Background: Studies addressing patients with type 2 myocardial infarction and myocardial injury, including the impact of using high-sensitivity (hs) cardiac troponin (cTn) assays on their incidence are needed.
Methods: Ours is a prospective, observational US cohort study. Consecutive emergency department patients with serial cTnI measurements were studied. Outcomes included 180-day mortality and major adverse cardiac events, including 2-year follow-up for those with myonecrosis.
Results: Among 1640 patients, using a contemporary cTnI assay, 30% (n = 497) had ≥1 cTnI >99 percentile, with 4.7% (n = 77), 8.5% (n = 140), and 17% (n = 280) classified as type 1 myocardial infarction, type 2 myocardial infarction, and myocardial injury, respectively. Compared with patients without myonecrosis, 180-day mortality was higher for type 2 myocardial infarction (4% vs 13%, P < .0001) (adjusted hazard ratio 2.7; 95% confidence interval, 1.6-4.8; P = .0005) and myocardial injury (4% vs 11%, P < .0001) (adjusted hazard ratio 1.8; 95% confidence interval, 1.1-3.0; P = .02), both with mortality >20% at 2 years. Predictors of 2-year mortality for type 2 myocardial infarction included age, congestive heart failure, and beta-blockers. Relative to the contemporary cTnI assay, hs-cTnI had less myonecrosis (30% vs 26%, P = .003) and acute myocardial infarction (13.2% vs 10.8%, P = .032), including fewer type 2 myocardial infarctions (8.5% vs 6.3, P = .01), with no difference in myocardial injury (17% vs 15%, P = .1).
Conclusions: cTnI increases are encountered in approximately a third of patients, the majority due to nonatherothrombotic conditions. Compared with patients without myonecrosis, type 2 myocardial infarction and myocardial injury have worse short-term outcomes, with mortality rates >20% at 2 years. hs-cTnI assay does not lead to more myocardial injury or infarction.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.amjmed.2017.05.049 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Echocardiographic phenotypes of diabetic myocardial disorder: evolution over 15 months follow-up in the ARISE-HF trial.
Cardiovasc Diabetol
January 2025
Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Background: Diabetic myocardial disorder (DbMD, evidenced by abnormal echocardiography or cardiac biomarkers) is a form of stage B heart failure (SBHF) at high risk for progression to overt HF. SBHF is defined by abnormal LV morphology and function and/or abnormal cardiac biomarker concentrations.
Objective: To compare the evolution of four DbMD groups based on biomarkers alone, systolic and diastolic dysfunction alone, or their combination.
Revolutionizing Heart Failure Therapy: Harnessing IVT mRNA and Fusion Protein Technology to Prolong rhBNP Half-Life.
Pharm Res
January 2025
Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Purpose: Recombinant human B-type natriuretic peptide (rhBNP) has been extensively proven to be an effective mean of heart failure (HF) therapy, but its clinical application is limited by its very short half-life. This study aims to combine in vitro transcribed mRNA (IVT mRNA) and fusion protein technology to develop a rhBNP-Fc mRNA drug with long half-life, high efficiency and few side effects to treat HF.
Methods: The rhBNP-Fc fusion mRNA with IgG4-Fc sequence was produced by IVT technology.
TFEB activator protects against ethanol toxicity-induced cardiac injury by restoring mitophagy and autophagic flux.
Biochim Biophys Acta Mol Basis Dis
January 2025
College of Life Sciences, Institute of Life Science and Green Development, Hebei University, Baoding 071002, China; The Key Laboratory of Zoological Systematics and Application, College of Life Sciences, Hebei University, Baoding 071002, China. Electronic address:
Excessive alcohol consumption is a major cause of alcoholic cardiomyopathy (ACM) and myocardial injury. This study aims to investigate the role of transcription factor EB (TFEB) in ethanol-induced cardiac anomalies using a murine model, AC16 human cardiomyocytes, and human plasma. Wild-type mice treated with a TFEB activator (Compound 1) or vehicle (25 mg/kg/d) were challenged with or without ethanol (3 g/kg/d, i.
View Article and Find Full Text PDFTrends in Cardiovascular Diseases and Costs Among Type 2 Diabetes Mellitus (T2DM) Patients in Malaysia: A Cohort Study of 240,611 Public Hospital Inpatients.
Cureus
December 2024
Public Health, Ministry of Health Malaysia, Kuala Lumpur, MYS.
Background: Identifying trends of hospital admissions and costs for cardiovascular disease events (CVDEs) is crucial for public health intervention and the economic burden for future clinical improvements and better outcomes. This study aims to define the admission trends and cost of CVDE among type 2 diabetes mellitus (T2DM) patients in Malaysia between 2014 and 2020. Methodology: An ecological study was conducted using hospital admission data taken from the Casemix database in public hospitals in Malaysia.
View Article and Find Full Text PDFCirculating autophagy regulator Rubicon is linked to increased myocardial infarction risk.
J Mol Cell Cardiol Plus
March 2025
Center for Clinical Investigation (CIC1436)/CARDIOMET, Rangueil University Hospital, Toulouse, France.
Background: The identification of new biomarkers that improve existing cardiovascular risk prediction models for acute coronary syndrome is essential for accurately identifying high-risk patients and refining treatment strategies. Autophagy, a vital cellular degradation mechanism, is important for maintaining cardiac health. Dysregulation of autophagy has been described in cardiovascular conditions such as myocardial ischemia-reperfusion injury, a key factor in myocardial infarction (MI).
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!