Associations of high-density lipoprotein cholesterol levels with the presence and severity of coronary atherosclerosis

Objective — To investigate the relationship between blood lipid levels with severity of coronary artery atherosclerosis in a Chinese population sample.Methods and results — According to coronary angiography results, 363patients (287men and 76women) with coronary artery atherosclerosis were divided into four groups: the single-vessel group (I, n=125), the double-vessel group (II, n=113), the triple-vessel group (III, n=107) and the multivessel group (IV, n=18).The severity of coronary artery atherosclerosis was quantified with a modified Gensini score on the basis of angiographic imaging. Serum triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), non-high density lipoprotein cholesterol (non-HDL-C) were measured before angiography in all groups. Levels of serum TC, LDL-C and non-HDL-C of the II, III and IV group were significantly higher than those of the I group (4.78 ± 0.82mmol/L and 4.87 ± 1.50mmol/L and 4.73 ± 0.99mmol/L vs. 4.38 ± 0.93mmol/L, 2.91 ± 0.68mmol/L and 2.74 ± 1.23mmol/L and 2.64 ± 0.84mmol/L vs. 2.30 ± 0.77mmol/L, 3.58 ± 0.75mmol/L and 3.59 ± 1.41mmol/L and 3.43 ± 0.94mmol/L vs. 3.17 ± 0.91mmol/L; p < 0.05); the mean levels of TC, LDL-C and non-HDL-C associated positively with the Gensini score.Conclusion — Serum lipid levels correlate positively with the severity of coronary artery atherosclerosis in a Chinese population sample. Patients with higher levels of serum TC, LDL-C and non-HDL-C have more severe coronary atherosclerosis, compared with those with low levels of serum TC, LDL-C and non-HDL-C.

We studied the relationship of cigarette smoking to the severity of coronary and thoracic aortic atherosclerosis in 116 men who received coronary angiography and transesophageal echocardiography. Severity of coronary atherosclerosis was assessed in terms of Gensini's score (GS), and that of thoracic aortic atherosclerosis was assessed by the average sclerotic length (ASL) and average sclerotic area (ASA). The plasma fibrinogen levels were significantly positively correlated with smoking, and fasting blood sugar levels tended to be positively associated with smoking. GS was inversely associated with serum levels of high density lipoprotein (HDL) cholesterol. ASL and ASA were positively associated with age, fasting blood sugar levels and plasma fibrinogen levels, and these associations were statistically significant. Analysis of covariance was used to examine the net association between cigarette smoking and GS, ASL or ASA controlling for age, total cholesterol, HDL cholesterol, fasting blood sugar and plasma fibrinogen. We found that GS, ASL, and ASA were all significantly increased with increasing number of cigarette years. Additional adjustment for other risk factors (triglyceride, uric acid, body mass index, alcohol use and hypertension) also showed a strong independent contribution of smoking to GS, ASL and ASA. We concluded that the cumulative exposure to cigarette smoking was an independent indicator of the severity of coronary atherosclerosis as well as thoracic aortic atherosclerosis.

The aim – to determine the influence of the pro-inflammatory state of cellular and humoral immunity on the severity of coronary atherosclerosis in patients with stable coronary artery disease.Materials and methods. 115 patients with coronary artery disease (stable angina of exertion in patients of functional class II–IV) were examined. When analyzing coronarograms, the number of affected vessels, the degree and localization of stenoses were taken into account. The total damage to the heart arteries was calculated. The control group consisted of 30 practically healthy individuals with intact coronary arteries. Immunological parameters were studied in peripheral blood taken on an empty stomach.Results. Multivariate stepwise linear regression analysis revealed a statistically significant complex effect of anti-vascular antibodies (B=0.34; p=0.003), anti-vLDL antibodies (B=0.23; p=0.04) and CIC (B=0.25; p=0.03) on the severity and prevalence of coronary atherosclerosis (F=5.9; p=0.001) with the greatest contribution of anti-vascular antibodies. The use of uncorrelated IL-6, IL-8 (pro-inflammatory cytokines) and MF mts (phagocyte system) in the regression analysis showed a statistically significant effect on the severity and prevalence of atherosclerosis according to SUAS (F=5.9; p=0.001), according to the number of affected CA (F=4.5; p=0.006). The total effect of TNFα (pro-inflammatory cytokine system) and NST NF and MC (phagocyte system) on SUAS (F=3.9; p=0.01) and the number of affected CA (F=3.6; p=0.02) was also revealed. A significant complex effect of uncorrelated inflammatory cytokines (IL-6, TNFα) and humoral immunity (Antibodies to vessels) on the severity and prevalence of coronary atherosclerosis was revealed (F=3.1; p=0.04).Conclusions. The severity and prevalence of coronary atherosclerosis in stable CHD is associated with the activity of the adaptive cellular, humoral, and innate phagocytic components of the immune system. The severity and prevalence of coronary atherosclerosis in patients with stable CHD is directly affected by the cytokine system – IL-6, IL-8 and IL-10; in the humoral immunity system – Antibodies to arterial wall components, Antibodies to oLDL and CIC. Simultaneous activation of proinflammatory cytokine systems, humoral immunity and phagocytes also have a direct cumulative effect on the severity and prevalence of coronary atherosclerosis.

Excision repair cross-complementing 1 (ERCC1) gene encodes ERCC1 protein, which is mainly responsible for the repair of DNA damage in different diseases including coronary artery atherosclerosis by acting as a rate-limiting element in nucleotide excision repair (NER). Using a three-stage case-control study with 3037 coronary artery disease (CAD) patients and 3002 controls, we investigated associations of three single nucleotide polymorphisms (SNPs) with CAD risk and severity of coronary artery atherosclerosis in Chinese Han population. In the discovery set, the variant allele T of rs11615 was significantly associated with higher CAD risk (adjusted OR = 1.27, P = 0.006) and severity of coronary artery atherosclerosis (adjusted OR = 1.54, P = 0.003). These associations were more remarkable in the merged set (adjusted OR = 1.23, P = 8 × 10−6 for CAD risk; adjusted OR = 1.36, P = 4.3 × 10−5 for severity of coronary artery atherosclerosis). And the expression level of ERCC1 was significantly higher in CAD cases than controls. Multiplicative interactions among SNP rs11615, alcohol drinking, history of T2DM, and history of hyperlipidemia could increase 5.06-fold risk of CAD (P = 1.59 × 10−9). No significant association of rs2298881 and rs3212986 with CAD risk was identified. Taken together, SNP rs11615 in ERCC1 gene might confer susceptibility to CAD and severity of coronary atherosclerosis in a Chinese Han population.

Chronic kidney disease (CKD) is considered to be associated with increased risk of coronary artery disease (CAD). To elucidate the associations between kidney dysfunction (KD) and the severity of coronary and aortic atherosclerosis, we performed aortic black-blood MRI in 149 patients (pts) (age 64±9 yrs) undergoing coronary angiography. Regarding MRI, 9 slices of thoracic and 9 slices of abdominal aorta were obtained at 12-mm intervals. Plaque extent in each slice was scored. Severity of aortic atherosclerosis was represented as the sum of scores. On coronary angiograms, severity of coronary atherosclerosis was represented as the numbers of stenotic vessels and segments. KD was evaluated by eGFR. RESULTS: The 149 pts were divided into tertiles by eGFR: 51±10 (T1), 60±3 (T2) and 86±12 ml/min/1.73 2 (T3). CKD (eGFR&lt;60) was present in 41 (28%) pts. CAD (&gt;50% stenosis) and thoracic and abdominal aortic plaques were found in 105 (70%), 95 (64%) and 136 (91%) pts, respectively. Regarding coronary atherosclerosis, the number of &gt;25% stenotic coronary segments correlated with eGFR (r=-0.25, P&lt;0.005). Stepwise decrease in the number of &gt;50% stenotic vessels was found depending on eGFR tertiles: 1.5±1.0 (T1), 1.3±1.2 (T2) and 0.9±0.8 (T3) (P&lt;0.025). In multivariate analysis, reduced eGFR was associated with the severity of coronary atherosclerosis independent of risk factors. Regarding aortic atherosclerosis, the severity of thoracic aortic atherosclerosis correlated with eGFR (r=-0.22, P&lt;0.01), but abdominal aortic atherosclerosis did not (P=NS). The severity of thoracic aortic atherosclerosis decreased stepwise with eGFR tertiles: 3.0 (median) (T1), 2.0 (T2) and 1.0 (T3) (P&lt;0.02), whereas the severity of abdominal atherosclerosis tended to decrease on eGFR tertiles: 8.0 (T1), 7.0 (T2) and 6.0 (T3) (P=NS). However, in multivariate analysis, reduced eGFR was not an independent factor for thoracic or abdominal aortic atherosclerosis. CONCLUSION: The severity of coronary and thoracic, but not abdominal, aortic atherosclerosis correlated with the degree of KD. However, KD was an independent factor for coronary atherosclerosis but not for aortic atherosclerosis. KD is more likely to be associated with coronary atherosclerosis than aortic atherosclerosis.

IntroductionA deficiency of 25-hydroxyvitamin D (25(OH)D) (the standard biomarker for vitamin D status) can have multiple impacts on the cardiovascular system. The aim of the study was to assess of the influence of 25(OH)D on severity of coronary atherosclerosis and lipid profile.Material and methodsThe study involved prospectively 637 patients subject to coronary catheterization. The stage of coronary atherosclerosis was assessed using the Coronary Artery Surgery Study score (CASSS). Plasma concentration of 25(OH)D was measured using an electrochemiluminescent immunoassay. The levels of total cholesterol (TC), high-density cholesterol (HDL-C) and triglycerides (TG) were measured using the enzymatic method, and the concentration of low-density cholesterol (LDL-C) was calculated with the Friedewald equation.ResultsThe average level of 25(OH)D was 15.85 ng/ml. A higher level of 25(OH)D was observed in men (16.28 ng/ml vs. 15.1 ng/ml; p = 0.027). The study did not reveal any significant correlation between the level of 25(OH)D and severity of coronary atherosclerosis. It was observed however that the increase of 25(OH)D level results in an increased number of patients without significant lesions in the coronary arteries. In the whole group of women and men in the age group of 70–80 years an inverse relationship was observed between the level of 25(OH) and the severity of coronary atherosclerosis. The whole study group showed a statistically significant inverse correlation of the 25(OH)D level with TC (p = 0.0057), LDL-C (p = 0.00037) and TG (p = 0.00017).ConclusionsWomen and men over 70 years showed an inverse correlation of the 25(OH)D level and the stage of coronary atherosclerosis. Deficiency of 25(OH)D affects the levels of TC, LDL-C and TG.

The aim. To assess the relationships between the degree of severity of coronary and carotid atherosclerosis and the functional liver condition in patients with stable angina pectoris and obesity. Research materials and methods. During the study, two groups of patients were formed. Group I was composed of patients with stable angina and obesity (n = 69), group II - patients with stable angina with a normal body mass index (BMI) (n = 35). Measures of liver function, carbohydrate and lipid metabolism, results of duplex scanning of extracranial brachiocephalic arteries (BCA DS), coronaroangiography (CAG) data were evaluated, and biomarker of hepatic steatosis (НSI) were calculated. The severity of coronary atherosclerosis was analyzed by Gensini score (GS). All patients underwent ultrasound of the liver (ultrasound). Results. In 100% of patients of group I, non-alcoholic hepatic steatosis was detected according to ultrasound. Biomarker of hepatic steatosis (HSI) proved to be more significant among group I patients, while confirming the presence of steatosis. In patients of group I, more significant hypertriglyceridemia was established. Atherosclerotic plaques (according to the BCA DS) were detected in 100% patients of group I and in 68,5% patients of group II. Pronounced stenosis of СCA (≥75% of vessel lumen) is established in 14,5% patients of group I, and is not found among patients of group II. The proportion of patients with significant СA stenosis (&gt; 70% vessel lumen) turned out to be greater in the I group, making up 69,5%, in the II group - 42,8% (χ2=6,9; р=0,009). The GS index values were more significant in patients of group I compared to group II (p = 0.01). Close correlation relationships have been identified between functional liver condition and the severity of coronary and carotid atherosclerosis. Biomarker of steatosis (HSI) have demonstrated their relationship with atherosclerotic lesions of ССA and CA. Conclusion. Against the background of impaired the functional liver condition in patients with stable stenocardia and obesity, more significant expression of coronary and carotid atherosclerosis is determined in comparison with patients with normal body mass index.

BackgroundCase-control Genome-Wide Association Studies (GWAS) have identified single nucleotide polymorphisms (SNPs) at the 9p21 locus as risk factors for coronary artery disease (CAD). The locus does not contain a clear candidate gene. Hence, the results of GWAS have raised an intense interest in delineating the basis for the observed association. We analyzed association of 4 SNPs at the 9p21 locus with the severity and progression of coronary atherosclerosis, as determined by serial quantitative coronary angiograms (QCA) in the well-characterized Lipoprotein Coronary Atherosclerosis Study (LCAS) population. The LCAS is a randomized placebo-control longitudinal follow-up study in patients with CAD conducted to test the effects of fluvastatin on progression or regression of coronary atherosclerosis.MethodsExtensive plasma lipid levels were measured at the baseline and 2 1/2 years after randomization. Likewise serial QCA was performed at the baseline and upon completion of the study. We genotyped the population for 4 SNPs, previously identified as the susceptibility SNPs for CAD in GWAS, using fluorogenic 5' nuclease assays. We reconstructed the haplotypes using Phase 2, analyzed SNP and haplotype effects using the Thesias software as well as by the conventional statistical methods.ResultsOnly Caucasians were included since they comprised 90% of the study population (332/371 with available DNA sample). The 4 SNPs at the 9p21 locus were in tight linkage disequilibrium, leading to 3 common haplotypes in the LCAS population. We found no significant association between quantitative indices of severity of coronary atherosclerosis, such as minimal lumen diameter and number of coronary lesions or occlusions and the 9p21 SNPs and haplotypes. Likewise, there was no association between quantitative indices of progression of coronary atherosclerosis and the SNPs or haplotypes. Similarly, we found no significant SNP or haplotype effect on severity and progression of coronary atherosclerosis.ConclusionWe conclude the 4 SNPs at the 9p21 locus analyzed in this study do not impart major effects on the severity or progression of coronary atherosclerosis. The effect size may be very modest or the observed association of the CAD with SNPs at the 9p21 locus in the case-control GWAS reflect involvement of vascular mechanisms not directly related to the severity or progression of coronary atherosclerosis.

BackgroundFibrinogen is a coagulation/inflammatory biomarker strongly associated with atherogenesis. However, no data is currently available regarding the association of fibrinogen level with the presence and severity of new-onset coronary atherosclerosis assessed by Gensini score (GS), particularly in Han Chinese with a large sample size.Methods and ResultsWe studied 2288 consecutive, new-onset subjects undergoing coronary angiography with angina-like chest pain. Clinical and laboratory data were collected. Coronary stenotic lesions were considered to be the incidence of coronary atherosclerosis. The severity of coronary stenosis was determined by the GS system. Data indicated that patients with high GS had significantly elevated fibrinogen level (p<0.001). The prevalence and severity of coronary atherosclerosis were dramatically increased according to fibrinogen tertiles. Spearman correlation analysis revealed a positive association between fibrinogen level and GS (r = 0.138, p<0.001). Multivariate logistic regression analysis demonstrated that plasma fibrinogen level was independently associated with high GS (OR = 1.275, 95% CI 1.082–1.502, p = 0.004) after adjusting for potential confounders. Moreover, fibrinogen level was also independently related to the presence of coronary atherosclerosis (fibrinogen tertile 2: OR = 1.192, 95% CI 0.889–1.598, p = 0.241; tertile 3: OR = 2.003, 95% CI 1.383–2.903, p <0.001) and high GS (fibrinogen tertile 2: OR = 1.079, 95% CI 0.833–1.397, p = 0.565; tertile 3: OR = 1.524, 95% CI 1.155–2.011, p = 0.003) in a dose-dependent manner. Receiver-operating characteristic curve analysis showed that the best fibrinogen cut-off value for predicting the severity of coronary stenosis was 3.21 g/L.ConclusionsHigher fibrinogen level is independently linked with the presence and severity of new-onset coronary atherosclerosis in Han Chinese population.

Background: Insulin resistance (IR) in patients with type 2 diabetes mellitus (T2DM) represents a predictor of coronary artery disease (CAD). However, how IR is able to impact the severity of coronary atherosclerosis in non-diabetic patients is unknown. Objectives. We investigated the relation between the IR and the extent and severity of coronary atherosclerosis in non-diabetic patients referred to coronary angiography (CA) Methods: Consecutive patients undergoing to CA for acute coronary syndromes or stable angina were analyzed. The IR was assessed by mean of the homeostasis model assessment of insulin resistance (HOMA-IR) whereas the SYNTAX score (SS) was used as index of the severity of coronary atherosclerosis Results: Overall, 126 patients were included, with a median SS of 12 (IQR 5.25–20.5). Patients were divided in four groups according to the distribution in quartiles of SS (SS1-2-3-4). A significant correlation between HOMA-IR and SS was observed, especially in women. A progressive increase of HOMA-IR was observed in parallel with the increasing severity (from SS1 to SS4) and extension (1-2-3-vessel disease) of coronary atherosclerosis. Multivariable analysis showed that the HOMA-IR was the strongest independent predictor of severe (SS4) and extensive (three-vessel disease) coronary atherosclerosis. Conclusion: Insulin resistance goes hand in hand with the extension and severity of coronary atherosclerosis in non-diabetic patients. The HOMA index is an independent predictor of three-vessel disease at CA. The HOMA index could be useful for risk stratification of CAD even in absence of T2DM.

Background It remains unclear as to why some individuals at low risk of cardiovascular disease (CVD) develop severe coronary atherosclerosis, while those at high CVD risk may remain free from coronary atherosclerosis. Purpose Using Coronary Computed Tomography Angiography (CCTA), we aimed to identify factors associated with absence and severe coronary atherosclerosis in subjects from the general population with very high and low-moderate CVD risk, respectively. Methods We assessed cross-sectionally a nationwide, multicenter population-based cohort, consisting of 30,154 individuals randomly recruited from the general population (age range 50-64 years, 51.4% women). Coronary calcified plaque burden was estimated by coronary artery calcium score (CACS) assessed by CCTA. Absent coronary atherosclerosis was defined as CACS 0 and severe coronary atherosclerosis was defined as CACS ≥301. We investigated only individuals with low-moderate (&amp;lt;5%) and very high CVD risk (≥10%) according to SCORE2 were included. Individuals with CACS 0 and prevalent CVD were excluded, as well as those with moderate CACS (1-300) or SCORE2 risk 5-9%. Out of 26 722 subjects with complete data on CACS and SCORE2, 13 075 were included. Logistic regression was performed adjusted for age and sex. Results The overall distribution of CACS in relation to SCORE2 CVD risk is illustrated in the Figure. Study characteristics are displayed in Table 1. Severe-extensive CACS in combination with low-moderate CVD risk was present in 2.3% (n=296). A further 2.3% (n=311) had very high CVD risk but CACS 0. Factors associated with CACS 0 despite a very-high estimated CVD risk included: lower age, being female, being born in Sweden, not having hypertension or hyperlipidemia, fewer pack-years of smoking, and lower waist circumference in men. On the contrary, severe-extensive CACS despite a low-moderate estimated CVD risk was associated with higher age, being male, being an ex-smoker, reporting more pack-years of smoking, having higher HbA1c, higher BMI, higher waist circumference, and prevalent hyperlipidemia and hypertension (Table 2). Conclusions We identified extreme cardiovascular risk phenotypes (subgroups) in the general population that either lacked coronary calcifications despite being at very high estimated CVD risk or had severe subclinical coronary atherosclerosis despite being at estimated low-moderate CVD risk. Further studies are warranted to elucidate putative enhancing or protective mechanisms explaining this unexpected phenomenon.

We investigated the association between atherosclerosis of the thoracic aorta and the severity and extent of coronary atherosclerosis detected by multidetector computed tomography (MDCT) coronary angiography. In 122 patients, atherosclerotic plaque was scored from 0 to 4 points by the percentage of the luminal surface at the cross-sectional area of proximal, mid, and distal segments of the descending aorta. Critical coronary atherosclerosis was defined as lesions causing >50% luminal narrowing. Atherosclerotic plaque score of the descending aorta was associated with the severity (noncritical: 2.95 +/- 1.45 vs critical: 4.09 +/- 2.25, P < .001) and extent of coronary atherosclerosis (Kruskal-Wallis test, P < .005). Logistic regression revealed that aortic plaque score was as an independent risk factor associated with the severity of coronary artery disease (OR 1.32, 95% CI 1.01-1.73, P <.05). Atherosclerotic plaque burden of the descending aorta was associated with the extent and severity of coronary atherosclerosis.

Aims: Tartrate-resistant acid phosphatase (TRACP)-5b and osteoprotegerin (OPG) are specific and sensitive markers of bone resorption in patients with rheumatoid arthritis (RA) and chronic kidney disease (CKD). The TRACP-5b level is associated with the severity of RA and CKD, while the OPG level is associated with the severity of coronary atherosclerosis and calcification, and can predict a poor outcome in patients with coronary artery disease (CAD). However, the impact of TRACP-5b on coronary atherosclerosis in CAD patients remains unclear.Methods: A total of 71 CAD patients (57 men, 14 women; mean age: 69.0 ± 9.7 years) and 28 age- and gender-matched healthy subjects were investigated. The number of diseased vessels (a marker of the severity of coronary atherosclerosis) and the Gensini score (a marker of the extent of coronary atherosclerosis), as well as the OPG and TRACP-5b levels were measured in CAD patients. The TRACP-5b levels were classified into quartiles.Results: The TRACP-5b levels were significantly higher in CAD patients than in healthy subjects. Patients with higher TRACP-5b levels had higher OPG levels and Gensini scores than those with lower TRACP-5b levels. Higher TRACP-5b levels were associated with an increased number of diseased vessels. A multivariate linear regression analysis showed that the OPG level and the number of diseased vessels or the Gensini score were significantly and independently associated with the TRACP-5b level.Conclusions: These data indicate that the TRACP-5b level is significantly associated with the OPG level and with the severity and extent of coronary atherosclerosis in CAD patients.

BackgroundInsulin-resistant subjects develop more severe and diffuse coronary artery atherosclerosis than insulin-sensitive controls but the mechanisms that mediate this atherosclerosis phenotype are unknown.Research ObjectiveTo determine the metabolic parameters that associate with the severity of coronary atherosclerosis in insulin resistant pigs fed a high fat/high NaCl diet.Key MethodsThe primary endpoint was severity of coronary atherosclerosis in adult pigs (Sus scrofa, n = 37) fed a high fat diet that also contained high NaCl (56% above recommended levels) for 1 year.Principal FindingsTwenty pigs developed severe and diffuse distal coronary artery atherosclerosis (i.e., severe = intimal area as a percent medial area > 200% in at least 2 coronary artery cross sections and diffuse distal = intimal area as a percent medial area ≥ 150% over 3 sections separated by 2 cm in the distal half of the coronary artery). The other 17 pigs had substantially less coronary artery atherosclerosis. All 37 pigs had blood pressure in a range that would be considered hypertensive in humans and developed elevations in total and LDL and HDL cholesterol, weight gain, increased backfat, and increased insulin resistance (Bergman Si) without overt diabetes. Insulin resistance was not associated with atherosclerosis severity. Five additional pigs fed regular pig chow also developed increased insulin resistance but essentially no change in the other variables and little to no detectible coronary atherosclerosis. Most importantly, the 20 high fat/high NaCl diet -fed pigs with severe and diffuse distal coronary artery atherosclerosis had substantially greater increases (p< 0.05) in oxidized LDL (oxLDL) and fructosamine consistent with increased protein glycation.ConclusionIn pigs fed a high fat/high NaCl diet, glycated proteins are induced in the absence of overt diabetes and this degree of increase is associated with the development of severe and diffuse distal coronary artery atherosclerosis.

The impact of glucose-6-phosphate dehydrogenase (G6PD) deficiency on coronary atherosclerosis has not been clearly investigated so far. We aimed to assess the effects of G6PD deficiency on the extent and complexity of coronary atherosclerosis in a large unselected cohort of consecutive patients with acute coronary syndromes (ACS). We studied 623 consecutive patients presenting with ACS and undergoing coronary angiography and percutaneous coronary intervention (PCI). G6PD activity was quantitatively measured in all individuals using a biochemical assay based on the G6PD/6GPD ratio in erythrocytes. Individuals were defined as deficient when the ratio was less than 0.80. The severity and complexity of coronary atherosclerosis were assessed by SYNTAX score at baseline angiography. Fifty-six patients (9%) showed G6PD deficiency. Severe (i.e. enzymatic activity < 0.10) G6PD deficiency was detected in 33 (5.3%) individuals, mainly of male sex (n = 32). Overall, the cardiovascular risk profile was similar between patients with G6PD deficiency and controls. Patients with G6PD deficiency showed similar severity and complexity of coronary atherosclerosis as compared to control patients; accordingly, the SYNTAX score (15 vs. 14.5, P = 0.90, respectively, in G6PD-deficent patients and controls), and all its components were similar between deficient individuals and controls. The only independent predictor of a SYNTAX score of more than 22 was patients' age (odds ratio 1.035, 95% confidence interval 1.018-1.051; P < 0.001). G6PD deficiency does not impact on the extent and complexity of coronary atherosclerosis assessed by coronary angiography in patents presenting with ACS.