scholarly journals Prospective evaluation of the role of routine cardiac troponin T measurement to identify left ventricular ejection fraction < 40% after first myocardial infarction

Heart ◽  
2003 ◽  
Vol 89 (5) ◽  
pp. 559-560 ◽  
Author(s):  
A C R Rao
2021 ◽  
Vol 41 (2) ◽  
Author(s):  
Ana C.A. Casarotti ◽  
Daniela Teixeira ◽  
Ieda M. Longo-Maugeri ◽  
Mayari E. Ishimura ◽  
Maria E.R. Coste ◽  
...  

Abstract Despite early reperfusion, patients with ST segment elevation myocardial infarction (STEMI) may present large myocardial necrosis and significant impairment of ventricular function. The present study aimed to evaluate the role of subtypes of B lymphocytes and related cytokines in the infarcted mass and left ventricular ejection fraction obtained by cardiac magnetic resonance imaging performed after 30 days of STEMI. This prospective study included 120 subjects with STEMI submitted to pharmacoinvasive strategy. Blood samples were collected in subjects in the first (D1) and 30th (D30) days post STEMI. The amount of CD11b+ B1 lymphocytes (cells/ml) at D1 were related to the infarcted mass (rho = 0.43; P=0.033), measured by cardiac MRI at D30. These B1 cells were associated with CD4+ T lymphocytes at D1 and D30, while B2 classic lymphocytes at day 30 were related to left ventricular ejection fraction (LVEF). Higher titers of circulating IL-4 and IL-10 were observed at D30 versus D1 (P=0.013 and P&lt;0.001, respectively). Titers of IL-6 at D1 were associated with infarcted mass (rho = 0.41, P&lt;0.001) and inversely related to LVEF (rho = −0.38, P&lt;0.001). After multiple linear regression analysis, high-sensitivity troponin T and IL-6 collected at day 1 were independent predictors of infarcted mass and, at day 30, only HDL-C. Regarding LVEF, high-sensitivity troponin T and high-sensitivity C-reactive protein were independent predictors at day 1, and B2 classic lymphocytes, at day 30. In subjects with STEMI, despite early reperfusion, the amount of infarcted mass and ventricular performance were related to inflammatory responses triggered by circulating B lymphocytes.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Toru Kondo ◽  
Naoki Shibata ◽  
shingo kazama ◽  
Yuki Kimura ◽  
Hideo Oishi ◽  
...  

Background: Fulminant myocarditis (FM) is a fatal disease that causes rapid-onset severe heart failure requiring inotropes or mechanical circulatory support (MCS). Because insufficient myocardial recovery requires durable left ventricular assist device or heart transplantation, the course of myocardial recovery should be predicted. Hypothesis: Cardiac troponins, which elevates due to myocardial damage, may associate with myocardial recovery in FM. Purpose: We aimed to investigate the relationship between cardiac troponin T (TnT) levels and myocardial recovery course in patients with FM. Method: We performed a retrospective medical record review of 19 patients with FM requiring MCS from May 2012 to January 2020. The serial changes of one-week left ventricular ejection fraction (LVEF) after MCS implantation according to TnT levels were evaluated. Results: Median age was 50 years and 10 patients were male. As for initial MCS, veno-arterial extracorporeal membrane oxygenation (VA-ECMO) with intra-aortic balloon pumping (IABP) were used in 13 patients, IABP in 4 patients, VA-ECMO in one patient, and impella 2.5 in one patient. Median peak TnT level within one week after MCS implantation were 4.43 (2.47 - 34.6) ng/mL. The patients were divided into High-TnT group and Low-TnT group according to median peak TnT level. All patients in both groups were alive until 7 days after MCS implantation, and LVEF on day 7 was significantly lower in the High-TnT group (Fig). TnT level was highest on day 1 and gradually decreased in the High-TnT group (Fig). Six patients died during hospitalization in the High-TnT group, in contrast, only one patient died in the Low-TnT group (p=0.020). Peak TnT level in patients with LVEF ≥30% (n=8) on day 7 was significantly lower than in patients with LVEF <30% (2.40 vs 13.5 ng/mL, p=0.012), however, other laboratory parameters showed no significant differences. Conclusion: Higher TnT level showed impaired myocardial recovery in patients with FM.


2018 ◽  
Vol 47 (5) ◽  
pp. 361-371 ◽  
Author(s):  
Qing Kuang ◽  
Ning Xue ◽  
Jing Chen ◽  
Ziyan Shen ◽  
Xiaomeng Cui ◽  
...  

Background: Chronic kidney disease (CKD) has been proposed to associate with decreased hydrogen sulfide (H2S) level. Nevertheless, the role of H2S in the pathogenesis of CKD has not been fully investigated. Our study aimed to investigate the plasma level of endogenous H2S in patients with different stages of CKD, and to identify the role of H2S in the progression of CKD and its relationship with cardiovascular diseases. Methods: A total of 157 non-dialysis CKD patients were recruited in our study, with 37 age- and sex-matched healthy individuals as control. Plasma concentration of H2S was measured with spectrophotometry. Sulfhemoglobin, the integration of H2S and hemoglobin, was characterized and measured by dual wavelength spectrophotometry. Serum levels of homocysteine (Hcy), cardiac troponin T (cTnT), and N-terminal pro B type natriuretic peptide were measured using automated analyzers. Conventional transthoracic echocardiography was performed and left ventricular ejection fraction (LVEF) was analyzed as a sensitive parameter of cardiac dysfunction. Results: The plasma H2S level (μmol/L) in CKD patients was significantly lower than those in healthy controls (7.32 ± 4.02 vs. 14.11 ± 5.24 μmol/L, p < 0.01). Plasma H2S level was positively associated with estimated glomerular filtration rate (eGFR; ρ = 0.577, p < 0.01) and negatively associated with plasma indoxyl sulfate concentration (ρ = –0.554, p < 0.01). The mRNA levels of cystathionine β-synthase and cystathionine γ-lyase, 2 catalytic enzymes of H2S formation, were significantly lower in blood mononuclear cells of CKD patients with respect to controls; however, the mRNA level of 3-mercaptopyruvate sulfurtransferase, as another H2S-producing enzyme, was significantly higher in CKD patients. The serum concentration of Hcy, acting as the substrate of H2S synthetase, was higher in the CKD group (p < 0.01). Specifically, the content of serum Hcy in CKD stages 3–5 patients was significantly higher than that in CKD stages 1–2, indicating an increasing trend of serum Hcy with the decline of renal function. Examination of ultrasonic cardiogram revealed a negative ­correlation between plasma H2S level and LVEF (ρ = –0.204, p < 0.05) in CKD patients. The H2S level also correlated negatively with cTnT concentration (ρ = –0.249, p < 0.01). Conclusions: Plasma H2S level decreased with the decline of eGFR, which may contribute to the cardiac dysfunction in CKD ­patients.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Konkal-Matt R Prasad ◽  
Ronald J Beyers ◽  
Yaqin Xu ◽  
Brent A French

Introduction: The wide tissue tropism exhibited by AAV provides for efficient gene transfer throughout the body, but targeting gene expression to cardiomyocytes is desirable for cardiac gene therapy. We hypothesized that targeted overexpression of extracellular superoxide dismutase (EcSOD) via the cardiac Troponin-T (cTnT) promoter would suffice to minimize left ventricular (LV) remodeling after myocardial infarction (MI). Methods: An AAV9 vector expressing EcSOD from the cTnT promoter (AcTnTEcSOD) was injected into 5 wk-old C57 mice via jugular vein (3x10 11 vp/mouse). Western blots, immunohistochemistry & in vitro SOD assays were used to measure EcSOD expression, distribution and activity. Cardiac magnetic resonance (CMR) imaging was performed at baseline (5 wks post-vector injection) and at days 1, 7 & 28 after MI to assess LV volumes (vol) & ejection fraction (EF) as compared to WT mice (n=4). Infarct (IF) sizes were also compared by DE on D1. Results: Systemic injection of the vector (AcTnTEcSOD) provided uniform EcSOD overexpression within cardiomyocytes (Panels A&B) and elevated total cardiac SOD activity by 5.6 fold (p<0.05). On D1 post-MI, IF sizes were similar in vector & WT groups (p=ns). The vector group had significantly lower end-diastolic vol at D7, D28 and lower end-systolic vol at D28 (all p<0.05 by ANOVA, Panels C&D), resulting in improved D28 EF over controls (p=0.02). Conclusions: Cardiac-specific overexpression of therapeutic genes can be achieved by combining highly-efficient AAV9 vectors with cardiac-specific promoters. AAV-mediated, cardiac-restricted overexpression of EcSOD from the cTnT promoter significantly reduces post-MI LV remodeling.


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