scholarly journals Ethnicity-Specific Changes in Cardiac Troponin T in Response to Acute Mental Stress and Ethnicity-Specific Cutpoints for the R Wave of the aVL Lead

2019 ◽  
Vol 188 (8) ◽  
pp. 1444-1455 ◽  
Author(s):  
Annemarie Wentzel ◽  
Leoné Malan ◽  
Roland von Känel ◽  
Nicolaas T Malan

Abstract Acute mental stressor–induced cardiac stress responses might contribute to excessive myocardial strain and resultant cardiovascular episode risk. We assessed ethnicity-specific acute cardiac stress (by measuring cardiac troponin T (cTnT) and N-terminal prohormone of brain natriuretic peptide) related to hemodynamic activity. The prospective Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) study was conducted during 2007–2008 in South Africa. In the cross-sectional phase of the SABPA study, 388 black and white participants underwent a 1-minute acute mental stressor, during which blood pressure was continuously measured. Fasting blood samples for cardiac stress markers were obtained before and 10 minutes after stress (% change). Resting 10-lead electrocardiogram measured the R wave of the aVL lead (RaVL). Black participants exhibited greater cardiac stress responses (P < 0.001), diastolic blood pressure, total peripheral resistance, and stroke volume compared with white participants, who displayed decreases in cardiac stress and increases in cardiac output. Prestress and stressor cTnT cutpoints of 4.2 pg/mL predicted 24-hour, daytime, and nighttime diastolic hypertension in black participants (P < 0.001). These cTnT cutpoints were associated with an ethnicity-specific RaVL cutpoint of 0.28 mV (odds ratio = 3.49, 95% confidence interval: 2.18, 5.83; P = 0.021). Acute mental stress elicited an α-adrenergic activation pattern and cardiac stress hyperreactivity only in black participants. Mental stress might increase the black population’s risk for ischemic episodes and heart disease.

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Andrea L Schneider ◽  
Andreea M Rawlings ◽  
A. R Sharrett ◽  
Alvaro Alonso ◽  
Thomas Mosley ◽  
...  

Introduction: Clinical cardiovascular disease is a major risk factor for cognitive impairment and dementia, but less is known about the association of subclinical myocardial damage (measured by highly sensitive cardiac troponin T [hs-cTnT]) with cognition and dementia in the general population. Hypothesis: We hypothesized that higher levels of hs-cTnT would be associated with lower cognitive test scores and increased risk of dementia. Methods: We conducted cross-sectional (1996-1998) and prospective (follow-up through 2009) analyses of 8,601 participants in the ARIC Study without a history of cardiovascular disease or stroke. Cognition was measured by 3 tests: Delayed Word Recall (DWR), Digit Symbol Substitution (DSS), and Word Fluency (WF). Dementia was defined using ICD-9 codes. Linear regression and Cox proportional hazards models were adjusted for demographic, lifestyle, and cardiovascular factors. Results: 66% of participants had detectable hs-cTnT (≥0.003 μg/L) (mean age 63; 59% female; 20% black). In cross-sectional analyses, higher hs-cTnT was associated with lower scores on DSS (p-trend <0.001) and WF (p-trend=0.002), but not DWR (p-trend=0.09) (Table). Similarly, hs-cTnT ≥0.014 μg/L (≥99th percentile) vs. <0.014 μg/L was associated with lower scores on DSS (-1.78 points [95% CI: -2.61, -0.95]) and WF (-1.04 words [95% CI: -2.00, -0.07]), but not on DWR. Over a median of 12 years, there were 338 incident dementia cases. In prospective analyses, higher baseline levels of hs-cTnT were associated with increased dementia risk (p-trend <0.001) (Table). Conclusion: Higher levels of hs-cTnT were associated with lower cognitive test scores at baseline and increased dementia risk during follow-up. Our results suggest that subclinical myocardial damage is associated with cognition and dementia. This association may be driven by shared risk factors for myocardial and cerebral injury or as a direct result of subclinical small vessel or cardiac disease; more work is needed to elucidate potential mechanisms.


2009 ◽  
Vol 9 (1) ◽  
Author(s):  
Pål H Brekke ◽  
Torbjørn Omland ◽  
Stein Harald Holmedal ◽  
Pål Smith ◽  
Vidar Søyseth

BMJ Open ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. e052004
Author(s):  
Alexander Dietl ◽  
Martina E Zimmermann ◽  
Caroline Brandl ◽  
Stefan Wallner ◽  
Ralph Burkhardt ◽  
...  

ObjectiveEuropean guidelines recommended a uniform upper reference limit of high-sensitivity cardiac troponin T (hsTnT) to rule out non-ST segment elevation myocardial infarction. Our study aimed to provide a hsTnT reference distribution and to assess the specificity of the 14 ng/L cut-off value in the mobile population ≥70 years of age.DesignA cross-sectional analysis was performed in the German AugUR study (Altersbezogene Untersuchungen zur Gesundheit der University of Regensburg).SettingStudy population was the mobile population aged 70+ years living in the city and county of Regensburg, Germany.ParticipantsA random sample was derived from the local population registries of residence. Of the 5644 individuals invited, 1133 participated (response ratio=20.1%). All participants came to the study centre and were mentally and physically mobile to conduct the protocol (face-to-face interview, blood draw and standardised transthoracic echocardiography). None of the participants was in an acute state of myocardial infarction.ResultsAmong the 1129 individuals with hsTnT measurements (overall median=10.0 ng/L(25th, 75th percentile)=(7.0, 15.0 ng/L)), hsTnT was higher among the older individuals and higher among men (men 70–74 years median=9.6 ng/L (7.2, 13.1 ng/L); men 90–95 years median=21.2 ng/L (14.6, 26.0 ng/L); women 70–74 years median=6.3 ng/L (4.7, 8.7 ng/L); and women 90–95 years median=18.0 ng/L (11.0, 21.0 ng/L)). In participants with impaired kidney function (eGFRcrea <60 mL/min/1.73 m2), hsTnT was elevated (median=13.6 ng/L (9.4, 20.6 ng/L)).Specificity of recommended upper reference limit, 14 ng/L, is 68%. Most false positives were among men aged >79 years (specificity=34%). In a healthy subgroup (n=96, none of the following: overt heart disease, impaired renal function, blood pressure >160/100 mm Hg, left ventricular hypertrophy and diastolic/systolic dysfunction), specificity was 90%.ConclusionIn the elderly population without acute myocardial infarction, hsTnT further increases with age showing different levels for men and women. The specificity of the 14 ng/L cut-off is considerably lower than 99%, even in healthy subjects.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N Kozhuharov ◽  
D Wussler ◽  
R Twerenbold ◽  
J Walter ◽  
J Du Fay De Lavallaz ◽  
...  

Abstract Background Better characterization of the different pathophysiological mechanisms involved in normotensive and hypertensive acute heart failure (AHF) might help to develop novel individualized treatment strategies. Methods The extent of hemodynamic cardiac stress and cardiomyocyte injury was quantified by measuring B-type natriuretic peptide (BNP) as well as high-sensitive cardiac troponin T (hs-cTnT) in 1,152 unselected patients presenting with AHF to the emergency department (derivation cohort). Systolic blood pressure (SBP) of 90 - 140 mmHg at presentation was used to define normotensive AHF. Findings regarding hemodynamic cardiac stress and cardiomyocyte injury were validated in a second independent AHF cohort (validation cohort; n=324). Results In the derivation cohort 667 (58%) patients had hypertensive AHF. Hemodynamic cardiac stress, as quantified by BNP levels, was significantly higher in normotensive AHF as compared to hypertensive AHF (1,105 pg/mL versus 827 pg/mL, p<0.001). In addition, the extent of cardiomyocyte injury, as quantified by hs-cTnT, was significantly higher in normotensive AHF as compared to hypertensive AHF (41 ng/L versus 33 ng/L, p<0.001). These findings were confirmed in the validation cohort. Table 1. Cardiac stress and myocardial necrosis as quantified by BNP and hs-cTnT plasma concentrations Overall Hypertensive AHF Normotensive AHF p-value BNP in pg/ml, median (IQR) 974 (536–1,712) 827 (448–1,419) 1,105 (611–1,956) <0.001 hs-cTnT in ng/L, median (IQR) 37 (22–67) 33 (19–59) 41 (24–71) <0.001 BNP = B-type natriuretic peptide; hs-cTnT = high-sensitivity cardiac Troponin T; IQR = inter-quartile range. Figure 1 Conclusion Biomarker profiling revealed that the extent of hemodynamic stress and cardiomyocyte injury is different in patients with normotensive and hypertensive AHF. This characterization could help to understand AHF phenotypes better, which in turn may lead to more specific management in future, thus improving the dismal prognosis in these patients. Acknowledgement/Funding European Union, Swiss National Science Foundation, Swiss Heart Foundation, Cardiovascular Research Foundation Basel, University of Basel


2020 ◽  
Vol 4 (3) ◽  
pp. 1-5
Author(s):  
Zaki Akhtar ◽  
James Dargan ◽  
David Gaze ◽  
Sami Firoozi ◽  
Paul Collinson ◽  
...  

Abstract Background Troponin is a crucial biomarker for the diagnosis of an acute coronary syndrome (ACS). It rises in response to myocardial injury from significant acute myocardial ischaemia caused by obstructive coronary artery disease [‘classical’ myocardial infarction (MI)]. However, raised levels have also been noted in conditions not recognized as classical ACS. This may include MI with non-obstructed coronary arteries such as takotsubo cardiomyopathy and other acute or chronic conditions such as pulmonary embolus or chronic kidney disease. This is commonly labelled as a ‘falsely elevated’ troponin although there is some myocardial strain to explain the rise, such as an increase in cardiac oxygen demand. True ‘falsely elevated’ troponin, characterized by a persistent elevation in the absence of cardiac injury does occur and thought to be secondary to an immunoglobulin-troponin complex (macrotroponin). Case summary A 53-year-old gentleman with a background of diabetes, hypertension, hypercholesterolaemia, and hepatitis B was admitted with chest pain and persistently elevated cardiac troponin T (cTnT) levels. Investigations revealed unobstructed coronary arteries and a structurally normal, well-functioning heart. Subsequent biochemical analysis found the persistently elevated cTnT secondary to macrotroponin T. Discussion Macrotroponin, an immunoglobulin-troponin bound complex should be considered as a differential diagnosis when the biochemistry is not reflective of the clinical picture. Early recognition requires effective collaboration with the biochemistry laboratory for accurate diagnosis.


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