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Objectives: Galectin-3 (Gal-3) is involved in cardiac inflammation and fibrosis, and is in use as a biomarker that indicates increased risk in heart failure. This study examined the relationship between Gal-3 levels and acute and old myocardial infarction (MI) in patients assessed by cardiac magnetic resonance (CMR) imaging. Methods: Group 1 consisted of 38 patients with ST-elevation MI and single-vessel disease treated with primary percutaneous coronary intervention (PCI). Group 2 consisted of 52 patients with prior complicated MI. Twenty-two controls were included. CMR was performed in group 1 at 2 days, 1 week, 2 months and 1 year following PCI and in group 2 at >4 years after MI. Results: Median Gal-3 was elevated in patients compared with controls, group 1: 11.93 ng/ml (IQR 6.34-17.52, p = 0.03), group 2: 12.96 (IQR 6.33-19.29, p = 0.03) and controls: 10.16 (IQR 5.59-14.73). Gal-3 levels did not change during acute MI, and there was no relationship between Gal-3 and infarct size, troponin-T, highsensitivity C-reactive protein, left-ventricular (LV) volumes or LV ejection fraction (LVEF) in group 1. In group 2, Gal-3 correlated modestly with MI size (r = 0.28, p < 0.05), LV end-diastolic volume index (r = 0.40, p < 0.01), LV end-systolic volume index (r = 0.43, p < 0.01) and LVEF (r = -0.39, p < 0.01). Conclusion: There was no relationship between Gal-3 levels and acute ischemic myocardial injury. A significant, modest relationship between Gal-3 levels, MI size and LV remodeling was only found in patients with old MI. [ABSTRACT FROM AUTHOR]

Abstract: Background: We assessed the time profiles and prognostic utility of circulating markers of collagen turnover (CTO) following acute myocardial infarction (MI). In contrast to previous studies, no patient had been pre-treated with inhibitors of the renin-angiotensin-aldosterone system (RAAS) at the time of initial assessment. Methods: Plasma levels of N-terminal fragment of type I collagen (PINP), carboxy-terminal telopeptide of type I collagen (ICTP), N-terminal fragment of type III collagen (PIIINP), matrix metalloproteinase-1(MMP-1) and tissue inhibitor of MMPs type-1 (TIMP-1) were assessed in 233 patients following acute MI. The CTO markers were initially assessed prior to treatment by either captopril or losartan, at a median of 3days following MI. In addition, blood samples were acquired at 1month, 1year and 2years following MI. Development of heart failure symptoms, all-cause and cardiovascular death were recorded as endpoints during two years of follow-up. Results: With the exception of PIIINP, all CTO markers demonstrated significant longitudinal changes following MI. At baseline, ICTP (p<0.0001) and TIMP-1 (p=0.01) levels were significantly elevated in patients who later died compared with survivors. In multivariable analysis only ICTP reached statistical significance as predictor of all cause death (p=0.048). In patients developing symptoms of heart failure during follow-up, ICTP was the only significantly elevated CTO marker (p<0.01). Conclusion: The present study supports a prognostic role for ICTP in both the acute and chronic phase following MI. [Copyright &y& Elsevier]

Studies of patients with acute myocardial infarction (MI) suggest that anterior transmural infarcts are associated with greater left ventricular (LV) remodeling compared with nontransmural nonanterior infarctions. It is unclear whether this relation also exists in long-term survivors of MI. Cardiac magnetic resonance imaging was used to explore the relation between myocardial scar size, localization, transmurality, and degree of long-term LV remodeling in patients with healed MI. Subjects were recruited from a registry of patients with healed MI who participated in the OPTIMAAL trial. Cardiac magnetic resonance imaging was performed to assess LV mass, volumes, LV ejection fraction, and myocardial scarring, adjusting for myocardial ischemia. Fifty-seven patients (mean age 69 ± 10 years mean ejection fraction 49 ± 13%) were studied 4.4 ± 0.4 years after MI. Anterior scar was found in 19 patients and nonanterior scar in 33, whereas 5 patients did not show myocardial scar. Transmural scar was evident in 36 patients. In the 52 patients with scar, average total scar size was 13 ± 8% of total LV mass. There was a strong linear relation between scar size and LV end-diastolic volume index (r = 0.81, p <0.0001), end-systolic volume index (r = 0.86, p <0.0001), and LV ejection fraction (r = −0.74, p <0.0001). In multivariate analysis, scar size was the strongest independent predictor of ejection fraction and LV volumes independently of scar localization and transmurality. In conclusion, in the studied cohort, there was a linear relation between scar size and ejection fraction and LV volumes. This relation was independent of scar location and transmurality. [Copyright &y& Elsevier]

Increased circulating chemokines have been reported during acute myocardial infarction and might give prognostic information about future ischemic events. However, data on the chemokine network in relation to infarct size and measures of left ventricular remodeling after successful percutaneous coronary intervention (PCI) are lacking. A total of 42 patients with first-time ST-segment elevation acute myocardial infarction with a single occluded vessel were recruited, and cardiac magnetic resonance was used for serial assessment (2, 7, and 60 days) of infarct size and left ventricular remodeling. The chemokines were analyzed before and after PCI. After PCI, high levels of CCL4, CXCL16, CXCL10, and, in particular, CXCL8 within the first week after PCI correlated positively with the degree of myocardial damage, as reflected by correlations with the maximum troponin T levels and infarct size after 2 months, as assessed by cardiac magnetic resonance, and with impaired myocardial function after 2 months as assessed by cardiac magnetic resonance and neurohormonal methods. In contrast, the plasma levels of CCL3 and CXCL7 during the first week correlated negatively with myocardial dysfunction after 2 months. In conclusion, our findings suggest a role for chemokines in both adaptive and maladaptive responses after myocardial infarction and might support a role for CCL4, CXCL16, CXCL10, and, in particular, CXCL8 in postmyocardial infarction reperfusion and remodeling. [Copyright &y& Elsevier]