The Stroke-Heart syndrome is a major chapter in neurocardiology. Both brain-heart and stroke-heart correlations are based on neurophysiological studies that define and describe the relation between the central autonomic system and cardiac function and it will be presented in this narrative review. The Stroke-Heart syndrome groups the entire spectrum of cardiac changes - clinical, ECG, echocardiographic, biological, morphological - that occur in the first 30 days from the onset of stroke, especially in the first days. Their presence significantly marks the evolution and prognosis of stroke. The damage resulted from hypothalamus-pituitary-adrenal axis activation and high catecholamine release (adrenergic storm) targets mainly the myocyte and the microcirculation.The Takotsubo syndrome and Stunned myocardium are distinct forms of neurogenic myocardial ischemia - with changes in ECG, parietal motility, and biological markers - usually reversible although evolution towards cardiac dysfunction is also possible. The concept of Stroke-Heart syndrome and the brain-heart correlation brought new scientific information regarding stress cardiomyopathy or neurogenic myocardial injury.
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http://dx.doi.org/10.2478/rjim-2023-0020 | DOI Listing |
Am J Prev Cardiol
March 2025
Department of Cardiology, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, Zhejiang, PR China.
Background And Aims: Atherosclerotic cardiovascular disease (ASCVD) is a leading cause of mortality, and while the association between the urinary albumin-to-creatinine ratio (UACR) and cardiovascular risk is recognized, the specific impact of UACR on the long-term survival of ASCVD patients remains not fully understood. The aim of this study is to investigate the influence of UACR on the long-term risk of all-cause mortality in patients with ASCVD.
Methods: This study included ASCVD patients from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018.
Exp Neurol
December 2024
Department of Anesthesiology, the Key Laboratory of Anesthesiology and Intensive Care Research of Heilongjiang Province, Second Affiliated Hospital of Harbin Medical University, Harbin, China. Electronic address:
Stroke induces cardiac dysfunction, which increases poststroke mortality and morbidity. An imbalance in the autonomic nervous system resulting from brain injury may serve as the underlying mechanism. The present study investigated whether transcutaneous auricular vagus nerve stimulation (taVNS) attenuates poststroke cardiac dysfunction by activating the parasympathetic nervous system.
View Article and Find Full Text PDFJ Am Heart Assoc
December 2024
Liverpool Centre for Cardiovascular Science at University of Liverpool, Liverpool John Moores University and Liverpool Heart & Chest Hospital Liverpool UK.
Heart
January 2025
Department of Neurology with Experimental Neurology and Center for Stroke Research Berlin (CSB), Charité - Universitätsmedizin Berlin, Berlin, Germany
Cardiovascular alterations are common in patients who had ischaemic stroke, haemorrhagic stroke and other acute brain disorders such as seizures. These cardiac complications are important drivers of morbidity and mortality and comprise blood-based detection of cardiomyocyte damage, ECG changes, heart failure and arrhythmia. Recently, the concept of a distinct 'stroke-heart syndrome' has been formulated as a pathophysiological framework for poststroke cardiac complications.
View Article and Find Full Text PDFJ Nanobiotechnology
November 2024
Department of Cardiothoracic Surgery, Huashan Hospital of Fudan University, 12 Wulumuqi Rd, Shanghai, 200040, China.
Background: Cardiovascular events secondary to stroke-collectively classified as stroke-heart syndrome-greatly impair the patient's prognosis, however its underlying mechanism has yet to be determined. To investigate the mechanism of central neuroinflammation and its effects on stroke-heart syndrome, a temperature-ultrasound responsive brain-targeted drug delivery system, DATS/MION-LPE, was synthesized to specifically study neuroinflammation in the mouse middle cerebral artery occlusion (MCAO) model.
Results: The specific polymer of DATS/MION-LPE can close the nanoparticle pores at 37 °C, restricting drug release in the circulation.
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