The appropriateness of coronary investigation in myocardial injury and type 2 myocardial infarction (ACT-2): A randomized trial design

Lambrakis, Kristina; French, John K.; Scott, Ian A; Briffa, Tom; Brieger, David; Farkouh, Michael E.; White, Harvey D.; Chuang, Anthony; Tiver, Kathryn; Quinn, Stephen; Kaambwa, Billingsley; Horsfall, Matthew; Morton, Erin; Chew, Derek P.

doi:10.1016/j.ahj.2018.09.016

Cited by 54 publications

(38 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…65 primary endpoint of all-cause mortality at 2 years. 68 Cost-effectiveness will be determined based on clinical events, quality of life, and resource utilization over 24 months. 68 Beyond those patients with ischemic myocardial injury, unfortunately, no consensus exists regarding routine management of patients with myocardial injury.…”

Section: Laboratory Data and Imagingmentioning

confidence: 99%

Myocardial Injury in the Era of High-Sensitivity Cardiac Troponin Assays

et al. 2019

View full text Add to dashboard Cite

Section: Laboratory Data and Imagingmentioning

confidence: 99%

Myocardial Injury in the Era of High-Sensitivity Cardiac Troponin Assays

et al. 2019

View full text Add to dashboard Cite

“…In contrast, myocardial injury is defined as an elevated troponin without evidence of myocardial ischaemia and is subdivided into acute and chronic injury depending on the presence or absence of an observed rise and/or fall in troponin levels, respectively (Thygesen et al, 2018). In patients with CKD, acute and chronic myocardial injury likely account for a substantial portion of troponin elevations (Janzon et al, 2016;Lambrakis et al, 2019;Taylor et al, 2007;Thygesen et al, 2010). Indeed, in two recent large randomised trials of hs-cTn in clinical practice involving 48,282 and 3,378 patients both acute and chronic myocardial injury was found to account for at least 30% of patients with ele-vated troponin (Chew et al, 2019;Shah et al, 2018).…”

Section: Myocardial Infarction Myocardial Injury and The Fourth Univmentioning

confidence: 99%

“…Currently, there are two ongoing randomised trials investigating the role of invasive coronary assessment in patients with myocardial injury: ACT-2 (The Appropriateness of Coronary investigation in myocardial injury and Type 2 myocardial infarction, AC-TRN12618000378224) (Lambrakis et al, 2019) and DEMAND MI (DEtermining the Mechanism of myocardial injury AND role of coronary disease in type 2 Myocardial Infarction, NCT03338504).…”

Section: Myocardial Injury and Potential Myocardial Therapiesmentioning

confidence: 99%

High-sensitivity troponin in chronic kidney disease: Considerations in myocardial infarction and beyond

Chuang,

Nguyen,

Kung

et al. 2020

Rev. Cardiovasc. Med.

View full text Add to dashboard Cite

Acute myocardial infarction (MI) represents one of the most common hospital encounters, with significant short-term and long-term morbidity and mortality, and frequently occurs in patients with chronic kidney disease (CKD). Cardiac troponin is an exquisitely sensitive biomarker for myocardial injury and plays an essential role in the diagnosis, risk-stratification, and management of MI. In 2017, the United States Food and Drug Administration approved Roche Diagnostics’ 5th generation high-sensitivity cardiac troponin (hs-cTn) for clinical use. Whilst the improved analytical sensitivity of these new high-sensitivity troponin assays facilitate early diagnosis of MI, it also frequently identifies troponin elevations above the conventional reference threshold in the context of non-coronary conditions such as renal dysfunction, and can represent a major diagnostic challenge to clinicians. Furthermore, the optimal management strategy of patients with troponin elevation and high comorbidity burden, a common issue in patients with CKD, remains undefined. In recent years, there has been substantial research and progress undertaken in this rapidly evolving area. In this review, we aim to provide clinicians with an overview of hs-cTn in the setting of CKD as well as an update on its application and the particular considerations involved in the management of myocardial infarction, stable coronary artery disease and myocardial injury in this high risk population.

show abstract

“…[1,2] MI is characterized by myocardial cell necrosis due to the prolonged insufficient coronary oxygen and nutrient supply. [3] As a selective b1-adrenoceptor antagonist, the inexpensive medication metoprolol has been regarded as a common cardiovascular medication for acute myocardial infarction (AMI), alleviating the ischaemia and reperfusion damage and reducing the risk of perioperative cardiac complications. [4] However, the essential mechanism through which metoprolol exerts its cardioprotective effects remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Metoprolol protects against myocardial infarction by inhibiting miR-1 expression in rats

Qin

Zhang

et al. 2020

Journal of Pharmacy and Pharmacology

View full text Add to dashboard Cite

Objectives Metoprolol is regarded as a first‐line medicine for the treatment of myocardial infarction (MI). However, the underlying mechanisms remain largely unknown. This study aimed to investigate the involvement of miR‐1 in the pharmacological function of metoprolol. Methods In vivo MI model was established by left anterior descending coronary artery (LAD) ligation. The effects of metoprolol on infarct size and cardiac dysfunction were determined by triphenyltetrazolium chloride staining and cardiac echocardiography, respectively. In vitro oxidative stress cardiomyocyte model was established by H2O2 treatment. The effect of metoprolol on the expression of miR‐1 and connexin43 (Cx43) was quantified by real‐time PCR and western blot, respectively. The intercellular communication was evaluated by lucifer yellow dye diffusion. Key findings Left anterior descending ligation‐induced MI injury was markedly attenuated by metoprolol as shown by reduced infarct size and better cardiac function. Metoprolol reversed the up‐regulation of miR‐1 and down‐regulation of Cx43 in MI heart. Moreover, in H2O2‐stimulated cardiomyocytes, overexpression of miR‐1 abolished the effects of metoprolol on Cx43 up‐regulation and increased intercellular communication, indicating that miR‐1 may be a necessary mediator for the cardiac protective function of metoprolol. Conclusions Metoprolol relieves MI injury via suppression miR‐1, thus increasing its target protein Cx43 and improving intercellular communication.

show abstract

The appropriateness of coronary investigation in myocardial injury and type 2 myocardial infarction (ACT-2): A randomized trial design

Abstract: Chew , The appropriateness of coronary investigation in myocardial injury and Type 2 myocardial infarction (ACT-2): A randomized trial design. Ymhj (2018),

Cited by 54 publications

References 19 publications

Myocardial Injury in the Era of High-Sensitivity Cardiac Troponin Assays

Myocardial Injury in the Era of High-Sensitivity Cardiac Troponin Assays

High-sensitivity troponin in chronic kidney disease: Considerations in myocardial infarction and beyond

Metoprolol protects against myocardial infarction by inhibiting miR-1 expression in rats

Contact Info

Product

Resources

About