Early AF recurrence peaks within the first few weeks after PVI, but continues at a lower level until the completion of monitoring. A blanking period of 3 months is justified to identify patients with AF recurrences that do not portend procedure failure. Freedom from AF in the first 2 weeks following ablation significantly predicts long-term AF freedom.

Genetic variation in folate-regulating enzymes contributes to the risk of cardiovascular disease (CVD). The cytoplasmic serine hydroxymethyltransferase (cSHMT) enzyme is proposed to regulate a key metabolic intersection in folate metabolism. We hypothesized that a variant in cSHMT (cSHMT 1420C-->T) affects CVD risk, and that the effect depends on a linked step in the metabolic pathway catalyzed by methylenetetrahydrofolate reductase (MTHFR). A nested case-control study of incident CVD was conducted within the all-male Normative Aging Study cohort. Of the incident CVD cases, 507 had DNA samples; 2 controls/case were selected by risk set sampling (matched on age and birth year). A significant gene-gene interaction (P-values 0.0013, 0.0064) was found between MTHFR and cSHMT, and there was little or no change in the coefficients in covariate-adjusted models. The effect of MTHFR 677C-->T genotype on CVD risk varied by cSHMT 1420C-->T genotype. Among men with cSHMT 1420C-->T TT genotype, the odds ratios (OR) for CVD risk for MTHFR 677C-->T CT and TT genotypes compared with the MTHFR 677C-->T CC genotype were 3.6 (95% CI, 1.7-7.8) and 10.6 (95% CI, 2.5-46.0), respectively. Among men with the cSHMT 1420C-->T CC/CT genotype, the corresponding ORs were 1.0 (95% CI, 0.8-1.2) and 1.3 (95% CI, 0.9-1.8). Plasma total homocysteine concentrations were highest in the subgroup of men with both polymorphisms, MTHFR 677C-->T TT and cSHMT 1420C-->T TT, consistent with a higher risk of CVD in this subgroup. A more complete understanding of the molecular mechanism awaits identification of the functional effect of the polymorphism.

Changes in serum lipid and lipoprotein concentrations occur frequently in disorders of thyroid function. LDL-cholesterol (LDL-C) oxidation susceptibility is higher in these patients than in normal population. This study aims at assessing lipids, lipoproteins, apolipoproteins and serum paraoxonase 1 (PON1) activity in patients with thyroid dysfunction. Ninety-nine patients with thyroid dysfunction, (49 hypothyroid and 50 hyperthyroid) were compared with 2 separately age- and sex-matched control groups. A fasting blood sample was obtained and serum total cholesterol, triglycerides, apolipoproteins A-I and B, and PON1 activity were measured. In hyperthyroid patients, significantly lower PON1 activity (45 +/- 23 vs 67 +/- 37 IU/ml, p<0.001), triglycerides (112 +/- 53 vs 166 +/- 130 mg/dl, p<0.05), apolipoprotein A-I (137 +/- 26 vs 154 +/- 21 mg/dl, p<0.001) and apolipoprotein B (75 +/- 18 vs 86 +/- 25 mg/dl, p<0.05) were found. Hypothyroid patients had lower PON1 activity (46 +/- 21 vs 64 +/- 32 IU/ml, p<0.005) compared with controls, and higher total cholesterol (224 +/- 69 vs 185 +/- 41 mg/dl, p<0.001), LDL-C (133 +/- 59 vs 93 +/- 36 mg/dl, p<0.001), and apolipoprotein B (107 +/- 37 vs 84 +/- 23 mg/dl, p<0.001). The results show significant changes of lipid levels in thyroid dysfunction. In addition, a significant reduction in PON1 activity was observed in both hyper- and hypothyroid patients. Increased LDL-C oxidation in thyroid dysfunction observed in other studies, at least to some extent, can be attributed to reduced PON1 activity.

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