Association between parental consanguineous marriage and the incidence, age of onset, and severity of coronary artery disease: a cross-sectional study in Iran
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The relationship of consanguineous marriage (CM) with cardiovascular conditions, particularly structural congenital heart diseases, has been well established. Although CM may influence genetic predisposition by increasing oligogenicity and genetic homogeneity, its association with coronary artery disease (CAD) remains uncertain. This study aimed to investigate the relationship between parental CM and the prevalence, age of onset, and severity of CAD.
Methods
In this cross-sectional study conducted between May 2021 and August 2022, a total of 13,151 patients undergoing coronary angiography at the Tehran Heart Center were enrolled. A structured questionnaire was used to collect demographic and anthropometric data, medical history, cardiovascular risk factors, previous angiographic findings, and parental kinship information. Analyses were performed using IBM SPSS ver. 23.0.
Results
Among 11,986 participants, 66.0% were male, with a mean age of 58.9±10.7 years. CAD was diagnosed in 9,083 individuals (75.8%). In total, 1,515 participants (12.6%) reported a history of parental CM. The prevalence of CAD was 3.2 percentage points higher in individuals with parental CM (P<0.001). Additionally, parental CM was associated with an earlier CAD by 2.4 years. However, no significant correlation was observed between parental CM and CAD severity.
Conclusion
Parental consanguinity is associated with a higher prevalence and earlier onset of CAD. These findings suggest that parental CM may be relevant in the context of CAD risk and should be considered in comprehensive CAD risk assessments, particularly in regions where consanguinity is common.
Coronary artery disease (CAD) is one of the most prevalent noncommunicable diseases and the leading cause of death worldwide. It occurs due to the accumulation of atherosclerotic plaques within the coronary arteries, which progressively obstruct blood flow, reduce oxygen delivery, and lead to myocardial ischemia [1,2]. Numerous risk factors influence the incidence, progression, and severity of CAD [3]. Identifying these risk factors and determining their prevalence are critical for timely diagnosis and risk stratification [4].
Typically, CAD risk factors are classified into two categories: modifiable and nonmodifiable. Modifiable risk factors include smoking, elevated total cholesterol, high low-density lipoprotein (LDL) levels, hypertension (HTN), diabetes mellitus (DM), high body mass index, psychological stress, poor dietary habits, and low vitamin D levels [3,5]. Nonmodifiable risk factors include advanced age, male sex, family history (FH) of CAD, and genetic predisposition [6].
Certain risk factors, particularly genetic factors, may be more prevalent in specific regions than other CAD risk factors observed in various communities [7,8]. Genetic variations and hereditary factors across populations contribute to these differences. A consanguineous marriage (CM), with its oligogenicity and homogeneity, further increases the dominance of genetic factors and significantly influences genetic inheritance. CM is a cultural, social, and religious phenomenon, and its prevalence varies from 80% in the Middle East to less than 1% in Western societies [9].
Notably, although the influence of genetics on CAD has been confirmed in studies [10,11], conflicting findings regarding the link exist between CM and CAD. Therefore, the current study aimed to assess the relationship between parental CM and the incidence, age of onset, and severity of CAD. To the best of our knowledge, this is the first and largest investigation addressing this association in an Iranian population undergoing coronary angiography.
Methods
Study design and population
This cross-sectional study investigated the association between parental CM and prevalence and clinical characteristics of CAD in patients undergoing coronary angiography at the Tehran Heart Center between May 2021 and August 2022. A structured questionnaire was used to collect demographic and anthropometric data, cardiovascular risk factors, medical history, angiographic findings, and parental kinship details. In total, 13,151 patients completed the questionnaire.
Eligible participants were adults referred for coronary angiography with a diagnosis of chronic coronary syndrome, non-ST-elevation acute coronary syndrome, or ST-elevation acute coronary syndrome. Exclusion criteria were failure to undergo angiography following referral, angiography performed solely for electrophysiological studies or interventions related to congenital heart disease, and incomplete or missing angiographic data. Accordingly, 523 patients who did not undergo angiography, 425 patients with angiography performed for other procedures, and 217 patients with incomplete data were excluded. Ultimately, 11,986 patients met the inclusion criteria and were included in the analysis (Figure 1).
The study protocol was approved by the Ethics Committee of the Tehran Heart Center (Approval ID. IR.TUMS.MEDICINE. REC.1400.919). Written informed consent was obtained from all patients before enrollment. The aims and potential benefits of the study were explained to all participants before inclusion. Participation was voluntary, and individuals were informed of their right to withdraw from the study at any time without consequences.
Definitions of cardiovascular risk factors
CAD was defined as the presence of atherosclerotic plaques causing more than 50% luminal stenosis in at least one coronary artery as determined by angiography [12]. Parental CM was defined as unions between first cousins, and their offspring, who are second cousins, and underwent coronary angiography [13]. DM was diagnosed based on glycated hemoglobin >48 mmol/mol, fasting blood sugar >126 mg/dL, or current use of glucose-lowering medications [7]. HTN was characterized by systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg on at least two separate occasions or by the current use of antihypertensive therapy [7]. Dyslipidemia (DLP) was identified by total cholesterol ≥200 mg/dL, LDL ≥130 mg/dL, or the ongoing use of lipid-lowering medications [10]. Smoking status was defined as a history of smoking at least 100 cigarettes over a lifetime. A positive FH of CAD was considered a first-degree relative with CAD diagnosed before the age of 55 years in males or 60 years in females [7].
Statistical analysis
Categorical variables are presented as frequencies with percentages, and continuous variables are expressed as means with standard deviations. Associations between parental CM and CAD as well as other cardiovascular risk factors were analyzed using univariate and multivariate logistic regression models. Multivariate models adjusted for age, sex, DM, HTN, DLP, smoking, and FH of CAD. Odds ratios (ORs) and 95% confidence intervals (CIs) were also determined. Statistical significance was set at a P-value less than 0.05. Analyses were performed using IBM SPSS ver. 23.0 (IBM Corp.).
Results
Among the 11,986 patients who underwent coronary angiography, 9,083 (75.8%) had more than 50% coronary artery stenosis and were categorized as having CAD. The remaining 2,903 patients (24.2%) had either normal coronary findings or less than 50% stenosis and were classified as non-CAD. Of the total population, 7,910 (66.0%) were male, of whom 6,441 (81.4%) belonged to the CAD group. In contrast, the sex distribution among non-CAD cases was nearly equal. Male sex was significantly associated with a higher prevalence of CAD (P<0.05).
The mean age of the overall study population was 58.9±10.7 years. On average, patients with CAD were 3.2 years younger than those without CAD, a statistically significant difference (P<0.05). HTN was the most prevalent cardiovascular risk factor, observed in 57.9% of patients, followed by DLP (50.7%). All conventional cardiovascular risk factors were significantly more frequent in individuals with CAD than in those without CAD (Table 1).
In total, 1,515 patients (12.6%) reported a history of parental CM, among whom 1,190 (78.5%) had CAD. Of 10,471 without such a history, 7,893 (75.4%) were diagnosed with CAD. The prevalence of CAD was 3.2 percentage points higher in the CM group than in the control group (P<0.001) (Figure 2). Furthermore, patients with CAD with a history of parental CM were on average 1.9 years younger than those without such a history (P<0.001). Among patients with CAD, HTN was less common in those with parental CM (51.3% vs. 61.6%). This inverse association remained significant in both univariate (OR, 0.85; P=0.020) and multivariate analyses (adjusted OR, 0.73; P<0.001), suggesting a potential link between parental CM and lower odds of HTN (Table 2).
Based on initial angiographic evidence of stenosis exceeding 50%, the mean age of CAD onset was 59.0±10.8 years. The average ages at first percutaneous coronary intervention and coronary artery bypass grafting were 59.9±10.6 and 60.6±10.4 years, respectively. Across clinical parameters, those with a history of parental CM experienced considerably earlier onset, with mean ages approximately 2 years younger than individuals without such a history (Table 3).
As shown in Table 3, patients with parental CM had a slightly higher frequency of normal coronary findings than those without CM (12.3% vs. 9.3%). Mild or minimal CAD was observed in 15.8% of patients with a history of parental consanguinity compared to 14.3% of those without such a history. Similarly, single-vessel disease was found in 24.7% and 23.4% of these groups, respectively. The prevalence of two-vessel and three-vessel diseases was slightly lower in the CM group (20.1% and 27.1%, respectively) than in the non-CM group (23.7% and 29.3%, respectively). However, after adjusting for confounding variables, none of these differences remained statistically significant (adjusted OR, 1.29; 95% CI, 0.64–1.73; P=0.806).
In this study, the unadjusted mean age at CAD onset was 59.0±10.8 years, which increased to 63.1±10.3 years after accounting for risk factors. A history of parental CM was linked to an earlier onset of CAD by 2.4 years. Among all evaluated determinants, a positive FH of CAD had the greatest association, with onset occurring approximately 4.9 years earlier. Smoking, DLP, and male sex were also related to earlier onset, reducing the age by 3.5, 3.0, and 2.6 years, respectively. Conversely, DM was linked to a slight delay of 0.2 years, while HTN was associated with a notably later onset of 2.0 years (P<0.001) (Figure 3).
As illustrated in Figure 4, when parental CM was considered a contributing factor, the estimated mean age at CAD onset decreased from 63.1 to 60.7 years. Among male patients with parental CM, the mean age decreased further to 58.1 years. Among those with multiple risk factors, including male sex, smoking, DLP, positive FH, and parental CM, the disease manifested 16.4 years earlier, with an average onset at 46.7 years.
Discussion
The global prevalence of CM varies widely due to a combination of religious, cultural, and socioeconomic factors. Religiously, CM is permitted in Islam and Judaism but is generally discouraged or prohibited in Christianity [14]. Culturally, it is more common in specific populations, particularly in South Asian and Indian communities. Additionally, CM is more prevalent among populations with a lower socioeconomic status. These factors contribute to its high prevalence in the Middle East, where it accounts for approximately 80% of marriages compared to less than 1% in Western and Eastern countries [9,15].
A well-recognized biological effect related to CM is increased homozygosity, which is linked to a higher likelihood of inherited genetic disorders at both familial and population levels. Chronic conditions have also been correlated with an increased risk such as various cancers and cardiovascular diseases [13,16,17]. Two primary models have been used to investigate the relationship between genetic variants and diseases: common variant association studies (CVAS) and genome-wide association studies, also known as rare variant association studies (RVAS). In CVAS, deoxyribonucleic acid sequence variants are present in sufficient numbers, making it feasible to analyze each variant individually and estimate its frequency in disease cases compared to controls. In contrast, rare variants occur infrequently, making it difficult to separately test the correlation of each variant. Therefore, RVAS require pooling these rare variants into groups and comparing their overall frequency distributions between cases and controls [18,19].
Previous studies have demonstrated associations between genetic factors and cardiovascular diseases, including structural congenital heart defects, and have identified numerous nucleotide polymorphisms and at least 58 genomic loci linked to CAD [20,21]. However, the number of studies that have specifically examined the relationship between CM and CAD is considerably greater.
In the present study, the prevalence of parental CM was 12.6%. After adjusting for other established CAD risk factors, CM correlated with a higher likelihood of CAD and an earlier age at onset. However, CM did not appear to be linked with the severity of CAD in our population. Youhanna et al. [22] similarly reported an association between CM and earlier CAD onset but found no significant effect on overall CAD risk. Notably, their analysis did not adjust for potential confounders, which may have partially explained the divergence in findings.
Several mechanisms may underlie the observed relationship between CM and a higher likelihood of CAD with earlier onset. Genetic evidence supports a biological link between consanguinity and the development of CAD. Increased homozygosity in consanguineous unions may unmask recessive alleles affecting lipid metabolism, endothelial function, and inflammatory pathways central to atherogenesis. Variants in genes such as apolipoprotein B (APOB), LDL receptor (LDLR), and proprotein convertase subtilisin/kexin type 9 (PCSK9) have been associated with abnormal plasma lipid levels and premature atherosclerosis. Similarly, polymorphisms in genes regulating nitric oxide synthesis and inflammatory cytokines may promote vascular inflammation and endothelial injury in genetically homogeneous populations. Furthermore, genome-wide studies have indicated that extended runs of homozygosity are linked to an increased burden of rare deleterious alleles associated with cardiovascular risk [23-26].
In addition to genetic mechanisms, several social and environmental factors may also play a role. CM is more common in communities with lower socioeconomic status and is a well-established risk factor for CAD [27]. Third, populations with high CM prevalence, such as those in many Middle Eastern countries, may share common lifestyle-related risk factors, including poor dietary habits and reduced physical activity [15].
Consistent with earlier studies [1,10,18], our findings demonstrated that positive FH, DLP, smoking, and male sex were associated with a higher likelihood of CAD and an earlier disease onset. Interestingly, patients with HTN exhibited a later onset of CAD, which may be explained by several factors. First, the average age of hypertensive individuals in our study was higher than the overall mean age at CAD onset [27-29]. Second, hypertensive patients often present with atypical chest pain, potentially delaying referral for angiographic evaluation [30]. Long-standing HTN may lead to the development of coronary collateral vessels, which can postpone the appearance of symptoms and thus delay the diagnosis [31,32]. Fourth, patients with HTN are more likely to receive primary preventive therapies, which may contribute to the later onset of CAD [27]. Similarly, DM was associated with a modest (although statistically insignificant) increase in the age of CAD onset. The same contributing factors may apply to patients with diabetes.
The findings of this study have several important implications for clinical practice and public health. First, individuals with a history of parental consanguinity may benefit from early cardiovascular screening for modifiable risk factors, including DLP, HTN, and DM, to facilitate timely preventive interventions. Second, targeted lifestyle interventions such as dietary modifications, regular physical activity, and smoking cessation should be emphasized in populations with high rates of consanguinity. Third, premarital and genetic counseling that includes assessment of FH of CAD can help at-risk couples make informed decisions and raise awareness about potential cardiovascular risks. Finally, public health programs in regions with prevalent CMs could integrate educational campaigns to promote cardiovascular health awareness and preventive strategies, ultimately contributing to the reduction of early onset CAD in these communities.
Study limitations
Our study has several limitations. First, its cross-sectional design prevents establishing causality between parental CM and CAD. Second, despite adjusting for known confounders, residual confounding from unmeasured genetic or environmental factors cannot be completely excluded. Third, the assessment of CAD severity in this study was based solely on the number of affected vessels. The absence of quantitative measures such as the SYNTAX or Gensini scores, represents a limitation and should be addressed in future research. Finally, information on medication use, healthcare utilization patterns, lifestyle factors, and socioeconomic status may not have been fully captured, which could have influenced the observed associations.
Conclusions
This study demonstrated that a history of parental CM was associated with a higher likelihood of CAD and an earlier age of disease onset. These findings highlight the relevance of parental CM in the context of CAD, particularly in regions where consanguinity is common. Accounting for parental consanguinity in early cardiovascular screening, lifestyle interventions, and premarital counseling may improve risk stratification and guide preventive strategies in high-risk populations.
Notes
Conflict of interest
No potential conflict of interest relevant to this article was reported.
Funding
None.
Data availability
Data of this research are available from the corresponding author upon reasonable request.
Sampling flowchart of the study to evaluate the correlation of parental consanguineous marriage (CM) and coronary artery disease (CAD). CAG, coronary angiography
Figure. 2.
Frequency of coronary artery disease (CAD) in patients with a history of parental consanguineous marriage (CM) was significantly higher than those without such a history.
Figure. 3.
The adjusted effects of coronary artery disease (CAD) risk factors on the age of CAD onset. Parental consanguineous marriage (CM) independently reduced the age of onset by 2.4 years. Family history (FH) of CAD had the strongest association, lowering the age of onset by 4.9 years, followed by smoking (3.5 years) and dyslipidemia (DLP; 3 years). Male sex was also associated with a 2.6-year earlier onset. DM, diabetes mellitus; HTN, hypertension.
Figure. 4.
The adjusted cumulative effect of coronary artery disease (CAD) risk factors on the age of disease onset. A patient who was male, had a positive family history (FH) of CAD, smoked, had parental consanguineous marriage (CM), and had dyslipidemia (DLP) was expected to develop CAD at 46.6 years of age, compared to 63.1 years in the absence of these risk factors.
Table 1.
Association of demographic characteristics and cardiovascular risk factors with CAD in patients undergoing coronary angiography
Characteristic
All patients (n=11,986)
CAD (n=9,083)
Non-CAD (n=2,903)
Univariable
Multivariable
OR (95% CI)
P-value
Adjusted OR (95% CI)
P-value
Age (y)
58.9±10.7
59.8±10.6
56.5±11
1.44 (1.25–1.72)
<0.001
1.33 (1.11–1.58)
<0.001
Sex (male)
7,910 (66.0)
6,441 (70.9)
1,469 (50.6)
1.51 (1.34–1.68)
<0.001
1.42 (1.29–1.57)
<0.001
Body mass index (kg/m2)
31.9±10.2
32.1±10.2
31.1±10.4
1.16 (1.11–1.27)
<0.001
1.09 (1.05–1.19)
0.014
Waistline (cm)
100.1±12.3
100.9±12.4
99.9±11.8
1.09 (1.02–1.23)
<0.001
1.01 (0.89–1.14)
0.128
Smoking
2,915 (24.3)
2,386 (26.3)
529 (18.2)
1.31 (1.15–1.52)
<0.001
1.11 (1.04–1.24)
<0.001
Dyslipidemia
6,080 (50.7)
5,051 (55.6)
1,029 (35.4)
1.83 (1.46–2.32)
<0.001
1.57 (1.33–1.83)
<0.001
Diabetes mellitus
4,796 (40.0)
3,957 (43.6)
839 (28.9)
1.68 (1.43–2.06)
<0.001
1.46 (1.27–1.72)
<0.001
Hypertension
6,937 (57.9)
5,475 (60.3)
1,462 (50.4)
1.45 (1.29–1.66)
<0.001
1.28 (1.14–1.47)
<0.001
Family history
2,208 (18.4)
1,746 (19.2)
462 (15.9)
1.23 (1.15–1.32)
<0.001
1.07 (1.01–1.18)
0.003
Values are presented as mean±standard deviation or number (%) unless otherwise stated.
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Association between parental consanguineous marriage and the incidence, age of onset, and severity of coronary artery disease: a cross-sectional study in Iran
Figure. 1. Sampling flowchart of the study to evaluate the correlation of parental consanguineous marriage (CM) and coronary artery disease (CAD). CAG, coronary angiography
Figure. 2. Frequency of coronary artery disease (CAD) in patients with a history of parental consanguineous marriage (CM) was significantly higher than those without such a history.
Figure. 3. The adjusted effects of coronary artery disease (CAD) risk factors on the age of CAD onset. Parental consanguineous marriage (CM) independently reduced the age of onset by 2.4 years. Family history (FH) of CAD had the strongest association, lowering the age of onset by 4.9 years, followed by smoking (3.5 years) and dyslipidemia (DLP; 3 years). Male sex was also associated with a 2.6-year earlier onset. DM, diabetes mellitus; HTN, hypertension.
Figure. 4. The adjusted cumulative effect of coronary artery disease (CAD) risk factors on the age of disease onset. A patient who was male, had a positive family history (FH) of CAD, smoked, had parental consanguineous marriage (CM), and had dyslipidemia (DLP) was expected to develop CAD at 46.6 years of age, compared to 63.1 years in the absence of these risk factors.
Graphical abstract
Figure. 1.
Figure. 2.
Figure. 3.
Figure. 4.
Graphical abstract
Association between parental consanguineous marriage and the incidence, age of onset, and severity of coronary artery disease: a cross-sectional study in Iran
Characteristic
All patients (n=11,986)
CAD (n=9,083)
Non-CAD (n=2,903)
Univariable
Multivariable
OR (95% CI)
P-value
Adjusted OR (95% CI)
P-value
Age (y)
58.9±10.7
59.8±10.6
56.5±11
1.44 (1.25–1.72)
<0.001
1.33 (1.11–1.58)
<0.001
Sex (male)
7,910 (66.0)
6,441 (70.9)
1,469 (50.6)
1.51 (1.34–1.68)
<0.001
1.42 (1.29–1.57)
<0.001
Body mass index (kg/m2)
31.9±10.2
32.1±10.2
31.1±10.4
1.16 (1.11–1.27)
<0.001
1.09 (1.05–1.19)
0.014
Waistline (cm)
100.1±12.3
100.9±12.4
99.9±11.8
1.09 (1.02–1.23)
<0.001
1.01 (0.89–1.14)
0.128
Smoking
2,915 (24.3)
2,386 (26.3)
529 (18.2)
1.31 (1.15–1.52)
<0.001
1.11 (1.04–1.24)
<0.001
Dyslipidemia
6,080 (50.7)
5,051 (55.6)
1,029 (35.4)
1.83 (1.46–2.32)
<0.001
1.57 (1.33–1.83)
<0.001
Diabetes mellitus
4,796 (40.0)
3,957 (43.6)
839 (28.9)
1.68 (1.43–2.06)
<0.001
1.46 (1.27–1.72)
<0.001
Hypertension
6,937 (57.9)
5,475 (60.3)
1,462 (50.4)
1.45 (1.29–1.66)
<0.001
1.28 (1.14–1.47)
<0.001
Family history
2,208 (18.4)
1,746 (19.2)
462 (15.9)
1.23 (1.15–1.32)
<0.001
1.07 (1.01–1.18)
0.003
Characteristic
All CAD patients (n=9,083)
With parental CM (n=1,190)
Without parental CM (n=7,893)
Univariable
Multivariable
OR (95% CI)
P-value
Adjusted OR (95% CI)
P-value
Age (y)
59.8±10.6
58.1±10.8
60.2±10.6
1.23 (1.11–1.44)
<0.001
1.14 (1.09–1.25)
<0.001
Sex (male)
6,441 (70.9)
753 (63.3)
5,688 (72.1)
1.02 (0.72–1.28)
0.284
1.08 (0.79–1.34)
0.126
Body mass index (kg/m2)
32.1±10.2
31.7±11.3
32.1±10.1
1.17 (0.96–1.37)
0.096
1.08 (0.84–1.18)
0.351
Waistline (cm)
100.1±12.3
100.2±11.3
99.9±12.8
1.06 (0.84–1.21)
0.520
1.01 (0.86–1.14)
0.741
Smoking
2,386 (26.3)
269 (22.6)
2,117 (26.8)
1.11 (0.85–1.42)
0.477
1.16 (0.94–1.39)
0.214
Dyslipidemia
7,052 (77.6)
851 (71.5)
6,201 (78.6)
1.13 (0.78–1.46)
0.727
1.24 (0.92–1.36)
0.154
Diabetes mellitus
3,957 (43.6)
476 (40.0)
3,481 (44.1)
1.01 (0.95–1.04)
0.948
1.07 (0.86–1.24)
0.756
Hypertension
5,475 (60.3)
610 (51.3)
4,865 (61.6)
0.85 (0.74–0.96)
0.020
0.73 (0.59–0.87)
<0.001
Family history
1,746 (19.2)
234 (19.7)
1,512 (19.2)
1.16 (1.02–1.34)
0.045
1.14 (0.94–1.28)
0.227
Variable
All patients (n=11,986)
With parental CM (n=1,515)
Without parental CM (n=10,471)
Univariable
Multivariable
OR (95% CI)
P-value
Adjusted OR (95% CI)
P-value
Age of first CAG
58.6±10.8
56.7±10.8
58.8±10.7
1.47 (1.14–1.84)
<0.001
1.24 (1.11–1.43)
<0.001
Age of first CAD
59.0±10.8
57.2±10.8
59.3±10.7
1.34 (1.21–1.68)
<0.001
1.31 (1.16–1.47)
<0.001
Age of first PCI
59.9±10.6
58.4±11.1
60.1±10.5
1.58 (1.18–2.06)
<0.001
1.27 (1.21–1.44)
<0.001
Age of first CABG
60.6±10.4
58.7±10.4
60.9±10.38
1.41 (1.09–1.83)
<0.001
1.37 (1.18–1.62)
<0.001
Underwent PCI
5,302 (44.2)
670 (44.3)
4,632 (44.2)
1.07 (0.87–1.31)
0.503
1.16 (0.74–1.41)
0.628
Underwent CABG
2,772 (23.1)
315 (20.8)
2,457 (23.5)
1.14 (0.76–1.53)
0.246
1.28 (0.94–1.57)
0.124
Severity of CAD
1.12 (1.06–1.19)
<0.001
1.29 (0.64–1.73)
0.806
Normal
1,164 (9.7)
186 (12.3)
978 (9.3)
Mild/minimal
1,739 (14.5)
239 (15.8)
1,500 (14.3)
SVD
2,821 (23.5)
374 (24.7)
2,447 (23.4)
2VD
2,785 (23.2)
304 (20.1)
2,481 (23.7)
3VD
3,477 (29.0)
412 (27.1)
3,065 (29.3)
Table 1. Association of demographic characteristics and cardiovascular risk factors with CAD in patients undergoing coronary angiography
Values are presented as mean±standard deviation or number (%) unless otherwise stated.
, Arash Jalali2
