Procollagen type III amino-terminal propeptide: a serum biomarker of left ventricular remodelling in paediatric dilated cardiomyopathy

AbstractBackgroundProcollagen type III amino-terminal propeptide is a collagen III cleavage product released in blood. The serum levels of this propeptide in adults with dilated cardiomyopathy are associated with cardiac remodelling and prognosis. The utility of procollagen type III amino-terminal propeptide as a biomarker in paediatric dilated cardiomyopathy is unknown.MethodsThis was a prospective, longitudinal study of children with dilated cardiomyopathy and changes in procollagen type III amino-terminal propeptide. The serum level of propeptide was measured serially, compared with paediatric normal values, and correlated with clinical status and left ventricular size and function on echocardiograms and cardiac magnetic resonance imaging.ResultsProcollagen type III amino-terminal propeptide was measured serially in 149 samples from 39 patients, age 9.0±6.4 years, followed up for 16.8±16.3 months. Procollagen type III amino-terminal propeptide in dilated cardiomyopathy was higher than in normal children. On multivariate analyses, procollagen type III amino-terminal propeptide had a positive correlation with left ventricular dilation, left ventricular end-diastolic diameter index (p<0.0001), and left ventricular end-diastolic diameter Z-score (p=0.0003), and a negative correlation with shortening fraction changes over time (p=0.001). Patients with myocarditis (n=12) had higher procollagen type III amino-terminal propeptide values than those with idiopathic dilated cardiomyopathy (n=20).ConclusionsProcollagen type III amino-terminal propeptide increases with left ventricular dilation and decreases with improvement in systolic function in paediatric dilated cardiomyopathy, indicating a role as a biomarker of cardiac remodelling in children. The diagnostic utility of procollagen type III amino-terminal propeptide to differentiate myocarditis from idiopathic dilated cardiomyopathy warrants further investigation.

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541: Association of Left Ventricular Dilation at Listing for Heart Transplant with Post-Listing and Early Post-Transplant Survival in Pediatric Dilated Cardiomyopathy

The Journal of Heart and Lung Transplantation ◽

10.1016/j.healun.2007.11.555 ◽

2008 ◽

Vol 27 (2) ◽

pp. S255

Author(s):

T.P. Singh ◽

L.A. Sleeper ◽

S. Lipshultz ◽

A. Cinar ◽

C. Canter ◽

...

Keyword(s):

Dilated Cardiomyopathy ◽

Heart Transplant ◽

Left Ventricular ◽

Ventricular Dilation ◽

Transplant Survival ◽

Post Transplant ◽

Left Ventricular Dilation

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Procollagen type III amino terminal peptide and myocardial fibrosis: A study in hypertensive patients with and without left ventricular hypertrophy

Revista Portuguesa de Cardiologia (English Edition) ◽

10.1016/j.repce.2015.05.007 ◽

2015 ◽

Vol 34 (5) ◽

pp. 309-314

Author(s):

Carlos dos Santos Moreira ◽

Fátima Serejo ◽

Paula Alcântara ◽

Vítor Ramalhinho ◽

J. Braz Nogueira

Keyword(s):

Left Ventricular Hypertrophy ◽

Myocardial Fibrosis ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Hypertensive Patients ◽

Type Iii ◽

Procollagen Type ◽

Amino Terminal

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Long-Term Effects of Delapril Hydrochloride on Procollagen Type III Amino-Terminal Peptide, Left Ventricular Mass and Left Ventricular Function in Hypertensive Patients

Japanese Circulation Journal ◽

10.1253/jcj.62.900 ◽

1998 ◽

Vol 62 (12) ◽

pp. 900-902 ◽

Cited By ~ 2

Author(s):

Munetoshi Matoba ◽

Takayoshi Asaji ◽

Shinobu Matsui ◽

Noboru Takekoshi

Keyword(s):

Left Ventricular Function ◽

Ventricular Function ◽

Left Ventricular Mass ◽

Left Ventricular ◽

Long Term Effects ◽

Hypertensive Patients ◽

Type Iii ◽

Procollagen Type ◽

Amino Terminal

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Left Ventricular Hypertrophy and Geometry in Untreated Essential Hypertension is Associated With Blood Levels of Aldosterone and Procollagen Type III Amino-Terminal Peptide

Circulation Journal ◽

10.1253/circj.71.716 ◽

2007 ◽

Vol 71 (5) ◽

pp. 716-721 ◽

Cited By ~ 31

Author(s):

Takao Nakahara ◽

Yoshifumi Takata ◽

Yoji Hirayama ◽

Kihiro Asano ◽

Hirotaka Adachi ◽

...

Keyword(s):

Essential Hypertension ◽

Left Ventricular Hypertrophy ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Blood Levels ◽

Type Iii ◽

Procollagen Type ◽

Amino Terminal

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Mitochondrial CaMKII causes metabolic reprogramming, energetic insufficiency, and dilated cardiomyopathy

10.1101/2020.02.13.947564 ◽

2020 ◽

Author(s):

Elizabeth D. Luczak ◽

Yuejin Wu ◽

Jonathan M. Granger ◽

Mei-ling A. Joiner ◽

Nicholas R. Wilson ◽

...

Keyword(s):

Dilated Cardiomyopathy ◽

Mechanical Performance ◽

Left Ventricular ◽

Metabolic Reprogramming ◽

Ventricular Dilation ◽

Over Expression ◽

Calmodulin Kinase ◽

Left Ventricular Dilation ◽

Myocardial Energetics ◽

Camkii Activation

AbstractDespite the clear association between myocardial injury, heart failure and depressed myocardial energetics, little is known about upstream signals responsible for remodeling myocardial metabolism after pathological stress. We found increased mitochondrial calmodulin kinase II (CaMKII) activation and left ventricular dilation in mice one week after myocardial infarction (MI) surgery. In contrast, mice with genetic mitochondrial CaMKII inhibition were protected from left ventricular dilation and dysfunction after MI. Mice with myocardial and mitochondrial CaMKII over-expression (mtCaMKII) had severe dilated cardiomyopathy and decreased ATP that caused elevated cytoplasmic resting (diastolic) Ca2+ concentration and reduced mechanical performance. We mapped a metabolic pathway that allowed us to rescue disease phenotypes in mtCaMKII mice, providing new insights into physiological and pathological metabolic consequences of CaMKII signaling in mitochondria. Our findings suggest myocardial dilation, a disease phenotype lacking specific therapies, can be prevented by targeted replacement of mitochondrial creatine kinase, or mitochondrial-targeted CaMKII inhibition.

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