Relation Between Connective Tissue Growth Factor and Cardiac Sympathetic Nerve Activity in Heart Failure in DCM Patients

Abstract

SummaryCardiac fibrosis is an important process of myocardial remodeling. Connective tissue growth factor (CTGF) is a cytokine that plays a key role in the occurrence of progressive fibrosis and excessive scarring. CTGF levels are increased in the failing heart. In addition, sympathetic nerve activity is enhanced in the failing heart, and exacerbates heart failure. To clarify the relation between cardiac sympathetic nerve activity and CTGF, we studied 35 (M/F = 28/7 patients) aged 57 ± 15 years with dilated cardiomyopathy (DCM). Cardiac sympathetic nerve activity was estimated from the total defect score (TDS) and from the H/M ratio and washout rate (WR) on I-123-MIBG imaging. Cardiac symptoms (NYHA class), exercise capacity (specific activity scale: SAS), brain natriuretic peptide (BNP), hemodynamics, and CTGF were assessed. There was a significant correlation between the CTGF and WR on I-123-MIBG (r = 0.45, P = 0.008). Also, a higher plasma CTGF level was associated with a lower SAS score (r = 0.51, P = 0.002), but not the TDS, H/M ratio, or BNP concentration. Moreover, a higher NYHA class and pulmonary artery wedge pressure were associated with a higher plasma CTGF level. The plasma CTGF level can be strongly related with cardiac sympathetic nerve activity in heart failure in DCM patients. (Int Heart J 2012; 53: 282-286)

Connective tissue growth factor dependent collagen gene expression induced by MAS agonist AR234960 in human cardiac fibroblasts

“…The levels of CTGF in tissue correlate with the degree and severity of fibrosis [ 11 , 36 ] as well as its role as a hypertrophic factor for cardiomyocytes [ 37 ]. The plasma CTGF level is also associated with HF in dilated cardiomyopathy patients [ 38 , 39 ]. Finding that cardiac fibroblasts produce CTGF and collagen downstream of MAS provides the basis for consideration of MAS blockade as a therapy for cardiac disease states, specifically to combat HF and fibrosis.…”

Late gadolinium enhancement on cardiac magnetic resonance combined with 123I- metaiodobenzylguanidine scintigraphy strongly predicts long-term clinical outcome in patients with dilated cardiomyopathy

“…In the HF status, the rein-angiotensin-aldosterone system was activated and the angiotensinⅡinduced expression of plasma connective tissue growth factor (CTGF) which was a cytokine that played a key role in the prognosis fibrosis, and expression of transforming growth factor-β(TGF-β) which caused cardiac fibrosis [25,26]. Moreover previous studies reported that, in DCM patients, these serum levels were strongly related with cardiac sympathetic nervous activity expressed by WR on 123 I-MIBG scintigraphy [27,28]. In this study, regardless of the presence or absence of LGE, the median of WR was higher than the control [14] both groups, however, WR was not significantly different between the presence and absence of LGE.…”

Relationship of postcontrast myocardial T1 value and delayed enhancement to reduced cardiac function and serious arrhythmia in dilated cardiomyopathy with left ventricular ejection fraction less than 35%

“…The myocardial T1 value was not correlated with BNP in our study. One previous study has shown that myocardial collagen turnover does not correlate with serum BNP in DCM patients with severe heart failure (29). Serum BNP is affected by stretching of myocytes and diastolic dysfunction as well as by myocardial ischemia, obesity, and other clinical factors (30).…”