[Collagen synthesis and heart failure]. / Síntesis de colágeno e insuficiencia cardíaca.

Little is known about collagen metabolism in heart failure, with or without left ventricular systolic dysfunction. We studied serum concentrations of the carboxy-terminal propeptide of procollagen type I (PIP), a marker of collagen type-I synthesis, and of the carboxy-terminal telopeptide of collagen type I (ICTP), a marker of collagen type-I degradation, in 70 patients admitted for heart failure (35 with depressed left ventricular systolic function and 35 with preserved left ventricular systolic function) and in 30 control subjects. Patients with kidney failure, liver disease, metabolic bone disease, rheumatic disease, recent (within 3 months) major trauma or surgery, or serious wounds were excluded. The concentration of the collagen synthesis marker, PIP, was higher in heart failure patients than control subjects, at 140+/-56.38 mg/L vs 113.66+/-36.6 microg/L, respectively (P=.01). However, there was no difference in the concentration of the collagen degradation marker, ICTP, between heart failure patients and control subjects, at 2.89+/-2.37 mg/L vs 2.26+/-1.7 microg/l, respectively. In heart failure patients, left ventricular systolic function had nonsignificant effect on the PIP or ICTP concentration.

Síntesis de colágeno e insuficiencia cardíaca / Collagen synthesis and heart failure

Se desconoce el metabolismo del colágeno en la insuficiencia cardíaca con y sin disfunción sistólica ventricular izquierda. Estudiamos las concentraciones de los marcadores de síntesis de colágeno tipo I (péptido C-terminal del procolágeno tipo I [PIP]) y de degradación (telopéptido del colágeno tipo I [CITP]) en un grupo de 70 pacientes tras un ingreso por insuficiencia cardíaca (35 con función ventricular izquierda deprimida y 35 con función ventricular conservada), así como en 30 individuos sanos. Excluimos a los pacientes con insuficiencia renal, enfermedad hepática, enfermedad autoinmunitaria o del metabolismo óseo, traumatismo mayor y cirugía reciente (< 3 meses) y heridas extensas. Encontramos mayores concentraciones del marcador de síntesis colágena (PIP)en los pacientes con insuficiencia cardíaca respecto al grupo control (140 ±56,38 frente a 113,66 ±36,6 µg/l; p= 0,01), sin que se apreciaran diferencias en el marcador de degradación (CITP) (2,89 ± 2,37 frente a 2,26 ± 1,7µg/l). No observamos diferencias significativas entre los valores medios de PIP y CITP en pacientes con insuficiencia cardíaca con función sistólica conservada frente adeprimida

Little is known about collagen metabolism in heart failure, with or without left ventricular systolic dysfunction. We studied serum concentrations of the carboxy-terminal propeptide of procollagen type I (PIP), a marker of collagentype-I synthesis, and of the carboxy-terminal telopeptideof collagen type I (ICTP), a marker of collagen type-I degradation, in 70 patients admitted for heart failure (35 with depressed left ventricular systolic function and 35 with preserved left ventricular systolic function) and in 30 control subjects. Patients with kidney failure, liver disease, metabolic bone disease, rheumatic disease, recent (within 3 months) major trauma or surgery, or serious wounds were excluded. The concentration of the collagen synthesis marker, PIP, was higher in heart failure patients thancontrol subjects, at 140±56.38 mg/L vs 113.66±36.6 µg/L, respectively (P=.01). However, there was no difference in the concentration of the collagen degradation marker, ICTP, between heart failure patients and control subjects, at 2.89±2.37 mg/L vs 2.26±1.7 µg/l, respectively. In heart failure patients, left ventricular systolic function had nosignificant effect on the PIP or ICTP concentration