Propeptide of procollagen type I (PIP) and outcomes in decompensated heart failure

Fj, Ruiz-Ruiz; Laiglesia, Fernando José Ruiz; Samperiz-Legarre, Pilar; Lasierra-Díaz, Pilar; Flamarique-Pascual, Álvaro; Morales-Rull, J.L.; Pérez-Calvo, Juan Ignacio

doi:10.1016/j.ejim.2006.09.014

Cited by 15 publications

(13 citation statements)

References 28 publications

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“…The interplay between body composition and depression as predictors of fibrosis markers requires further investigation. Most studies (Querejeta et al, 2004; Laviades et al, 1998; Ruiz-Ruiz et al, 2007; Cicoira et al, 2004; Izawa et al, 2005; Schwartzkopff et al, 2002), including the present study (Barash et al, 2009), have found elevated fibrosis markers in heart failure patients versus matched controls. However, the functional disease severity based on NYHA classification does not appear to be a strong predictor of fibrosis markers (Cavallari et al, 2007).…”

Section: Discussionsupporting

confidence: 44%

“…Type I and III collagens are the predominant fibrillar collagens in normal and diseased myocardium (de Souza, 2002). Serum markers of type I and III collagen are associated with hypertensive cardiac disease and heart failure progression, independent of hypertension and left ventricular (LV) hypertrophy (Querejeta et al, 2004; Laviades et al, 1998; Ruiz-Ruiz et al, 2007; Cicoira et al, 2004; Izawa et al, 2005; Schwartzkopff et al, 2002). Biomarkers of fibrosis include carboxyterminal propeptide of procollagen type I (PIP), a marker of type I collagen synthesis; carboxyterminal telopeptide of type I collagen (CITP), a marker of degradation of type I collagen; and aminoterminal propeptide of procollagen III (PIIINP), a marker of synthesis and degradation of type III collagen (Weber, 1997; Cuspidi et al, 2006; Klappacher et al, 1995).…”

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confidence: 99%

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Association between depressive symptoms and fibrosis markers: The Cardiovascular Health Study

Kop

Kuhl

Barasch

et al. 2010

Brain, Behavior, and Immunity

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Objective-Fibrosis plays an important role in heart failure (HF) and other diseases that occur more frequently with increasing age. Depression is associated with an increased risk of heart failure and other age-related diseases. This study examined the association between depressive symptoms and fibrosis markers in adults aged 65 years and above.Methods-Fibrosis markers and depressive symptoms were assessed in 870 participants (age=80.9 ±5.9, 49% women) using a case-control design based on heart failure status (307 HF patients and 563 age-and sex-matched controls, of whom 284 with CVD risk factors (hypertension, diabetes mellitus, or hypercholesterolemia) and 279 controls without these CVD risk factors). Fibrosis markers were procollagen type I (PIP), type I collagen (CITP), and procollagen type III (PIIINP). Inflammation markers included C-reactive protein, white blood cell counts and fibrinogen. Depression was assessed using the Center for Epidemiological Studies-Depression (CES-D) scale using a previously validated cut-off point for depression (CES-D ≥ 8). Covariates included: demographic and clinical variables.Results-Depression was associated with higher levels of PIP (median=411.0, inter quartile range (IQR)=324.4-472.7 ng/mL vs. 387.6, IQR=342.0-512.5 ng/mL, p=0.006) and CITP (4.99, vs. 4.53,.22 μg/L, p=0.024), but not PIIIINP (4.07, IQR = 2.75-5.54 μg/mL vs. 3.58, IQR=2.71-5.01 μg/mL, p=0.29) compared to individuals without depression. Inflammation markers were also elevated in depressed participants (CRP, p=0.014; WBC, p=0.075; fibrinogen, p=0.074), but these inflammation markers did not account for the relationship between depression and fibrosis markers.Conclusions-Depression is associated with elevated fibrosis markers and may therefore adversely affect heart failure and other age-related diseases in which extra-cellular matrix formation plays a pathophysiological role.Corresponding Author: Willem J. Kop, University of Maryland Baltimore, 22 South Greene Street, Ste. 3B08, Baltimore, MD 21201, Phone: 410-328-2063, FAX: 410-328-4382, wkop@medicine.umaryland.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Fibrosis contributes to cardiovascular disease progression in general and heart failure in particular. Myocardial fibrosis and subsequent cardiac remodelling occurs in heart failure because of increased collagen production and collagen deposition as a result of pressure overload, myocardial ischemia, as well as neurohormonal activation (including the reninagiotensin-aldosterone axis and sympathetic nervous system activation) (Gonzalez et al., 200...

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Section: Discussionsupporting

confidence: 44%

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confidence: 99%

Association between depressive symptoms and fibrosis markers: The Cardiovascular Health Study

Kop

Kuhl

Barasch

et al. 2010

Brain, Behavior, and Immunity

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“…Cicoira et al reported on 101 individuals with HF (mean age 62 ± 9 years) and found that in patients with a LVEF < 31%, a serum level >4.7 mcg/L of PIIINP was associated with a higher mortality and rate of hospitalization for HF as compared with the other patients (7). Ruiz-Ruiz et al found in 111 patients (age = 73 ± 8 years) with decompensated HF that a higher level of PIP was associated with a increased mortality and readmission rate (26), and Rossi et al reported on 106 patients (age = 64 ±6 years) with dilated cardiomyopathy that a higher serum level of PIIINP was associated with a restrictive mitral inflow pattern and 2-fold higher mortality than those with a non-restrictive pattern (27). In RALES (16), which enrolled 261 elderly patients with EF < 35% in NYHA class III and IV, those with baseline PIIINP > 3.85 μg/L had a higher relative risk of death and /or HF hospitalization.…”

Section: Discussionmentioning

confidence: 99%

The Relationship Between Serum Markers of Collagen Turnover and Cardiovascular Outcome in the Elderly

Barasch

Gottdiener

Aurigemma

et al. 2011

Circ: Heart Failure

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Background The deposition of collagen fibrils in the myocardial extracellular matrix increases with age and plays a key role in the pathophysiology of heart failure (HF). We sought to determine the predictive value of serum markers of collagen turnover for incident HF and cardiovascular (CV) morbidity, mortality and all-cause mortality in elderly individuals. Methods and Results In 880 participants in the Cardiovascular Health Study (mean age 77 ± 6 yrs, 48% female), serum levels of carboxyl-terminal peptide of procollagen type I (PIP), carboxyl-terminal telopeptide of collagen type I (CITP), and amino-terminal peptide of procollagen type III (PIIINP) were measured in 4 groups: HF with reduced ejection fraction (HFREF; n=146, EF < 55%); HF with preserved EF (HFPEF; n=175, EF ≥ 55%), controls with CV risk factors but not HF (CVD; n = 280) and healthy controls free of CV disease (n=279). Relationships between these serum markers and outcome at follow-up of 12 ± 4 years (range, 3-17 years) was determined in six models including those adjusted for conventional risk factors, renal function, NT-proBNP and agents which interfere with collagen synthesis. For the entire cohort, in unadjusted and adjusted models, both PIIINP and CITP were associated with myocardial infarction, incident HF, hospitalization for HF, cardiovascular and all-cause mortality. In healthy controls, CITP and PIIINP were associated with all-cause death. In controls with risk factors, CITP was associated with incident HF, and in participants with HFPEF, CITP was associated with hospitalization for HF. No collagen biomarker was associated with outcome in participants with HFREF, and PIP was not associated with outcome in the cohort or its subgroups. Conclusions In both healthy and elderly individuals with CV disease at risk of developing HF, CITP and PIIINP are significantly associated with multiple adverse cardiac outcomes including myocardial infarction, HF and death. Clinical Trial Registration URL: http://www.chs-nhlbi.org. Unique Identifier: NCT00005133.

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“…described PIP levels of 116.60 ± 3.52 ng/mL for HFpEF patients and 67.67 ± 4.35 ng/mL for controls. Serum PIP was described to independently predict HF episodes, readmission and death and a single serum measurement of PIP may have prognostic value in patients presenting with decompensated HF . Treatment effects of torasemide had previously been described to range from a 20% to 25% PIP decrease under torasemide .…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, a net release of PIP from the heart into the circulation has been reported in patients with hypertensive heart disease and HF, suggesting a cardiac origin for systemic serum PIP in this condition . Some studies have described further associations between serum PIP levels and outcomes or disease state …”

Section: Introductionmentioning

confidence: 95%

Investigating a biomarker‐driven approach to target collagen turnover in diabetic heart failure with preserved ejection fraction patients. Effect of torasemide versus furosemide on serum C‐terminal propeptide of procollagen type I (DROP‐PIP trial)

Trippel

Linthout

Westermann

et al. 2017

European J of Heart Fail

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Propeptide of procollagen type I (PIP) and outcomes in decompensated heart failure

Cited by 15 publications

References 28 publications

Association between depressive symptoms and fibrosis markers: The Cardiovascular Health Study

Association between depressive symptoms and fibrosis markers: The Cardiovascular Health Study

The Relationship Between Serum Markers of Collagen Turnover and Cardiovascular Outcome in the Elderly

Investigating a biomarker‐driven approach to target collagen turnover in diabetic heart failure with preserved ejection fraction patients. Effect of torasemide versus furosemide on serum C‐terminal propeptide of procollagen type I (DROP‐PIP trial)

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