Study population

Sampling procedures for this study have been described previously in detail . Briefly, the study comprised 316 patients who underwent coronary angiography because of myocardial infarction ( n = 113), angina ( n = 169), thoracic pain ( n = 18) or heart failure ( n = 16) in the Cardiology Department at Sahloul University Hospital, Sousse, Tunisia. Patients were subdivided into two groups: those with SCS and those without SCS. SCS patients were those who had significant coronary artery stenosis, which was defined as a luminal narrowing of ≥ 50% in at least one major coronary artery. Patients without SCS were those without any significant coronary artery stenosis (< 50%).

Data on lifestyle factors were collected using an interviewer-administered questionnaire, which included questions about personal history, presence of disease, drug intake (if any), cigarette smoking and alcohol consumption. Patients taking lipid-lowering drugs were excluded. Diabetes mellitus was defined as fasting glucose > 7 mmol/L or currently receiving antidiabetic medication. The smoking status of an individual was assigned ‘yes’ if they were smoking currently or had given up < 3 months previously. Hypertension was defined as blood pressure > 140/90 mmHg or currently on antihypertensive medication. Dyslipidaemia was defined as low-density lipoprotein cholesterol (LDL-C) concentration ≥ 4.1 mmol/L and/or HDL-C concentration ≤ 1 mmol/L and/or triglyceride concentration ≥ 1.71 mmol/L. Informed consent was taken from all the participants. The study was approved by the local medical ethics committee.

Measurement of serum lipids and apolipoproteins

After overnight fasting and before coronary angiography, blood was collected from each subject. Serum total cholesterol, triglyceride and HDL-C concentrations were determined by a standard method using the Synchrom CX7 Clinical System (Beckman, Fullerton, CA, USA). LDL-C concentration was calculated using the Friedewald formula when the triglyceride concentration was < 4 mmol/L; otherwise, LDL-C concentration was measured directly using the Synchrom CX7 Clinical System (Beckman, Fullerton, CA, USA). Serum ApoAI and apolipoprotein B (ApoB) concentrations were determined using the IMMAGE Immunochemistry System (Beckman, Fullerton, CA, USA), based on immunonephelometric quantitation. ApoB/ApoAI and total cholesterol/HDL-C ratios were calculated. We considered elevation of these atherogenicity ratios as > 0.86 and > 4.5, respectively, and hypoApoAI as ≤ 0.9 g/L.

DNA extraction and ABCA1 genotyping

Genomic DNA was extracted from ethylenediaminetetraacetic acid-treated whole blood samples using a salting-out method . The genotypes for each ABCA1 polymorphism (G1051A [R219K], G2706A [V771M], G2868A [V825I] and –565C/T [–477C/T]) were determined by polymerase chain reaction-restriction fragment length polymorphism analysis. The G1051A and –565C/T polymorphisms were genotyped following Assmann and Nofer ; the G2706A and G2868A polymorphisms were genotyped as described by Miller and Miller . The polymerase chain reaction was carried out using a deoxyribonucleic acid thermal cycler (LP×2 Thermal Cycler, Thermo Electron Corporation, Milford, NE, USA). After initial denaturation at 95 °C for 5 min, the polymerase chain reaction was carried out for 35 cycles, each cycle comprising a denaturation at 95 °C for 45 s, an annealing temperature as described previously [1,2] for 45 s and 72 °C for 45 s, with a final extension time of 7 min at 72 °C. Shortly, each polymerase chain reaction product of G1051A, G2706A, G2868A and –565C/T polymorphisms was digested using StyI (2U), BsaAI (2U), BsaI (3U) and AciI (2U), respectively. Polymerase chain reaction products and the digested products were resolved by 2% agarose gel electrophoresis and visualized by ethidium bromide staining.

Statistical analysis

Statistical analysis was performed by SPSS 16.0 for Windows. The biological variables were compared by one-way analysis of variance then by Student’s t -test or Fisher’s exact test and their values were reported as means ± standard deviations. A chi-square analysis was performed to determine the Hardy–Weinberg equilibrium of the polymorphism studied in both groups with one degree of freedom. Genotype and allele frequencies were compared by a chi-square test. Pairwise linkage disequilibrium coefficients were expressed as D’, which is the ratio of unstandardized coefficient to its minimal/maximal value, and estimated using a single nucleotide polymorphism analyser programme . Odds ratios (ORs) were calculated as a measure of the association of the each ABCA1 genotype with the phenotype. For each OR, two-tailed p values and 95% confidence intervals (CIs) were calculated; p was considered to be significant when it was < 0.05. Adjusted ORs for potential confounders were determined using logistic regression analysis and corresponding p values were reported.

Population characteristics

Clinical and biochemical characteristics of the study population are given in Table 1 . Patients with SCS had significantly lower HDL-C ( p = 0.040) and ApoAI (p = 0.009) concentrations, significantly higher triglyceride concentrations ( p = 0.022) and a higher ApoB/ApoAI ratio ( p = 0.036) than patients without SCS. All variables with a p value < 0.25 between the two studied groups were considered as confounding factors for further OR adjustment.

ABCA1 genotypes

The prevalence of the four ABCA1 polymorphisms (G1051A, G2706A, G2868A and –565C/T) was evaluated in 316 subjects. Each of these polymorphisms was found to be in the Hardy–Weinberg equilibrium. Genotype and allele frequencies are shown in Table 2 . The prevalence of homozygous individuals for the G2706 allele was significantly higher ( p = 0.009) in the SCS group. No mutated genotype for this polymorphism was found in the group without SCS. No significant difference was observed in genotype frequencies between the two groups for the other three polymorphisms. No allele frequency difference was observed between patients with versus without SCS for any polymorphism.

Table 2

ABCA1 genotypes and allele frequencies among patients with and without SCS in a Tunisian population.

ABCA1 SNPs		With SCS ( n = 212)			Without SCS ( n = 104)		p	With SCS	Without SCS	p
G1051A	GG	GA	AA	GG	GA	AA	0.68	A-allele frequency		0.95
%	40	47.7	12.3	35.6	50.9	13.5		0.64	0.61
G2706A	GG	GA	AA	GG	GA	AA	0.009	A-allele frequency		0.89
%	91	8.5	0.5	80	20	0		0.05	0.1
G2868A	GG	GA	AA	GG	GA	AA	0.77	A-allele frequency		0.98
%	76.9	22.6	0.5	79.8	19.2	1		0.12	0.11
–565C\T	CC	CT	TT	CC	CT	TT	0.60	T-allele frequency		0.95
%	24.5	52.9	22.6	27.9	54.8	17.3		0.49	0.45

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