Relation between use of antiinflammatory agents and left ventricular free wall rupture during acute myocardial infarction

doi:10.1016/0002-9149(87)90817-4

The American Journal of Cardiology

Volume 59, Issue 4, 1 February 1987, Pages 363-364

https://doi.org/10.1016/0002-9149(87)90817-4 Get rights and content

Abstract

In this retrospective study we examined the relation between corticosteroid and nonsteroidal anti-inflammatory drug (NSAID) usage in an autopsy series of patients with left ventricular (LV) free wall rupture during acute myocardial infarction (AMI).

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Cited by (92)

Steroids and myocardial infarction: Investigating safety and short-term mortality in critical post-myocardial infarction patients
2024, American Journal of the Medical Sciences
Conventionally, in the pre-percutaneous intervention era, free wall rupture is reported to be a major concern for using steroids in myocardial infarction (MI) patients. Therefore, the aim of this study was to evaluate the safety of the use of steroids in critically ill post-MI patients in terms of hospital course and short-term (up to 180-day) mortality.
We included patients admitted to CCU diagnosed with MI, undergone revascularization, critically ill, and requiring mechanical ventilator (MV) support. The hospital course and short-term (up to 180-day) mortality were independently compared between steroid and non-steroid cohorts and propensity-matched non-steroid cohorts.
A total of 312 patients were included, out of which steroids were used in 93(29.8%) patients during their management. On periodic bedside echocardiography, no free wall rupture was documented in the steroid or non-steroid cohort. When compared steroids with a propensity-matched non-steroid cohort, MV duration >24 h was 66.7% vs. 59.1%; p = 0.288, major bleeding was 6.5% vs. 3.2%; p = 0.305, need for renal replacement therapy was 9.7% vs. 8.6%; p = 0.799, in-hospital mortality was 35.5% vs. 23.7%; p = 0.077, and 180-day mortality was 48.4% vs. 41.9%; p = 0.377, respectively. The hazard ratio was 1.22 [95% CI: 0.80 to 1.88] compared to the propensity-matched non-steroid cohort. The ejection fraction (%) was found to be the independent predictor of 180-day mortality with an adjusted odds ratio of 0.92 [95% CI: 0.86 to 0.98].
In conclusion, using steroids is safe in post-MI patients with no significant increase in short-term mortality risk.
Identification of molecular signatures in acute myocardial infarction based on integrative analysis of proteomics and transcriptomics
2023, Genomics
Myocardial infarction (MI) is one of the most serious cardiovascular diseases, characterized by a rapid and irreversible decline in myocardial function. Early detection of patients with MI and prolonging the optimal therapeutic window of acute myocardial infarction (AMI) are particularly important. This study aimed to identify the diagnostic biomarkers and novel therapeutic targets for acute myocardial infarction.
We generated the AMI mouse models by ligating the proximal left anterior descending coronary artery. Six time points—Sham, AMI 10-min, 1-h, 6-h, 24-h, and 72-h—were chosen to examine the molecular changes that occur during the AMI process. RNA-seq and DIA-MS were performed on the infarcted left ventricular tissues of AMI mice at each time point. Co-expression pattern genes were screened from myocardial infarction samples at different time points by time-series analysis. Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were used to examine these genes. Using the Interactive Gene/Protein Retrieval Tool (STRING) database, the protein-protein interaction network (PPI) was constructed and the hub genes were identified. In order to evaluate the diagnostic value of hub genes, a receiver operating characteristic (ROC) curve was constructed. An independent data set, GSE163772, confirmed the diagnostic value of hub genes further.
We obtained the expression profiles at different time points after the occurrence of heart failure through high-throughput sequencing, and found 167 genes with similar expression patterns through time series analysis. The immune response and immune-related pathways had the greatest enrichment of these genes. Among them, Itgb2 Syk, Tlr4, Tlr2, Itgax, and Lcp2 may play key roles as hub genes. Combined with the results of proteomic analysis, it was found that the expression of Coro1a in both omics increased with time. The results of external validation showed that TLR2, ITGAX, and LCP2 had good predictive ability for AMI diagnosis.
Itgb2, Syk, Tlr4, Tlr2, Itgax, Lcp2 and Coro1a are considered to be the seven key genes significantly associated with AMI. Our results may provide potential targets for the prevention of adverse ventricular remodeling and the treatment of AMI.
Genetic Deletion of Galectin-3 Alters the Temporal Evolution of Macrophage Infiltration and Healing Affecting the Cardiac Remodeling and Function after Myocardial Infarction in Mice
2020, American Journal of Pathology
Citation Excerpt :
Studies in animals reported that the inhibition of the reparative process can reduce the infarct size and improve the evolution of the VR.44,45 However, the early use of anti-inflammatory drugs after infarction promoted the thinning and expansion of the infarct zone in animals and increased the incidence of cardiac rupture in patients.46 Thus, a defect in the healing process or an increase in the infarct size and parietal stress were the main determinants of the expansion and the appearance of adverse clinical events, heart failure, and death.22
We studied the role of galectin-3 (Gal-3) in the expression of alternative activation markers (M2) on macrophage, cytokines, and fibrosis through the temporal evolution of healing, ventricular remodeling, and function after myocardial infarction (MI). C57BL/6J and Gal-3 knockout mice (Lgals3^-/-) were subjected to permanent coronary ligation or sham. We studied i) mortality, ii) macrophage infiltration and expression of markers of alternative activation, iii) cytokine, iv) matrix metalloproteinase-2 activity, v) fibrosis, and vi) cardiac function and remodeling. At 1 week post-MI, lack of Gal-3 markedly attenuated F4/80+ macrophage infiltration and significantly increased the expression of Mrc1 and Chil1, markers of M2 macrophages at the MI zone. Levels of IL-10, IL-6, and matrix metalloproteinase-2 were significantly increased, whereas tumor necrosis factor-α, transforming growth factor-β, and fibrosis were remarkably attenuated at the infarct zone. In Gal-3 knockout mice, scar thinning ratio, expansion, and cardiac remodeling and function were severely affected from the onset of MI. At 4 weeks post-MI, the natural evolution of fibrosis in Gal-3 knockout mice was also affected. Our results suggest that Gal-3 is essential for wound healing because it regulates the dynamics of macrophage infiltration, proinflammatory and anti-inflammatory cytokine expression, and fibrosis along the temporal evolution of MI in mice. The deficit of Gal-3 affected the dynamics of wound healing, thus aggravating the evolution of remodeling and function.
Pretreatment of carprofen impaired initiation of inflammatory- and overlapping resolution response and promoted cardiorenal syndrome in heart failure
2019, Life Sciences
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) are commonly used to control pain, inflammation, and limit the cardinal signs of injury in humans. However, prolonged use of NSAIDs increases the risk of heart attack (myocardial infarction; MI) and the subsequent risk of heart and renal failure. The molecular and cellular mechanism of action for this adverse effect, particularly along the cardiorenal network, is incomplete. To define the mechanism, carprofen (CAP), an NSAID was administered at the dose of 5 mg/kg to C57BL/6 male mice for two weeks. After last dose of CAP treatment mice were subjected to permanent occlusion of coronary artery that induces irreversible cardiac remodeling while maintaining naive and MI-controls. After MI, cardiac pathology and dysfunction were confirmed, along with additional measurements of kidney function, histology, and injury markers, such as plasma creatinine. CAP treatment increased plasma creatinine levels and subsequently, myocardial structural disorganization increased. Kidney neutrophil gelatinase associated lipocalin (NGAL) and protein expression were increased post-MI. After two weeks CAP treatment, the expression of pyrogenic pro-inflammatory cytokines TNF-α and IL-1β was increased compared to non-CAP treated mice, indicative of amplified inflammatory response. There was also evidence that renal injury of both the post-CAP treatment controls and post-CAP MI were much greater than the non-CAP treated naïve controls, as serum creatinine and NGAL levels were elevated along with obvious structural impairment of the glomerulus. Therefore, CAP treatment tampers with the acute inflammatory response that promotes cardiorenal syndrome and non-resolving inflammation post-MI in acute heart failure.
Inhaled corticosteroid/long-acting bronchodilator treatment mitigates STEMI clinical presentation in COPD patients
2018, European Journal of Internal Medicine
Patients with myocardial infarction and concomitant COPD are at increased risk of poor clinical outcomes, including death, as compared to patients without COPD.
To investigate and compare the severity of the clinical presentation of ST-segment elevation myocardial infarction (STEMI) and of the short-(7 days) and long-term-(end of follow up) mortality in COPD patients treated with inhaled corticosteroids (ICS)/long-acting bronchodilator (LABD) - either long-acting beta2 agonist (LABA) or long-acting muscarinic antagonist (LAMA) - vs. any other inhaled treatments.
Data from the REAL (Registro Angioplastiche dell'Emilia-Romagna) Registry were obtained from a large prospective study population of 11,118 patients admitted to hospital for STEMI.
From January 2003 to June 2009 we identified 2032 COPD patients admitted to hospital for STEMI. Eight hundred and twenty (40%) COPD patients were on ICS/LABD treatment (of which 55% on ICS/LABA) prior to admission. After adjustment for potential confounding factors, ICS/LABD treatment before STEMI was an independent predictor of reduced risk of pulmonary oedema and cardiogenic shock (OR 0.5, 95%CI 0.3–0.72, p < 0.01; OR 0.7, 95%CI 0.4–0.9, p = 0.03, respectively). ICS/LABD treatment was associated to reduced 7-days mortality (OR 0.54, 95%CI 0.29–0.98, p = 0.045) compared to other inhaled regimens. ICS/LABD-treated did not affect long-term (median 4 years) mortality. After hospital discharge, the proportion of ICS/LABD treated patients decreased significantly at 6 months and afterwards after the STEMI episode.
Our data provide preliminary evidence that in COPD patients ICS/LABD treatment reduces the severity of STEMI acute-phase clinical manifestations compared to other inhaled treatments.
2017 AHA/ACC Clinical Performance and Quality Measures for Adults With ST-Elevation and Non–ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology/American Heart Association Task Force on Performance Measures
2017, Journal of the American College of Cardiology

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Brief reportRelation between use of antiinflammatory agents and left ventricular free wall rupture during acute myocardial infarction

Abstract

Am J Cardiol

Am J Med

Wound healing II. Injury and abnormal repair

N Engl J Med

Brief report
Relation between use of antiinflammatory agents and left ventricular free wall rupture during acute myocardial infarction