Journal of Community Medicine & Public Health (ISSN: 2577-2228)

Article / research article

"Risk Factors Associated with Cardiovascular Diseases among Adults Attending the Primary Health Care Centers in Qatar, a Cross-Sectional Study"

A.Jaleel A.Latif Zainel*, Ahmed Sameer Al Nuaimi, Mohamed Ahmed Syed, Hamda Abdulla A/Qotba

Department of Clinical Research, Directorate of Clinical Affairs, Primary Health Care Corporation, Doha, Qatar

*Corresponding author: A.Jaleel A.Latif Zainel, Lead Principal Investigator, Department of Clinical Research Directorate of Clinical Affairs, Primary Health Care Corporation, P.O. Box 26555 Doha, Qatar

Received Date: 03 February, 2020; Accepted Date: 19 February, 2020; Published Date: 26 February, 2020

Abstract

Introduction/Aim: In Qatar, prevalence of risk factors of cardiovascular diseases significantly higher compared to many other countries. It is therefore critical to understand the associations between selected risk factors and having cardiovascular diseases (Any cardiac disease including coronary, thrombotic/hemorrhagic and peripheral vascular diseases) as we aimed by this study.

Materials and Methods: Cross-sectional study design was used. Data for individuals aged ≥18 and who visited primary health care canters in Qatar during 2017 were extracted from electronic medical records and analysed.

Results: The adjusted model of analysis confirmed that the increase in age especially over the age of sixty (adjusted OR of 6.65) represents the most potent risk factor for cardiovascular diseases occurring among study’s participants. Being male gender, Northern African, Western Asian, Southern Asian, Qatari increased the risk of cardiovascular disease unevenly with adjusted OR of 1.36, 1.45, 1.42, 1.31 and 1.15 respectively. Having a high blood pressure almost doubled the risk of cardiovascular disease developing (adjusted OR of 1.83). Unlike expected, the high triglycerides component failed to show any significant contribution to risk of having cardiovascular disease with adjusted OR of 0.86. For each one-factor increase in the count of metabolic syndrome components, the risk of having the outcome is multiplied by 21%.

Conclusion: The study provides essential epidemiological data required by decision makers. Although not nationally representative, this study is suggestive of a higher risk of cardiovascular diseases occurring among an older population, men and in Northern African, Western Asian and Southern Asian nationalities, as well as having high blood pressure, insulin resistance and low serum HDL. More studies are needed to establish which public health interventions are likely to be effective in Qatar. Currently, efforts should be contextualized and should target the key epidemiological features.

Keywords

Adult; Cardiovascular diseases; Primary health care; Qatar; Risk factor

Introduction

Cardiovascular Disease (CVD) are a group of major disorders of the heart and the arterial circulation supplying the heart, brain and the peripheral tissues. Accordingly, the main components of CVDs are ischemic heart disease, stroke, heart failure, peripheral arterial disease, and a number of other cardiac and vascular conditions, constitute the leading cause of global mortality and are a major contributor to reduced quality of life. They are common in the general population, affecting mainly adults past the age of 60 years [1-3].

Many risk factors for CVD are modifiable by specific preventive measures. In a study covered patients from 52 countries, nine potentially modifiable factors accounted for over 90 percent of the population-attributable risk of a first myocardial infarction (MI): smoking, dyslipidemia, hypertension, diabetes, abdominal obesity, psychosocial factors, lack of daily consumption of fruits and vegetables, regular alcohol consumption, and lack of regular physical activity [4]. In addition to age and gender, most patients with CVD have at least one established or borderline risk factor [5-7].

Coronary Heart Disease (CHD) represent about one-half of the total cases of CVD. Based on the Framingham Heart Study of 7733 participants aged 40 to 94 and were initially free of CHD, the lifetime risk for individuals at age 40 was 49 percent in men and 32 percent in women [8].

Although many evidences showing that death rates from CVD, CHD, and stroke have declined in the United States since 1975, CVD and its related complications remain highly prevalent and expensive to treat [9]. CVD is the leading cause of death in most developed countries, as well as its prevalence is rapidly increasing in developing countries [10].

In 2017, CVD caused an estimated 17.8 million deaths worldwide, corresponding to 330 million years of life lost and another 35.6 million years lived with disability [2,3].

Unfortunately, information related to CVD in Qatar is limited, however many studies have tried to cover some important aspects related to these conditions relatively. A study on Non-Communicable Diseases (NCDs) in Qatar indicated that CVD is on the top of diseases burden economically. Same study demonstrated that the risk factors of CVD can be traced mainly to lifestyle-patterns such as tobacco use, fatty food and physical inactivity [11]. A cross-sectional study conducted on school children aged 6-11 years old concluded that overweight and obese children screened using International Obesity Task Force reference values are at increased risk of CVD in adulthood [12]. When the data registry of all patients admitted between 1982 and 1990 to the Coronary Care Unit at the main general in Qatar with the diagnosis of documented acute MI is reviewed, the results showed that 86.6% of cases were among men with a mean age of 51 years. Among the cases, 62% were smokers, 29% had diabetes, and 20% had hypertension. Being older age and female gender were associated with higher mortality [13].

In this study, we have tried to explore the magnitude of participating of specific factors in the risk of developing any CVD as an outcome among adults using the governmental funded primary health care centers in Qatar.

Materials and Methods

Study design and settings

A cross-sectional study used ready raw data (secondary data from the electronic medical records “EMR”) in the data analysis to get the results. Essentially, data have been collected through the health centers affiliated with the Primary Health Care Corporation (PHCC) in the State of Qatar. PHCC is the largest primary care provider in the country publicly with 30 health centres (all accredited by Accreditation Canada International).

Study population and data collection

The study population includes both Qataris and non-Qataris registered at a PHCC health centre, aged ≥18 and who visited a health centre between 1 January 2017 and 31 December 2017. Required data were extracted from the EMR for the defined population.

Definitions and data analysis

The definition of having CVD was based on a list of SNOMED codes and its ICD-10 translated counterpart which is used in the PHCC-EMR (appendix 1). The National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) component definitions was adapted for the definition of the five components of Metabolic syndrome (MetS) used in this study based on the data available in the PHCC-EMR system (Table 1) [14]. All data were analyzed using the Statistical Package for the Social Sciences (SPSS) statistical software package.

Ethical considerations

Study’s team have assured the privacy of subjects and the confidentiality of the data, as all the collected data for the study purpose were anonymised. None of the subjects’ personal information was available to the research team. Overall, the study was conducted with integrity according to generally accepted ethical principles and was approved by the PHCC’s independent ethics committee (PHCC/RS/18/02/003).

Results

In univariate modeling (Table 2), the older age, male gender and the Asian, North African and Qatari nationalities increased the risk of having CVD (Any cardiac disease including coronary, thrombotic/hemorrhagic and peripheral vascular diseases). The five selected risk factors (components of MetS) contributed towards the risk of having CVD with high blood pressure and insulin resistance being the largest contributors. Having metabolic syndrome increased the risk by 2.5 times while accumulating more risk factors accounting for metabolic syndrome significantly increased the risk of having CVD.

The multivariate modelling (Table 3) showed a similar pattern of association between increasing age, male gender, Asian, Qatari and North African nationalities, risk factors and count of MetS components and increased risk of having CVD. The magnitude of risk estimates for each explanatory variable included in the model after adjustment is lower than its counterparts in unadjusted model. In addition, the high triglycerides component failed to show any significant contribution to risk of having CVD after adjusting for other factors. For each one factor increase in the count of MetS components the risk of having the outcome is multiplied by 21%.

Discussion

The prevalence of identified risk factors of CVD has changed over time because of increased awareness and changes in kind of diet and lifestyle. It can be said that the results of this study partly support the fact that the leading modifiable risk factors which estimated to be responsible for more than half of cardiovascular mortality are hypercholesterolemia, diabetes, hypertension, obesity, and smoking [20,21]. On the other hand, this study support that the absence of major risk factors predicts a much lower risk of CVD [22].

Our study has shown that CVD increased with increasing in age, in a multiple regression analysis of our data the adjusted odd ratio was 2.42 among age group of 40-59 increased to 6.65 among people aged 60 and above compared to age group of 18-39. When a study analyzed the situation of cardiovascular mortality in industrialized countries, the results showed a tendency for mortality change, either positively or negatively, it was quicker in younger age groups than in older ones. These varying levels and trends in CVD mortality have been caused by differences in risk factors prevalence and operating in each country, affecting the incidence of CVDs and their prognosis [23]. Age alone contribute to the development of CVD as have shown in a cohort of more than 3.6 million individuals aged 40 years or older who had screened for CVD, the prevalence of any vascular disease increased significantly with each decade of life (2% in 40-50 years old, 3.5% in 51- 60, 7.1% in 61-70, 13% in 71-80, 22.3% in 81-90, 32.5% in 91-100 years old). After adjusting for traditional risk factors, each additional decade of life was associated with an approximate doubling of the risk of vascular disease, exactly as ours [24]. Systolic blood pressure and isolated systolic hypertension are major CHD risk factors at all ages and in both genders [25]. In the Framingham study, patients <50 years of age, diastolic blood pressure was the strongest predictor of CHD risk; in those 50 to 59 years of age, all three blood pressure indices (systolic, diastolic, and pulse pressure) were comparable predictors of CHD risk, while in those ≥60 years of age, pulse pressure was the strongest predictor [26].

This study indicated that CVD more prevalent among male compared to female with adjusted odd ratio of 1.36. Several population studies have identified male gender as a risk factor for higher rates of CVD and CVD-related mortality [27-29]. This fact has been supported by a study included 7733 participants where lifetime risk of CHD at age 40 years was 48.6% for men and 31.7% for women. At age 70 years, lifetime risk was 34.9% for men and 24.2% for women [8]. Similar findings have been reported in a meta-analysis of 18 cohorts involving over 250,000 men and women [30]. Contrary to the results of this research, the trends of cardiovascular mortality were much more promising in females than in males as shown in a different study [23].

In this study, we discussed the relation between the five elements of metabolic syndrome and having CVDs, these five elements were previously defined within the study.

When we conducted a multiple logistic regression model to evaluate the independent association of insulin resistance as a risk factor for having CVD, the results showed an adjusted odd ratio of 1.31 for having such cases. This outcome was reinforced by findings of many international researches. Results of 20 years of surveillance of the Framingham cohort relating CVD to diabetes, showed increase in some CVD by two to three times. The relative impact was greatest for intermittent claudication (IC) and congestive heart failure (CHF) compares to CHD [31]. Another study has shown that presence of DM was highly related (P<0.01) to the development of first CHD events [21].

Obesity is associated with several risk factors for cardiovascular morbidity and mortality, including hypertension, insulin resistance and glucose intolerance, hypertriglyceridemia, and reduced HDL cholesterol [32-34]. In our study being obese increased the risk of CVD relatively with adjusted odd ratio of 1.13 compared to non-obese individuals. This result supported by an analysis of data from 4780 adults in the Framingham Offspring Study, where obesity significantly and independently predicted the occurrence of CHD and cerebrovascular disease after adjusting for traditional risk factors [21].

This work has explored that increasing in blood pressure has almost doubled the prevalence of CVD compared to people with normal blood pressure. This was supported by a study where people with blood pressure ≥140/90 mm Hg or those receiving blood pressure-lowering drugs had 63.3% lifetime risk of overall CVD at age of 30 years compared with 46.1% for those with normal blood pressure, as well as the group of high blood pressure developed CVD five years earlier [35]. Another study has showed that decreasing in systolic blood pressure by 10 mmHg was associated with specific level of decreasing in risk of stroke and ischemic heart disease [36]. In this context, many studies have confirmed that high blood pressure act as a well-established risk factor for adverse cardiovascular outcomes, including mortality from Coronary Heart Disease (CHD) and stroke [4,35,37,38]. Furthermore, higher systolic blood pressure act as predictors for first CHD and cerebrovascular events [21].

When we have discussed the relation between lipid profile as risk factor and occurring of CVD, we found inconsistent or conflicted results. As having of a high serum triglyceride acted as a protective factor from CVDs occurring (adjusted odd ratio of 0.86). On the other hand, having a low serum HDL associated with higher CVDs (adjusted odd ratio of 1.28). These findings were supported in many studies, but there are also many others that opposed those results.

In some studies, the prevalence of dyslipidemia has been increased in patients with premature CHD, being as high as 75 to 85 percent compared with approximately 40 to 48 percent in age-matched controls without CHD [39,40]. In a study, dyslipidemia accounted for 49 percent of the population-attributable risk of a first Myocardial Infarction (MI) [4]. Using statins has reduced in total and LDL cholesterol levels which in turn have reduced coronary events and mortality when given for primary and secondary prevention as indicated in different studies [41-43].

Low serum HDL cholesterol can occur as sole lipid abnormality or, more often, in association with hypertriglyceridemia or elevated LDL particles or Apo lipoprotein B levels [40]. Isolated low HDL cholesterol, a condition that occurs when HDL cholesterol is <50 mg/dL in women and <40 mg/dL in men, and triglycerides and LDL cholesterol are <100 mg/dL, predicts an increased risk for cardiovascular events in population studies [44,45]. Based on data from the Framingham Heart Study, the risk for MI increases by about 25 percent for every 5 mg/dL (0.13 mmol/L) decrement in serum HDL cholesterol below median values for men and women [46]. The rate of MI death was 33% lower in the highest HDL cholesterol quartile as compared with the lowest one [47]. Not all studies have found that HDL cholesterol is predictive of future events in patients with established CVD treated with statin therapy. In a cohort study of 6111 patients with CVD treated with intensive lipid lowering, HDL cholesterol was not associated with recurrent vascular events irrespective of LDL cholesterol level [48]. Despite the substantial body of evidence of an inverse relationship between HDL cholesterol and cardiovascular event risk, low levels of HDL cholesterol have not been established as causative of this relationship or with the development of atherosclerosis [49].

Elevated triglyceride levels are associated with and appear to be implicated in the pathogenesis of atherosclerosis and CVD. Several studies have shown a positive relationship between hypertriglyceridemia and atherosclerotic cases in contrast to our finding [50-53]. So, elevated triglyceride levels are independently associated with increased risk of CVD events [54,55]. In two large prospective studies, the combined adjusted odds ratio was 1.7 for CHD comparing individuals in the top third of serum triglyceride levels with those in the bottom third [56]. In a study of 14,000 untreated males, aged 26 to 45 years who had serum triglycerides measured five years ago, triglycerides at first measurement were strongly and independently associated with CHD risk when comparing those in the highest level with those in the lowest [57]. Hypertriglyceridemia is associated with increased mortality in patients with known CHD as indicated in two different studies [58,59]. Other two large studies found that increased non-fasting triglyceride levels are associated with an increased risk for ischemic stroke [60,61].

From the above, we find that the risk factors associated with CVDs are many and vary between societies, origins and different nationalities, as the results of our research showed, in addition to many previous international researches.

Conclusion

The study provides essential epidemiological data required by decision makers. Although not nationally representative, this study is suggestive of a higher risk of cardiovascular diseases occurring among an older population, men and in Northern African, Western Asian and Southern Asian nationalities, as well as having high blood pressure, insulin resistance and low serum HDL. More studies are needed to establish which public health interventions are likely to be effective in Qatar. Currently, efforts should be contextualized and should target the key epidemiological features.

Acknowledgement

The authors thank all members of the Electronic Medical Records system in the Primary Health Care Corporation provided us with the data required for this research. The authors also thank Dr. Hanan Al Mujalli; the executive director of Clinical Affairs Directorate for her continuous support and care.


Components

NCEP ATP III definition

Study definition

Rationale

Insulin resistance

Fasting blood sugar (FBS) over 100 mg/dl.

·        Insulin Resistance (Serum Fasting Glucose>=100 mg/dl or HbA1c>=5.56) or

·        A diagnosis of T2DM

           HbA1c is an important marker and enhances the detection of hyperglycaemia for the diagnosis for MetS [15-18]

High Blood Pressure

Blood pressure over 130/85 mmHg

·         Blood pressure over 130/85 mmHg or

 

·         A diagnosis of hypertension

Same definition used

Obesity

Waist circumference over 40 inches (men) or 35 inches (women)

·    Waist circumference over 102              centimetres (men) and 94                  centimetres (women) 

·         or

·   Body Mass Index (BMI) >=30             kg/m2)

·         Waist circumference are specific for each population therefore waist circumference for the Qatari population was used from a published study [19]

·         BMI value was shown by International Diabetes Federation to be a specific enough criterion to represent central obesity without the need for waist circumference measurements

High serum triglycerides

Fasting triglyceride level over 150 mg/dl

Fasting triglyceride level over 150 mg/dl

Same definition used

Low serum HDL

Fasting high-density lipoprotein (HDL) cholesterol level less than 40 mg/dl (men) or 50 mg/dl (women)

Fasting high-density lipoprotein (HDL) cholesterol level less than 40 mg/dl (men) or 50 mg/dl (women)

Same definition used

    
Table 1: Metabolic Syndrome component definitions.

Explanatory variables

Total

No.

Cardiovascular diseases

Odds ratio

95% CI OR

P

No.

%

Age group (years)

 

18-39

44576

509

1.1

Ref

40-59

60598

2313

3.8

3.4

(3.12 - 3.78)

<0.001

60+

22767

2635

11.6

11.3

(10.29 - 12.47)

<0.001

Total

127941

5457

4.3

 

 

 

Gender

 

Female

70853

2289

3.2

Ref

Male

57088

3168

5.5

1.8

(1.67 - 1.86)

<0.001

Nationality category

 

Others

9054

253

2.8

Ref

Qatar

45854

1722

3.8

1.4

(1.19 - 1.55)

<0.001

Northern Africa

21397

956

4.5

1.6

(1.41 - 1.87)

<0.001

Southern Asia

32205

1607

5

1.8

(1.6 - 2.09)

<0.001

Western Asia (excluding Qatar)

19431

919

4.7

1.7

(1.5 - 1.99)

<0.001

Obesity (BMI>=30 kg/m2 or central obesity)

 

Negative

64400

2406

3.7

Ref

Positive

63541

3051

4.8

1.3

(1.23 - 1.37)

<0.001

High Blood Pressure (Systolic or Diastolic) or hypertensive

 

Negative

60183

1058

1.8

Ref

Positive

67758

4399

6.5

3.9

(3.62 - 4.16)

<0.001

Low serum HDL (<1.04 mmol/L in male and <1.3 mm in female)

 

Negative

65899

2355

3.6

Ref

Positive

62042

3102

5

1.4

(1.34 - 1.5)

<0.001

High serum Triglycerides (>=1.7 mmol/L)

 

Negative

89568

3660

4.1

Ref

Positive

38373

1797

4.7

1.2

(1.09 - 1.22)

<0.001

Insulin Resistance (Serum Fasting Glucose>=100 mg/dl or HbA1c>=5.56) or DM

 

Negative

50841

986

1.9

Ref

Positive

77100

4471

5.8

3.1

(2.9 - 3.34)

<0.001

Metabolic Syndrome

 

Negative

65379

1644

2.5

Ref

Positive

62562

3813

6.1

2.5

(2.37 - 2.67)

<0.001

Count of positive criteria for Metabolic Syndrome

 

0

13471

179

1.3

Ref

1

22030

436

2

1.5

(1.26 - 1.78)

<0.001

2

29878

1029

3.4

2.6

(2.25 - 3.11)

<0.001

3

31830

1628

5.1

4.0

(3.43 - 4.67)

<0.001

4

22122

1483

6.7

5.3

(4.56 - 6.24)

<0.001

5

8610

702

8.2

6.6

(5.58 - 7.79)

<0.001

    
Table 2: The risk of having cardiovascular disease (Any cardiac disease including coronary, thrombotic/hemorrhagic and peripheral vascular diseases) by selected explanatory variables.

Explanatory variables

Adjusted OR

P

Age group (years)

 

 

40-59 years of age compared to '18-39 years of age'

2.42

<0.001

60+ years of age compared to '18-39 years of age'

6.65

<0.001

Male gender compared to female

1.36

<0.001

Nationality category

 

 

Qatar compared to 'Others'

1.15

0.045

Northern Africa compared to 'Others'

1.45

<0.001

Southern Asia compared to 'Others'

1.31

<0.001

Western Asia (excluding Qatar) compared to 'Others'

1.42

<0.001

Risk factors (Metabolic Syndrome elements)

 

 

Insulin Resistance (Serum Fasting Glucose>=100 mg/dl or HbA1c>=5.56) compared to those with no insulin resistance

1.31

<0.001

Being obese (BMI>=30 kg/m2 or central obesity) compared to non-obese

1.13

<0.001

Having a high Blood Pressure (Systolic or Diastolic) or hypertensive compared to those with normal Blood Pressure

1.83

<0.001

Having a low serum HDL (<1.04 mmol/L in male and <1.3 mm in female) compared to those with normal HDL

1.28

<0.001

Having a high serum Triglycerides (>=1.7 mmol/L) compared to those with normal triglycerides

0.86

<0.001

Constant

0.005

 

Count of positive criteria for Metabolic Syndrome

1.21

<0.001


Table 3: Multiple logistic regression model evaluating the independent association of selected risk factors with having cardiovascular diseases (Any cardiac disease including coronary, thrombotic / hemorrhagic and peripheral vascular diseases) as an outcome.

References

  1. Labarthe DR (2011) Epidemiology and Prevention of Cardiovascular Diseases: A Global Challenge. Second edition. Jones & Bartlett Publishers, USA.
  2. GBD 2017 DALYs and HALE Collaborators (2018) Global, regional, and national disability-adjusted life-years (DALYs) for 359 diseases and injuries and healthy life expectancy (HALE) for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet 392: 1859-1922.
  3. GBD 2017 Causes of Death Collaborators (2018) Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet 392: 1736-1788.
  4. Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, et al. (2004) Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 364: 937-952.
  5. Greenland P, Knoll MD, Stamler J, Neaton JD, Dyer AR, et al. (2003) Major risk factors as antecedents of fatal and nonfatal coronary heart disease events. JAMA 290: 891-897.
  6. Khot UN, Khot MB, Bajzer CT, Sapp SK, Ohman EM, et al. (2003) Prevalence of conventional risk factors in patients with coronary heart disease. JAMA 290: 898-904.
  7. Vasan RS, Sullivan LM, Wilson PW, Sempos CT, Sundstrom J, et al. (2005) Relative importance of borderline and elevated levels of coronary heart disease risk factors. Ann Intern Med 142: 393-402.
  8. Lloyd-Jones DM, Larson MG, Beiser A, Levy D (1999) Lifetime risk of developing coronary heart disease. Lancet 353: 89-92.
  9. Cooper R, Cutler J, Desvigne-Nickens P, Fortmann SP, Friedman L, et al. (2000) Trends and disparities in coronary heart disease, stroke, and other cardiovascular diseases in the United States: findings of the national conference on cardiovascular disease prevention. Circulation 102: 3137-3147.
  10. Benjamin EJ, Muntner P, Alonso A, Bittencourt MS, Callaway CW, et al. (2019) Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association. Circulation 139: e56-e528.
  11. Al-Kaabi SK, Atherton A (2015) Impact of noncommunicable diseases in the State of Qatar. Clinicoecon Outcomes Res 7: 377-385.
  12. Rizk NM, Yousef M (2012) Association of lipid profile and waist circumference as cardiovascular risk factors for overweight and obesity among school children in Qatar. Diabetes Metab Syndr Obes 5: 425-432.
  13. Chaikhouni A, Chouhan L, Pomposiello C, Banna A, Mahrous F, et al. (1993) Myocardial Infarction in Qatar: The First 2515 Patients. Clin Cardiol 16: 227-230.
  14. Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, et al. (2005) Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 112: 2735-2752.
  15. Osei K, Rhinesmith S, Gaillard T, Schuster D (2003) Is glycosylated hemoglobin A1c a surrogate for metabolic syndrome in nondiabetic, first-degree relatives of African-American patients with type 2 diabetes? J Clin Endocrinol Metab 88: 4596-4601.
  16. Ong KL, Tso AW, Lam KS, Cherny SS, Sham PC, et al. (2010) Using glycosylated hemoglobin to define the metabolic syndrome in United States adults. Diabetes care 33: 1856-1858.
  17. Lorenzo C, Wagenknecht LE, Hanley AJ, Rewers MJ, Karter AJ, et al. (2010) A1C between 5.7 and 6.4% as a marker for identifying pre-diabetes, insulin sensitivity and secretion, and cardiovascular risk factors: the Insulin Resistance Atherosclerosis Study (IRAS). Diabetes care 33: 2104-2109.
  18. Siu PM, Yuen QS (2014) Supplementary use of HbA1c as hyperglycemic criterion to detect metabolic syndrome. Diabetol Metab Syndr 6: 119.
  19. Al-Thani MH, Al-Thani AA, Cheema S, Sheikh J, Mamtani R, et al. (2016) Prevalence and determinants of metabolic syndrome in Qatar: results from a National Health Survey. BMJ Open 6: e009514.
  20. Patel SA, Winkel M, Ali MK, Narayan KM, Mehta NK (2015) Cardiovascular mortality associated with 5 leading risk factors: national and state preventable fractions estimated from survey data. Ann Intern Med 163: 245-253.
  21. Wilson PW, Bozeman SR, Burton TM, Hoaglin DC, Ben-Joseph R, et al. (2008) Prediction of first events of coronary heart disease and stroke with consideration of adiposity. Circulation 118: 124-130.
  22. Stamler J, Stamler R, Neaton JD, Wentworth D, Daviglus ML, et al. (1999) Low risk-factor profile and long-term cardiovascular and noncardiovascular mortality and life expectancy: findings for 5 large cohorts of young adult and middle-aged men and women. JAMA 282: 2012-2018.
  23. Uemura K, Pisa Z (1988) Trends in cardiovascular disease mortality in industrialized countries since 1950. World Health Stat Q 41: 155-178.
  24. Savji N, Rockman CB, Skolnick AH, Guo Y, Adelman MA, et al. (2013) Association between advanced age and vascular disease in different arterial territories: a population database of over 3.6 million subjects. J Am Coll Cardiol 61: 1736-1743.
  25. James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, et al. (2014) 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA 311: 507-520.
  26. Franklin SS, Larson MG, Khan SA, Wong ND, Leip EP, et al. (2001) Does the relation of blood pressure to coronary heart disease risk change with aging? The Framingham Heart Study. Circulation 103: 1245-1249.
  27. Tunstall-Pedoe H, Kuulasmaa K, Mahonen M, Tolonen H, Ruokokoski E, et al. (1999) Contribution of trends in survival and coronary-event rates to changes in coronary heart disease mortality: 10-year results from 37 WHO MONICA project populations. Monitoring trends and determinants in cardiovascular disease. Lancet 353: 1547-1557.
  28. D'Agostino RB Sr, Vasan RS, Pencina MJ, Wolf PA, Cobain M, et al. (2008) General cardiovascular risk profile for use in primary care: the Framingham Heart Study. Circulation 117: 743-753.
  29. Kappert K, Bohm M, Schmieder R, Schumacher H, Teo K, et al. (2012) Impact of sex on cardiovascular outcome in patients at high cardiovascular risk: analysis of the Telmisartan Randomized Assessment Study in ACE-Intolerant Subjects With Cardiovascular Disease (TRANSCEND) and the Ongoing Telmisartan Alone and in Combination With Ramipril Global End Point Trial (ONTARGET). Circulation 126: 934-941.
  30. Berry JD, Dyer A, Cai X, Garside DB, Ning H, et al. (2012) Lifetime risks of cardiovascular disease. N Engl J Med 366: 321-329.
  31. Kannel WB, McGee DL (1979) Diabetes and cardiovascular disease. The Framingham study. JAMA 241: 2035-2038.
  32. Eckel RH, York DA, Rossner S, Hubbard V, Caterson I, et al. (2004) Prevention Conference VII: Obesity, a worldwide epidemic related to heart disease and stroke: executive summary. Circulation 110: 2968-2975.
  33. Calle EE, Thun MJ, Petrelli JM, Rodriguez C, Heath CW Jr. (1999) Body-mass index and mortality in a prospective cohort of U.S. adults. N Engl J Med 341: 1097-1105.
  34. Tirosh A, Shai I, Afek A, Dubnov-Raz G, Ayalon N, et al. (2011) Adolescent BMI trajectory and risk of diabetes versus coronary disease. N Engl J Med 364: 1315-1325.
  35. Rapsomaniki E, Timmis A, George J, Pujades-Rodriguez M, Shah AD, et al. (2014) Blood pressure and incidence of twelve cardiovascular diseases: lifetime risks, healthy life-years lost, and age-specific associations in 1.25 million people. Lancet 383: 1899-1911.
  36. Lawes CM, Rodgers A, Bennett DA, Parag V, Suh I, et al. (2003) Blood pressure and cardiovascular disease in the Asia Pacific region. J Hypertens 21: 707-716.
  37. Miura K, Daviglus ML, Dyer AR, Liu K, Garside DB, et al. (2001) Relationship of blood pressure to 25-year mortality due to coronary heart disease, cardiovascular diseases, and all causes in young adult men: the Chicago Heart Association Detection Project in Industry. Arch Intern Med 161: 1501-1508.
  38. Lewington S, Clarke R, Qizilbash N, Peto R, Collins R (2002) Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet 360: 1903-1913.
  39. Roncaglioni MC, Santoro L, D'Avanzo B, Negri E, Nobili A, et al. (1992) Role of family history in patients with myocardial infarction. An Italian case-control study. GISSI-EFRIM Investigators. Circulation 85: 2065-2072.
  40. Genest JJ Jr, Martin-Munley SS, McNamara JR, Ordovas JM, Jenner J, et al. (1992) Familial lipoprotein disorders in patients with premature coronary artery disease. Circulation 85: 2025-2033.
  41. Shepherd J, Cobbe SM, Ford I, Isles CG, Lorimer AR, et al. (1995) Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. N Engl J Med 333: 1301-1307.
  42. Downs JR, Clearfield M, Weis S, Whitney E, Shapiro DR, et al. (1998) Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TexCAPS. Air Force/Texas Coronary Atherosclerosis Prevention Study. JAMA 279: 1615-1622.
  43. Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford JD, et al. (1996) The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators. N Engl J Med 335: 1001-1009.
  44. Huxley RR, Barzi F, Lam TH, Czernichow S, Fang X, et al. (2011) Isolated low levels of high-density lipoprotein cholesterol are associated with an increased risk of coronary heart disease: an individual participant data meta-analysis of 23 studies in the Asia-Pacific region. Circulation 124: 2056-2064.
  45. Bartlett J, Predazzi IM, Williams SM, Bush WS, Kim Y, et al. (2016) Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor? New Insights From the Framingham Offspring Study. Circ Cardiovasc Qual Outcomes 9: 206-212.
  46. Castelli WP (1983) Cardiovascular disease and multifactorial risk: challenge of the 1980s. Am Heart J 106: 1191-1200.
  47. Acharjee S, Boden WE, Hartigan PM, Teo KK, Maron DJ, et al. (2013) Low levels of high-density lipoprotein cholesterol and increased risk of cardiovascular events in stable ischemic heart disease patients: A post-hoc analysis from the COURAGE Trial (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation). J Am Coll Cardiol 62: 1826-1833.
  48. van de Woestijne AP, van der Graaf Y, Liem AH, Cramer MJ, Westerink J, et al. (2013) Low high-density lipoprotein cholesterol is not a risk factor for recurrent vascular events in patients with vascular disease on intensive lipid-lowering medication. J Am Coll Cardiol 62: 1834-1841.
  49. Rosenson RS (2016) The High-Density Lipoprotein Puzzle: Why Classic Epidemiology, Genetic Epidemiology, and Clinical Trials Conflict? Arterioscler Thromb Vasc Biol 36: 777-782.
  50. Ballantyne CM, Grundy SM, Oberman A, Kreisberg RA, Havel RJ, et al. (2000) Hyperlipidemia: diagnostic and therapeutic perspectives. J Clin Endocrinol Metab 85: 2089-2112.
  51. Hodis HN, Mack WJ (1995) Triglyceride-rich lipoproteins and the progression of coronary artery disease. Curr Opin Lipidol 6: 209-214.
  52. Mack WJ, Krauss RM, Hodis HN (1996) Lipoprotein subclasses in the Monitored Atherosclerosis Regression Study (MARS). Treatment effects and relation to coronary angiographic progression. Arterioscler Thromb Vasc Biol 16: 697-704.
  53. Hodis HN, Mack WJ, Dunn M, Liu C, Liu C, et al. (1997) Intermediate-density lipoproteins and progression of carotid arterial wall intima-media thickness. Circulation 95: 2022-2026.
  54. Thompson WG, Gau GT (2009) Hypertriglyceridemia and its pharmacologic treatment among US adults--invited commentary. Arch Intern Med 169: 578-579.
  55. Rosenson RS, Davidson MH, Hirsh BJ, Kathiresan S, Gaudet D (2014) Genetics and causality of triglyceride-rich lipoproteins in atherosclerotic cardiovascular disease. J Am Coll Cardiol 64: 2525-2540.
  56. Sarwar N, Danesh J, Eiriksdottir G, Sigurdsson G, Wareham N, et al. (2007) Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies. Circulation 115: 450-458.
  57. Tirosh A, Rudich A, Shochat T, Tekes-Manova D, Israeli E, et al. (2007) Changes in triglyceride levels and risk for coronary heart disease in young men. Ann Intern Med 147: 377-385.
  58. Haim M, Benderly M, Brunner D, Behar S, Graff E, et al. (1999) Elevated serum triglyceride levels and long-term mortality in patients with coronary heart disease: the Bezafibrate Infarction Prevention (BIP) Registry. Circulation 100: 475-482.
  59. Sprecher DL, Pearce GL, Cosgrove DM, Lytle BW, Loop FD, et al. (2000) Relation of serum triglyceride levels to survival after coronary artery bypass grafting. Am J Cardiol 86: 285-288.
  60. Bansal S, Buring JE, Rifai N, Mora S, Sacks FM, et al. (2007) Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA 298: 309-316.
  61. Freiberg JJ, Tybjaerg-Hansen A, Jensen JS, Nordestgaard BG (2008) Nonfasting triglycerides and risk of ischemic stroke in the general population. JAMA 300: 2142-2152.

Citation: Zainel AA, Al Nuaimi AS, Syed MA, A/Qotba HA (2020) Risk Factors Associated with Cardiovascular Diseases among Adults Attending the Primary Health Care Centers in Qatar, a Cross-Sectional Study. J Community Med Public Health 4: 171. DOI: 10.29011/2577-2228.100071

free instagram followers instagram takipçi hilesi