Cardiac Troponin T: Its Role in the Diagnosis of Clinically Suspected Acute Myocarditis and Chronic Dilated Cardiomyopathy in Children

Soongswang, Jarupim; Durongpisitkul, Kritvikrom; Ratanarapee, S; Leowattana, Wattana; Nana, Arth; Laohaprasitiporn, Duangmanee; Akaniroj, S.; Limpimwong, N.; Kangkagate, Charuwan

doi:10.1007/pl00021005

Cited by 41 publications

(29 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, in the case of several abnormal cardiac conditions in which cardiac muscle undergoes active necrosis (including cardiomyopathy), troponin T is released into the bloodstream and can be detected at high levels in the serum (26). We measured the resting serum troponin T levels in the dysferlin-null mice of 2 age groups (30 and 70 to 90 weeks old) ( Figure 3K).…”

Section: Figurementioning

confidence: 99%

Dysferlin-mediated membrane repair protects the heart from stress-induced left ventricular injury

Han¹,

Bansal²,

Miyake³

et al. 2007

J. Clin. Invest.

158

190

View full text Add to dashboard Cite

Dilated cardiomyopathy is a life-threatening syndrome that can arise from a myriad of causes, but predisposition toward this malady is inherited in many cases. A number of inherited forms of dilated cardiomyopathy arise from mutations in genes that encode proteins involved in linking the cytoskeleton to the extracellular matrix, and disruption of this link renders the cell membrane more susceptible to injury. Membrane repair is an important cellular mechanism that animal cells have developed to survive membrane disruption. We have previously shown that dysferlin deficiency leads to defective membrane resealing in skeletal muscle and muscle necrosis; however, the function of dysferlin in the heart remains to be determined. Here, we demonstrate that dysferlin is also involved in cardiomyocyte membrane repair and that dysferlin deficiency leads to cardiomyopathy. In particular, stress exercise disturbs left ventricular function in dysferlin-null mice and increases Evans blue dye uptake in dysferlin-deficient cardiomyocytes. Furthermore, a combined deficiency of dystrophin and dysferlin leads to early onset cardiomyopathy. Our results suggest that dysferlin-mediated membrane repair is important for maintaining membrane integrity of cardiomyocytes, particularly under conditions of mechanical stress. Thus, our study establishes what we believe is a novel mechanism underlying the cardiomyopathy that results from a defective membrane repair in the absence of dysferlin. IntroductionDilated cardiomyopathy is the most common type of cardiomyopathy, a condition that can often progress into heart failure and sudden death. Many cases of dilated cardiomyopathy have a genetic etiology. Indeed, inherited forms of idiopathic dilated cardiomyopathy account for at least 30% of dilated cardiomyopathy cases. These are a major cause of severe heart failure and necessitate heart transplantation (1). A number of genes encoding sarcomeric and cytoskeletal proteins have been identified as being responsible for dilated cardiomyopathy: cardiac actin, cardiac troponin T, β-myosin heavy chain, α-tropomyosin, α-actinin, titin, metavinculin, and desmin (reviewed in ref. 2). Mutations in genes such as dystrophin (3, 4), α-sarcoglycan (5), β-sarcoglycan (6), γ-sarcoglycan (7), and δ-sarcoglycan (8, 9), which encode proteins involved in linking the cytoskeleton, sarcolemma, and extracellular matrix, have also been identified as causes of some familial dilated cardiomyopathy. Such mutations lead to the disruption of the cytoskeleton-sarcolemma-extracellular matrix link and thus render the sarcolemma more susceptible to contraction-induced injury (10-12).The plasma membrane provides a physical barrier between the extracellular and intracellular environments, and the maintenance of this barrier is crucial for cell survival; however, plasma-membrane disruption occurs physiologically in certain types of cells,

show abstract

Section: Figurementioning

confidence: 99%

Dysferlin-mediated membrane repair protects the heart from stress-induced left ventricular injury

Han¹,

Bansal²,

Miyake³

et al. 2007

J. Clin. Invest.

158

190

View full text Add to dashboard Cite

show abstract

“…Prevalence: While Tn is often raised in idiopathic DCM, several studies have shown that it is lower than in myocarditis and TnT but not hs-TnT might be useful in distinguishing these conditions [58][59][60][61] (Table 5). Patients with ischaemic cardiomyopathy have greater levels of TnI than DCM patients at hospital presentation but levels are more likely to remain elevated at 3 months in DCM.…”

Section: Dilated Cardiomyopathymentioning

confidence: 99%

Measurement of Troponin in Cardiomyopathies

2016

View full text Add to dashboard Cite

Troponins are thin myofilament proteins that regulate the contraction of cardiac and skeletal muscle. The cardio-specific troponin I (TnI) and T (TnT) proteins are sensitive and specific biomarkers of myocardial injury which over the past twenty years have revolutionised the diagnosis and management of myocardial infarction. With the advent of high sensitivity assays the role for cardiac troponins is possibly expanding. Elevated levels are associated with adverse cardiovascular events and mortality in heart failure and the general population. Studies in cardiomyopathies are generally small with <200 patients, but serum troponin levels can be chronically raised and detect subclinical myocyte damage. This review examines all major published studies of cardiac troponin measurement in cardiomyopathies. There is considerable variability among studies regarding assays used and definitions of abnormal results but elevated troponin levels are almost invariably related to poor prognosis and their negative predictive value is important.

show abstract

“…A number of studies have been conducted examining troponin release during myocarditis, DCM or heart failure in patients (Smith et al, 1997;Brandt et al, 2001;Imazio et al, 2008;Miller et al, 2007;Peacock et al, 2008). Troponin I and T have also been found to predict the severity of myocarditis and the short-term prognosis in children with acute and fulminant myocarditis and DCM (Soongswang et al, 2002;Al-Biltagi et al, 2010). Overall, troponin levels were found to increase in relation to the severity of myocardial inflammation or ventricular wall stress caused by remodeling (Agewall et al, 2011;Miller et al, 2007).…”

Section: Troponins I and Tmentioning

confidence: 99%