Exercise Training Increases Serum Cardiac Troponin T Independent of Left Ventricular Mass

Author(s):  
Zhaowei Kong ◽  
Haifeng Zhang ◽  
Jinlei Nie ◽  
Li Wen ◽  
Qingde Shi ◽  
...  

AbstractThe purpose of this study was to determine whether exercise training mediated cardiac troponin T (cTnT) and whether this was associated with increases in left ventricular mass (LVM). Fifty-four sedentary obese women were randomised to high-intensity interval training (HIIT, repeated 4–min cycling at 90% V̇O2max interspersed with 3–min rest), work-equivalent continuous aerobic training (CAT, continuous cycling at 60% V̇O2max) or a control group (CON). Resting serum cTnT was assessed using a high-sensitivity assay before and after 12 weeks of training. LVM was determined from 2D echocardiography at the same timepoints. Both HIIT and CAT induced a similar elevation (median 3.07 to 3.76 ng.l−1, p<0.05) in resting cTnT compared with pre-training and the CON (3.49 to 3.45 ng.l−1, p>0.05). LVM index in HIIT increased (62.2±7.8 to 73.1±14.1 g.m−2, p<0.05), but not in CAT (66.1±9.7 to 67.6±9.6 g.m−2, p>0.05) and CON (67.9±9.5 to 70.2±9.1 g.m−2, p>0.05). Training-induced changes in resting cTnT did not correlate with changes in LVM index (r=−0.025, p=0.857). These findings suggest that twelve weeks of either HIIT or CAT increased resting cTnT, but the effects were independent of any changes in LVM in sedentary obese women.

2003 ◽  
Vol 49 (12) ◽  
pp. 2020-2026 ◽  
Author(s):  
Junnichi Ishii ◽  
Wei Cui ◽  
Fumihiko Kitagawa ◽  
Takahiro Kuno ◽  
Yuu Nakamura ◽  
...  

Abstract Background: Recent studies have suggested that cardiac troponin T (cTnT) and troponin I may detect ongoing myocardial damage involved in the progression of chronic heart failure (CHF). This study was prospectively designed to examine whether the combination of cTnT, a marker for ongoing myocardial damage, and B-type natriuretic peptide (BNP), a marker for left ventricular overload, would effectively stratify patients with CHF after initiation of treatment. Methods: We measured serum cTnT, plasma BNP, and left ventricular ejection fraction (LVEF) on admission for worsening CHF [New York Heart Association (NYHA) functional class III to IV] and 2 months after initiation of treatment to stabilize CHF (n = 100; mean age, 68 years). Results: Mean (SD) concentrations of cTnT [0.023 (0.066) vs 0.063 (0.20) μg/L] and BNP [249 (276) vs 753 (598) ng/L], percentage increased cTnT (&gt;0.01 μg/L; 35% vs 60%), NYHA functional class [2.5 (0.6) vs 3.5 (5)], and LVEF [43 (13)% vs 36 (12)%] were significantly (P &lt;0.01) improved 2 months after treatment compared with admission. During a mean follow-up of 391 days, there were 44 cardiac events, including 12 cardiac deaths and 32 readmissions for worsening CHF. On a stepwise Cox regression analysis, increased cTnT and BNP were independent predictors of cardiac events (P &lt;0.001). cTnT &gt;0.01 μg/L and/or BNP &gt;160 ng/L 2 months after initiation of treatment were associated with increased cardiac mortality and morbidity rates. Conclusion: The combination of cTnT and BNP measurements after initiation of treatment may be highly effective for risk stratification in patients with CHF.


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.


2021 ◽  
Author(s):  
Muzheng Li ◽  
Zhijian Wu ◽  
Ilyas Tudahun ◽  
Qiuzhen Lin ◽  
Na Liu ◽  
...  

Abstract Aims: The level of serum carbohydrate antigen 125 (CA 125) elevated is a common finding in patients with cardiac amyloidosis in clinical practice. It is unclear whether CA 125 is correlated with cardiac amyloidosis. The aim of this study was to systematically evaluate the clinical implications of CA 125 elevation in patients with cardiac amyloidosis.Methods and Results: We enrolled 101 patients diagnosed with cardiac amyloidosis at the Second Xiangya Hospital, 41 patients with acute decompensated heart failure (AHF) and 39 patients with multiple myeloma (MM) who were confirmed to have no cardiac amyloidosis served as control group, respectively. In 101 patients with cardiac amyloidosis, 58 (57%) patients had elevated serum CA 125 levels, which the mean age was 61.2 ± 11.4 years. Patients with high CA 125 were more likely to present with polyserositis ( 79.3% vs 60.5%, p = 0.03) , higher levels of hemoglobin (117.22 ± 21.87 g/L vs. 106.07 ± 25.15 g/L, p = 0.01), serum potassium (4.17 ± 0.49 mmol/L vs. 3.98 ± 0.41 mmol/L, p = 0.05), low density lipoprotein-cholesterol (2.98 ± 1.65 mmol/L vs. 2.22 ± 1.10 mmol/L, p = 0.01), and cardiac troponin T (115 pg/mL vs. 59.52 pg/mL, p = 0.005) . The serum CA 125 levels were significantly higher in cardiac amyloidosis than AHF and MM. The median overall survival for patients with elevated and normal serum CA125 were 5 and 20 months, respectively (p = 0.012). According to multivariate Cox hazard analysis, CA 125 (HR 1.002, 95%CI 1.000-1.004, p = 0.020) contributed to all-cause mortality. The time-dependent receiver operating characteristic was used to reflect the accuracy of different biomarkers in predicting overall survival at various time points by the area under the curve (AUC). CA 125 has no worse prediction accuracy than cardiac troponin T, NT-proBNP and LDH according to the AUC.Conclusions: The prevalence of elevated serum CA 125 levels is more than 50% in patients with cardiac amyloidosis. As an independent prognostic predictor, highly serum CA 125 values indicated the lower overall survival and the accuracy of predicting prognosis was not inferior to the other biomarkers.


Sign in / Sign up

Export Citation Format

Share Document