Clinical, serum cardiac troponin T and echocardiographic evaluation for prediction of late doxorubicin cardiotoxicity

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 9536-9536
Author(s):  
E. C. Benites ◽  
M. G. Paiva ◽  
A. M. Cappellano ◽  
O. M. Felix ◽  
S. B. Marinelli ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Troponin T ◽  
Elevated Serum ◽  
Clinical Signs ◽  
Dobutamine Stress ◽  
Left Ventricular ◽  
Cardiac Troponin T ◽  
Group A ◽  
Group B ◽  
Serum Cardiac Troponin

9536 Background: To evaluate whether clinical signs or symptoms of congestive heart failure, serial assessment of systolic and diastolic cardiac function by low dose dobutamine stress echo (LDSE) and serum cardiac troponin T (cTnT) can predict doxorubicin (DOXO) cardiotoxicity. Methods: Twenty five patients with osteosarcoma enrolled in the Brazilian osteosarcoma treatment group study 2000, from january 2000 to may 2004, were studied with LDSE (>5μg/kg/min) before chemotherapy, 160 mg/m2 DOXO and after 160 mg/m2 DOXO. cTnT were measured before and during DOXO infusion. Cardiotoxicity was defined as shortening fraction (SF) less than 30% assessed by rest echo 1 to 6 months off chemotherapy. Group A comprised those without cardiotoxicity (16 patients, 10 male, 14.3 ± 4.7 years) whereas group B included those with a SF < 30% (9 patients, 6 male, 15.4 ± 3 years). Elevated serum cTnT was defined as seric levels above 0.01ng/ml. Results: Patients were submitted to a mean 3.4 LDSE and a mean of 32.5 serum cTnT. One patient (group B) presented clinical manifestation of cardiotoxicity. There was no statistical difference of elevated serum cTnT between the group B and group A (87.5% vs 46.2%; p=0,06). Left ventricular dimensions by M- MODE and transmitral Doppler inflow diastolic parameters were not significantly different between the two groups. Resting SF showed comparable values in both groups until cumulative doses of DOXO reached 160mg/m2, then the resting SF in group B was significant lower than group A (27% ± 2 and 34.1% ± 2, p<0.01). During dobutamine infusion, SF and ΔSF (dobutamine-rest) were significantly lower in group B as compared to group A at a DOXO dose 160mg/m2 (SF 36.1%±3,4 and ΔSF 2.1±2.3 vs. SF 45.2%±4.9 and ΔSF 9.4±3; p< 0.01 and p < 0.01) as well as at a DOXO dose > 160mg/m2 (30.3%±3 and 3.1±1.9 vs. 40.8%±5.9 and 7.2±4.2;p<0.01 and p<0.01). Conclusions: This study suggests that LDSE is more reliable than cTnT and clinical evaluation for predicting future subclinical cardiotoxicity,even at lower doxorubicin dose. No significant financial relationships to disclose.

Abstract 810: Impact of Elevated Plasma Matrix Metalloproteinase-2 on Prognosis in Hypertrophic Cardiomyopathy: Evidence from Long-Term Follow-Up of Genotyped Patients

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Eiichi Masuta ◽  
Hidekazu Ino ◽  
Noboru Fujino ◽  
Katsuharu Uchiyama ◽  
Kenshi Hayashi ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Cardiac Events ◽  
Group A ◽  
Group B

Background: Previous studies suggest that production of matrix metalloproteinase-2 (MMP-2) which is responsible for cardiac remodeling could determine prognosis of hypertrophic cardiomyopahty (HCM). However, few data exist regarding the importance of MMP-2 production in clinical settings. Therefore, we determined MMP-2 levels correlated to prognosis in HCM with sarcomere gene mutations. Methods and Results: Echocardiography and determination of plasma MMP-2 levels by enzyme-linked immunoassay were simultaneously performed in 31 HCM patients (22 women, mean age 56±12 years) with sarcomere protein gene mutation including 22 for cardiac troponin I, 5 for cardiac myosin binding-protein C, 3 for cardiac troponin T and 1 for beta-myosin heavy chain. Major cardiac events such as hospitalization due to congestive heart failure or ventricular fibrillation and mortality were prospectively examined for follow-up period of 48.4±29.1 months. When patients were divided into two groups (Group A: MMP-2 ≥800 ng/ml n=16 and Group B: MMP-2<800ng/ml n=15), there was no differences in mean age (59.4±11.7 year vs 53.1±11.3 year, p=0.13). On echocardiograms, interventricular septal thickness in group A (11.7±4.2 mm) was smaller than that in group B (15.9±4.8 mm, p<0.05) and percent fractional shortening (FS) was significantly impaired in group A (24.8±12.5%) in comparison with that in group B (37.7±8.1%, p=0.002). There was negative correlation between the MMP-2 levels and FS (p<0.001, r=0.76). The frequency of cardiac events was significantly higher in group A (10 patients of 16 patients) than in group B (1 patient of 15 patients, p=0.0012). Importantly, 5 patients of group A died, although none of groupB patients did (p=0.018). Conclusion: These results demonstrate that the high plasma concentration of MMP-2 (≥800 ng/ml) could be a predictor of prognosis in HCM with sarcomere mutations probably through reflecting impaired left ventricular function.

scholarly journals Correlation of cardiac troponin T level, clinical parameters and myocardial ischaemia in perinatal asphyxia

2013 ◽  
Vol 40 (2) ◽  
pp. 165-168
Author(s):  
CC Uzodimma ◽  
CAN Okoromah ◽  
E Ekure ◽  
CV Ezeaka ◽  
FO Njokanma
Keyword(s):  
Clinical Judgment ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Perinatal Asphyxia ◽  
Elevated Serum ◽  
Clinical Signs ◽  
Heart Rhythm ◽  
Cardiac Troponin T ◽  
Arterial Blood ◽  
Pulse Volume

Introduction: Resource limitation in developing countries may preclude access to cardiac troponin-T assay thereby necessitating reliance on clinical judgment for identification of hypoxic myocardial cellular injury.Objectives: To relate selected clinical signs with elevated serum cardiactroponin-T in asphyxiated term neonates.Methods: Asphyxia was identified by low umbilical arterial blood pH . 7.20 and low five minute Apgar score . 6 while controls were term, non.asphyxiated neonates. All babies were examined for heart rate,heart rhythm irregularities, peripheral pulse volume, respiratory rate,pallor, cyanosis, heart murmur and sensorium.Results: Thirty term, asphyxiated neonates and their matched controlswere studied. Central cyanosis, reduced pulse volume, pallor, depressedsensorium; tachycardia and tachypnea were all associated with increased odds ratios for abnormal cardiac troponin.T levels.Conclusion: Clinicians working in resource.limited health facilitiesshould have a high index of suspicion for myocardial cellular injurywhen these signs are elicited.Keywords: neonates, asphyxia, troponin-T, myocardial injury

Serum Cardiac Troponin T and Creatine Kinase–MB Elevations in Murine Autoimmune Myocarditis

Circulation ◽  
1995 ◽  
Vol 92 (7) ◽  
pp. 1927-1932 ◽  
Author(s):  
Kurt Bachmaier ◽  
Johannes Mair ◽  
Felix Offner ◽  
Christian Pummerer ◽  
Nikolaus Neu
Keyword(s):  
Creatine Kinase ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Cardiac Troponin T ◽  
Autoimmune Myocarditis ◽  
Creatine Kinase Mb ◽  
Serum Cardiac Troponin

scholarly journals Prognostic Value of Combination of Cardiac Troponin T and B-Type Natriuretic Peptide after Initiation of Treatment in Patients with Chronic Heart Failure

2003 ◽  
Vol 49 (12) ◽  
pp. 2020-2026 ◽  
Author(s):  
Junnichi Ishii ◽  
Wei Cui ◽  
Fumihiko Kitagawa ◽  
Takahiro Kuno ◽  
Yuu Nakamura ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Functional Class ◽  
Cardiac Troponin T ◽  
Cardiac Events ◽  
Nyha Functional Class

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.

Abstract 3809: Cardiac-Specific Overexpression of EcSOD Using an AAV9 Vector in Combination with the Cardiac Troponin-T Promoter Inhibits LV Remodeling after Myocardial Infarction

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Konkal-Matt R Prasad ◽  
Ronald J Beyers ◽  
Yaqin Xu ◽  
Brent A French
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Left Ventricular ◽  
The Body ◽  
Cardiac Troponin T ◽  
Sod Activity ◽  
Western Blots ◽  
Systemic Injection ◽  
Lv Remodeling

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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