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

Abstract

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.

Cardiotrophin-1: A new predictor of atrial fibrillation relapses after successful cardioversion

“…Two experimental studies revealed the importance of CT-1 in the pathogenesis of atrial myocardial fibrosis and developing arrhythmias over the release of high concentrations of calcium during diastole [16,17]. There are evidence that CT-1 plasma levels can be elevated in patients with hypertension [20], coronary artery disease [21,22], and heart failure [23]. A recent experimental study indicated that CT-1 accelerates the development of atherosclerotic lesions by stimulating the inflammasome, foam cell formation associated with CD36 and acyl-CoA: cholesterol acyltransferase-1 upregulation in macrophages, and migration, proliferation, and collagen-1 production in vascular smooth muscle cells [24].…”

Cardioprotective growth factors

“…102 Myocardial stretch from cardiac dilatation is responsible for the overexpression of CT-1 in the failing hearts. 103 Interestingly, CT-1 has been detected in human plasma, 104 and its levels are increased in a variety of cardiac conditions including stable and unstable angina, 105 acute myocardial infarction, 106 aortic stenosis, 107 mitral regurgitation, 108 left ventricular hypertrophy, 109 and left ventricular systolic dysfunction. 110,111 Further work is required to determine the pathophysiological significance of these findings.…”

Plasma Cardiotrophin‐1 Levels are Associated With Hypertensive Heart Disease: A Meta‐Analysis

“…Full text assessment of the 23 potentially relevant articles resulted in further exclusion of 5 studies (Figure ). The reasons for exclusion were as follows: Plasma CT‐1 levels were not reported, not measured, not interpretable, or not reported for patients with left ventricular systolic dysfunction …”

“…Eighteen studies were included in the meta‐analysis. Fourteen studies had a case‐control design and 4 were prospective cohort studies . For analysis of prospective cohort studies, the baseline CT‐1 levels were used.…”