• Users Online: 291
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 9  |  Issue : 3  |  Page : 102-106

Coronary artery disease among young drivers (<40 years): Occupational hazard or air pollution driving it?


1 Department of Cardiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bengaluru, Karnataka, India
2 Department of Cardiology, Vijan Hospital, Nashik, Maharashtra, India

Date of Submission25-May-2020
Date of Acceptance21-Jul-2020
Date of Web Publication26-Sep-2020

Correspondence Address:
Dr. Laxmi H Shetty
Department of Cardiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bengaluru, Karnataka
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JCPC.JCPC_35_20

Rights and Permissions
  Abstract 


Aims: To study clinico-social, biochemical and angiographic profile of patients presenting with premature coronary artery disease (PCAD) who are drivers by profession. To highlight the impact of occupational hazard and air pollution in them. Subjects and Methods: Of 3450 patients registered in the PCAD registry till date, 755 (21.88%) were found to satisfy the inclusion criteria. The data was analyzed by statistical software R version 3.5.0. Further analysis of smokers versus nonsmokers was done. Results: The average age of the group was 33.10 years. Almost all 754 (99.8%) were males, of which 323 (42.78%) smoked. The group had 83 (10.95%) diabetics and 71 (9.4%) hypertensives. Around 99 (13.11%) had a family history of coronary artery disease (CAD). Majority of them, 440 (58.27%), were urban drivers with average driving of 10 h/day. In the group, 482 (63.8%) had abnormal body mass index (BMI) and 539 (71.41%) had abdominal obesity. Low HDL was seen in 508 (67%) patients. ST-elevation myocardial infarction was the most common presentation in 415 (54.96%). Obstructive atherosclerotic CAD was seen in 217 (34.22%). Further analysis of smokers versus nonsmokers showed that hypertension, diabetes, and abnormal BMI were less common among nonsmokers, indicating the probable role of air pollution in them. Conclusions: Occupational hazard due to the stress related to prolonged driving hours, obesity, smoking and the possible role of air pollution are the important cardiovascular (CV) risks which come to light in this group of patients. Furthermore, the majority of them presented with predominant thrombotic lesions, however, smokers, who also had other CV risk factors, presented more often with obstructive atherosclerotic CAD.

Keywords: Air pollution, driver, occupation and heart disease, premature coronary artery disease, prospective observational study


How to cite this article:
Patil RS, Shetty LH, Vijan V, Cheekatla LN, Thomas TJ, Singh H, Raghu T R, Manjunath C N. Coronary artery disease among young drivers (<40 years): Occupational hazard or air pollution driving it?. J Clin Prev Cardiol 2020;9:102-6

How to cite this URL:
Patil RS, Shetty LH, Vijan V, Cheekatla LN, Thomas TJ, Singh H, Raghu T R, Manjunath C N. Coronary artery disease among young drivers (<40 years): Occupational hazard or air pollution driving it?. J Clin Prev Cardiol [serial online] 2020 [cited 2020 Oct 30];9:102-6. Available from: https://www.jcpconline.org/text.asp?2020/9/3/102/296185




  Introduction Top


Premature coronary artery disease (PCAD) by definition occurs at a younger age (before the age of 55 years in men and 65 years in women).[1] In its severe form, PCAD occurs below the age of 40 years.[2]

Atherosclerosis is a chronic inflammatory condition that starts from young age itself.[3] Studies have shown that atherosclerotic plaques or their precursors could be seen even in children younger than 10 years.[4] During later life, the effects of a sedentary lifestyle, coupled with unhealthy nutrition, smoking, alcohol consumption, obesity, and family history of cardiovascular (CV) disease, accelerates atherosclerotic disease.[4] Recently, air pollution is also emerging as a major CV risk factor.[5],[6]

There are two important aspects to be considered among drivers. First, the occupational hazard associated with long and irregular driving hours and second the impact of air pollution over and above the conventional CV risks in them.

Occupational hazard

Drivers are commonly exposed to many unhealthy working conditions such as long hours, irregular shift work, sleep disturbances, stressful conditions, and harmful exposures to environmental pollution.[7],[8],[9],[10],[11] Furthermore, prolonged sitting and physical inactivity can lead to the development of hypertension, diabetes mellitus, and obesity.[12],[13],[14],[15] Drivers are classified as a high-risk group for work-related stress.[16] Many studies have recently confirmed certain relationships between occupational stress, hypertension, and heart diseases.[17],[18]

Air pollution

Recently, many epidemiological and clinical studies have increasingly shown that air pollution is associated with an increased CV disease risk.[6],[19] The most important link between air pollution and heart disease is the particulate matter (PM). The constituents of air pollution are PM PM 2.5 and PM 0.1 particles with aerodynamic diameters (Ads) <2.5 and <0.1 μm, respectively. These penetrate the alveolocapillary membrane of the lung and enter the bloodstream.[20],[21] There they can cause an increase in heart rate, blood pressure, fibrinogen, and blood coagulation factors. They also increase inflammatory mediators like C-reactive protein) and decrease the heart rate variability, which in turn causes myocardial ischemia, malignant ventricular arrhythmias, increased acute clot formation triggering acute coronary syndromes.[20],[21] Furthermore, long-term exposure to environmental pollutants increases the probability to develop atherosclerosis and ischemic heart disease.[10],[11],[22]

There are several studies highlighting the CV risk, occupational stress, and air pollution in drivers. However, there is a paucity of data on drivers presenting with PCAD. What drives it, is it only occupational stress? and or air pollution? needs to be answered. Identifying the high-risk factors among occupational drivers is very important for the early detection and prevention of CV diseases, more so PCAD. Hence, the study is an attempt to answer some of these questions and bring forward the risk factors favoring occupational stress and air pollution.

Settings and design

PCAD Registry is a Prospective ongoing descriptive observational study in Indian populations <40 years of age with Coronary Artery Disease (CAD). It was started on April 1, 2017.


  Subjects And Methods Top


The PCAD registry is a prospective multisite descriptive observational study examining a cohort of young Indian adults aged ≤40 years with CAD, from the point of index admission to a period of 5 years. This is registered under the Clinical Trials Registry of India (CTRI/2018/03/012544).

This registry included all patients with index admission for ischemic heart disease, as proven by:

  1. Documented episode of the acute coronary syndrome and
  2. Chronic stable angina with documented evidence of CAD. Patients with:


    1. with myocarditis, cardiomyopathies, and pulmonary embolism
    2. previously diagnosed cases of CAD or on medications such as antiplatelets and statins; and
    3. with chronic kidney disease, liver failure, and steroids were excluded from the study.


Once admitted into the hospital, patients who satisfied the entry criteria for the age group and occupation were selected. Demographic factors such as age, gender, address, socioeconomic factors such as income, marital history, religion were noted. Risk factor profiles such as the presence of smoking, diabetes, hypertension, physical activity, family history of CAD, and average hours of driving were all recorded. Clinical presentation to hospital, the primary method of management (thrombolysis in STEMI patients), course in hospital, and echo on admission were also documented. Total cholesterol and triglycerides (TGs) were estimated using commercially available kits (Accurex Biomedical Pvt. Ltd., Mumbai, Maharashtra, India). Measurement of direct Low-Density Lipoprotein-cholesterol (LDL-C) was done by enzymatic homogeneous colorimetric assay using Cobas Gen3. C502 analyzer.

Body mass was measured using a portable electronic scale to the nearest 0.1 kg. Height was measured to the nearest 0.1 cm using a portable wall-mounted stadiometer. Waist (just above the iliac crest) and hip (the widest part of the hips at the middle of the pelvis) circumferences were measured to the nearest 0.1 cm. Body mass index (BMI) was calculated as body weight (kg) divided by height squared (m). Coronary angiographic profile and mode of intervention (if any) were all documented.

Statistical methods

The qualitative data were summarized by count and percentage, while quantitative data were tabulated by descriptive statistics such as mean, median, standard deviation, interquartile range, minimum, and maximum. The data were analyzed using R statistical analysis and computing language version 3.5.1 (R core team, 2018), which is released under the GNU General Public License, version 2, published by the Free Software Foundation. The “P” value was derived by Chi-square calculator with Yates correction and value of <0.001 was considered statistically significant.


  Results Top


The PCAD registry has 3450 patients so far, of which 755 (21.88%) were drivers by profession and hence included in the analysis.

Demographic characteristics

The average age of the group was 33.10 years Of which 294 (38.94%) were aged 36–40 years, 275 (36.4%) were aged 31–35 years, 149 (19.7%) were aged 26–30 years and only 37 (4.9%) were below 25 years [Figure 1].
Figure 1: Age distribution of patients in the study

Click here to view


Almost all 754 (99.8%) were males, of which 323 (42.78%) smoked. The group had 83 (10.95%) diabetics and 71 (9.4%) hypertensives. Around 99 (13.11%) had a family history of CAD. The majority of them 440 (58.27%) were urban drivers (Bangalore city) with average driving of 10 h/day. The group had 25 (3.31%) graduates, 90 (11.9%) were educated up to 12th STD, 288 (38.14%) up to 10 STD, and 34 (4.5%) of them did not receive any formal education. The group had 647 (85.69%) Hindus. Only 30 (3.97%) patients were vegetarians.

Risk factor characteristics

Physical parameters showed that 254 patients (33.66%) had normal BMI, whereas 228 patients (30.19%) had high BMI (181 overweight, 47 obese), 254 patients (33.75%) were overweight according to the revised BMI classification for South Asian Indians. Going by waist-hip ratio definition, 539 patients (71.41%) had abdominal obesity [Table 1]. Almost all reported a sedentary lifestyle. Mean total cholesterol of the entire study population was 166.956 ± 47.11, LDL was 117.75 ± 84.81 mg/dl, HDL was 32.376 ± 9.64, TG was 194.166 ± 87.11. Among lipid parameters, 49 (6.4%) had high total cholesterol, 508 (67%) had low HDL, 88 (11.65%) had high LDL cholesterol, and 222 patients (29.4%) had high triglycerides [Figure 2].
Table 1: Risk factor profile of patients

Click here to view
Figure 2: Distribution of conventional lipid parameters in the study group. HDL: High Density Lipoprotein, LDL: Low Density Lipoprotein

Click here to view


Clinical and angiographic characteristics

ST-elevation myocardial infarction (STEMI) was the most common presentation in 415 (54.96%) patients and unstable angina/Non-ST elevation myocardial infarction (MI) was seen in 102 patients (13.50%). Furthermore, 195 patients (25.82%) had a delayed STEMI presentation (Evolved MI), 19 patients (2.51%) had spontaneous resolution of MI, and 6 (0.8%) patients presented with chronic stable angina.

In the group, 634 of 755 (83.9%) patients underwent coronary angiogram. Of which 257 (40.54%) patients had recanalized coronaries, 217 (34.22%) had obstructive CAD, 93 (14.67%) had nonobstructive CAD, 43 (6.78%) had thrombotic lesions, and 24 patients (3.78%) had normal coronaries. Left ventricular (LV) ejection fraction showed normal systolic function (>55%) in 333 patients (44.10%), mild LV systolic dysfunction (45%–54%) in 200 (26.5%) patients, moderate LV dysfunction (30%–45%) in 130 (17.2%) patients, while it was severe LV dysfunction (<30%) in 92 (11.92%) patients.

Of 755 (66.88%) patients, 505 were continued on optimal medical therapy, 217 (28.71%) patients underwent revascularization (211 PTCA, 6 CABG). Twenty-eight (3.71%) patients received triple antithrombotic therapy for predominant thrombotic lesions and were advised to repeat angiogram on follow-up. Eight (1.05%) patients underwent intracoronary thrombolysis with tenecteplase/urokinase. Among the group, 12 patients went into cardiogenic shock due to severe pump failure and died.

Further analysis of smokers versus non-smokers showed that a history of diabetes hypertension, abnormal BMI, and the presence of atherosclerotic obstructive CAD was statistically significant (P < 0.001) in smokers [Table 2]. P < 0.001 was considered significant.
Table 2: Subgroup analysis of smokers versus nonsmokers

Click here to view



  Discussion Top


There are two important aspects to be considered among drivers. One is the occupational hazard and second, the impact of air pollution over and above the conventional CV risks.

Evidence for occupational hazard

Drivers are commonly exposed to many unhealthy working conditions such as long working hours, irregular shift work times, sleep disturbances, and stressful conditions.[7],[8],[9],[10],[11] They are classified as a high-risk group for work-related stress.[16] Many studies have confirmed links between occupational stress, hypertension, and heart diseases.[17],[18] Most patients in our group reported occupational stress, with average driving hours of 10 h per day, which was more than the usual prescribed by International Labour organization in their Hours of Work and Rest Periods (Road Transport) Recommendation, 1979 and also the Motor transport workers act of 1961 of the Indian government.[23] Furthermore, prolonged sitting and physical inactivity can cause hypertension, diabetes mellitus, dyslipidemia, and obesity.[12],[13],[14],[15] An abnormal BMI was noted in 63.8% of patients and almost 71.4% satisfied the criteria for abdominal obesity. Almost all the patients reported a sedentary lifestyle. The predominant form of dyslipidemia observed was low HDL cholesterol in 67% and high triglycerides in 29.4%, which is more common in the population presenting with PCAD more so, Indians with the exception of LDL which was increased only in 11.6% in our group.[24],[25]

Evidence for air pollution

Drivers also face harmful exposure to environmental pollution.[10],[11] Several studies have shown that high concentrations of fine PM and traffic-related air pollution in metropolitan cities are associated with hypertension, diabetes, and acceleration of atherosclerosis, which predispose to CV diseases.[10],[26],[27],[28],[29]

We further classified the study group into smokers and nonsmokers. It is well known that smoking is a major CV risk factor for CAD in the young, more so in Indians, and was also seen in 42.7% of patients in our group.[30],[31] We hypothesized that this classification would neutralize the effect of smoking and help in the analysis of data pertaining only to air pollution in the nonsmoker group. The other conventional risk factors such as diabetes, hypertension, obesity, dyslipidemia and family history of CAD were compared between these two groups. The presence of hypertension, diabetes, and abnormal BMI was statistically significant (P < 0.001) among smokers, indicating that air pollution was probably the major underlying risk factor in nonsmokers. Family history of CAD and Low HDL levels were equally comparable in both groups, with air pollution acting as an additional driver over and above the conventional risk factors. Some authors noted that even short-term exposure to PM 2.5 may trigger acute coronary events such as STEMI but not non-STEMI.[32],[33],[34] Similar observations were noted in our group where presentation to hospital as STEMI or evolved MI (delayed presentation of STEMI) was seen in 80.7%, and was also statistically significant in the nonsmoker group. Only 13.5% presented with non-STEMI/UA. A small number of patients presented with chronic stable angina (0.8%).

In the group, 40.5% had recanalized coronaries (post thrombolysis), 6.7% had thrombotic lesions indicating an overall hypercoagulable state due to smoking and air pollution. However, atherosclerotic obstructive CAD was seen in 34.2% and was statistically significant in the smoker's group. This observation could be because the smokers subgroup had more conventional risk factors. Most patients (70.5%) had either normal or mild LV dysfunction at discharge. Similar to other studies on patients with premature CAD.[35],[36]

Limitations of the study

  1. Actual occupational stress assessment using stress questionnaire was not done; however, the same was inferred from average hours of driving/day
  2. Number of years of driving was not documented
  3. The actual air pollution risk could not be ascertained directly; however, indirect evidence was obtained after excluding smokers by doing a subgroup analysis.



  Conclusion Top


Asian Indians have the highest risk of PCAD. A cause of concern in developing countries like India is the incomplete detection, treatment, and control of CAD risk factors. Adequate measures have to be taken by policymakers to reduce air pollution and its ill effects. Screening for CV risk factors and proper education of drivers regarding their occupational risks is important. Furthermore, to ensure strict enforcement of labor laws so that the work stress can be significantly reduced, thereby decreasing CV risk.

Acknowledgment

We would like to thank Research Coordinator, Mrs. Rani B J, and Research Assistant Mr. Prateesh, for technical help.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Farmer JA, Grotto AN. Dyslipidaemia and other risk factors for coronary artery disease. In: Braunwald E, editor. Braunwald's Heart Disease: A Text Book of Cardiovascular Disease. Vol. 5. Philadelphia: W.B. Saunders and Co.; 1997. p. 1126-60.  Back to cited text no. 1
    
2.
Bansal SK, Agarwal S, Daga MK. Advanced atherogenic index for the assessment of consolidated lipid risk in premature coronary artery disease patients in India. J Lab Physicians 2016;8:77-84.  Back to cited text no. 2
[PUBMED]  [Full text]  
3.
Mellies M, Glueck CJ. Lipids and the development of atherosclerosis in schoolchildren. J Paediatr Gastroenterol Nutr 1983;2:5298–03.  Back to cited text no. 3
    
4.
da Luz Giroldo M, Villela Baroncini LA, Champoski AF, Carla A, Biazon B, Isolane A, et al. Household cardiovascular screening in adolescents from high-risk families. Atherosclerosis 2013;226:286-90.  Back to cited text no. 4
    
5.
Franklin BA, Brook R, Pope CA III. Air pollution and cardiovascular disease. Curr Probl Cardiol 2015;40:207-38.  Back to cited text no. 5
    
6.
Brook RD, Rajagopalan S, Pope CA 3rd, Brook JR, Bhatnagar A, Diez-Roux AV, et al. Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation 2010;121:2331-78.  Back to cited text no. 6
    
7.
Bawa MS, Srivastav M. Study the epidemiological profile of taxi drivers in the background of occupational environment, stress and personality characteristics. Indian J Occup Environ Med 2013;17:108-13.  Back to cited text no. 7
[PUBMED]  [Full text]  
8.
Wu S, Deng F, Niu J, Huang Q, Liu Y, Guo X. Association of heart rate variability in taxi drivers with marked changes in particulate air pollution in Beijing in 2009. Environ Health Perspect 2008;118:87-91.  Back to cited text no. 8
    
9.
Kaushal K. Understanding epidemiological correlates: A comment on study the epidemiological profile of taxi drivers in the background of occupational environment, stress, and personality characteristics. Indian J Occup Environ Med 2014;18:36.  Back to cited text no. 9
[PUBMED]  [Full text]  
10.
Brucker N, Charão MF, Moro AM, Ferrari P, Bubols G, Sauer E, et al. Atherosclerotic process in taxi drivers occupationally exposed to air pollution and co-morbidities. Environ Res 2014;131:31-8.  Back to cited text no. 10
    
11.
Elshatarat RA, Burgel BJ. Cardiovascular risk factors of taxi drivers. J Urban Health 2016;93:589-606.  Back to cited text no. 11
    
12.
Apantaku-Onayemi F, Baldyga W, Amuwo S, Adefuye A, Mason T, Mitchell R, et al. Driving to better health: Cancer and cardiovascular risk assessment among taxi cab operators in Chicago. J Health Care Poor Underserved 2012;23:768-80.  Back to cited text no. 12
    
13.
Kurosaka K, Daida H, Muto T, Watanabe Y, Kawai S, Yamaguchi H. Characteristics of coronary heart disease in Japanese taxi drivers as determined by coronary angiographic analyses. Ind Health 2000;38:15-23.  Back to cited text no. 13
    
14.
Gany FM, Gill PP, Ahmed A, Acharya S, Leng J. Every disease…man can get can start in this cab”: Focus groups to identify south Asian taxi drivers' knowledge, attitudes and beliefs about cardiovascular disease and its risks. J Immigr Minor Health 2012;15:986-92.  Back to cited text no. 14
    
15.
Burgel BJ, Gillen M, White MC. Health and safety strategies of urban taxi drivers. J Urban Health 2012;89:717-22.  Back to cited text no. 15
    
16.
Kompier M. Bus Drivers: Occupational Stress and Stress Prevention. Geneva: International Labour Office; 1996. p. 5-8.  Back to cited text no. 16
    
17.
Cohen S, Janicki-Deverts D, Miller GE. Psychological stress and disease. JAMA 2007;298:1685-7.  Back to cited text no. 17
    
18.
Pickering TG, Devereux RB, James GD, Gerin W, Landsbergis P, Schnall PL, et al. Environmental influences on blood pressure and the role of job strain. J Hypertens Suppl 1996;14:S179-85.  Back to cited text no. 18
    
19.
Pope CA 3rd, Burnett RT, Thurston GD, Thun MJ, Calle EE, Krewski D, et al. Cardiovascular mortality and long-term exposure to particulate air pollution: Epidemiological evidence of general pathophysiological pathways of disease. Circulation 2004;109:71-7.  Back to cited text no. 19
    
20.
Pope III CA. Particulate air pollution, C-reactive protein, and cardiac risk. Europ Heart J 2001;22:1149-50.  Back to cited text no. 20
    
21.
Luttmann-Gibson H, Suh HH, Coull BA, Dockery DW, Sarnat SE, Schwartz J, et al. Systemic inflammation, heart rate variability and air pollution in a cohort of senior adults. Occup Environ Med 2010;67:625-30.  Back to cited text no. 21
    
22.
Kaufman JD. Prospective study of particulate air pollution exposures, subclinical atherosclerosis, and clinical cardiovascular disease: The multi-ethnic study of atherosclerosis and air pollution (MESA Air). Am J Epidemiol 2012;176:825-37.  Back to cited text no. 22
    
23.
The meeting of experts, the ILO Governing Body. Guidelines on the promotion of decent work and road safety in the transport sector. MERTS Rev 2019;9:1-53.  Back to cited text no. 23
    
24.
Goel PK, Bharti BB, Pandey CM, Singh U, Tewari S, Kapoor A, et al. A tertiary care hospital-based study of conventional risk factors including lipid profile in proven coronary artery disease. Indian Heart J 2003;55:234-40.  Back to cited text no. 24
    
25.
Mohan V, Deepa R, Rani SS, Premalatha G; Chennai Urban Population Study (CUPS No. 5). Prevalence of coronary artery disease and its relationship to lipids in a selected population in South India: The Chennai urban population study (CUPS no 5). J Am Coll Cardiol 2001;38:682-7.  Back to cited text no. 25
    
26.
Schwartz J. Particulate air pollution and daily mortality: A synthesis. Public Health Rev 1991;19:39-60.  Back to cited text no. 26
    
27.
Pope CA 3rd, Dockery DW. Epidemiology of particle effects. In: Holgate ST, Samet JM, Koren HS and Maynard RL, editors. Air Pollution and Health. San Diego, Calif: Academic Press; 1999. p. 673-705.  Back to cited text no. 27
    
28.
Schwartz J. Air pollution and hospital admissions for heart disease in eight U.S. counties. Epidemiology 1999;10:17-22.  Back to cited text no. 28
    
29.
Seaton A, MacNee W, Donaldson K, Godden D. Particulate air pollution and acute health effects. Lancet 1995;345:176-8.  Back to cited text no. 29
    
30.
Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. Lancet 2004;364:937-52.  Back to cited text no. 30
    
31.
Gupta R, Gupta VP, Prakash H, Sarna M, Sharma AK. Hindu-Muslim differences in the prevalence of coronary heart disease and risk factors. J Indian Med Assoc 2002;100:227-30.  Back to cited text no. 31
    
32.
Peters A, von Klot S, Heier M, Trentinaglia I, Cyrys J, Hörmann A, et al. Particulate air pollution and nonfatal cardiac events. Part I. Air pollution, personal activities, and onset of myocardial infarction in a case-crossover study. Res Rep Health Eff Inst 2005;124:1-66.  Back to cited text no. 32
    
33.
Mustafic H, Jabre P, Caussin C, Murad MH, Escolano S, Tafflet M, et al. Main air pollutants and myocardial infarction: A systematic review and meta-analysis. JAMA 2012;307:713-21.  Back to cited text no. 33
    
34.
Pope CA 3rd, Muhlestein JB, Anderson JL, Cannon JB, Hales NM, Meredith KG, et al. Short-term exposure to fine particulate matter air pollution is preferentially associated with the risk of st-segment elevation acute coronary events. J Am Heart Assoc 2015;4:1-10.  Back to cited text no. 34
    
35.
Cole JH, Miller JI 3rd, Sperling LS, Weintraub WS. Long-term follow-up of coronary artery disease presenting in young adults. J Am Coll Cardiol 2003;41:521-8.  Back to cited text no. 35
    
36.
Christus T, Shukkur AM, Rashdan I, Koshy T, Alanbaei M, Zubaid M, et al. Coronary artery disease in patients aged 35 or less – A different beast? Heart Views 2011;12:7-11.  Back to cited text no. 36
[PUBMED]  [Full text]  


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Subjects And Methods
Results
Discussion
Conclusion
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed158    
    Printed7    
    Emailed0    
    PDF Downloaded25    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]