Coping and Cardiac Troponin T – A Risk for Hypertension and Sub-Clinical ECG Left Ventricular Hypertrophy: The SABPA Study

The aim of this study was to estimate the impact and prevalence of left ventricular geometric alterations and systolic and diastolic dysfunction in hemodialysis patients, as well as the relationship with cardiac troponin as a marker of myocardial damage. Methods: 31 patients (pts), 19 males and 12 females, age 58.1±16.4 (26 on hemodialysis, 5 on peritoneal dialysis) and 31 healthy normal controls were enrolled. Echocardiography measurements were carried out according to the American Society of Echocardiography recommendations. Left ventricular mass was calculated, according to the Devereux formula and indexed to height and weight 2.7. Doppler echocardiography was performed to study diastolic function by measurements of isovolumetric relaxation period (IVRT), E wave deceleretion time (DTE) and E/A ratio. Cardiac troponin was measured by a third generation electrochemiluminescence immunoassay. Statistical analysis was performed using the t-test for between-group comparisons and the Pearson and Spearman’s tests to investigate correlations; p values of <0.05 were considered statistically significant. Results: Eccentric hypertrophy was the most frequent pattern (n=17; 55%), followed by normal cardiac geometry (n=7; 23%), and concentric hypertrophy (n=5; 16%). Only 6% of pts (n=2) showed concentric remodelling. Systolic dysfunction was present in terms of endocardial parameters in 3 pts (9%) (fractional shartening <25%, EF<50%), but in terms of midwall myocardial shortening in 51% (n=16). Diastolic dysfunction was present in 87% (n=27) with a pattern of impaired relaxation (in 5 without left ventricular hypertrophy). E/A was negatively correlated with age (r=-0.41, p=0.02); DTE was positively correlated with posterior wall thickness (r=0.36, p=0.05) and interventricular septum thickness (r=0.45, p=0.01); cardiac troponin was positively correlated with age (r=0.50, p=0.00), left ventricular mass (r=0.41, p=0.02), posterior wall thickness (r=0.41; p=0.02) and interventricular septum thickness (r=0.39, p=0.03) but not with diastolic dysfunction parameters. No significant difference was found in terms of duration of dialysis between patients with normal left ventricular geometry and those with left ventricular hypertrophy, but a significant difference in age was found (p=0.03). Pts with diastolic dysfunction had more frequent hypotensive episodes during dialysis (p <0.01). Conclusion: Impaired geometry and cardiac function is frequently observed in pts undergoing hemodialysis. Diastolic dysfuction is associated to a geometric pattern of left ventricular hypetrophy, although it can be an isolated initial manifestation of myocardial damage. Depressed midwall myocardial shortening can discriminate left ventricular dysfunction better than traditional endocardial systolic indexes.

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Association of High-Sensitivity Cardiac Troponin T and N-Terminal Pro-Brain-Type Natriuretic Peptide With Left Ventricular Structure: J-HOP Study

Journal of Clinical Hypertension ◽

10.1111/jch.12321 ◽

2014 ◽

Vol 16 (5) ◽

pp. 354-361 ◽

Cited By ~ 2

Author(s):

Satoshi Hoshide ◽

Michiaki Nagai ◽

Yuichiro Yano ◽

Joji Ishikawa ◽

Kazuo Eguchi ◽

...

Keyword(s):

Natriuretic Peptide ◽

Cardiac Troponin ◽

Troponin T ◽

High Sensitivity ◽

Left Ventricular ◽

Cardiac Troponin T ◽

Left Ventricular Structure ◽

Ventricular Structure

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

Clinical Chemistry ◽

10.1373/clinchem.2003.021311 ◽

2003 ◽

Vol 49 (12) ◽

pp. 2020-2026 ◽

Cited By ~ 66

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 (>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 <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 <0.001). cTnT >0.01 μg/L and/or BNP >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.

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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 ◽

10.1161/circ.118.suppl_18.s_488-c ◽

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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Factors associated with baseline and serial changes in circulating NT-proBNP and high-sensitivity cardiac troponin T in a population-based cohort (Dallas Heart Study)

Biomarkers in Medicine ◽

10.2217/bmm-2021-0055 ◽

2021 ◽

Author(s):

Christopher W Puleo ◽

Colby R Ayers ◽

Sonia Garg ◽

Ian J Neeland ◽

Alana A Lewis ◽

...

Keyword(s):

Body Composition ◽

Cardiac Troponin ◽

Troponin T ◽

High Sensitivity ◽

Left Ventricular ◽

Cardiac Troponin T ◽

C Reactive Protein ◽

Reactive Protein ◽

Heart Study ◽

Dallas Heart Study

Aim: N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin T (hs-cTnT) associate with structural heart disease and heart failure risk in individuals without known cardiovascular disease (CVD). However, few data are available regarding whether factors influencing levels of these two biomarkers are similar or distinct. We performed serial measurement of NT-proBNP and hs-cTnT in a contemporary multiethnic cohort with extensive phenotyping, with the goal of identifying their respective biological determinants in a population without known or suspected CVD. Methods: We evaluated 1877 participants of the Dallas Heart Study who had NT-proBNP and hs-cTnT measured and were free from clinical CVD at the each of its two examinations (2000–2002 and 2007–2009). Variables collected included demographic and risk factors, high-sensitivity C-reactive protein, body composition via dual-energy x-ray absorptiometry, coronary artery calcium by computed tomography, and cardiac dimensions and function by cardiac MRI. Linear regression was used to identify associations of these factors with each biomarker at baseline and with changes in biomarkers over follow-up. Results: NT-proBNP and hs-cTnT were poorly correlated at baseline (Spearman rho 0.083, p = 0.015), with only moderate correlation between change values (rho 0.18, p < 0.001). hs-cTnT positively associated and NT-proBNP inversely associated with male gender and black race. At baseline, both NT-proBNP and hs-cTnT associated with left ventricular end-diastolic volume and wall thickness, but only NT-proBNP associated with left atrial size. Changes in cardiac dimensions between phases were more strongly associated with changes in NT-proBNP than hs-cTnT. NT-proBNP was more strongly associated with high-sensitivity C-reactive protein and measures of body composition than hs-cTnT. Conclusion: Among individuals without CVD in the general population, NT-proBNP and hs-cTnT are nonredundant biomarkers that are differentially associated with demographic and cardiac factors. These findings indicate that hs-cTnT and NT-proBNP may reflect different pathophysiological pathways.

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Altered ventricular mechanics after 60 min of high-intensity endurance exercise: insights from exercise speckle-tracking echocardiography

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00917.2014 ◽

2015 ◽

Vol 308 (8) ◽

pp. H875-H883 ◽

Cited By ~ 16

Author(s):

Glenn M. Stewart ◽

Akira Yamada ◽

Luke J. Haseler ◽

Justin J. Kavanagh ◽

Gus Koerbin ◽

...

Keyword(s):

Mean Arterial Pressure ◽

Cardiac Troponin ◽

Troponin T ◽

High Sensitivity ◽

Left Ventricular ◽

Cardiac Troponin T ◽

Low Intensity ◽

Exercise Challenge ◽

Exercise Induced ◽

Low Intensity Exercise

Transient reductions in myocardial strain coupled with cardiac-specific biomarker release have been reported after prolonged exercise (>180 min). However, it is unknown if 1) shorter-duration exercise (60 min) can perturb cardiac function or 2) if exercise-induced reductions in strain are masked by hemodynamic changes that are associated with passive recovery from exercise. Left ventricular (LV) and right ventricular global longitudinal strain (GLS), LV torsion, and high-sensitivity cardiac troponin T were measured in 15 competitive cyclists (age: 28 ± 3 yr, peak O2 uptake: 4.8 ± 0.6 l/min) before and after a 60-min high-intensity cycling race intervention (CRIT60). At both time points (pre- and post-CRIT60), strain and torsion were assessed at rest and during a standardized low-intensity exercise challenge (power output: 96 ± 8 W) in a semirecumbent position using echocardiography. During rest, hemodynamic conditions were different from pre- to post-CRIT60 (mean arterial pressure: 96 ± 1 vs. 86 ± 2 mmHg, P < 0.001), and there were no changes in strain or torsion. In contrast, during the standardized low-intensity exercise challenge, hemodynamic conditions were unchanged from pre- to post-CRIT60 (mean arterial pressure: 98 ± 1 vs. 97 ± 1 mmHg, not significant), but strain decreased (left ventricular GLS: −20.3 ± 0.5% vs. −18.5 ± 0.4%, P < 0.01; right ventricular GLS: −26.4 ± 1.6% vs. −22.4 ± 1.5%, P < 0.05), whereas LV torsion remained unchanged. Serum high-sensitivity cardiac troponin T increased by 345% after the CRIT60 (6.0 ± 0.6 vs. 20.7 ± 6.9 ng/l, P < 0.05). This study demonstrates that exercise-induced functional and biochemical cardiac perturbations are not confined to ultraendurance sporting events and transpire during exercise that is typical of day-to-day training undertaken by endurance athletes. The clinical significance of cumulative exposure to endurance exercise warrants further study.

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