Better Prognosis in Overweight/Obese Coronary Heart Disease Patients With High Plasma Levels of Leptin

Abstract

Background and aimThe involvement of leptin in atherosclerosis is very complex, including inflammation, the oxidative stress and thrombosis. Leptin has atherogenic and also antiatherogenic actions. In obesity elevated leptin levels are not sufficient to prevent disturbances of energy balance, suggesting that obese people are leptin resistant. The aim of the study was to investigate the relationship between baseline plasma levels of leptin and the incidence of new ischemic events in patients with CHD.MethodsPlasma levels of leptin in fifty nine consecutive patients (29 men and 30 women) with CHD hospitalized in the County Emergency Clinical Hospital of Cluj-Napoca were measured using commercially available ELISA at admission. Patients with active infectious disease, neoplasia, acute coronary syndrome, stroke, hepatic or renal failure and severe heart failure were excluded The relationship between leptin levels and incident cardiovascular events (angina, nonfatal myocardial infarction or heart failure) over two years follow-up was studied using MEDCALC version 9.6.Results73.6% patients with CHD were overweight or suffered of obesity. There were no significant differences between women and men regarding the plasma levels of leptin, the body mass index (BMI), the number of rehospitalizations, rehospitalizations/patient, diabetes mellitus, hypertension or dyslipidemia. Only in women plasma levels of leptin are correlated with BMI. As compared with men with overweight and obesity (BMI≥25kg/m2), plasma levels of leptin were significantly higher in women with overweight and obesity (3905.97±463.91 pg/ml vs 1835.17±533.9 pg/ml) (p<0.002). Patient gender could not be demonstrated to influence prognosis. During the two years we recorded one or more readmissions in 26 patients (44%). The analysis of time till readmission using Kaplan-Meier curves, showed that leptin level (cut-off 2000 pg/ml, HR 0.38, 95% CI 0.17–0.83; p=0.01) and BMI (cut-off 28 kg/m2, HR 0.3164, 95% CI 0.145–0.0689; p<0.01) were significantly associated with prognosis.ConclusionPatients with plasma levels of leptin >2000 pg/ml and BMI >28kg/m2 had a better prognosis, suggesting a protective role of leptin in overweight/mild obesity.

Usefulness of the Adipokines as Biomarkers of Ischemic Cardiac Dysfunction

“…Its importance as a protective factor is not yet clarified, although it was suggested that hyperleptinemia might not be directly linked to atherogenesis, but it might reflect and be a consequence of a state of leptin resistance. The obesity paradox was described, and it represents only a small part of the complex molecular system that controls and promotes the inflammation and its effect on blood vessels [ 42 – 44 ].…”

“…It appears that high levels of leptin promote the production of other inflammatory mediators such as tumor necrosis factor, interleukin-2, and interleukin-6 and increase the production of the reactive oxygen radicals. Leptin stimulates the proliferation and hypertrophy of smooth muscle cells within the vessel wall and the accumulation of cholesterol esters in foam cells, particularly if associated with hyperglycemia [ 42 , 45 ]. It is well known that all these effects contribute to endothelial dysfunction and promote the development and progression of atherosclerotic lesions, but it is not yet clear if leptin itself can induce the atherosclerotic process or it is only a marker of the biological context in which the vascular lesions are produced.…”

Serum level of apelin-13 negatively correlated with NT-proBNP in heart failure patients

“…The apelin and its receptor (APJ receptor) is one of the molecular systems which counteracts the negative effects of aldosterone on the myocardial cells and limits the inflammatory reactions and the oxidative stress that are increased in chronic, severe, heart failure. Although apelin is also synthesized in the adipose tissue and was listed as adipocytokine and studied as one [8][9][10][11], its major site of synthesis and target is the endothelium and the cardiovascular system. It is the most potent endogenic positive inotropic agent and is a positive regulator of angiotensin converting enzyme type 2, and so it is a RAAS antagonist [12,13].…”

Severe degenerative aortic stenosis with preserved ejection fraction does not change adipokines serum levels

“…Generally, leptin, which is a mediator of the long-term regulation of energy balance, suppresses food intake [34]. Subjects with high plasma leptin levels have a better prognosis, thus suggesting a protective role of leptin in overweight/mild obesity [35]. On the other hand, overweight and obesity are associated with hyperleptinemia secondary to an impaired sensitivity of leptin receptors [36].…”