Background: Acute ischaemic or haemorrhagic cerebrovascular events may produce myocardial damage. Cardiac troponin I is an indicator of cardiac cell injury with very high sensitivity and specificity.
Material And Methods: We measured troponin I in 149 acute stroke patients admitted to the stroke unit of Trondheim University Hospital, Norway, in January to June 1999.
Results: 40 patients (27%) had troponin I values at 0.4 microgram/l or higher, indicating myocardial injury. 10 patients (6.7%) had troponin I values above 2.0 micrograms/l. Similarly, the mean value of CK-MB vas higher in the patients with myocardial injury, and these patients had more often ECG findings suggesting myocardial ischaemia. Patients with myocardial injury had a higher rate of previous TIA and heart failure. ECG showed atrial fibrillation in 13 of 39 patients with myocardial damage. Patients with detectable levels of troponin I had more embolic brain infarctions than thrombotic brain infarctions. Patients with myocardial injury did more often have abnormal values of CRP. 9 of 10 patients with troponin I-values above 2.0 micrograms/l had abnormal CRP values. No differences in glycosylated haemoglobin, cholesterol, heart rate, blood pressure or body temperature were found. Patients with the highest troponin I values had lower systolic blood pressure, and a higher heart rate, but these differences were not statistically significant. Patients with troponin I values above 2.0 micrograms/l had lower functional and neurological scores at admittance. Patients with myocardial injury were more often discharged to nursing homes.
Interpretation: Many patients with an acute stroke have at the same time a myocardial injury, determined by elevated troponin I values.
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FASEB J
January 2025
National Key Laboratory of Space Medicine, China Astronaut Research and Training Center, Beijing, China.
Microgravity-induced cardiac remodeling and dysfunction present significant challenges to long-term spaceflight, highlighting the urgent need to elucidate the underlying molecular mechanisms and develop precise countermeasures. Previous studies have outlined the important role of miRNAs in cardiovascular disease progression, with miR-199a-3p playing a crucial role in myocardial injury repair and the maintenance of cardiac function. However, the specific role and expression pattern of miR-199a-3p in microgravity-induced cardiac remodeling remain unclear.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Department of Vascular & Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Purpose: Cardiomyocyte death is a major cytopathologic response in acute myocardial infarction (AMI) and involves complex inflammatory interactions. Although existing reports indicating that mixed lineage kinase domain-like protein (MLKL) is involved in macrophage necroptosis and inflammasome activation, the downstream mechanism of MLKL in necroptosis remain poorly characterized in AMI.
Methods: MLKL knockout mice (MLKL), RIPK3 knockout mice (RIPK3), and macrophage-specific MLKL conditional knockout mice (MLKL) were established.
Sci Rep
January 2025
Department of Radiotherapy, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
To investigate how PD-L1 monoclonal antibodies (mAbs) affect the left ventricular function in mice with myocardial infarction (MI) and through what mechanisms they exert their effects. In vivo experiments were conducted using 27 female BALB/c mice, which were divided equally into 3 groups. Cardiac function was assessed by ultrasound.
View Article and Find Full Text PDFInt J Cardiol
January 2025
School of Medicine, Northeast Ohio Medical University, Rootstown, OH, USA. Electronic address:
Int Immunopharmacol
January 2025
Department of Critical Care Medicine, the Affiliated Hospital of Qingdao University, Qingdao 266000 Shandong, China. Electronic address:
Esmolol has been demonstrated to mitigate inflammation damage and T lymphocyte apoptosis in septic cardiomyopathy. It has been established that the activation of α7 nicotinic acetylcholine receptor (nAChR) by cluster of differentiation 4(CD4) T lymphocytes expressing choline acetyltransferase (ChAT) can prevent excessive inflammation and reduce splenocyte apoptosis in septic cardiomyopathy. Given the similar anti-inflammatory effects, we hypothesized that esmolol might be associated with α7 nAChR and thereby exert its cardioprotective functions.
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