Serum type III procollagen peptide levels in coronary artery disease (a marker of atherosclerosis)

Abstract

The known shift in collagen synthesis from procollagen type I to type III in patients with atherosclerosis, suggested measurement of serum procollagen III peptide (PIIIP) levels in patients with coronary artery disease (CAD). Two groups of patients were studied: group I--thirty-six patients with CAD (male, mean age 56.9 +/- 7.5 years, hospitalized for coronary angiography. Risk factors included 16 patients with high blood pressure, four diabetics, 31 smokers and 15 with hypercholesterolaemia. Five patients had no significant lesions, seven had one vessel with over 50% stenosis, 10 had two vessels and 14 had three vessels. Group II--35 patients (male, mean age 39.4 +/- 13.3 years), with normal physical examination and ECG according to WHO criteria, formed the control group: the risk factors included nine patients with high blood pressure, 14 smokers and one with hypercholesterolaemia. Procollagen III peptide levels were determined by radioimmunoassay. In group I, PIIIP levels were 26.8 +/- 16 ng ml-1 vs. 10.4 +/- 3.2 for group II. Sixty-one per cent of group I had pathological levels of PIIIP with an absence of correlation with the severity of atherosclerosis or risk factors. Only 2.8% of patients in group II had pathological levels. Procollagen III peptide determination would appear to be a sensitive, specific and predictive test for atherosclerosis in patients with CAD.

Collagen: scaffold for repair or execution

“…As a natural consequence, interest has risen in serological monitoring of collagen metabolism during various aspects of cardiovascular disease. Serum levels of PIIINP in atherosclerotic patients apparently differ from those of controls [31]. Furthermore, elevated levels of serum PICP and PIIINP in hypertensive patients appear to be normal after 6 months of ACE inhibitor therapy [32].…”

Telomere length and replicative aging in human vascular tissues.

“…Unfortunately, current markers for the progression of atherosclerosis or for the propensity of an individual to develop atherosclerosis do not directly address this issue. For example, endothelium-derived type III collagen (13), von Willebrand's factor VIII (14), cholesterol, triglycerides, apolipoprotein B (11), lipoprotein(a) (15)(16)(17), endothelin (18), and heparinreleasable platelet factor 4 (19) are associated with atherogenesis and can be detected in the plasma but have not been linked directly to cell aging. A similar situation exists for other markers (20)(21)(22), including restriction fragment length polymorphisms associated with susceptible individuals (23,24).…”

Efficacy of Steroid Therapy for Pacing Failure in a Patient with Chronic Myocarditis

“…To date, the serum P-III-P value has been used as a marker for diagnosing and determining the fibrosis in liver disease (10). That value is known to increase in hypertensive ventricular hypertrophy, dilated cardiomyopathy and acute myocardial infarction (up to 4 months) (11)(12)(13)(14). In heart disease, the P-III-P also is considered to imply fibrosis of the heart.…”