The relationship between serum fibrosis markers and restrictive ventricular filling in patients with heart failure with reduced ejection fraction: A technetium-99m radionuclide ventriculography study

Abstract

Myocardial fibrosis leads to a restrictive diastolic filling pattern of the left ventricle which is associated with a poor prognosis in patients with heart failure. We investigated the relationship between cardiac fibrosis and restrictive filling pattern of the left ventricle measured by Tc99m left ventriculography in patients with chronic symptomatic heart failure. Serum cardiac extracellular matrix markers including type I and III aminoterminal propeptide of procollagen (PINP and PIIINP), matrix metalloproteinase-2,9 (MMP-2,9), and tissue inhibitor of MMP-1 (TIMP-1) were analyzed. Fifty-one (39 males) patients were enrolled. Their median age was 51.8 years, and median left ventricular ejection fraction was 31.9%. Time to peak filling rate of the left ventricle was significantly correlated with serum levels of the three cardiac extracellular matrix markers (TIMP-1, PIIINP, and MMP-2). The patients with a restrictive diastolic filling pattern of the left ventricle (time to peak filling rate = 154 ms) had significantly higher levels of these extracellular matrix markers. In receiver operating characteristic curve analysis, areas under the curve of PIIINP, TIMP-1, and MMP-2 were 0.758, 0.695, and 0.751 to predict the presence of a restrictive pattern. In C-statistics, all three cardiac extracellular matrix markers significantly increased the area under the curve after adding creatinine. In net reclassification improvement and integrated discrimination improvement models, PIIINP and MMP-2 significantly improved the predictive power of age, creatinine and brain natriuretic peptide. In conclusion, serum extracellular matrix markers are significantly correlated with restrictive diastolic filling pattern of the left ventricle in patients with heart failure.

Impact of polyphenols on heart failure and cardiac hypertrophy: clinical effects and molecular mechanisms

“…HF occurs under different pathological circumstances, including MI ( 23 ), valvular inadequacy ( 24 ), hypertension ( 25 ), cardiomyopathy ( 26 ), diabetes ( 27 ), and autoimmune diseases ( 28 ). Heart loss of function is primarily due to abnormal remodeling after the defects in cardiomyocytes' cellular metabolisms ( 29 – 31 ). Following hemodynamic alterations, compensatory mechanisms help maintain the heart's function, like the renin-angiotensin process, the sympathetic nervous system, and other neurohormonal mechanisms ( 32 ).…”

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 ].…”

Improved medical expenditure and survival with integration of traditional Chinese medicine treatment in patients with heart failure: A nationwide population-based cohort study

“…Heart failure (HF) is a common cause of morbidity and mortality [ 1 – 3 ]. The prevalence of HF is increasing worldwide due to both an aging population and significant advances in the management of associated comorbidities, such as ischemic heart disease, arrhythmia, diabetes mellitus, stroke, and hypertension [ 4 , 5 ].…”