Increased Collagen Type I Synthesis in Patients With Heart Failure of Hypertensive Origin

Abstract

Background-We investigated whether increased collagen type I synthesis and deposition contribute to enhancement of myocardial fibrosis and deterioration of cardiac function in patients with hypertensive heart disease (HHD). Methods and Results-We studied 65 hypertensives with left ventricular hypertrophy subdivided into 2 groups: 34 patients without heart failure (HF) and 31 patients with HF. Transvenous endomyocardial biopsies of the interventricular septum were performed to quantify the amount of fibrotic tissue and the extent of collagen type I deposition. The carboxy-terminal propeptide of procollagen type I (PIP), an index of collagen type I synthesis, was measured by radioimmunoassay in serum samples from the coronary sinus and the antecubital vein. Compared with normotensives, the amount of collagen tissue, the extent of collagen type I deposition, and coronary and peripheral PIP were increased (PϽ0.01) in the 2 groups of hypertensives. These parameters were also increased (PϽ0.01) in HF hypertensives compared with non-HF hypertensives. Coronary PIP was higher (PϽ0.01) than peripheral PIP in hypertensives but not in normotensives. The amount of collagen tissue was inversely correlated with the ejection fraction and directly correlated with both coronary and peripheral PIP in all hypertensives. Conclusions-These findings suggest that an excess of cardiac collagen type I synthesis and deposition may be involved in the enhancement of myocardial fibrosis that accompanies the development of HF in HHD. In addition, our data show that the heart secretes PIP via the coronary sinus into the peripheral circulation in patients with HHD. Thus, PIP determined in peripheral blood can be a useful marker of myocardial fibrosis in these patients.

Spironolactone improves diastolic function in the elderly

“…16 Higher levels of PICP were recently reported in hypertensives with than in those without heart failure. 17 Markedly elevated baseline PICP levels in our study indicated that significant fibrosis was present in our elderly with diastolic dysfunction. After 4 months of treatment with spironolactone, PICP levels decreased significantly from baseline values.…”

Structure and Mechanical Properties of Soft Tissues during Selected Pathological Processes

“…Those situations can be associate to impaired degradation of collagen type I. Conformational changes of this protein also occur in people with heart failure. As a result of proteins modification, increasing of collagen type I content is observed [40], What lead to change of tissue stiffness? It is worth mentioning that in arterial vessels, protein structure also can be altered during pathological processes.…”

“…The above considerations allow to conclude that stiffness tissue modification are not one-way process. In the case of the heart, the liver or even abnormal wound healing, the impaired function of the degradation can be the reason [38][39][40]. However, skin diseases modifications of lipid conformations can be the source of problems.…”

Time course of serum collagen types I and III metabolism products after reperfused acute myocardial infarction in patients with and without systemic hypertension

“…[11][12][13][14] This excess of myocardial collagen is primarily a result of the uncoupling between increased synthesis and unchanged or decreased degradation of collagen type I fibres. 18 However, patients with coronary heart disease have been excluded from these studies, 11-14 so it is not clear if a different pattern of interstitial remodelling may be present in the first months after AMI in patients with antecedent hypertension.…”

“…[11][12][13][14] Accordingly, we serially measured serum products collagen types I and III turnover, which constitute the bulk of cardiac ECCM, 15 and LV volumes and function in a consecutive sample of patients successfully treated with primary percuta-neous coronary intervention (PCI) for a first AMI with LV systolic dysfunction. The purpose of this study was to evaluate if a different pattern of ECCM and LV remodelling is present in patients with antecedent hypertension compared with those without hypertension.…”