Search

Epidemiological studies indicate a positive relation between iron status and coronary artery disease (CAD) risk The HFE C282Y allele is associated with increased iron status and higher CAD risk. We investigated whether HFE C282Ymight be a CAD risk factor in Curaçao in a case-control study design. The patient group comprised 42 men and 10 women. Fifty-four men and 30 women without history of CAD served as age and gender matched controls. HFE C282Y genotypes were established using sequence-specific priming polymerase chain reaction. None of the investigated subjects were homozygous for HFE C282Y, whereas 5/52 (9.6%) CAD patients and 1/84 controls (1.2%) were heterozygous for HFE C282Y (p = 0.03). The HFE C282Y mutation was 8.8 fold (95% CI 1.001, 77.8; p = 0.049) more prevalent in CAD patients than in controls. The HFE C282Y allele frequency in Curaçao is higher than that of African populations, but comparable with that of Jamaica. We conclude that Curaçao CAD patients have somewhat higher frequency of HFE C282Y heterozygosity than controls, and that the HFE C282Y allele frequency in the Curaçao population is higher than might be expected in persons of African descent. The consequences of HFE C282Y heterozygosity as CAD risk factor are as yet uncertain, since there is no proof that iron lowering reduces CAD risk.

Patients with coronary artery disease are advised to augment their dietary linoleic acid intakes at the expense of saturated fatty acids. We investigated whether the dietary linoleic acid intake of 57 patients with coronary artery disease (47 males, 10 females; ages 61 +/- 10 years) in Curaçao is higher as compared with 77 controls (51 males, 26 females; ages 56 +/- 7 years). For this, we measured plasma cholesterol ester fatty acids, which reflect the dietary fatty acid composition of the preceding weeks. Patients with coronary artery disease and controls had minor differences in cholesterol ester fatty acids. Their cholesterol ester linoleic acid content suggests that the dietary polyunsaturated/saturated fatty acid ratio is far below 1. Comparison with data reported for The Netherlands, Greenland and Crete showed that the dietary fatty acid composition in Curaçao is typically Western with a high intake of saturated fatty acids, a low intake of monounsaturated fatty acids and the consumption of linoleic acid as the predominant polyunsaturated fatty acid. Intake of long chain polyunsaturated fatty acids from fatty fish is low. Reduction of dietary saturated fatty acids, augmentation of fish consumption, and an increase of the alpha-linolenic/linoleic acid ratio are likely to be of benefit to both primary and secondary prevention from coronary artery disease in Curaçao.

We studied lipids, apolipoprotein-E (apo-epsilon) genotypes and other coronary artery disease (CAD) risk factors of 67 CAD patients (male/female ratio 5) in Curaçao. Compared with 57 controls, male CAD patients had higher cholesterol, triglycerides, LDL-cholesterol, apo-B and decreased HDL-cholesterol and HDL-cholesterol/cholesterol concentrations. Other CAD risk factors were: increased fasting glucose and HbA1c concentrations, decreased creatinine clearance, and increased prevalences of lipoprotein (a) concentration > 500 mg/l, renal disease, hyperhomocysteinaemia, diabetes mellitus type II (DM-II), positive CAD family history and cigarette smoking. Male CAD patients had higher plasma alpha-tocopheroleq. Compared with 29 female controls, female CAD patients had higher fasting plasma glucose and HbA1c concentrations, and prevalence of DM-II. Predicting factors for CAD development in the whole CAD group were: DM-II, cigarette smoking, apo-epsilon 3/epsilon 4 and apo-epsilon 4/epsilon 4 Apo-epsilon 4 was associated with lower HDL- and higher LDL-cholesterol concentrations. There is a need for local studies on improvement of diabetic control, reference values of lipoprotein (a) and homocysteine concentrations, on apolipoprotein (a) phenotypes, causes of hyperhomocysteinaemia, and dietary influences on CAD development in subjects who carry the apo-epsilon 4 allele.