Plasma Cardiotrophin-1 Levels Research Articles

Endothelial dysfunction in patients with myocardial ischemia or infarction and nonobstructive coronary arteries.

The syndromes of myocardial infarction/myocardial ischemia with No Obstructive Coronary Artery Disease (MINOCA/INOCA) are seen more and more often. Endothelial dysfunction (ED) leading to ischemic events has been reported in many of these patients. We aimed to compare patients with MINOCA and INOCA regarding brachial artery flow-mediated endothelium-dependent vasodilation (flow-mediated dilation [FMD]) and plasma concentration of cardiotrophin-1 (CT-1). We included 42 patients with MINOCA and 38 patients with INOCA. Endothelial function was assessed by measuring FMD% and nitroglycerin-mediated dilatation (NMD%) in the brachial artery. The plasma level of CT-1 was determined by solid-phase enzyme-linked immunosorbent assay. FMD% was significantly lower in MINOCA than in INOCA patients (6.45 ± 2.65 vs 8.94 ± 3.32, P < .001), without significant difference in NMD% (10.69 ± 3.19 vs 12.16 ± 3.69, P = .06). Plasma CT-1 levels were not significantly different: 40.1 pg/mL (22.5-102.1) vs 37.2 pg/mL (23.5-67.2), P = .53. Our results suggest worse ED in MINOCA than in INOCA patients, but demonstrated no difference in CT-1 levels between patients with stable and unstable ischemic heart disease and normal coronary arteries.

Plasma cardiotrophin-1 levels are associated with hypertensive heart disease: a meta-analysis.

Cardiotrophin-1 (CT-1) is a member of the interleukin 6 cytokine superfamily. Plasma CT-1 levels have been associated with heart failure and hypertension in small independent studies. Whether plasma CT-1 levels are associated with progression of hypertensive heart disease is poorly understood. The authors carried out a meta-analysis using published studies and electronic databases. Relevant data were extracted using standardized algorithms. Additional data were obtained directly from investigators when indicated. A total of 18 studies were included that reported on association between CT-1 level and hypertension (n=8), cardiac hypertrophy (n=9), and heart failure (HF) (n=10). The serum levels of CT-1 were significantly higher in patients with hypertension (standard mean difference [SMD], 0.85; 95% confidence interval [CI], 0.64-1.06 fmol/mL), left ventricular hypertrophy (SMD, 0.88; 95% CI 0.60-1.17 fmol/mL), or HF (SMD, 0.66; 95% CI, 0.51-0.80 fmol/mL) compared with controls. Subgroup analysis revealed CT-1 levels to be highest in patients with hypertension-induced hypertrophy with HF, followed by patients with hypertension-induced left ventricular hypertrophy without HF (SMD, 0.52; 95% CI, 0.30-0.75 fmol/mL), patients with hypertension without left ventricular hypertrophy (SMD, 0.67; 95% CI, 0.46-0.88 fmol/mL) as compared with normotensive patients (SMD, 0.74; 95% CI, 10.45-1.04 fmol/mL). Increased plasma CT-1 levels are associated with risk for HF in hypertensive patients. CT-1 may serve as a novel biomarker in determining prognosis in hypertensive patients.

Serum Cardiotrophin-1 and IL-6 Levels in Patients with Obstructive Sleep Apnea Syndrome

Obstructive sleep apnea syndrome (OSAS) is associated with increased rates of cardiovascular diseases (CVD). Basic mechanisms involved in the increased cardiovascular risk of OSAS remain unclear. Inflammation has been shown to potentially play a critical role in this association. The aim of the present study was to investigate the level of cardiotrophin-1 (CT-1) in patients with OSAS. Forty-eight newly diagnosed OSAS patients and 37 nonapneic controls were enrolled in this study. Demographic data, cigarette smoking status, previous history of chronic diseases including CVD and metabolic diseases and drugs, and habits were obtained by a standardized questionnaire. All patients underwent polysomnographic evaluation. The mean age was 48.3 ± 12.3 (24-74) years in OSAS group. Median apnea-hypopnea index was 23.6 (6-91.8) and median body mass index was 30.4 (24.2-49.4) in the OSAS group. Plasma CT-1 levels in OSAS and control groups, respectively, were 12.03 ± 1.08 and 11.85 ± 1.18 pg/ml. There was no significant difference in the plasma levels of CT-1 and IL-6 between the OSAS group and the controls.

Effect of cardiac resynchronization therapy on cardiotrophin-1 circulating levels in patients with heart failure

Cardiotrophin-1 (CT-1) is a member of the interleukin (IL-6) family of cytokines. Plasma CT-1 levels correlate with the left ventricle mass index in patients with dilatated cardiomyopathy and congestive heart failure (CHF). The aim of this paper was to evaluate CT-1 plasma levels, before and after cardiac resynchronization therapy CRT, and to characterizeits prognostic role in patients with CHF. Fifty-two consecutive patients (M/F = 39/13; 56 ± 11 years old) underwent clinical and echocardiographic evaluation, and blood sample collection at baseline. The same evaluation was repeated 6.4 ± 0.79 months after CRT. Patients with a decreased LV end-systolic volume by at least 15% (reverse remodeling) were considered echo responders to CRT. Twenty-nine patients (56%) were responders to CRT. After CRT, only 15 patients (29%) showed increased CT-1 after CRT. They were all non responders to CRT. A multivariate, logistic model showed CT-1 as an independent predictor of CRT echo response (p = 0.005; OR 0.97). During follow-up (18 ± 7 months), 21 cardiac events in 18 patients occurred. A Cox multivariable model showed plasma BNP pre-CRT (p = 0.02; CI 1.2-5.6; OR 3.1) and CT1 post-CRT (p = 0.01; CI 1.4-4.3; OR 2.7) as independent predictors of cardiac events. Analysis of CT-1 plasma levels deserves future consideration for larger, longitudinal studies in patients with CHF.

The human heart releases cardiotrophin-1after coronary artery bypass grafting with cardiopulmonary bypass

Objectives. Cardiotrophin-1 (CT-1) is closely linked to many cardiovascular diseases, such as myocardial infarction and heart failure, and exhibits cardioprotective effect in ischemia-reperfusion injury. The present study was designed to investigate the course of CT-1 in patients undergoing on-pump coronary artery bypass grafting (CABG), and to evaluate the relationship between plasma CT-1 levels and postoperative cardiac function. Methods. Twenty-four patients undergoing elective CABG were studied. Radial artery blood samples were collected before cardiopulmonary bypass (CPB), 5 min and 20 min after reperfusion, and 1 h, 6 h, 12 h and 24 h after CPB. Coronary sinus blood samples were collected before CPB, 5 min and 20 min after reperfusion. Plasma CT-1 levels were measured using the ELISA method. Hemodynamic data were collected. Results. Peripheral CT-1 levels did not change significantly postoperatively. Trans-myocardial CT-1 levels increased significantly 5 min and 20 minutes after reperfusion as compared to baseline. A weak positive correlation (r = 0.408, p = 0.048) was found between trans-myocardial CT-1 levels at 20 min after reperfusion and CI at 12 h after CPB. Conclusions. The heart secretes CT-1 after ischemic injury. The precise effect of CT-1 in CABG needs further investigation.

Cardiotrophin-1 plasma levels are associated with the severity of hypertrophy in hypertrophic cardiomyopathy

AimsCardiotrophin-1 (CT-1) is a cytokine that induces hypertrophy in cardiomyocytes and is associated with left ventricular hypertrophy (LVH) in hypertensive patients. The objective of this study was to evaluate whether plasma CT-1 is associated with hypertrophic cardiomyopathy (HCM).Methods and resultsThe study was performed in 124 patients with HCM. All patients underwent a full clinical evaluation and an echocardiogram. Left ventricular hypertrophy was evaluated by the measurement of the maximal LV wall thickness and the Spirito's LVH score. Plasma CT-1 was measured by an enzyme-linked immunosorbent assay. Compared with controls, patients with HCM exhibited higher (P < 0.001) plasma CT-1 levels. Significant correlations were found between CT-1 and maximal LV wall thickness (r = 0.284, P = 0.001) and the Spirito's LVH score (r = 0.287, P = 0.006) in HCM patients. In addition, the levels of CT-1 were higher (P = 0.02) in patients with severe LVH (maximal LV wall thickness ≥30 mm) than in patients with mild or moderate LVH (maximal LV wall thickness <30 mm).ConclusionsThese findings show that plasma CT-1 is associated with the severity of LVH in patients with HCM. Further studies are required to ascertain whether CT-1 is a diagnostic biomarker of this cardiomyopathy.

Cardiotrophin-1 in Patients with Acute Myocardial Infarction

Problem statement: Myocardial infarction is the combined result of environmental and personal factors. Prothrombotic factors might play an important role in this phenomenon. Inflammation plays a pivotal role in atherosclerosis and coronary heart disease. Cardiotrophin-1 (CT-1), a member of the IL-6 family of cytokines, was identified as a growth factor for cardiac myocytes that induces cardiomyocyte hypertrophy and stimulates cardiac fibroblasts, protects myocytes from cell death. This study was designed to investigate whether plasma concentration of Cardiotrophin-1 (CT-1), in patients who had the first acute myocardial infarction and to analyze their relationship with traditional cardiovascular risk factors. Approach: This study was carried out on 45 patients with Acute Myocardial Infarction (AMI) in their first 24 h of admission as case group and 36 healthy matched individuals were studied as the control. Plasma level of cardiotrophin-1 was determined by enzyme-linked immunosorbent assay and the results were compared. Results: Plasma CT-1 levels in the patients with AMI on admission 615.279±5.109 pmol L-1 were significantly higher than those in the control group 534.767±6.750 pmol L-1 (p = 0.001). Plasma CT-1 level was not correlated with diabetes mellitus, hyperlipidemia, sex, age and smoking. Conclusion: Our findings suggested that high plasma CT-1 level in patients with AMI is indicative of hypercoagulable state that is not related to the traditional cardiovascular risk factors.

Response to Cardiotrophin-1 in Adolescents: Impact of Obesity and Blood Pressure

We read with interest the letter from Jung et al1 providing data on the potential impact of overweight/obesity and blood pressure on cardiotrophin-1 (CT-1) levels in adolescents. We saw that they found no differences in plasma CT-1 levels between overweight/obese and normal-weight adolescents and neither overweight/obesity indices nor HBA1c and adiponectin correlated with plasma levels of CT-1. In our study, the high plasma CT-1 in morbidly obese patients might possibly be attributable both to the degree of …

Association of Increased Plasma Cardiotrophin-1 With Left Ventricular Mass Indexes in Normotensive Morbid Obesity

To the Editor: We read with great interest the article by Lopez et al,1 who hypothesize that cardiotrophin-1 (CT-1), a cytokine that induces cardiomyocyte growth, may be abnormally upregulated in hypertensive patients with inappropriate left ventricular mass (LVM), suggesting that an excess of CT-1 may contribute to inappropriate left ventricular growth. This possibility is supported by the finding of a correlation between CT-1 levels and the observed LVM/predicted LVM ratio, independent from concentric left ventricular hypertrophy (LVH). de Simone et al2 suggested that, other than hemodynamic load, the process that yields to inappropriate LVH can also depend on the protracted activity over time of cytokines, among other nonhemodynamic factors. The observation by Lopez et al1 that CT-1 levels were high in treated patients in whom inappropriate LVM persisted …

Plasma cardiotrophin-1 following acute myocardial infarction: relationship with left ventricular systolic dysfunction

The glycoprotein 130 (gp 130) signalling pathway is important in the development of heart failure. Cardiotrophin-1 (CT-1), a cytokine acting via the gp 130 pathway, is involved in the process of ventricular remodelling following acute myocardial infarction (AMI) in animals. The aims of the present study were to examine the profile of plasma CT-1 following AMI in humans, and its relationship with echocardiographic parameters of left ventricular (LV) systolic function. Serial measurements of plasma CT-1 levels were made in 60 patients at 14-48 h, 49-72 h, 73-120 h and 121-192 h following AMI and at a later clinic visit. LV function was assessed using a LV wall motion index (WMI) score on admission (WMI-1) and at the clinic visit (WMI-2). Compared with values in control subjects (29.5+/-3.6 fmol/ml), the plasma CT-1 concentration was elevated in AMI patients at 14-48 h (108.1+/-15.1 fmol/ml), 49-72 h (105.2+/-19.7 fmol/ml), 73-120 h (91.2+/-14.9 fmol/ml) and 121-192 h (118.8+/-22.6 fmol/ml), and at the clinic visit (174.9+/-30.9 fmol/ml) (P<0.0001). Levels were higher following anterior compared with inferior AMI. For patients with anterior AMI, CT-1 levels were higher at the clinic visit than at earlier times. WMI-1 correlated with CT-1 at all times prior to hospital discharge (P<0.05). On best subsets analysis, the strongest correlate with WMI-1 was CT-1 level at 49-72 h (R(2)=20%, P<0.05). In conclusion, plasma levels of CT-1 are elevated soon after AMI in humans and rise further in the subsequent weeks in patients after anterior infarction. CT-1 measured soon after AMI is indicative of LV dysfunction, and this cytokine may have a role in the development of ventricular remodelling and heart failure after AMI.

Elevated circulating cardiotrophin-1 in heart failure: relationship with parameters of left ventricular systolic dysfunction

Cardiotrophin-1 (CT-1) is a cytokine that has been implicated as a factor involved in myocardial remodelling. The objective of the present study was to establish the relationship between circulating levels of CT-1 and measures of left ventricular size and systolic function in patients with heart failure. We recruited 15 normal subjects [six male; median age 60 years (range 30–79 years)] and 15 patients [11 male; median age 66 years (range 43–84 years)] with a clinical diagnosis of heart failure and echocardiographic left ventricular systolic dysfunction (LVSD). Echocardiographic variables (left ventricular wall motion index, end-diastolic and -systolic volumes, stroke volume, fractional shortening) and plasma CT-1 levels were determined. In patients with LVSD [median wall motion index 0.6 (range 0.3–1.4)], CT-1 was elevated [median 110.4 fmol/ml (range 33–516 fmol/ml)] compared with controls [wall motion index 2 in all cases; median CT-1 level 34.2 fmol/ml (range 6.9–54.1 fmol/ml); P &lt; 0.0001]. Log CT-1 was correlated with log wall motion index (r = -0.76, P &lt; 0.0001), log left ventricular end-systolic volume (r = 0.54, P &lt; 0.05), stroke volume (r = -0.60, P = 0.007) and log fractional shortening (r = -0.70, P = 0.001). In a multivariate model of the predictors of log wall motion index, the only significant predictor was log CT-1 (R2 = 56%, P = 0.006). This is the first assessment of the relationship between plasma CT-1 levels and the degree of LVSD in humans, and demonstrates that CT-1 is elevated in heart failure in relation to the severity of LVSD.

Elevated circulating cardiotrophin-1 in heart failure: relationship with parameters of left ventricular systolic dysfunction

Cardiotrophin-1 (CT-1) is a cytokine that has been implicated as a factor involved in myocardial remodelling. The objective of the present study was to establish the relationship between circulating levels of CT-1 and measures of left ventricular size and systolic function in patients with heart failure. We recruited 15 normal subjects [six male; median age 60 years (range 30-79 years)] and 15 patients [11 male; median age 66 years (range 43-84 years)] with a clinical diagnosis of heart failure and echocardiographic left ventricular systolic dysfunction (LVSD). Echocardiographic variables (left ventricular wall motion index, end-diastolic and -systolic volumes, stroke volume, fractional shortening) and plasma CT-1 levels were determined. In patients with LVSD [median wall motion index 0.6 (range 0.3-1.4)], CT-1 was elevated [median 110.4 fmol/ml (range 33-516 fmol/ml)] compared with controls [wall motion index 2 in all cases; median CT-1 level 34.2 fmol/ml (range 6.9-54.1 fmol/ml); P<0.0001]. Log CT-1 was correlated with log wall motion index (r=-0.76, P<0.0001), log left ventricular end-systolic volume (r=0.54, P<0.05), stroke volume (r=-0.60, P=0.007) and log fractional shortening (r=-0.70, P=0.001). In a multivariate model of the predictors of log wall motion index, the only significant predictor was log CT-1 (R(2)=56%, P=0.006). This is the first assessment of the relationship between plasma CT-1 levels and the degree of LVSD in humans, and demonstrates that CT-1 is elevated in heart failure in relation to the severity of LVSD.