The combination of carboxy‐terminal propeptide of procollagen type I blood levels and late gadolinium enhancement at cardiac magnetic resonance provides additional prognostic information in idiopathic dilated cardiomyopathy – A multilevel assessment of myocardial fibrosis in dilated cardiomyopathy

Raafs, Anne; Verdonschot, Job A.J.; Henkens, Michiel T.H.M.; Adriaans, Bouke P.; Wang, Ping; Derks, Kasper; Hamid, Myrurgia Abdul; Knackstedt, Christian; Empel, Vanessa van; Dı́ez, Javier; Rocca, Hans‐Peter Brunner‐La; Brunner, Han G.; González, Arantxa; Bekkers, Sebastiaan C.A.M.; Heymans, Stéphane; Hazebroek, Mark

doi:10.1002/ejhf.2201

Cited by 42 publications

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“…In a study including 209 patients with dilated cardiomyopathy, different markers of fibrosis were assessed. Late gadolinium enhancement at cardiovascular magnetic resonance and the biomarker carboxy‐terminal propeptide of procollagen type I had additive prognostic value 10 …”

Section: Diagnosis and Prognosismentioning

confidence: 97%

“…Late gadolinium enhancement at cardiovascular magnetic resonance and the biomarker carboxy-terminal propeptide of procollagen type I had additive prognostic value. 10 Higher levels of circulating dipeptidyl peptidase 3 (DPP3) were related with mortality in patients with cardiogenic shock and DPP3 inhibition can improve haemodynamics. 11,12 Boorsma et al 13 showed that high DPP3 levels are associated with higher renin and aldosterone concentrations and poorer outcomes.…”

Section: Biomarkersmentioning

confidence: 99%

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June 2021 at a glance: focus on epidemiology, biomarkers and medical treatment

Tomasoni

Adamo

Metra

2021

European J of Heart Fail

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The epidemiology of heart failure (HF) is still unsettled, above all in European countries, because of marked differences in coding and management modalities. To date, most of our data came from analyses of dedicated studies and trials. 1,2 The Heart Failure Association (HFA) Atlas is a novel European data set, developed to provide a contemporary description of HF epidemiology and management. 3,4 The median incidence of HF was 3.2 [interquartile range (IQR) 2.66-4.17] cases per 1000 person-years; the median HF prevalence was 17.20 (IQR 14.30-21) cases per 1000 people and the median number of HF hospitalizations was 2671 (IQR 1771-4317) per million people, annually. A large heterogeneity among different countries both with respect to epidemiology and management was shown. 3 Diagnosis and prognosis Endomyocardial biopsyTreatment of cardiomyopathies and myocarditis remains challenging. [5][6][7] Indications to endomyocardial biopsy needed to be updated accordingly and this issue hosts a consensus document developed by HFA, HF Society of America and Japanese HF Society. 8 Evidence-based medical treatment is still underused in patients with HF and reduced ejection fraction. 23,24 In a HFA consensus document, Rosano et al. 25 identified nine patient profiles which may inform treatment choices. These profiles include patients with atrial fibrillation, low blood pressure, tachycardia, chronic kidney disease, hyperkalaemia, congestion, or pre-discharge status. A strategy of rapid sequencing of evidence-based treatment was also proposed to optimize medical treatment. 26

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Section: Diagnosis and Prognosismentioning

confidence: 97%

Section: Biomarkersmentioning

confidence: 99%

June 2021 at a glance: focus on epidemiology, biomarkers and medical treatment

Tomasoni

Adamo

Metra

2021

European J of Heart Fail

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“…In this issue of the Journal, Raafs and colleagues quantified fibrosis in 209 patients with DCM using (i) CMR non‐invasive late gadolinium enhancement (LGE), (ii) invasive endomyocardial biopsy (EMB) with determination of CVF, and (iii) circulating levels of PICP and PIIINP 10 . The authors found that PICP (but not PIIINP) was positively correlated with myocardial fibrosis as determined by CMR‐LGE (R 2 = 0.39) and by EMB‐CVF, particularly among severely symptomatic patients with reduced ejection fraction (R 2 = 0.68).…”

Section: Figurementioning

confidence: 99%

Circulating levels of procollagen type I carboxy‐terminal propeptide reflect myocardial fibrosis

Ferreira

2021

European J of Heart Fail

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This article refers to 'The combination of carboxyterminal propeptide of procollagen type I blood levels and late gadolinium enhancement at cardiac magnetic resonance provides additional prognostic information in idiopathic dilated cardiomyopathy -A multilevel assessment of myocardial fibrosis in dilated cardiomyopathy' by A.G. Raafs et al., published in this issue on pages 933-944.Myocardial fibrosis is a consequence of a profound change in the architecture and composition of the cardiac extra-cellular matrix affecting the structure and function of the heart. Non-specific insults to the cardiovascular system (e.g. hypertension, diabetes, ageing, ischaemia, genetic alterations) may dysregulate various cell types and signalling pathways, ultimately resulting in myocardial fibrosis. 1,2 Once established, myocardial fibrosis is strongly associated with a poor prognosis, including in patients with idiopathic dilated cardiomyopathy (DCM). 3,4 Despite the sound pathophysiological background and prognostic impact of myocardial fibrosis, its assessment remains challenging in clinical practice. Circulating markers reflecting collagen synthesis are under investigation as potential means for evaluating myocardial fibrosis non-invasively. In this regard, procollagen type I carboxy-terminal propeptide (PICP) may directly reflect the synthesis of collagen type 1 because it is produced during the conversion of procollagen type I to collagen type I in a 1:1 ratio. 1 Furthermore, serum PICP levels have been correlated with total myocardial collagen volume fraction (CVF) (assessed in myocardial samples with collagen-specific staining) in patients with hypertension, heart failure and DCM. 4,5 Another potential marker of collagen synthesis is N-terminal propeptide of type III collagen (PIIINP). PIIINP is generated from the conversion of procollagen type III into collagen type III and has been correlated with the amount of collagen type III fibres in the myocardium of heart failure patients, but itThe opinions expressed in this article are not necessarily those of the Editors of the European Journal of Heart Failure or of the European Society of Cardiology.

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“…These molecules have been observed to be considerably correlated to the progression of myocardial fibrosis in patients with ischemic heart disease and NIDCM [ 7 , 8 ]. Additionally, their increased sera levels are able to predict MACEs in patients with HF and preserved left ventricle (LV) ejection fractions (LVEFs) [ 4 , 16 ]. However, their role in patients with NIDCM is not entirely clear.…”

Section: Introductionmentioning

confidence: 99%

The Role of Circulating Collagen Turnover Biomarkers and Late Gadolinium Enhancement in Patients with Non-Ischemic Dilated Cardiomyopathy

et al. 2022

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Background: Myocardial scarring is a primary pathogenetic process in nonischemic dilated cardiomyopathy (NIDCM) that is responsible for progressive cardiac remodeling and heart failure, severely impacting the survival of these patients. Although several collagen turnover biomarkers have been associated with myocardial fibrosis, their clinical utility is still limited. Late gadolinium enhancement (LGE) determined by cardiac magnetic resonance imaging (CMR) has become a feasible method to detect myocardial replacement fibrosis. We sought to evaluate the association between collagen turnover biomarkers and replacement myocardial scarring by CMR and, also, to test their ability to predict outcome in conjunction with LGE in patients with NIDCM. Method: We conducted a prospective study on 194 patients (48.7 ± 14.3 years of age; 74% male gender) with NIDCM. The inclusion criteria were similar to those for the definition of NIDCM, performed exclusively by CMR: (1) LV dilation with an LV end-diastolic volume (LVEDV) of over 97 mL/m2; (2) global LV dysfunction, expressed as a decreased LVEF of under 45%. CMR was used to determine the presence and extent of LGE. Several collagen turnover biomarkers were determined at diagnosis, comprising galectin-3 (Gal3), procollagen type I carboxy-terminal pro-peptide (PICP) and N-terminal pro-peptide of procollagen type III (PIIINP). A composite outcome (all-cause mortality, ventricular tachyarrhythmias, heart failure hospitalization) was ascertained over a median of 26 months. Results: Gal3, PICP and PIIINP were considerably increased in those with LGE+ (p < 0.001), also being directly correlated with LGE mass (r2 = 0.42; r2 = 0.44; r2 = 0.31; all p < 0.001). Receiver operating characteristic (ROC) analysis revealed a significant ability to diagnose LGE, with an area under the ROC of 0.816 for Gal3, 0.705 for PICP, and 0.757 for PIIINP (all p < 0.0001). Kaplan–Meier analysis showed that at a threshold of >13.8 ng/dL for Gal3 and >97 ng/dL for PICP, they were able to significantly predict outcome (HR = 2.66, p < 0.001; HR = 1.93, p < 0.002). Of all patients, 17% (n = 33) reached the outcome. In multivariate analysis, after adjustment for covariates, only LGE+ and Gal3+ remained independent predictors for outcome (p = 0.008; p = 0.04). Nonetheless, collagen turnover biomarkers were closely related to HF severity, providing incremental predictive value for severely decreased LVEF of under 30% in patients with NIDCM, beyond that with LGE alone. Conclusions: In patients with NIDCM, circulating collagen turnover biomarkers such as Gal3, PICP and PIIINP are closely related to the presence and extent of LGE and can significantly predict cardiovascular outcome. The joint use of LGE with Gal3 and PICP significantly improved outcome prediction.

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Cited by 42 publications

References 42 publications

June 2021 at a glance: focus on epidemiology, biomarkers and medical treatment

June 2021 at a glance: focus on epidemiology, biomarkers and medical treatment

Circulating levels of procollagen type I carboxy‐terminal propeptide reflect myocardial fibrosis

The Role of Circulating Collagen Turnover Biomarkers and Late Gadolinium Enhancement in Patients with Non-Ischemic Dilated Cardiomyopathy

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