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ObjectiveLeft ventricular diastolic dysfunction (LVDD) is considered a precursor of diabetic cardiomyopathy, while the metabolic syndrome (MetS) is associated with an increased risk of cardiovascular morbidity and mortality. This study aimed to evaluate the association between LVDD, MetS and glucose metabolism disturbances classifi ed by oral glucose tolerance testing (oGTT).Methods and resultsThe presence of LVDD was evaluated in 166 subjects with normal ejection fraction, 43 (26%) of whom had type 2 diabetes at inclusion. In subjects without diabetes, an oGTT was performed. The MetS was diagnosed as indentifi ed by the NCEPIII-criteria, while LVDD was verifi ed and graded according to the current guidelines.MetS was diagnosed in 97 (59%) patients, 44% of whom had known diabetes. The prevalence of LVDD was 68% in subjects with MetS vs. 19% in patients without MetS, respectively (P< 0.001). A severe form of LVDD was observed in 34% and 15% of patients with and without MetS, respectively (P= 0.001), whereupon the prevalence of mild and severe diastolic dysfunction increased with the number of MetS criteria (P= 0.001). In the MetS group, early diastolic tissue relaxation velocity (E´) was signifi cantly reduced (6.9 ± 1.8 cm/s vs. 7.7 ± 2.1 cm/s; P= 0.009) and the E/E´ ratio was signifi cantly higher (10.5 ± 3.9 vs. 9.1 ± 3.0 cm/s, P= 0.015) as compared to the group without MetS (n = 69).ConclusionMetS was associated with a higher prevalence and severity of LVDD, whereupon coexisting diabetes aggravates these fi nding. Patients displaying MetS with concomitant LVDD might represent a target population in which appropriate medical care for early heart failure prevention should be initiated

Objective —The development of left ventricular remodelling (LVR) after acute myocardial infarction (AMI) is a predictor of heart failure and mortality.The extracellular matrix (ECM) is highly susceptible to ischaemic injury. Laminin and collagen type VI (CVI) contribute to ECM formation in the infarct zone.To determine whether these markers can be detected in blood samples, we measured laminin and CVI in patients with AMI and control subjects.Methods —A total of 60patients scheduled for coronary angiography and 31patients with AMI were included.We subdivided the patients into three groups: (1) AMI, (2) stable coronary artery disease (CAD) and (3) exclusion of CAD. Laminin and CVI serum concentrations were recorded using the ELISA-technique.Results —Laminin was significantly higher in patients with AMI than in subjects with stable CAD (36.5 vs. 23.9, P<0.01) or without CAD (36.5 vs. 24.6ng/ml, P<0.05). CVI-levels were significantly elevated in patients with AMI compared to subjects without CAD (7.5ng/ml vs. 5.4ng/ml, P<0.05) or stable CAD (7.5ng/ml vs. 5.7ng/ml, P=0.01). Laminin and CVI were significantly higher in patients with severely reduced left ventricular function. Laminin and CVI values were significantly correlated (r=0.6).Conclusion— Our data suggest that laminin and CVI serum levels can be potential surrogate parameters of ECM remodelling after AMI.We hypothesize that serum laminin reflects early ECMremodelling involved in the process of postischaemic tissue degradation and repair, and CVI may be a marker of collagen denaturation and shifts in the collagen phenotype ratios.