Diagnostic and Prognostic Role of Troponin and Brain Natriuretic Peptide in Pediatric Patients With Cardiomyopathy in Correlation to Echocardiography Findings

NCT ID: NCT06348732

Last Updated: 2024-04-05

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

NOT_YET_RECRUITING

Total Enrollment

65 participants

Study Classification

OBSERVATIONAL

Study Start Date

2024-09-01

Study Completion Date

2025-11-30

Brief Summary

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This study aims to assess the the role of cardiac biomarkers (troponin and ProBNP) in pediatric Patients with all types of cardiomyopathy in correlation with echocardiography findings .

Detailed Description

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Cardiomyopathy are structural or functional abnormalities of the myocardium not secondary to congenital, valvular, hypertensive, pulmonary, or coronary heart diseases .

Cardiomyopathy has traditionally been classified into three types based on anatomic and functional features: hypertrophy, dilated, and restrictive. In 1995, two other categories were added by the World Health Organization (WHO), namely, arrhythmical right ventricular cardiomyopathy (dysplasia) (ARVC \& ARCD) and unclassified cardiomyopathy .

Over the ensuing years, however, other organizations have proposed or classified cardiomyopathy that emphasize the genetics aspect of the disease.

The original three types of cardiomyopathy are functionally different from one another, and demands of therapy also are different .

In recent years, biomarkers have emerged as important tools for diagnosis, risk stratification and therapeutic decision making in cardiovascular diseases .

Cardiac troponins in particular have become the cornerstone for diagnostic work up of patients with cardiomyopathy. Currently, several promising new biomarkers are under scientific investigation.

Most of these new biomarkers, however, are not yet suitable for clinical application, with exception of B-type natriuretic peptide (BNP) and its N-terminal fragment (NT-ProBNP).

Both markers have proven their diagnostic usefulness in a great number of studies and thus have progressed from bench to clinical application .

This study aims to summarize existing data concerning troponins and NT-ProBNP measurement in pediatric with cardiomyopathy and to outline how these markers can be integrated into clinical routine.

\* THE BIOLOGY OF TROPONIN: The 3-unit troponin complex (troponin I, T and C) along with tropomyosin is located on the actin filament and is essential for calcium -mediated regulation of skeletal and cardiac muscle contraction. There is tissue - specific isoforms of troponin I, T and C.

Because the cardiac isoform of troponin C is shared by slow-twitch skeletal muscles, troponin C does not have cardiac specificity and thus is not used in assays of the diagnosis of cardiac injury .

There is one cardiac troponin I (cTn I) isoform in myocardial tissue. This isoform has post-translation tail of 32 amino acids on the N-terminus. This sequence and the 42% and 45% dissimilarity with sequences of other isoforms have made possible the generation of highly specific monoclonal anti-bodies without cross-reactivity with other non-cardiac forms .

Subtypes of troponin (cardiac I and T) are sensitive and specific indicators of heart muscle damage (myocardium).

\* B-type natriuretic peptide (BNP) and NT-proBNP in clinical routine: B-type natriuretic peptide, which is also called brain-type natriuretic peptide (BNP), was first described in 1988 after isolation from porcine brain. However, it was soon found to originate mainly from the heart, representing a cardiac hormone.

BNP belongs to the natriuretic peptide family together with other structurally similar peptides, namely atrial natriuretic peptides (ANP), C-type natriuretic peptide (CNP), and Urodilatin .

The natriuretic peptides have in common a characteristic biochemical structure which consists of a 17 amino acid ring and a disulfide bridge between two cysteine molecules. The major source of BNP synthesis and secretion is the ventricular myocardium.

Whereas ANP is stored in granules and can be released immediately after stimulation, only small amounts of BNP are stored in granules and rapid gene expression with de novo synthesis of the peptide is the underlying mechanism of the regulation of BNP secretion .

BNP is synthesized as a prohormone (proBNP) comprising 108 amino acids. Upon release into the circulation it is cleaved in equal proportions into the biologically active 32 amino acid BNP, which represents the C-terminal fragment, and the biologically inactive 76 amino acid N-terminal fragment (NT-proBNP).

Both molecules are constantly released and can be detected in the blood. The main stimulus for increased BNP and NT-proBNP synthesis and secretion is myocardial wall stress .

Conditions

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Cardiomyopathies

Study Design

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Observational Model Type

CASE_CROSSOVER

Study Time Perspective

CROSS_SECTIONAL

Eligibility Criteria

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Inclusion Criteria

Patients more than one month old and younger than 18 years old with any types of cardiomyopathy admitted at Assiut University Children Hospital.

\-

Exclusion Criteria

Patients aged more than 18 years old.

* Patients aged less than one month old .
* Patients with congenital heart diseases .
* Patients with other chronic diseases as : ( chronic kidney diseases , chronic lung diseases, chronic blood diseases and immune deficiency )
* Patients with acute myocarditis secondary to viral infection .
Minimum Eligible Age

1 Month

Maximum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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Assiut University

OTHER

Sponsor Role lead

Responsible Party

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Mahmoud Ramadan Badawi Hussein

principal investigator

Responsibility Role PRINCIPAL_INVESTIGATOR

Central Contacts

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mahmoud ramadan badawy Hussein, MASTER

Role: CONTACT

+2 01098131360

HEKMA SAAD FARGHALY, DOCTORATE

Role: CONTACT

+2 01091251040

References

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Hamada T, Kubo T, Kitaoka H, Hirota T, Hoshikawa E, Hayato K, Shimizu Y, Okawa M, Yamasaki N, Matsumura Y, Yabe T, Takata J, Doi YL. Clinical features of the dilated phase of hypertrophic cardiomyopathy in comparison with those of dilated cardiomyopathy. Clin Cardiol. 2010 Jul;33(7):E24-8. doi: 10.1002/clc.20533.

Reference Type BACKGROUND
PMID: 20641106 (View on PubMed)

Ikeda H, Imaizumi T. [Prognosis of hypertrophic and dilated cardiomyopathy]. Nihon Rinsho. 2000 Jan;58(1):86-92. Japanese.

Reference Type BACKGROUND
PMID: 10885294 (View on PubMed)

Other Identifiers

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biomarkers in cardiomyopathy

Identifier Type: -

Identifier Source: org_study_id

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