ArticleJournal of the American College of Cardiology2018
Troponin Release and Reversible Left Ventricular Dysfunction After Transient Pressure Overload.
Article in Journal of the American College of Cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 138 citations in OpenAlex.
- Echocardiographic derived pulmonary artery wedge pressure is associated with mortality, heart hospitalizations, and functional capacity in chronic systolic heart failure: insights from the HF-ACTION trial.Journal of echocardiography · 2024Trial
- Preoperative N-terminal pro-B-type natriuretic peptide and myocardial injury after stopping or continuing renin-angiotensin system inhibitors in noncardiac surgery: a prespecified analysis of a phase 2 randomised controlled multicentre trial.British journal of anaesthesia · 2024Trial
- Discontinuation vs. continuation of renin-angiotensin system inhibition before non-cardiac surgery: the SPACE trial.European heart journal · 2024Trial
- How Much Is Too Much? Cardiac Biomarkers After Cardiac Surgery: A Debate With No End in Sight?Journal of the American Heart Association · 2026Article
- Reductions in myocardial interstitial fibrosis are dissociated from LV chamber stiffness in swine with repetitive pressure overload.American journal of physiology. Heart and circulatory physiology · 2026Article
- When the heart cannot keep pace: case report of acute myocarditis in a recreational marathon runner.European heart journal. Case reports · 2026Article
- Mitochondrial DNA-Mediated Immune Activation After Resuscitation From Cardiac Arrest.Journal of the American Heart Association · 2026Article
- Article
- Myocardial stunning: mechanisms, molecular insights, and gaps in knowledge.Bioscience reports · 2025Review
- Utilizing saliva for non-invasive detection of exercise-induced myocardial injury with point-of-care cardiac troponin-I.Scientific reports · 2025Article
- Splenic modulation of the early inflammatory response to regional and global ischemia/reperfusion injury in swine.American journal of physiology. Heart and circulatory physiology · 2025Article
- The Pathophysiology of Cardiac Troponin Release and the Various Circulating Cardiac Troponin Forms-Potential Clinical Implications.Journal of clinical medicine · 2025Review
- Persistent Fibrosis and Left Ventricular Chamber Stiffening Despite Cessation of Repetitive Pressure Overload in Swine.JACC. Basic to translational science · 2025Article
- Impact of High Intensity Contact Physical Activity During a Match on Echocardiographic Parameters and High-Sensitivity Troponin I in Competitive Rugby Players.Journal of clinical medicine · 2025Article
- Delta troponin does not distinguish acute coronary syndrome in emergency department patients with renal impairment and an initial positive troponin.Journal of the American College of Emergency Physicians open · 2024Article
- Role of Antitroponin Antibodies and Macrotroponin in the Clinical Interpretation of Cardiac Troponin.Journal of the American Heart Association · 2024Review
- Anti-apoptotic and antioxidant mechanisms may underlie the abrogative potential ofToxicology reports · 2024Article
- Negative Impact of Acute Reloading after Mechanical Left Ventricular Unloading.Journal of cardiovascular translational research · 2024Article
- Early Diagnosis of Cardiovascular Diseases in the Era of Artificial Intelligence: An In-Depth Review.Cureus · 2024Review
- Clinical Interpretation of Serum Troponin in the Era of High-Sensitivity Testing.Diagnostics (Basel, Switzerland) · 2024Review
5 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe authors previously demonstrated that brief ischemia elicits cardiac troponin I (cTnI) release and myocyte apoptosis in the absence of necrosis. It remains uncertain whether other pathophysiological stresses can produce apoptosis and transient cTnI release without ischemia.
objectivesThis study sought to determine whether a transient increase in left ventricular (LV) preload elicits cTnI release in the absence of ischemia.
methodsPropofol-anesthetized swine (N = 13) received intravenous phenylephrine (PE) (300 μg/min) for 1 h to increase left ventricular end-diastolic pressure (LVEDP) to ∼30 mm Hg. Serial cTnI and echocardiographic function were assessed for 24 h, and myocardial tissue was analyzed for apoptosis and necrosis.
resultsPE infusion increased systolic blood pressure from 137 ± 14 mm Hg to 192 ± 11 mm Hg (mean ± SD; p < 0.001) and increased LVEDP from 17 ± 2 mm Hg to 30 ± 5 mm Hg (p < 0.001). Myocardial flow measurements demonstrated no evidence of ischemia. Hemodynamics normalized rapidly after PE, but LV ejection fraction remained depressed (32 ± 21% vs. 58 ± 7%; p < 0.01) with normalization after 24 h (51 ± 16%; p = 0.31). Baseline transcoronary cTnI release was low (16 ± 20 ng/l) but increased to 856 ± 956 ng/l (p = 0.01) 1 h after LVEDP elevation. Circulating cTnI rose above the 99th percentile within 30 min and remained elevated at 24 h (1,462 ± 1,691 ng/l). Pathological analysis demonstrated myocyte apoptosis at 3 h (31.3 ± 11.9 myocytes/cm
conclusionsTransient elevations of LVEDP lead to cTnI release, apoptosis, and reversible stretch-induced stunning in the absence of ischemia. Thus, preload-induced myocyte injury may explain many cTnI elevations seen in the absence of clinical signs or symptoms of myocardial ischemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.