Background: The serum concentration of cardiac enzymes may be influenced by mechanical and electrical trauma due to cardiopulmonary resuscitation (CPR) attempts. This could complicate the determination of whether an acute myocardial infarction (AMI) had occurred. In this study, only patients without any of the known confounding factors affecting cardiac enzyme release were included, and the specific time course and patterns of serum cardiac enzyme levels after resuscitation were evaluated. The purpose is to help clinicians distinguish between spontaneous myocardial damage and that induced by CPR.
Methods And Results: This prospective, observational study was performed in the emergency department on eight patients surviving cardiac arrest. They were selected for not having heart disease, chest trauma or septic shock; and not receiving defibrillation. The median (range) duration of return of spontaneous circulation (ROSC) was 13 min (5-30 min). Cardiac enzyme measurements were taken immediately after ROSC and every 6h thereafter. Although cardiac troponin I (cTnI) level reached as high as 62.6 ng/ml at 24 h in one patient, five of the eight (62.5%) patients had their cTnI level fall below the normal reference range (i.e. 2 ng/ml) by 30 h. The time to maximum and peak concentration of cTnI was 16.50+/-10.99 h and 16.85+/-21.50 ng/ml, respectively. Both MB creatine kinase (CKMB) and total creatine kinase (CK) levels were above their normal reference ranges. In addition, the CKMB/CK ratio exceeded 5% in all patients at any time point during this study.
Conclusion: In this study, the influence of resuscitative procedures - defibrillation excluded - on the release of cardiac enzymes were examined. During 30 h after ROSC cTnI level exhibited a bell-shaped configuration, which is distinct from that after AMI; whereas the enzymatic activities of CKMB and CK, as well as CKMB/CK ratio, were constantly higher than normal. This chronological pattern of cardiac enzyme levels may help physicians differentiate primary cardiac disease from other aetiologies in out-of-hospital cardiac arrests.
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http://dx.doi.org/10.1016/j.resuscitation.2005.07.018 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Innovative Genomics Institute, University of California, Berkeley, CA 94720.
The widespread application of genome editing to treat and cure disease requires the delivery of genome editors into the nucleus of target cells. Enveloped delivery vehicles (EDVs) are engineered virally derived particles capable of packaging and delivering CRISPR-Cas9 ribonucleoproteins (RNPs). However, the presence of lentiviral genome encapsulation and replication proteins in EDVs has obscured the underlying delivery mechanism and precluded particle optimization.
View Article and Find Full Text PDFFASEB J
January 2025
Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Lung cancer progression is characterized by intricate epigenetic changes that impact critical metabolic processes and cell death pathways. In this study, we investigate the role of histone lactylation at the AIM2 locus and its downstream effects on ferroptosis regulation and lung cancer progression. We utilized a combination of biochemical assays, including chromatin immunoprecipitation (ChIP), quantitative real-time PCR (qRT-PCR), and western blotting to assess histone lactylation levels and gene expression.
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Am J Physiol Regul Integr Comp Physiol
December 2024
Curtin University, Curtin Medical Research Institute (Bentley, WA, AUSTRALIA).
Physical activity improves myocardial structure, function and resilience via complex, incompletely defined mechanisms. We explored effects of 1-2 wks swim training on cardiac and systemic phenotype in young male C57Bl/6 mice. Two wks forced swimming (90 min twice daily) resulted in cardiac hypertrophy (22% increase in heart:body weight, P<0.
View Article and Find Full Text PDFCells
December 2024
Laboratory of Cardiovascular Science, Intramural Research Program, National Institute on Aging, National Institute of Health, Baltimore, MD 21224, USA.
The spontaneous firing of the sinoatrial (SA) node, the physiological pacemaker of the heart, is generated within sinoatrial nodal cells (SANCs) and is regulated by a "coupled-clock" pacemaker system, which integrates a "membrane clock", the ensemble of ion channel currents, and an intracellular "Ca clock", sarcoplasmic reticulum-generated local submembrane Ca releases via ryanodine receptors. The interactions within a "coupled-clock" system are modulated by phosphorylation of surface membrane and sarcoplasmic reticulum proteins. Though the essential role of a high basal cAMP level and PKA-dependent phosphorylation for basal spontaneous SANC firing is well recognized, the role of basal CaMKII-dependent phosphorylation remains uncertain.
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