Impaired hemodynamic response to tilt, handgrip and Valsalva manoeuvre in patients with takotsubo syndrome

Stępniewska, Anna; Budnik, Monika; Krzemiński, K; Niewiadomski, Wiktor; Gąsiorowska, Anna; Opolski, Grzegorz; Kochanowski, Janusz; Mieczkowska, Katarzyna; Żukowska, Katarzyna; Szepietowska, Katarzyna; Kowalik, Robert

doi:10.1016/j.autneu.2019.102555

Cited by 4 publications

(2 citation statements)

References 21 publications

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“…This may be significant since they can help evaluate autonomic system function. An inadequate autonomic system response to stress might weaken the heart’s ability to pump blood, which can impede pressure response [ 128 ].…”

Section: Diagnosismentioning

confidence: 99%

Takotsubo Syndrome: The Secret Crosstalk between Heart and Brain

Schino¹,

Bezzeccheri²,

Russo³

et al. 2023

Rev. Cardiovasc. Med.

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An acute, transient episode of left ventricular dysfunction characterizes Takotsubo syndrome. It represents about 2% of all cases of acute coronary syndrome (ACS), and occurs predominantly in postmenopausal women, generally following a significant physical or emotional stressor. It can be diagnosed based on clinical symptoms and the absence of coronary artery disease on angiography. Ventriculography remains the gold standard for the diagnosis. Despite its transitory characteristic Takotsubo syndrome should not be considered a benign condition since complications occur in almost half of the patients, and the mortality rate reaches 4-5%. Lately, it has been revealed that Takotsubo syndrome can also lead to permanent myocardial damage due to the massive release of catecholamines that leads to myocardial dysfunction. Different mechanisms have been advanced to explain this fascinating syndrome, such as plaque rupture and thrombosis, coronary spasm, microcirculatory dysfunction, catecholamine toxicity, and activation of myocardial survival pathways. Here are still several issues with Takotsubo syndrome that need to be investigated: the complex relationship between the heart and the brain, the risk of permanent myocardial damage, and the impairment of cardiomyocyte. Our review aims to elucidate the pathophysiology and the mechanisms underlying this complex disease to manage the diagnostic and therapeutic algorithms to create a functional synergy between physicians and patients.

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Section: Diagnosismentioning

confidence: 99%

Takotsubo Syndrome: The Secret Crosstalk between Heart and Brain

Schino¹,

Bezzeccheri²,

Russo³

et al. 2023

Rev. Cardiovasc. Med.

View full text Add to dashboard Cite

show abstract

“…The aforementioned study’s results could be considered important, because thanks to these noninvasive tests, we may indirectly assess autonomic system function, so by extension, recreate common real-life situations. An impaired pressor response may be caused by heart weakness in pumping function caused by an inadequate autonomic system reaction to stress [ 45 ].…”

Section: Low-grade Inflammatory Processmentioning

confidence: 99%

Pathophysiology of Takotsubo Syndrome as A Bridge to Personalized Treatment

Budnik

Piątkowski

Ochijewicz

et al. 2021

JPM

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Takotsubo syndrome (TTS) consists of transient dysfunction of the left and/or right ventricle in the absence of ruptured plaque; thrombus or vessel dissection. TTS may be divided into two categories. Primary TTS occurs when the cause of hospitalization is the symptoms resulting from damage to the myocardium usually preceded by emotional stress. Secondary TTS occurs in patients hospitalized for other medical; surgical; anesthetic; obstetric or psychiatric conditions who have activation of their sympathetic nervous system and catecholamines release- they develop TTS as a complication of their primary condition or its treatment. There are several hypotheses concerning the cause of the disease. They include decrease in estrogen levels; microcirculation dysfunction; endothelial dysfunction and the hypothesis based on the importance of the brain-heart axis. More and more researches concern the importance of genetic factors in the development of the disease.To date; no effective treatment or prevention of recurrent TTS has been found. Only when the pathophysiology of the disease is fully known; personalized treatment will be possible.

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NeuroAiDTM-II (MLC901) Promoted Neurogenesis by Activating the PI3K/AKT/GSK-3β Signaling Pathway in Rat Spinal Cord Injury Models

Anjum,

Yazid,

Daud

et al. 2024

Biomedicines

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Traumatic damage to the spinal cord (SCI) frequently leads to irreversible neurological deficits, which may be related to apoptotic neurodegeneration in nerve tissue. The MLC901 treatment possesses neuroprotective and neuroregenerative activity. This study aimed to explore the regenerative potential of MLC901 and the molecular mechanisms promoting neurogenesis and functional recovery after SCI in rats. A calibrated forceps compression injury for 15 s was used to induce SCI in rats, followed by an examination of the impacts of MLC901 on functional recovery. The Basso, Beattie, and Bresnahan (BBB) scores were utilized to assess neuronal functional recovery; H&E and immunohistochemistry (IHC) staining were also used to observe pathological changes in the lesion area. Somatosensory Evoked Potentials (SEPs) were measured using the Nicolet® Viking Quest™ apparatus. Additionally, we employed the Western blot assay to identify PI3K/AKT/GSK-3β pathway-related proteins and to assess the levels of GAP-43 and GFAP through immunohistochemistry staining. The study findings revealed that MLC901 improved hind-limb motor function recovery, alleviating the pathological damage induced by SCI. Moreover, MLC901 significantly enhanced locomotor activity, SEPs waveform, latency, amplitude, and nerve conduction velocity. The treatment also promoted GAP-43 expression and reduced reactive astrocytes (GFAP). MLC901 treatment activated p-AKT reduced p-GSK-3β expression levels and showed a normalized ratio (fold changes) relative to β-tubulin. Specifically, p-AKT exhibited a 4-fold increase, while p-GSK-3β showed a 2-fold decrease in T rats compared to UT rats. In conclusion, these results suggest that the treatment mitigates pathological tissue damage and effectively improves neural functional recovery following SCI, primarily by alleviating apoptosis and promoting neurogenesis. The underlying molecular mechanism of this treatment mainly involves the activation of the PI3K/AKT/GSK-3β pathway.

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Impaired hemodynamic response to tilt, handgrip and Valsalva manoeuvre in patients with takotsubo syndrome

Cited by 4 publications

References 21 publications

Takotsubo Syndrome: The Secret Crosstalk between Heart and Brain

Takotsubo Syndrome: The Secret Crosstalk between Heart and Brain

Pathophysiology of Takotsubo Syndrome as A Bridge to Personalized Treatment

NeuroAiDTM-II (MLC901) Promoted Neurogenesis by Activating the PI3K/AKT/GSK-3β Signaling Pathway in Rat Spinal Cord Injury Models

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