Serum Concentration of Procollagen Type III Amino-Terminal Peptide is Increased in Patients with Successfully Repaired Coarctation of the Aorta with Left Ventricular Hypertrophy

Abstract

Pathological left ventricular hypertrophy (LVH) with myocardial fibrosis is an independent risk factor for cardiovascular mortality. Previous studies indicated that patients with coarctation of the aorta (CoA) have increased left ventricular mass (LVM) including LVH, even after successful CoA repair. It is unclear whether the increased LVM is pathological one with cardiac fibrosis. Group A consisted of 17 patients with successfully repaired CoA. Group B consisted of 17 postoperative subjects who matched the age and postoperative periods of group A. Group C comprised 28 subjects for the geometric standard of the left ventricle. The LVM index (LVMI) and the relative wall thickness (RWT) of group A and B were compared with the values of 17 age-matched subjects from group C. The serum concentration of procollagen type III amino-terminal peptide (P-III-P), a biomarker for myocardial fibrosis, in group A was compared with the concentration in group B. The correlations between the serum P-III-P concentration and LVMI and RWT were studied in group A and non-A group. In group A, RWT and LVMI were significantly higher than those in group C (0.37 ± 0.05 vs. 0.31 ± 0.02, p < 0.01; 44.8 ± 11.2 vs. 36.5 ± 7.6, p = 0.04, respectively), and the serum P-III-P concentration was significantly higher than that in group B (1.59 ± 0.74 vs. 1.07 ± 0.33, p = 0.04). Serum P-III-P concentrations were well correlated with RWT and LVMI (r = 0.89, p < 0.01; r = 0.63, p < 0.01, respectively) in group A. LVH in patients with successfully repaired CoA may have an abnormal pathogenesis associated with myocardial fibrosis.

Liver Fibrosis Markers Represent Central Venous Pressure in Post-pubertal Patients With Congenital Heart Disease

“…However, CHD patients are prone to concomitant hepatic congestion and ischemia. In addition to cases of hepatic congestion, liver fibrosis markers have been reported to be elevated in cases of increased systemic-to-pulmonary blood flow ratios or myocardial fibrosis [ 16 , 17 ]. Although it is very important to monitor the fibrotic status of the liver in patients with CHD, it is difficult to set a predictive cutoff value for liver fibrosis markers.…”

The Diabetic Cardiorenal Nexus

“…Among chronic dialysis patients, concentric left ventricular hypertrophy was associated with a lower prevalence of cardiovascular events than eccentric hypertrophy and was more responsive to size reduction with angiotensin-converting enzyme inhibition [204,205]. The explanation for this finding may be related to the relative impact of ACE inhibition on muscle as opposed to collagen, which is found in higher serum [205] and arterial tissue [206] concentrations in hypertension. Collagen synthesis as measured by levels of mRNA and protein may be delineated in endo-myocardial biopsies of hypertensive heart disease with or without heart failure [207].…”

Roles of Biomarkers in Myocardial Fibrosis

“…This shows that the increase in serum PIIINP levels could reflect cardiac fibrosis to some extent, which was of prognostic value and was related to clinical stage. Additionally, PIIINP levels were positively correlated with diastolic dysfunction in patients with HF with reduced ejection fraction (HFrEF) [ 26 ], with left ventricular mass index (LVMI), and with relative wall thickness (RWT) in patients with successfully repaired coarctation of the aorta (CoA) with left ventricular hypertrophy [ 27 ]. It was also inversely associated with diastolic function in patients with hypertension [ 28 ].…”