Georgios K. Liakos

Long-chain n-3 PUFA from fish oils are known to have anti-inflammatory effects. We evaluated the effect of alpha-linolenic acid (ALA), precursor of n-3 fatty acids, on serum inflammatory markers and soluble cellular adhesion molecules (sCAM) of dyslipidaemic males, relative to their background diet. Participants were assigned to two groups, based upon food intake patterns: (a) twenty-one dyslipidaemic subjects who habitually ate a Mediterranean-Cretan-type diet; (b) nineteen dyslipidaemic subjects who normally ate a Westernised Greek diet. All were supplemented with 8.1 g ALA/d for 12 weeks. We determined serum amyloid A (SAA), C-reactive protein (CRP), macrophage colony-stimulating factor (MCSF), IL-6, soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 and soluble E-selectin concentrations at the beginning and the end of the ALA supplementation period. Serum baseline concentrations of inflammatory markers and sCAM were similar across the diet groups. Type of diet had a significant impact on the response of inflammatory markers to ALA supplementation. The Westernised Greek diet group showed a reduction in SAA (P<0.001), CRP (P=0.002), MCSF (P=0.005) and IL-6 (P=0.04) concentrations. The Mediterranean-Cretan-type background diet group showed a significant reduction only in MCSF concentrations (P=0.003). The sVCAM-1 concentrations were significantly reduced in both the Westernised Greek diet group (P=0.001) and the Mediterranean-Cretan-type diet group (P<0.001). The present study demonstrated that ALA supplementation lowered the serum concentrations of inflammatory markers more profoundly when the background diet was rich in saturated fatty acids and poor in MUFA.

INTRODUCTION: Inflammation has a major role in atherosclerosis and the acute phase C-reactive protein (CRP) is elevated after acute myocardial infarction. Inflammation is also implicated in autonomic nervous system control. Heart rate variability (HRV) has been used as a marker of abnormal autonomic activity after myocardial infarction. Our purpose was to investigate the relation between CRP levels and autonomic tone in patients after acute ST-segment elevation myocardial infarction. METHODS: We studied prospectively 98 patients. CRP and the cardiac enzymes CK, CK-MB, and troponin-I were measured for a total of 72 hours and 24-hour Holter ECG recordings for HRV analysis were acquired before hospital discharge. RESULTS: The natural logarithm of CRP levels was inversely correlated with the following logarithmic transformed indices of HRV in the time and in the frequency domain: SDNN, standard deviation of all normal R-R intervals, (r = -0.40, p < 0.001); SDANN index, standard deviation of the average normal R-R intervals for 5-minute segments, (r = -0.46, p < 0.001); SDNN index, mean of the standard deviation of all normal R-R intervals for 5-minute segments (r = -0.41, p < 0.001); total power (TP) (r = -0.38, p < 0.001); high frequency power (HF) (r = -0.31, p < 0.01); low frequency power (LF) (r = -0.45, p < 0.001). The strong inverse relation between CRP and SDNN, SDANN, SDNN index, LF and TP persisted after adjustment for left ventricular function. CONCLUSIONS: Increased levels of circulating CRP after acute myocardial infarction are associated with attenuated HRV indices, suggesting a possible relationship between inflammation and cardiac autonomic balance.