Background: We studied the dynamics of QT dispersion in patients with acute myocardial infarction, and compared them with those in controls.
Methods And Results: Serial electrocardiograms of patients admitted to our institute with acute myocardial infarction were analyzed for QT dispersion, and compared with those of healthy age- and sex-matched controls. QT dispersion from 12 leads was measured as maximum QT minus minimum QT interval in ms. The mean QT dispersion of 114 +/- 29.6 ms was significantly higher in patients with acute myocardial infarction on admission as compared to 51.45 +/- 5.56 ms in controls (p < 0.001). QT dispersion showed a dynamic change in patients with acute myocardial infarction who were thrombolyzed, being 109.11 +/- 5.77 ms, 87.59 +/- 5.88 ms, 75.89 +/- 18.33 ms, and 68.20 +/- 12.66 ms on admission, post-thrombolysis, and on days 3 and 7, respectively. During a similar time period, nonthrombolyzed patients showed a QT dispersion of 132.38 +/- 36.04 ms, 130.47 +/- 34.42 ms, 111.11 +/- 24.94 ms, and 106.25 +/- 27.64 ms, respectively: the difference between the 2 groups at all periods was significant (p < 0.01). Mean QT dispersion values in patients who developed ventricular tachycardia or ventricular fibrillation were significantly higher than in patients who did not develop ventricular tachycardia or ventricular fibrillation (p < 0.01).
Conclusions: Mean QT dispersion is significantly increased after acute myocardial infarction, and shows a dynamic decrease with time, the difference being more marked in thrombolyzed patients. Mean QT dispersion levels are higher in patients with ventricular tachycardia and ventricular fibrillation compared to patients with acute myocardial infarction without these arrhythmias. The changes in QT dispersion are dynamic, and it may serve as a non-invasive marker of susceptibility to malignant ventricular arrhythmias.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Acute myocardial infarction (MI) is a leading cause of death worldwide. Although with current treatment, acute mortality from MI is low, the damage and remodeling associated with MI are responsible for subsequent heart failure. Reducing cell death associated with acute MI would decrease the mortality associated with heart failure.
View Article and Find Full Text PDFNuclear receptor 4A1 Regulates Mitochondrial Homeostasis in Cardiac Post-Ischemic Injury by Controlling Mitochondrial Fission 1 Protein-Mediated Fragmentation and Parkin-Dependent Mitophagy.
Int J Biol Sci
January 2025
Department of Cardiovascular Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China 510120.
The close interaction of mitochondrial fission and mitophagy, two crucial mechanisms, is key in the progression of myocardial ischemia-reperfusion (IR) injury. However, the upstream regulatory mechanisms governing these processes remain poorly understood. Here, we demonstrate a marked elevation in Nr4a1 expression following myocardial IR injury, which is associated with impaired cardiac function, heightened cardiomyocyte apoptosis, exacerbated inflammatory responses, and endothelial dysfunction.
View Article and Find Full Text PDFThe Appropriate Utilization of Beta-Blockers in Acute Coronary Syndrome Patients: An Improvement Initiative.
Cureus
December 2024
Cardiology, Tata Main Hospital, Jamshedpur, IND.
Background and objective Beta-blockers are a cornerstone in the management of acute coronary syndrome (ACS), effectively reducing myocardial oxygen demand, preventing recurrent ischemia, and lowering the risk of arrhythmias and reinfarction. Despite several established guidelines, such as those by the American College of Cardiology/American Heart Association (ACC/AHA), advocating their use within 24 hours for eligible patients, beta-blockers remain underutilized in clinical practice. This study aimed to analyze beta-blocker utilization patterns in ACS management and evaluate the impact of targeted improvement initiatives on their appropriate use in eligible ACS patients.
View Article and Find Full Text PDFCardiac cells and mesenchymal stem cells derived extracellular vesicles: a potential therapeutic strategy for myocardial infarction.
Front Cardiovasc Med
December 2024
Department of Cardiology, Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Despite improvements in clinical outcomes of acute myocardial infarction (AMI), mortality rates remain high, indicating the need for further understanding of the pathogenesis and developing more effective cardiac protection strategies. Extracellular vesicles (EVs) carry proteins and noncoding RNAs (ncRNAs) derived from different cardiac cell populations, mainly including cardiomyocytes, endothelial cells, endothelial progenitor cells, cardiac progenitor cells, cardiosphere-derived cells, immune cells, fibroblasts and cardiac telocytes have vital roles under both physiological and pathological process such as myocardial infarction (MI). The content of EVs can also indicate the status of their parental cells and serve as a biomarker for monitoring the risk of cardiac injury.
View Article and Find Full Text PDFSleep-disordered breathing does not directly affect early cardiac rehabilitation efficacy after myocardial infarction.
Kardiol Pol
January 2025
Department of Electrocardiology and Heart Failure, Medical University of Silesia in Katowice, Katowice, Poland.
Background: Sleep-disordered breathing (SDB) impairs exercise capacity after myocardial infarction (MI).
Aims: This study aimed to evaluate the impact of SDB on the efficacy of post-MI cardiac rehabilitation (CR).
Methods: The study evaluated consecutive patients up to 28 days after MI who participated in outpatient CR as part of the Polish Managed Care after Acute Myocardial Infarction program.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!