The Story of a Broken Heart: Takotsubo Cardiomyopathy

Hussein, Mohamed Toufic El; Kilfoil, Lauren

doi:10.1016/j.jen.2020.12.014

Cited by 2 publications

(3 citation statements)

References 25 publications

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“…It was usually caused by severe stress. For clinical examination, echocardiograph shows apical or mid-left ventricular dyskinesia and troponin and NT-proBNP will elevate (91)(92)(93). A melanoma patient present takotsubo syndrome after ICIs combination therapy, and echocardiograph showed apical motion with ballooning, electrocardiogram showed V2-V6 ST elevation 1-2 mm.…”

Section: Takotsubo Syndromementioning

confidence: 99%

Advances in immune checkpoint inhibitors induced-cardiotoxicity

Peng²,

Wu³

et al. 2023

Front. Immunol.

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Immune checkpoint inhibitors (ICIs) are approved as the first-line drug for treating many cancers and has shown significant survival benefits; however, it also causes immune-related adverse events (irAEs) while activating the immune system, involving multiple organs. Among them, cardiovascular immune-related adverse events (CV-irAE) are rare, but common causes of death in ICIs treated cancer patients, which manifest as myocardial, pericardial, vascular and other cardiovascular toxicities. Therefore, it is important that irAEs, especially CV-irAE should be carefully recognized and monitored during the whole ICIs treatment because early detection and treatment of CV-irAE can significantly reduce the mortality of such patients. Consequently, it is urgent to fully understand the mechanism and management strategies of CV-irAE. The effects of ICIs are multifaceted and the exact mechanism of CV-irAE is still elusive. Generally, T cells identify tumor cell antigens as well as antigen in cardiomyocytes that are the same as or homologous to those on tumor cells, thus causing myocardial damage. In addition, ICIs promote formation of cardiac troponin I (cTnI) that induces cardiac dysfunction and myocardial dilatation; moreover, ICIs also increase the production of cytokines, which promote infiltration of inflammation-linked molecules into off-target tissues. Currently, the management and treatment of cardiovascular toxicity are largely dependent on glucocorticoids, more strategies for prevention and treatment of CV-irAE, such as predictive markers are being explored. This review discusses risk factors, potential pathophysiological mechanisms, clinical manifestations, and management and treatment of CV-irAE, guiding the development of more effective prevention, treatment and management strategies in the future.

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Section: Takotsubo Syndromementioning

confidence: 99%

Advances in immune checkpoint inhibitors induced-cardiotoxicity

Peng²,

Wu³

et al. 2023

Front. Immunol.

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“…Abnormalities in ECGs were shown in most Takotsubo patients and were associated with ST segment abnormalities [7, 9a, 9b, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25,26 27, 28] , prolonged QT intervals [29,30,31,32,33,34,35] , tachyarrhythmias [36] , and more extensive repolarization [16,37] . Prolonged QTc intervals during a Takotsubo episode is associated with a high risk of cardiovascular rehospitalization were reported [38] .…”

Section: Mechanical Stress Varied Membrane Potentials Influence On Th...mentioning

confidence: 99%

“…The depth and spread of T-waves and QTc duration provide increased diagnostic confidence in nonobstructive coronary patients [39] . The significantly prolonged precordial T wave is altered by the spatial dispersion of ventricular repolarization [36] , which may be associated with ST segment elevation [30,19] and probable with ST depression in aVR and chest-led PR [36] . In mechanically lengthening cardiac muscle fibers, the cellular membrane depolarizes in a specific pattern, which significantly lasts the decay period of the repolization phase (Figure 2) [40] ; however, the action potential conduction velocity does not significantly change [41] .…”

Section: Mechanical Stress Varied Membrane Potentials Influence On Th...mentioning

confidence: 99%

Mechanical stress concealed force enhancement and ionic transient membrane potential and metabolism in akinesia of stress cardiomyopathy

Chen

Wang

Yang

et al. 2022

Preprint

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Stress cardiomyopathy is a unique heart syndrome that is characterized by reversible left ventricular apical wall motion abnormalities and is commonly known as Takotsubo syndrome. In transient left ventricular apical ballooning, myocardium lengthening stress is in a high energy-demand state. The increased passive tension and force enhancement conducted asynergically are associated with severe hypokinesis on the ventricular wall and reduced the blood ejection fraction. Ventricular myocardial deformation and global longitudinal strain have significant mechanotemporal alteration characteristics. Membrane potential dominant mechanisms related to akinesia are considered from multiple effects of variation of calcium transients, myocardium metabolism, which is relative to the ST segment lift in an ECG, and in the weakness of contraction of the ventricular muscle. Ventricular filling, not pressure,-determine the strengthening from stretching; thus, in stress cardiomyopathy, ventricular apical ballooning (takotsubo-shaped ventricle) strengthens the mechanical stress on the wall. Muscle fiber tolerance of lengthening is a high energy consumption process. Ventricular apical akinesia further aggravates passive tension. Depleted ATP and high inorganic phosphate inhibit Ca 2+-activated development, terminates the crossbridge detachment process in its early stage, and facilitates the occurrence of myogenic force enhancement. Comprehensive analysis of the above mechanisms, in lengthening stress, increased cardiac fibers energy demand, and Ca 2+ transient variation interruption of the diastolic cycle, delayed the onset of systole and aggravated the occurrence of apical ballooning in stress cardiomyopathy.

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The Story of a Broken Heart: Takotsubo Cardiomyopathy

Cited by 2 publications

References 25 publications

Advances in immune checkpoint inhibitors induced-cardiotoxicity

Advances in immune checkpoint inhibitors induced-cardiotoxicity

Mechanical stress concealed force enhancement and ionic transient membrane potential and metabolism in akinesia of stress cardiomyopathy

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