Beta-blockers and renin-angiotensin system inhibitors in acute myocardial infarction managed with inhospital coronary revascularization

Sim, Hui-Wen; Zheng, Huili; Richards, A. Mark; Chen, Ruth W; Sahlén, Anders; Yeo, Khung‐Keong; Tan, Jennifer K.; Chua, Terrance; Tan, Huay Cheem; Yeo, Tiong Cheng; Ho, Hee Hwa; Liew, Boon-Wah; Foo, Ling Li; Lee, Chi‐Hang; Hausenloy, Derek J.; Chan, Mark Y.

doi:10.1038/s41598-020-72232-y

Cited by 16 publications

(10 citation statements)

References 29 publications

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“…In this regard and through its effects in modulating post-MI remodeling, tropoelastin therefore bears some similarity to drugs historically used as subacute therapeutics, such as angiotensin converting enzyme inhibitors. 62 Following the subacute effects of MI and during progressive heart failure, the heart undergoes compensatory LV dilatation. 63 Therefore, to understand the effects of tropoelastin in a more chronic setting, future studies will likely concentrate on injecting tropoelastin 2 to 3 weeks post-MI with longer term (≥6 months) functional studies to elucidate its effects on LV dilatation.…”

Section: Discussionmentioning

confidence: 99%

Tropoelastin Improves Post-Infarct Cardiac Function

Hume

Kanagalingam

Deshmukh

et al. 2023

Circulation Research

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BACKGROUND: Myocardial infarction (MI) is among the leading causes of death worldwide. Following MI, necrotic cardiomyocytes are replaced by a stiff collagen-rich scar. Compared to collagen, the extracellular matrix protein elastin has high elasticity and may have more favorable properties within the cardiac scar. We sought to improve post-MI healing by introducing tropoelastin, the soluble subunit of elastin, to alter scar mechanics early after MI. METHODS AND RESULTS: We developed an ultrasound-guided direct intramyocardial injection method to administer tropoelastin directly into the left ventricular anterior wall of rats subjected to induced MI. Experimental groups included shams and infarcted rats injected with either PBS vehicle control or tropoelastin. Compared to vehicle treated controls, echocardiography assessments showed tropoelastin significantly improved left ventricular ejection fraction (64.7±4.4% versus 46.0±3.1% control) and reduced left ventricular dyssynchrony (11.4±3.5 ms versus 31.1±5.8 ms control) 28 days post-MI. Additionally, tropoelastin reduced post-MI scar size (8.9±1.5% versus 20.9±2.7% control) and increased scar elastin (22±5.8% versus 6.2±1.5% control) as determined by histological assessments. Ribonucleic acid sequencing analyses of rat infarcts showed that tropoelastin injection increased genes associated with elastic fiber formation 7 days post-MI and reduced genes associated with immune response 11 days post-MI. To show translational relevance, we performed immunohistochemical analyses on human ischemic heart disease cardiac samples and showed an increase in tropoelastin within fibrotic areas. Using ribonucleic acid sequencing we also demonstrated the tropoelastin gene ELN is upregulated in human ischemic heart disease and during human cardiac fibroblast-myofibroblast differentiation. Furthermore, we showed by immunocytochemistry that human cardiac fibroblast synthesize increased elastin in direct response to tropoelastin treatment. CONCLUSIONS: We demonstrate for the first time that purified human tropoelastin can significantly repair the infarcted heart in a rodent model of MI and that human cardiac fibroblast synthesize elastin. Since human cardiac fibroblasts are primarily responsible for post-MI scar synthesis, our findings suggest exciting future clinical translation options designed to therapeutically manipulate this synthesis.

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Section: Discussionmentioning

confidence: 99%

Tropoelastin Improves Post-Infarct Cardiac Function

Hume

Kanagalingam

Deshmukh

et al. 2023

Circulation Research

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“…The American College of Cardiology have proposed several conditions to be considered as atherosclerotic cardiovascular disease risk enhancers, including inflammatory disease such as rheumatoid arthritis or human immunodeficiency virus infection [ 28 ]. Established risk scores have also been shown to underestimate cardiovascular risk within these specific patient populations [ 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 ]. Hence, we propose that further research is needed to ascertain the value of adding cancer as a variable to the ASCVD score, as well as to identify and include relevant cancer-related variables to improve its applicability within patients with prior cancer.…”

Section: Discussionmentioning

confidence: 99%

“…The Singapore Myocardial Infarction Registry consists of data from patients diagnosed with AMI from 2007 across all hospitals within the country. Specialized coordinators collected data including patient demographics, clinical presentation, medications, laboratory and procedural parameters [ 15 ]. As individual-level blood pressure values were only available within the registry from 2017, data on blood pressure was extracted from hospital-level databases from two centers and merged with the national registry for the years 2007 to 2016.…”

Section: Methodsmentioning

confidence: 99%

Prior Cancer Is Associated with Lower Atherosclerotic Cardiovascular Disease Risk at First Acute Myocardial Infarction

et al. 2022

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Background: Patients with cancer are at increased risk of acute myocardial infarction (AMI). It is unclear if the Atherosclerotic Cardiovascular Disease (ASCVD) risk score at incident AMI is reflective of this higher risk in patients with prior cancer than those without. Methods: We linked nationwide AMI and cancer registries from 2008 to 2019. A total of 18,200 eligible patients with ASCVD risk score calculated at incident AMI were identified (1086 prior cancer; 17,114 no cancer). Results: At incident AMI, age-standardized mean ASCVD risk was lower in the prior cancer group (18.6%) than no cancer group (20.9%) (p < 0.001). Prior to incident AMI, smoking, hypertension, hyperlipidemia and diabetes mellitus were better controlled in the prior cancer group. However post-AMI, prior cancer was associated with lower guideline-directed medical therapy usage and higher all-cause mortality (adjusted hazard ratio 1.85, 95% confidence interval 1.66–2.07). Conclusions: AMI occurred despite better control of cardiovascular risk factors and lower age-standardized estimated mean 10-year ASCVD risk among patients with prior cancer than no cancer. Prior cancer was associated with lower guideline-directed medical therapy post-AMI and higher mortality.

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“…In a recent study, Rodriguez-Palomares et al concluded that assessment of left ventricular remodeling at 6 months did not increase the prognostic value of the principal cardiac magnetic resonance (CMR) derived variables provided by early CMR 23 . Since access to CMR is limited, we believe that this nomogram, once validated, could offer a widely available, low-cost alternative to predict patients at risk of developing pathologic left ventricular remodeling and we are doing so in a very early stage of myocardial infarction (12 hours after reperfusion has been achieved) despite administering optimal medical therapy and revascularization 24 .…”

Section: Discussionmentioning

confidence: 99%

Nomogram Containing Simple Routine Clinical and Biochemical Parameters Can Predict Pathologic Ventricular Remodeling in STEMI Patients

Vinter¹

2021

ACC

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Heart failure is the leading cause of morbidity and mortality worldwide, with ischemic heart disease being one of the most important etiologic factors. Heart failure develops due to ventricular remodeling, which leads to increases in left ventricular end-systolic and end-diastolic volumes. In this prospective observational study, we included 101 patients with first episode of ST-segment elevation myocardial infarction in whom percutaneous coronary intervention was conducted within 12 h and Thrombolysis in Myocardial Infarction III flow was achieved. The aim was to determine which clinical and biochemical parameters can help predict pathologic ventricular remodeling 1 year after myocardial infarction. We created a nomogram based on routinely used blood tests and vital parameters which showed highest correlation with pathologic ventricular remodeling. The nomogram included NTproBNP value 12 h after reperfusion, aspartate transaminase value 12 h after reperfusion, systolic blood pressure value on admission, and culprit coronary artery. We performed ROC analysis which yielded great predictive value of the nomogram. The area under curve was 0.907 (95% CI 0.842-0.973). The nomogram value of -3.54 had 91.4% sensitivity and 74.0% specificity. We believe that this nomogram, once validated, could offer a widely available, low-cost option that would help identify patients at risk of developing pathologic left ventricular remodeling and achieve this at a very early stage of myocardial infarction (12 h after reperfusion has been achieved).

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Beta-blockers and renin-angiotensin system inhibitors in acute myocardial infarction managed with inhospital coronary revascularization

Cited by 16 publications

References 29 publications

Tropoelastin Improves Post-Infarct Cardiac Function

Tropoelastin Improves Post-Infarct Cardiac Function

Prior Cancer Is Associated with Lower Atherosclerotic Cardiovascular Disease Risk at First Acute Myocardial Infarction

Nomogram Containing Simple Routine Clinical and Biochemical Parameters Can Predict Pathologic Ventricular Remodeling in STEMI Patients

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