Plasma levels and leucocyte RNA expression of adipokines in young patients with coronary artery disease, in metabolic syndrome and healthy controls.

OBJECTIVES: Little is known about the role of adipokines in the pathogenesis of coronary artery disease in young patients. The aims of this study were to compare serum levels of adipokines and expression of adipokines in peripheral blood leukocytes in patients with premature coronary artery disease (CAD), metabolic syndrome and healthy individuals. DESIGN AND METHODS: Sixty-five patients with premature CAD (men 18-45years old and women 18-55years old) formed the study group. The control groups were 75 patients with metabolic syndrome and 50 healthy individuals. For each group, RNA expression in peripheral blood leukocytes was determined for 24 different adipokines and 11 adipokines were examined in serum. RESULTS: In individuals with CAD, serum visfatin levels were significantly higher than in metabolic syndrome and healthy controls (2.3 vs. 1.6 vs. 0.7µg/L, P<0.001) while both omentin-1 (92.9 vs. 587.0 vs. 552.3µg/L, P<0.001) and ZAG2 (45.5 vs. 72.5 vs. 77.1mg/L, P<0.001) levels were lower. The receiver operating curve (ROC) analysis for testing the validity of these adipokines in the diagnosis of CAD compared to control groups provided the following areas under the curve (AUC): omentin-1 AUC 0.97 (cut-off ≤222µg/L), ZAG2 AUC 0.89 (cut-off ≤51.7mg/L) and visfatin AUC 0.74 (cut-off ≥1.0µg/L) (P<0.001 in all cases). Visfatin and omentin-1 serum levels did not differ between the acute phase of myocardial infarction and the chronic phase of CAD. In patients with CAD, we found no significant relation between mRNA expression and adipokine concentration. CONCLUSION: Serum omentin-1, visfatin and ZAG2 could serve as biomarkers of premature CAD in young apparently healthy people.

Adipokines and cardiovascular disease: A comprehensive review.

Adipokines are peptides that signal the functional status of adipose tissue to the brain and other target organs. In adipose tissue dysfunction, adipokine secretion is altered, and this can contribute to a spectrum of obesity-associated conditions including cardiovascular disease. Some adipokines have anti-inflammatory and cardioprotective effects (omentin, apelin, adiponectin). Others are pro-inflammatory with negative impact on cardiovascular function (leptin, visfatin, resistin, adipocyte fatty-acid-binding protein). In the first part, this article reviews the endocrine functions of adipose tissue in general, effects of the distribution and composition of fat tissue, and the roles of cortisol and the renin-angiotensin-aldosterone system in the development of the inflammatory state of addipose tissue. In the second part, the known cardiovascular effects of different adipokines and their clinical potential are discussed in detail.

Omentin-1 levels in patients with premature coronary artery disease, metabolic syndrome and healthy controls. Short communication.

OBJECTIVES: Omentin-1 is an adipokine which could have a protective role against the manifestation of atherosclerosis. Only limited data are available on omentin-1 serum values in patients with premature clinical manifestations of atherosclerosis. DESIGN AND METHODS: We tested omentin-1 in human serum by ELISA method in 61 individuals with a premature manifestation of coronary artery disease (CAD), 40 patients with metabolic syndrome and 40 healthy control subjects. RESULTS: Omentin-1 serum levels were significantly lower in patients with CAD (103.1±62.7 mg/L) compared to metabolic syndrome (668.2±339.6 mg/L) and healthy subjects (623.0±373.5 mg/L) (P < 0.01). In CAD patients, omentin-1 serum levels did not differ between patients sampled in the acute phase of myocardial infarction (n = 28; 110.3±82.4 mg/L) and in the chronic phase several months or years after myocardial infarction (n = 33; 97.0±39.3 mg/L) (P = 0.41). We found a weak positive correlation between omentin-1 and body mass index (r = 0.21, P = 0.014). No significant correlation was found between peak cardiac troponin T and omentin-1 (correlation coefficient r = 0.118, P = 0.406). CONCLUSION: Serum omentin-1 seems to be a useful biomarker of coronary artery disease across the whole age spectrum.

Echocardiographic assessment of global longitudinal right ventricular function in patients with an acute inferior ST elevation myocardial infarction and proximal right coronary artery occlusion.

Right ventricular (RV) myocardial infarction (MI) is a frequent concomitant of an acute inferior MI. We set out to determine the diagnostic value of speckle tracking echocardiography in comparison with cardiac magnetic resonance (CMR) for RV stunning and scar prediction. 55 patients (66 ± 11 years) with an acute inferior ST elevation MI who underwent percutaneous coronary intervention (PCI) of an occlusion in the proximal right coronary artery were prospectively enrolled. An echocardiography was done on the day of presentation and on the 5th day thereafter. A CMR was subsequently performed 1 month after the MI. The CMR was used to differentiate between the group with RV scar (n = 26) and without RV scar (n = 29). RV peak systolic longitudinal strain (RV-LS) at presentation determined RV scar (-21.1 ± 5.1% vs. -9.9 ± 4.6%, p < 0.0001). The RV-LS correlated with the scar extent (r = 0.83, p < 0.0001). RV-LS > -15.8% had a sensitivity of 92% and a specificity of 83% in RV scar prediction (AUC 0.93). RV-LS was superior to TAPSE and TDI in determining the presence of RV scar. According to RV-LS values at presentation and on the 5th day, 3 subgroups were defined: G1-normal deformation (RV-LS <-20%), G2-RV stunning (baseline RV-LS >-20%, 5th day RV-LS <-20%) and G3-persistent RV dysfunction (unchanged RV-LS > -20%). In G1, there was neither RV scar nor clinically relevant hypotension. In G2, 58% of patients developed RV scar and 36% had hypotension. In the G3, 83% developed RV scar and 55% had hypotension. The myocardial deformation analysis could provide an early prediction of RV scar. It allowed the patients to be divided into subgroups with normal RV function, stunning and persistent RV dysfunction.