Erythrocyte membrane trans-fatty acid index is positively associated with a 10-year CHD risk probability.

Industry-generated trans-fatty acids (TFA) are detrimental to risk of CHD, but ruminant-originated TFA have been reported as neutral or equivocal. Therefore, the total TFA amount should not be the only factor considered when measuring the effects of TFA. In the present study, we addressed whether a version of the TFA index that unifies the effects of different TFA isomers into one equation could be used to reflect CHD risk probability (RP). The present cross-sectional study involved 2713 individuals divided into four groups that represented different pathological severities and potential risks of CHD: acute coronary syndrome (ACS, n 581); chronic coronary artery disease (CCAD, n 631); high-risk population (HRP, n 659); healthy volunteers (HV, n 842). A 10-year CHD RP was calculated. Meanwhile, the equation of the TFA index was derived using five TFA isomers (trans-16 : 1n-7, trans-16 : 1n-9, trans-18 : 1n-7, trans-18 : 1n-9 and trans-18 : 2n-6n-9), which were detected in the whole blood, serum and erythrocyte membranes of each subject. The TFA index and the 10-year CHD RP were compared by linear models. It was shown that only in the erythrocyte membrane, the TFA isomers were significantly different between the groups. In the ACS group, industry-generated TFA (trans-16 : 1n-9, trans-18 : 1n-9 and trans-18 : 2n-6n-9) were the highest, whereas ruminant-originated TFA (trans-16 : 1n-7 and trans-18 : 1n-7), which manifested an inverse relationship with CHD, were the lowest, and vice versa in the HV group. The TFA index decreased progressively from 7·12 to 5·06, 3·11 and 1·92 in the ACS, CCAD, HRP and HV groups, respectively. The erythrocyte membrane TFA index was positively associated with the 10-year CHD RP (R 2 0·9981) and manifested a strong linear correlation, which might reflect the true pathological severity of CHD.

Dilatation as a marker of pulmonary veins initiating atrial fibrillation.

BACKGROUND: The pulmonary veins (PVs) have been shown to trigger paroxysmal atrial fibrillation. The relationship of anatomical dimensions versus arrhythmogenicity has not been assessed. METHODS: The diameters of four PVs were measured by selective PV angiography before ablation in 39 consecutive patients (23 male, mean age 46 years) with only one (25 patients) or two (14 patients) arrhythmogenic PVs (ArPVs). After ablation of ArPVs, no patient had recurrence of atrial fibrillation from the remaining PVs. Comparisons were performed variously between ArPV and non-ArPV, and within and across both groups. RESULTS: ArPVs were distributed as follows; left superior PV: 40%, left inferior PV: 28%, right superior PV: 26%, and right inferior PV: 6%. Statistical comparisons showed that (1) Triggers of atrial fibrillation were located in the largest PV in 72% of patients, (2) For each PV, the mean diameter of ArPV was significantly larger than that of non-ArPV (p < 0.05), (3) No significant difference was observed in the diameter of the four different ArPVs (range 16.2 +/- 1.3 to 17.2 +/- 4.4). CONCLUSIONS: In patients with atrial fibrillation initiated from one or two ArPVs, the diameters of ArPVs were significantly larger than those of non-ArPVs irrespective of the specific PV concerned, which might imply a possible role of PV dilatation in the arrhythmogenesis.