CCR-EPUB-104029
doi: 10.2174/1573403X16666200129114330
pmc: PMC8226199
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
188-203Informations de copyright
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
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