Background And Aims: We have demonstrated that an increased peak serum C-reactive protein (CRP) level after acute myocardial infarction (AMI) was a major predictor of left ventricular (LV) remodeling. We sought to clarify the effect of aging on the postinfarction inflammatory response and LV remodeling.
Methods: We studied 102 patients who underwent primary angioplasty for a first anterior Q-wave AMI. Serum CRP levels, plasma neurohormones and interleukin-6 (IL-6) levels, and LV volume by left ventriculography were serially measured. Patients were divided into two groups according to their age (>or=70 years, n=33; <70 years, n=69).
Results: There was no difference in use of cardiovascular drugs and coronary angiographic findings. Older patients had a greater increase in LV end-diastolic volume during 2 weeks after AMI (p=0.0007) and a higher peak CRP level (12.4+/-7.3 vs. 5.5+/-4.2 mg/dl, p<0.0001), although peak CK level was comparable between the two groups. Plasma atrial natriuretic peptide, brain natriuretic peptide and IL-6 levels were higher in older patients at 2 weeks and 6 months after AMI.
Conclusions: Augmented and prolonged activation of the inflammatory system after AMI was observed in older patients, in association with exaggerated LV remodeling. Aging may adversely affect LV remodeling through modification of the inflammatory response after AMI.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1159/000089542 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Associations Between Plasma Levels of NLRP3 Protein, Interleukin-1 Beta and Features of Acute ST-Elevation Myocardial Infarction.
J Pers Med
November 2024
Department of Clinical Laboratory Diagnostics, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, 634012 Tomsk, Russia.
Background: Phenotyping inflammation in ST-elevation myocardial infarction (STEMI) is a challenge for modern cardiology. NLRP3 inflammasome is a proven predictor of adverse outcomes in cardiovascular disease, but its specificity in stratifying inflammatory activity in patients with myocardial infarction (MI) has not been demonstrated. The aim of this paper is to describe the levels of NLRP3 protein and IL-1β concentrations and their changes in dynamics and associations with clinical, laboratory and instrumental characteristics of patients with STEMI.
View Article and Find Full Text PDFTubuloside A alleviates postmyocardial infarction cardiac fibrosis by inhibiting TGM2: Involvement of inflammation and mitochondrial pathway apoptosis.
Int Immunopharmacol
December 2024
Department of Cardiology, Donghai People's Hospital Affiliated to Kangda College of Nanjing Medical University, Donghai People's Hospital, Lianyungang 222300, China. Electronic address:
Article Synopsis
- Cardiac fibrosis following a myocardial infarction (MI) can lead to serious complications, including heart failure and death; this study examined the effects of tubuloside A (TA) on this condition.
- Results showed that TA significantly reduced mortality, improved heart function, and decreased fibrosis and injury in rats after MI, especially at higher doses.
- The study identified that TA directly inhibits the enzyme TGM2, which plays a role in fibrosis, and acts through pathways that reduce inflammation and prevent cell death, suggesting TA as a promising drug for treating post-MI cardiac complications.
Gut microbiota-related modulation of immune mechanisms in post-infarction remodelling and heart failure.
ESC Heart Fail
October 2024
University Hospital St Josef-Hospital Bochum, Cardiology and Rhythmology, Ruhr University Bochum, Bochum, Germany.
The immune system has long been recognized as a key driver in the progression of heart failure (HF). However, clinical trials targeting immune effectors have consistently failed to improve patient outcome across different HF aetiologies. The activation of the immune system in HF is complex, involving a broad network of pro-inflammatory and immune-modulating components, which complicates the identification of specific immune pathways suitable for therapeutic targeting.
View Article and Find Full Text PDFSalvaging myocardial infarction with nanoenzyme-loaded hydrogels: Targeted scavenging of mitochondrial reactive oxygen species.
J Control Release
November 2024
National Engineering Research Center for Biomaterials, College of Biomedical Engineering, Sichuan university, Chengdu 610064, China. Electronic address:
Myocardial infarction resulting from coronary artery atherosclerosis is the leading cause of heart failure, which represents a significant global health burden. The limitations of conventional pharmacologic thrombolysis and flow reperfusion procedures highlight the urgent need for new therapeutic strategies to effectively treat myocardial infarction. In this study, we present a novel biomimetic approach that integrates polyphenols and metal nanoenzymes, inspired by the structure of pomegranates.
View Article and Find Full Text PDFMineralocorticoid Receptor Blocker Prevents Mineralocorticoid Receptor-Mediated Inflammation by Modulating Transcriptional Activity of Mineralocorticoid Receptor-p65-Signal Transducer and Activator of Transcription 3 Complex.
J Am Heart Assoc
September 2024
Department of Cardiovascular Medicine Graduate School of Medical Sciences, Kumamoto University Kumamoto Japan.
Background: Mineralocorticoid receptor (MR) induces cardiac inflammation cooperatively with nuclear factor-κB and signal transducer and activator of transcription 3 (STAT3); MR blockers exert anti-inflammatory effects. However, the underlying mechanism remains unclear. We investigated the anti-inflammatory effect of esaxerenone, a novel MR blocker, in experimental myocardial infarction (MI) and its underlying mechanisms.
View Article and Find Full Text PDFWant 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!