Dietary Fatty Acids and Sodium Intake Cytokines LVH and CHF

Beyond the well-known effect of high sodium intake on the clinical course of CHF (and the occurrence of acute episodes of decompensation), another important issue is the role of diet in the development of left ventricular hypertrophy (LVH), a major risk factor for CHF (and also SCD), as well as for cardiovascular and all-cause mortality and morbidity.

The cause of LVH is largely unknown. Whereas male gender, obesity, heredity, and insulin resistance may explain some of the variance in LVH, hypertension (HBP) is generally regarded as the primary culprit. Thus, the risks associated with LVH and HBP are intimately linked. Recent data also suggested that low dietary intake of polyun-saturated fatty acids and high intake of saturated fatty acids, as well as HBP and obesity, at age 50 predicted the prevalence of LVH 20 years later. Although the source of saturated fatty acids is usually animal fat, the source of unsaturated fatty acids in that specific Scandinavian population and at that time was less clear and there was no adjustment for other potential dietary confounders such as magnesium, potassium, calcium, and sodium. Thus this study did not provide conclusive data regarding the dietary lipid determinants of LVH. However, it does suggest that dietary fatty acids may be involved in the development of LVH and that this "diet-heart connection" may partly explain the harmful effect of animal saturated fatty acids on the heart.

Another "diet-heart connection" in the context of advanced CHF relates to the recent theory that CHF also is a low-grade chronic inflammatory disease with elevated circulating levels of cytokines and cytokine receptors that are otherwise independent predictors of mortality. High-dose ACE inhibition with enalapril, a treatment that reduces mechanical overload and shear stress (two stimuli for cytokine production in patients with CHF), was recently shown to decrease both cytokine bioactivity and left ventricular wall thickness. Finally, various anti-cytokine and immunomodulating agents were shown to have beneficial effect on heart function and clinical functional class in patients with advanced CHF, suggesting a causal relationship between high cytokine production and CHF. This also suggests that there is a potential for therapies altering cytokine production in CHF. In that regard, it has been shown that dietary supplementation with n-3 fatty acids (either fish oil or vegetable oil rich in n-3 fatty acid) reduces cytokine production at least in healthy volunteers. An inverse exponential relationship between leukocyte n-3 fatty acid content and cytokine production by these cells was found, most of the reduction in cytokine production being seen with eicosapentaenoic acid in cell membrane lower than 1%, a level obtained with rather moderate n-3 fatty acid supplementation. However, further studies are warranted to test whether (and at which dosage) dietary n-3 fatty acids might influence the clinical course of CHF through an anti-cytokine effect.

Sodium intake is the environmental factor that is currently most suspected of influencing blood pressure and the prevalence of HBP. However, the full damaging potential of high sodium intake for the heart (and also the kidney) seems to be largely independent of the pressor effect of sodium. Animal experiments and clinical studies have consistently shown that high sodium intake is a pow erful and independent determinant of LVH and that such an arterial-pressure-independent effect of salt is not confined to the heart.

Whereas the long-term effect of a reduced sodium intake after a recent AMI is unknown, in particular on LVH, experts claim that even a 50mmol reduction in the daily sodium intake would reduce the average systolic blood pressure by at least 5 mmHg (in patients aged over 50 years) and CHD mortality by about 16%. Thus, as regards the damaging effect of high sodium intake on the heart, and despite the lack of strong data showing the beneficial effect of reducing sodium intake in that specific group of patients, we believe that cardiologists should extend their dietary counseling about sodium not only to patients with HBP or CHF but also to all post-infarction patients.

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