Association between admission systolic blood pressure and major adverse cardiovascular events in patients with acute myocardial infarction

Abstract Background Controversy exists regarding the use of beta-blockers (BBs) among patients with acute myocardial infarction (AMI) in contemporary reperfusion era. Previous studies predominantly focused on beta-blockers prescribed at discharge, and the effect of long-term adherence to beta-blocker on major adverse cardiovascular events (MACE) remains unclear. Objective To explore the association between long-term beta-blocker use patterns and MACE among contemporary AMI patients. Methods We enrolled 7860 patients with AMI, who were discharged alive and prescribed with BBs based on CAMI registry from January 2013 to September 2014. Patients were divided into two groups according to BBs use pattern: Always users group (n=4476) were defined as patients reporting BBs use at both 6- and 12-month follow-up; Inconsistent users group were defined as patients reporting at least once not using BBs at 6- or 12-month follow-up. Primary outcome was defined as MACE at 24-month follow-up, including all-cause death, non-fatal MI and repeat-revascularization. Multivariable cox proportional hazards regression model was used to assess the association between BBs and MACE. Results Baseline characteristics are shown in table 1. At 2-year follow-up, 518 patients in inconsistent users group (15.6%) and 548 patients in always users group (12.3%) had MACE. After multivariable adjustment, inconsistent use of BBs was associated with higher risk of MACE (HR: 1.323, 95% CI: 1.171–1.493, p<0.001). Table 1 Baseline characteristics Variable Always user (N=4476) Inconsistent user (N=3384) P value Age (years) 60.6±12.0 61.2±12.2 <0.001 Male 3381 (75.7%) 2461 (74.3%) 0.084 Diabetes 892 (20.0%) 610 (18.4%) 0.003 Hypertension 2372 (53.2%) 1543 (46.6%) <0.001 Dyslipidemia 244 (5.5%) 126 (3.8%) <0.001 Prior myocardial infarction 351 (7.9%) 232 (7.0%) <0.001 Heart failure 88 (2.0%) 63 (1.9%) <0.001 Chronic obstructive pulmonary disease 66 (1.5%) 60 (1.8%) <0.001 Current smoker 2054 (46.1%) 1579 (47.8%) 0.179 Left ventricular ejection fraction (%) 53.7±11.48 54.0±10.9 <0.001 Major Adverse Cardiovascular Events 548 (12.3%) 518 (15.6%) <0.001 Conclusions Our results showed consistent BBs use was associated with reduced risk of MACE among patients with AMI managed by contemporary treatment. Acknowledgement/Funding CAMS Innovation Fund for Medical Sciences (CIFMS) (2016-I2M-1-009)

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S100a8/a9 Signaling Causes Mitochondrial Dysfunction and Cardiomyocyte Death in Response to Ischemic/Reperfusion Injury

Circulation ◽

10.1161/circulationaha.118.039262 ◽

2019 ◽

Vol 140 (9) ◽

pp. 751-764 ◽

Cited By ~ 20

Author(s):

Yulin Li ◽

Boya Chen ◽

Xinying Yang ◽

Congcong Zhang ◽

Yao Jiao ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Percutaneous Coronary Intervention ◽

Cardiovascular Events ◽

Ischemia Reperfusion ◽

Coronary Intervention ◽

Major Adverse Cardiovascular Events ◽

Mouse Heart ◽

Early Reperfusion ◽

Percutaneous Coronary

Background: Myocardial ischemia-reperfusion (MI/R) injury is a significant clinical problem without effective therapy. Unbiased omics approaches may reveal key MI/R mediators to initiate MI/R injury. Methods: We used a dynamic transcriptome analysis of mouse heart exposed to various MI/R periods to identify S100a8/a9 as an early mediator. Using loss/gain-of-function approaches to understand the role of S100a8/a9 in MI/R injury, we explored the mechanisms through transcriptome and functional experiment. Dynamic serum S100a8/a9 levels were measured in patients with acute myocardial infarction before and after percutaneous coronary intervention. Patients were prospectively followed for the occurrence of major adverse cardiovascular events. Results: S100a8/a9 was identified as the most significantly upregulated gene during the early reperfusion stage. Knockout of S100a9 markedly decreased cardiomyocyte death and improved heart function, whereas hematopoietic overexpression of S100a9 exacerbated MI/R injury. Transcriptome/functional studies revealed that S100a8/a9 caused mitochondrial respiratory dysfunction in cardiomyocytes. Mechanistically, S100a8/a9 downregulated NDUF gene expression with subsequent mitochondrial complex I inhibition via Toll-like receptor 4/Erk–mediated Pparg coactivator 1 alpha/nuclear respiratory factor 1 signaling suppression. Administration of S100a9 neutralizing antibody significantly reduced MI/R injury and improved cardiac function. Finally, we demonstrated that serum S100a8/a9 levels were significantly increased 1 day after percutaneous coronary intervention in patients with acute myocardial infarction, and elevated S100a8/a9 levels were associated with the incidence of major adverse cardiovascular events. Conclusions: Our study identified S100a8/a9 as a master regulator causing cardiomyocyte death in the early stage of MI/R injury via the suppression of mitochondrial function. Targeting S100a8/a9-intiated signaling may represent a novel therapeutic intervention against MI/R injury. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT03752515

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