Abstract
Background
The proportion of the mainland Chinese population with premature ST-segment elevation myocardial infarction is significantly elevated. Young patients with ST-segment elevation myocardial infarction have a different risk factor profile and clinical outcome compared with elder patients, and may also differ as compared to young patients in Western populations.
Methods
We analyzed a total of 9462 consecutive ST-segment elevation myocardial infarction patients, and recruited 341 consecutive cases who had survived their first ST-segment elevation myocardial infarction at the age less than 40 years, and followed-up these patients for 5 years.
Results
The most prevalent risk factor in young Chinese ST-segment elevation myocardial infarction patients was smoking (307/341, 90.03%) and male gender (328/341, 96.19%), although young patients had fewer traditional risk factors of acute myocardial infarction than the control group [(1.63 ± 1.03) vs. (2.38 ± 1.15), p < 0.01]. The number of affected vessels in cases was significantly less than in the elder control group (p < 0.01). During the follow-up, blood lipids and blood pressure of most patients reached the target level, while 42.10% of patients reported continuation of smoking. Multivariable data analysis showed that persistence of smoking (OR: 3.784, 95% CI: 1.636-8.751, p < 0.01) was the most significant prognostic factor of cardiac events after adjusting for various confounding factors.
Conclusions
We demonstrated that cigarette smoking is the most prevalent factor among the avoidable cardiovascular risk factors for young ST-segment elevation myocardial infarctions in China. Accordingly, continued smoking is the most powerful predictor for the recurrence of cardiac events in young Chinese patients with ST-segment elevation myocardial infarction.
Keywords: Premature myocardial infarction, Prognosis, Risk factor
INTRODUCTION
Young people represent a minority of patients who sustain acute myocardial infarction. It is estimated that less than 2% of all acute myocardial infarctions are patients under 40 years of age. In recent years, the proportion of premature acute myocardial infarction in our geographic area has gradually increased.1,2 Young Chinese patients with acute myocardial infarction have a different risk factor profile and long-term clinical outcome compared with young patients in Western society.3-6 However, there are conflicting data regarding the clinical profile and prognostic predictors of young Chinese survivors of acute myocardial infarction, especially for the Chinese Han population. The primary objective of this study was to explore the clinical profile and long-term prognostic factors of young Chinese patients who had survived their first ST-segment elevation myocardial infarction at ≤ 40 years of age, and provide evidence for the prevention of acute myocardial infarction in this young Chinese population.
METHODS
Study population
We analyzed a total of 341 consecutive young ST-segment elevation myocardial infarction patients (≤ 40 years) at our institute from January 2001 to January 2013. This study was conducted in accordance with the declaration of Helsinki, and with approval from the Ethics Committee of the Chinese People’s Liberation Army General Hospital. Written informed consent was obtained from all participants. A subset of 341 ST-segment elevation myocardial infarction patients (≥ 40 years) was chosen randomly as control group 1 to match the young ST-segment elevation myocardial infarction group; the matching factors included the year of hospital admission and whether occurrence of cardiogenic shock on admission. Additionally, we used the same method to randomly select another group of age-matched 341 patients (≤ 40 years) who were excluded the diagnosis of coronary artery disease (CAD) by coronary angiography as control group 2.
Clinical evaluation and treatment
Diagnosis of ST-segment elevation myocardial infarction was based on the concurrence of chest pain or symptoms compatible with acute heart failure or unexplained syncope and ST-segment elevation ≥ 1 mm in 2 inferior leads or ≥ 2 mm in 2 precordial leads. All patients with ST-segment elevation myocardial infarction received aspirin, clopidogrel, statin, subcutaneous low molecular weight heparin, β-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor blocker based on ST-segment elevation myocardial infarction guideline,7 unless there were apparent drug contraindications. All patients underwent coronary angiography [primary percutaneous coronary intervention (PCI) (78.89%) or delayed PCI (21.11%)] and left ventriculography. Coronary artery stenosis was defined as greater than 50% reduction in lumen diameter of any of the three coronary arteries or their primary branches. We provided a comparative analysis between young ST-segment elevation myocardial infarction patients and control patients by traditional Framingham risk factors and other clinical manifestations. We evaluated the presence of hypertension (defined according to the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure),8 hyperlipidaemia (defined according to the National Cholesterol Education Program Adult Treatment Panel III Guidelines),9 diabetes mellitus (defined according to the Guidelines of American Diabetes Association),10 smoking status (heavy smoker was defined as patients who smoked regularly at least twenty cigarettes per day for at least ten years, smoker was defined as patients who smoked regularly for at least six months) as conventional coronary risk factors.11 Peripheral blood samples were collected from patients within 12 h of admission.
Follow-up
Overall, 170 out of 341 young ST-segment elevation myocardial infarction patients agreed to be followed-up, and voluntarily signed the informed consent. Patients were followed-up for 5 years, and every patient was followed-up at one month intervals by trained cardiologists. All patients had been given the suggestion to undertake secondary prevention of ST-segment elevation myocardial infarction according to the guidelines7 in every follow-up. It was an observational research study, with the primary endpoints being cardiac death, readmissions for acute coronary syndrome and revascularization because of clinical deterioration. Events that occurred during their initial hospitalization were not included in primary endpoints. Persistent smokers were defined as patients who smoked before the onset of ST-segment elevation myocardial infarction and continued to smoke during follow-up regularly at least five cigarettes per day.
Statistical analysis
The means of normally distributed variables were compared using the Student’s t-test, and χ2 analysis was used for comparison of the distribution of risk factors between groups. Long-term prognostic predictors were calculated using multivariable logistic regression models. The Mann-Whitney U test was used for those with abnormal distribution. Additionally, Kaplan-Meier curves were used to show the prognosis of these young patients. Statistical analysis was performed using SPSS software (version 19.0 SPSS Inc, Chicago, IL, USA). Statistical significance was set at p < 0.05.
RESULTS
Baseline clinical characteristics
We analyzed a total of 9462 consecutive ST-segment elevation myocardial infarction patients at our institute from January 2001 to January 2013. A total of 341 young consecutive ST-segment elevation myocardial infarction patients (≤ 40 years) were enrolled in our study, accounting for 3.60% of all ST-segment elevation myocardial infarction patients. There has been a progressive increase in the incidence of ST-segment elevation myocardial infarction among younger patients in recent years: 2001 to 2003, 2.80% (41 of 1466); 2004 to 2006, 3.52% (69 of 1958); 2007 to 2009, 3.66% (90 of 2456); 2010 to 2012, 3.94% (141 of 3582) (Figure 1). There were 12 patients that died during the acute phase of ST-segment elevation myocardial infarction with in-hospital mortality of 3.53%, while the total in-hospital mortality was 6.16% in the control group. The baseline characteristics of young ST-segment elevation myocardial infarction patients and control cases of eldly patients are presented in Table 1 and Table 2. Compared with the control group (60.06 ± 13.12 years old), young patients with ST-segment elevation myocardial infarction had an average age of 36.34 ± 4.01 years, and male gender was more often present in the young ST-segment elevation myocardial infarction group than in the control group (94.72% vs. 83.87%, p < 0.01). Among the 341 young ST-segment elevation myocardial infarction patients, 117 (34.31%) patients had hypertension, 100 (29.32%) patients had hypercholesterolemia, 37 (10.85%) patients had diabetes mellitus. Furthermore, the most prevalent traditional risk factor was smoking (307/341, 90.03%). Young ST-segment elevation myocardial infarction patients were characterized by a higher proportion of heavy smoking and a lower proportion of metabolic disorder. Young patients with ST-segment elevation myocardial infarction had significantly fewer traditional risk factors of CAD than the control group [(1.63 ± 1.03) vs. (2.38 ± 1.15), p < 0.01]. The majority of young ST-segment elevation myocardial infarction patients (n = 178) had one-vessel disease, especially in the left anterior descending. The number of affected vessels in cases were significantly less than the control group (p < 0.01). Notably, coronary angiography after application of thrombus aspiration in primary PCI revealed “normal” in some young ST-segment elevation myocardial infarction patients (28/341, 8.21%). Additionally, “normal” lesion in primary PCI are rare in the elderly control group (7/341, 2.05%).
Figure 1.
Progressive rise in the incidence of young ST-segment elevation myocardial infarction patients over the years.
Table 1. Risk factors of CAD in young and elder ST-segment elevation myocardial infarction patients .
| Risk factors of coronary artery disease | Young cases (n = 341) | Control group 2 (n = 341) | Control group 1 (n = 341) |
| Sex (male/female) | 323/18*# | 176/165 | 286/55 |
| Age (years) | 34.34 ± 4.01* | 34.34 ± 4.01 | 60.06 ± 13.12 |
| Current Smoker [n (%)] | 307 (90.03)*# | 121 (35.48) | 201 (58.94) |
| Heavy Smoker [n (%)] | 252 (73.90)*# | 82 (24.05) | 178 (52.20) |
| Obese [n (%)] | 70 (20.53) | 79 (23.17) | 62 (18.18) |
| History of hypertension [n (%)] | 117 (34.31)*# | 55 (16.13) | 177 (51.91) |
| History of hypercholesterolemia [n (%)] | 100 (29.32) | 78 (22.87) | 113 (33.14) |
| History of diabetes mellitus [n (%)] | 37 (10.85) | 29 (8.50) | 84 (24.63) |
| Family history [n (%)] | 43 (12.61) | 30 (8.80) | 32 (9.38) |
| LDL-C (mmol/L) | 2.56 ± 0.94# | 2.27 ± 0.85 | 2.53 ± 0.94 |
| The number of Framingham CAD risk factors per patient | 1.63 ± 1.03*# | 1.15 ± 0.85 | 2.38 ± 1.15 |
| In-hospital mortality | 12 (3.53)*# | 0 (0) | 21 (6.16) |
* Different from control group 1 at p < 0.05; # Different from control group 2 at p < 0.05.
CAD, coronary artery disease; LDL-C, low-density lipoprotein cholesterol.
Table 2. Coronary angiographic result in young STEMI patients .
| Young STEMI patients (n = 341) | Control group 1 (n = 341) | |
| Culprit vessel | ||
| LM (%) | 3 (0.88) | 5 (1.47) |
| LAD (%) | 202 (59.24) | 197 (57.77) |
| LCX (%) | 72 (21.11) | 70 (20.52) |
| RCA (%) | 64 (18.77) | 69 (20.23) |
| Single vessel lesion (%) | 178 (52.20)* | 122 (35.78) |
| Double vessel lesion (%) | 81 (23.75) | 102(29.91) |
| Triple vessel lesion (%) | 82 (24.05)* | 117 (34.31) |
* Different from control group at p < 0.05.
LAD, left anterior descending; LCX, left circumflex; LM, left main coronary artery; RCA, right coronary artery; STEMI, ST-segment elevation myocardial infarction.
Predictors of cardiac events
During the follow-up, 6 patients were lost to follow-up due to several reasons (denied to participate, wrong addresses), and some patients who were admitted from 2009 to 2012 have not yet completed follow-up. Therefore, a total 170 survivors have completed 5 years of follow-up of young patients with first ST-segment elevation myocardial infarction, and 32 patients (18.82%) presented cardiac events during the follow-up period. There have been 21 patients (12.35%) who developed recurrent acute myocardial infarction and readmitted to hospital, and 11 (6.47%) patients had a revascularization procedure because of deterioration of the clinical syndrome of angina pectoris (six PCI and five coronary artery bypass grafting). Overall, there were 6 deaths with the mortality of 3.53% in five years, while mortality of eldly patients in control group was 11.45%.
The differences of clinical manifestations between the cardiac events group and the non-cardiac events group are shown in Table 3. The median time elapsing between patients discharge and occurrence of cardiac events was 2.8 years. Blood pressure, cholesterol and glucose were controlled well in more than 80% of young ST-segment elevation myocardial infarction patients, while 42.10% patients didn’t quit smoking although they were quite aware of its harmful effects. Consequently, patients with a cardiac event were more likely to be persistent smokers, compared with those without events (75.00% vs. 22.46%, p < 0.01). Hypertension was not controlled well in the cardiac events group. No differences were observed regarding the other risk factors and drug treatment during follow-up between the two groups. Furthermore, logestic regression analysis showed that persistence of smoking [odds ratio (OR): 3.784, 95% confidence interval (CI): 1.636-8.751, p < 0.01] was the most significant predictor of cardiac events during follow-up after adjusting for various confounding factors, which is shown in Table 4.
Table 3. Clinical characteristics of the study population according to the recurrence of cardiac events .
| Cardiac events | Yes (n = 32) | No (n = 138) |
| Males [n (%)] | 29 (90.62) | 133 (96.38) |
| Age (years) | 34.56 ± 4.59 | 34.51 ± 4.90 |
| Persistent smokers [n (%)] | 21 (65.62)* | 43 (31.16) |
| Hypertension [n (%)] | 11 (34.38) | 45 (32.61) |
| Blood pressure < 140/90 mmHg during the follow-up [n (%)] | 28 (87.50)* | 120 (86.95) |
| Hyperlipemia [n (%)] | 11 (34.38) | 32 (23.19) |
| LDL < 100 mg/dl during the follow-up [n (%)] | 26 (81.25) | 115 (83.33) |
| Diabetes mellitus [n (%)] | 5 (15.63) | 8 (5.79) |
| Glycated hemoglobin < 6% during the follow-up [n (%)] | 31 (96.88) | 135 (97.83) |
| Family history [n (%)] | 4 (12.50) | 15 (10.87) |
| Antiplatelet treatment [n (%)] | 32 (100) | 138 (100) |
| Statin [n (%)] | 32 (100) | 130 (94.20) |
| β-blockers [n (%)] | 30 (93.75) | 132 (95.65) |
| ACEI/ARB [n (%)] | 28 (87.50) | 116 (84.06) |
* Different from event-free group at p < 0.05.
ACEI/ARB, angiotensin converting enzyme inhibitor/angiotensin receptor blocker; LDL-C, low-density lipoprotein cholesterol.
Table 4. Relative risk for recurrent cardiac events during follow-up period in young survivors of ST-segment elevation myocardial infarction in logistic regression .
| Risk factors | OR | p value | 95% CI |
| Age at first event (years) | 0.971 | 0.532 | 0.884-1.066 |
| Males sex | 0.341 | 0.191 | 0.068-1.709 |
| Persistence of smoking | 3.784 | 0.002 | 1.636-8.751 |
| Hypercholesterolaemia | 1.092 | 0.847 | 0.446-2.676 |
| Hypertension | 1.565 | 0.355 | 0.605-4.046 |
| Diabetes | 2.440 | 0.174 | 0.673-8.845 |
CI, confidence interval; OR, odds ratio.
The relationship of smoke and recurrent cardiac events
A full 42.10% (64/152) of all smokers continued to smoke at follow-up and were smoking an average of 22.5 cigarettes per day. Follow-up data were available for 98% of patients. Patients who continued smoking had a greater probability of having events compared with those who quit smoking (p < 0.01). Use of Kaplan-Meier curves presents cardiac events curves in persistent smokers versus smokers who quit (Figure 2). The patients who continued smoking had 4.81 times higher risk of cardiac events (cardiovascular death, recurrent myocardial infarction, or emergency revascularization) than the control group.
Figure 2.
Kaplan-Meier curves of up to 5 years of follow-up for those young patients who continued smoking and those who quit smoking after first ST-segment elevation myocardial infarction.
DISCUSSION
Our study indicated that 3.60% of patients with ST-segment elevation myocardial infarction are under 40 years of age, and there has been an increasing incidence of ST-segment elevation myocardial infarction year after year. The incidence of young patients with acute myocardial infarction has increased by 40.7% compared with the ten years ago in our hospital. In fact, taken as a whole, the incidence of young acute myocardial infarction in China has increased progressively.1
Many young Chinese patients with ST-segment elevation myocardial infarction have identifiable risk factors that are different from those found in Western populations.12-14 Western young patients have a higher level of low-density lipoprotein cholesterol and triglyceride levels compared with Chinese patients.12 Non-HDL cholesterol is more strongly associated with premature CAD in Western young patient populations than in the Chinese population. Additionally, patients in Western societies were more likely to be obese,13 a characteristic more often present in Western patients than in Chinese patients. The frequency of risk factors in the young patients differs from those in their elder counterparts as well. Male sex and current smoking were more prevalent in young patients than in elder patients, and the young patients had a higher level of low-density lipoprotein cholesterol compared with their elder counterparts in our study, a result which is consistent with previous research in the West.14
What reason could explain this trend in young Chinese patients in the last 10 years? Smoking habit is the most prevalent risk factor in young ST-segment elevation myocardial infarction patients in our study. In fact, 90.03% of young ST-segment elevation myocardial infarction patients were smokers, while hypertension, diabetes, hyperlipidemia and obesity which are associated with metabolic disorder were obviously less prevalent in young ST-segment elevation myocardial infarction patients. Our research indicated that the average number of CAD risk factors was (1.63 ± 1.03) in young patients and (2.38 ± 1.15) in controls. The traditional Framingham risk score underestimates cardiovascular risk in the young acute myocardial infarction population.15 Furthermore, our research further suggests that cigarette smoking plays a more important role in the occurrence of ST-segment elevation myocardial infarction in young patients than in elderly patients. Active smoking and passive smoking promotes ST-segment elevation myocardial infarction through various pathophysiological mechanisms: it reduces the biosynthesis of nitric oxide, induces epicardial coronary endothelial dysfunction, causes inflammatory reaction and coronary spasm, releases catecholamines and increases thrombosis capacity.16 Severe endothelial dysfunction occurs in young Chinese acute ST-segment elevation myocardial infarction patients and correlates with TIMI score.17 Tobacco use is one of the most important causes of acute myocardial infarction globally, especially in young men.18 Genetic factors also contribute to the development of ST-segment elevation myocardial infarction in young patients,19-21 and smoking could further increase the risk of acute myocardial infarction related to gene variants.22 The tendency of ST-segment elevation myocardial infarction patients getting younger is accompanied by an increasing proportion of young smokers in China. Currently, the average age of first smoking has been decreasing, with an average age of 21. An estimated 72% of Chinese individuals over the age of 15 have been exposed to tobacco, including those exposed to second-hand smoke.23,24 There has been a significant surge in the number of young Chinese smokers in the last 20 years or thereabouts, which may contribute to the rise of youth ST-segment elevation myocardial infarctions.
The clinical manifestations in young ST-segment elevation myocardial infarction patients are also different from those found in elderly patients. Most young people do not experience a warning before onset, and the first attack often leads to large infarct size due to lack of coronary collateral circulation.25,26 Young ST-segment elevation myocardial infarction is characterized by a less diffuse atherosclerotic lesions, primarily due to the elevated presence of single-vessel disease (52.20% vs. 35.78%) and lower in-hospital mortality (3.53% vs. 6.16%) compared to elderly patients; these results are consistent with the previously reported literature.27
The prevalence of young ST-segment elevation myocardial infarction remains high, which is in part attributable to the high smoking rates found in the young population. Our research further showed that quitting smoking is the most important predictor of prognosis for ST-segment elevation myocardial infarction. Other studies have shown a 20-40% reduction in crude relative risk (RR) of cardiovascular events for patients with CAD who quit smoking compared with those who continue smoking.18,28 Our research indicated that quitting smoking reduced the recurrence of cardiovascular events for young ST-segment elevation myocardial infarction patients by as much as 75%. Unfortunately, although smoking was the most prevalent avoidable risk factor in our study, it was not well controlled, and actual cessation rates were only 58%. Smoking cessation improves endothelial function of acute myocardial infarction patients, and as little as two weeks of smoking cessation can ameliorate the enhanced platelet aggregability in long-term smokers, possibly by decreasing oxidative stress.29 These findings justify the need for an intense and aggressive strategy of smoking cessation for secondary prevention of premature ST-segment elevation myocardial infarction. Primary preventive measures intended to inhibit our youth from adopting tobacco use should be implemented na-tionally. The younger the ST-segment elevation myo-cardial infarction patients are, the more benefit they could obtain from smoking cessation.
Our study did have limitations. We collected data on 341 young ST-segment elevation myocardial infarction cases from a single center over a period of 12 years, and there may be associated selection bias. Some cases were lost in follow-up, and withdraw bias may be the primary limitation of our study. The patients who were lost during follow-up are typically poorly compliant; therefore, we may have underestimated the incidence of cardiac events as well as the role of smoking on recurrent cardiac events.
CONCLUSIONS
Our investigation demonstrated that cigarette smoking is the most prevalent factor among the avoidable cardiovascular risk factors for young ST-segment elevation myocardial infarction patients in China. Furthermore, persistence of smoking is the most powerful predictor for the recurrence of cardiac events in young Chinese patients with ST-segment elevation myocardial infarction. Smoking cessation is a manifestly important consideration to help prevent or reduce the prevalence of this disease in a young Han Chinese population.
Acknowledgments
First, I would like to show my deepest gratitude to my supervisor, Dr. Gai Luyue, an extremely responsible and resourceful professor, who has provided me with valuable guidance in every stage of clinical research. Second, I should extend my thanks to Dr. Li lu for assistance in English writing. This research received no specific grant from any funding agency, commercial or not-for-profit sectors.
CONFLICT OF INTEREST
The authors declare that they have no conflict of interest.
REFERENCES
- 1.Chen YL, Bhasin A, Youssef AA, et al. Prognostic factors and outcomes in young Chinese patients with acute myocardial infarction undergoing primary coronary angioplasty. Int Heart J. 2009;50:1–11. doi: 10.1536/ihj.50.1. [DOI] [PubMed] [Google Scholar]
- 2.Jinnouchi H, Sakakura K, Wada H, et al. Clinical features of myocardial infarction in young Japanese patients. Int Heart J. 2013;54:123–128. doi: 10.1536/ihj.54.123. [DOI] [PubMed] [Google Scholar]
- 3.Jamil G, Jamil M, Alkhazraji H, et al. Risk factor assessment of young patients with acute myocardial infarction. Am J Cardiovasc Dis. 2013;3:170–174. [PMC free article] [PubMed] [Google Scholar]
- 4.Incalcaterra E, Caruso M, Lo Presti R, Caimi G. Myocardial infarction in young adults: risk factors, clinical characteristics and prognosis according to our experience. Clin Ter. 2013;164:e77–e82. doi: 10.7417/CT.2013.1535. [DOI] [PubMed] [Google Scholar]
- 5.Bajaj S, Shamoon F, Gupta N, et al. Acute ST-segment elevation myocardial infarction in young adults: who is at risk? Coron Artery Dis. 2011;22:238–244. doi: 10.1097/MCA.0b013e3283452e7f. [DOI] [PubMed] [Google Scholar]
- 6.Iqbal MP, Mehboobali N, Tareen AK, et al. Association of body iron status with the risk of premature acute myocardial infarction in a Pakistani population. PLoS One. 2013;8:e67981. doi: 10.1371/journal.pone.0067981. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction; a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of patients with acute myocardial infarction) J Am Coll Cardio. 2004;44:E1–E211. doi: 10.1016/j.jacc.2004.07.014. [DOI] [PubMed] [Google Scholar]
- 8.Jones DW, Hall JE. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure and evidence from new hypertension trials. Hypertension. 2004;43:1–3. doi: 10.1161/01.HYP.0000110061.06674.ca. [DOI] [PubMed] [Google Scholar]
- 9.Grundy SM, Cleeman JI, Merz CN, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation. 2004;110:227–239. doi: 10.1161/01.CIR.0000133317.49796.0E. [DOI] [PubMed] [Google Scholar]
- 10.American Diabetes Association. Standards of medical care in diabetes-2013. Diabetes Care. 2013;36(Suppl 1):S11–S66. doi: 10.2337/dc13-S011. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Cesaroni G, Forastiere F, Agabiti N, et al. Effect of the Italian smoking ban on population rates of acute coronary events. Circulation. 2008;117:1183–1188. doi: 10.1161/CIRCULATIONAHA.107.729889. [DOI] [PubMed] [Google Scholar]
- 12.Goliasch G, Oravec S, Blessberger H, et al. Relative importance of different lipid risk factors for the development of myocardial infarction at a very young age (≤ 40 years of age) Eur J Clin Invest. 2012;42:631–636. doi: 10.1111/j.1365-2362.2011.02629.x. [DOI] [PubMed] [Google Scholar]
- 13.Chua SK, Hung HF, Shyu KG, et al. Acute ST-elevation myocardial infarction in young patients: 15 years of experience in a single center. Clin Cardiol. 2010;33:140–148. doi: 10.1002/clc.20718. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14.Huang J, Qian HY, Li ZZ, Zhang JM. Comparison of clinical features and outcomes of patients with acute myocardial infarction younger than 35 years with those older than 65 years. Am J Med Sci. 2013;346:52–55. doi: 10.1097/MAJ.0b013e318265e33e. [DOI] [PubMed] [Google Scholar]
- 15.Zarich S, Luciano C, Hulford J, Abdullah A. Prevalence of metabolic syndrome in young patients with acute MI: does the Framingham risk score underestimate cardiovascular risk in this population? Diab Vasc Dis Res. 2006;3:103–107. doi: 10.3132/dvdr.2006.012. [DOI] [PubMed] [Google Scholar]
- 16.Lavi S, Prasad A, Yang EH, et al. Smoking is associated with epicardial coronary endothelial dysfunction and elevated white blood cell count in patients with chest pain and early coronary artery disease. Circulation. 2007;115:2621–2627. doi: 10.1161/CIRCULATIONAHA.106.641654. [DOI] [PubMed] [Google Scholar]
- 17.Chen SM, Tsai TH, Hang CL, et al. Endothelial dysfunction in young patients with acute ST-elevation myocardial infarction. Heart Vessels. 2011;26:2–9. doi: 10.1007/s00380-010-0017-0. [DOI] [PubMed] [Google Scholar]
- 18.Teo KK, Ounpuu S, Hawken S, et al. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet. 2006;368:647–658. doi: 10.1016/S0140-6736(06)69249-0. [DOI] [PubMed] [Google Scholar]
- 19.Zintzaras E, Kitsios G. Identification of chromosomal regions linked to premature myocardial infarction: a meta-analysis of whole-genome searches. J Hum Genet. 2006;51:1015–1021. doi: 10.1007/s10038-006-0053-x. [DOI] [PubMed] [Google Scholar]
- 20.Rallidis LS, Gialeraki A, Merkouri E, et al. Reduced carriership of 4G allele of plasminogen activator inhibitor-1 4G/5G polymorphism in very young survivors of myocardial infarction. J Thromb Thrombolysis. 2010;29:497–502. doi: 10.1007/s11239-009-0398-z. [DOI] [PubMed] [Google Scholar]
- 21.Rallidis LS, Gialeraki A, Komporozos C, et al. Role of methyl-enetetrahydrofolate reductase 677C->T polymorphism in the development of premature myocardial infarction. Atherosclerosis. 2008;200:115–120. doi: 10.1016/j.atherosclerosis.2007.12.016. [DOI] [PubMed] [Google Scholar]
- 22.Liu PY, Li YH, Chao TH, et al. Synergistic effect of cytochrome P450 epoxygenase CYP2J2*7 polymorphism with smoking on the onset of premature myocardial infarction. Atherosclerosis. 2007;195:199–206. doi: 10.1016/j.atherosclerosis.2006.11.001. [DOI] [PubMed] [Google Scholar]
- 23.Zhang J, Ou JX, Bai CX. Tobacco smoking in China: prevalence, disease burden, challenges and future strategies. Respirology. 2011;16:1165–1172. doi: 10.1111/j.1440-1843.2011.02062.x. [DOI] [PubMed] [Google Scholar]
- 24.Troost JP, Barondess DA, Storr CL, et al. An updated global picture of cigarette smoking persistence among adults. J Epidemiol Glob Health. 2012;2:135–144. doi: 10.1016/j.jegh.2012.06.003. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25.D’Ascenzo F, Moretti C, Omedè P, et al. Cardiac remote ischaemic preconditioning reduces periprocedural myocardial infarction for patients undergoing percutaneous coronary interventions. EuroIntervention. 2014;9:1463–1471. doi: 10.4244/EIJV9I12A244. [DOI] [PubMed] [Google Scholar]
- 26.Jennings RB, Wagner GS. Roles of collateral arterial flow and ischemic preconditioning in protection of acutely ischemic myocardium. J Electrocardiol. 2014;47:491–499. doi: 10.1016/j.jelectrocard.2014.04.015. [DOI] [PubMed] [Google Scholar]
- 27.Pineda J, Marín F, Roldán V, et al. Premature myocardial infarction: clinical profile and angiographic findings. Int J Cardiol. 2008;126:127–129. doi: 10.1016/j.ijcard.2007.02.038. [DOI] [PubMed] [Google Scholar]
- 28.Critchley JA, Capewell S. Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. JAMA. 2003;290:86–97. doi: 10.1001/jama.290.1.86. [DOI] [PubMed] [Google Scholar]
- 29.Johnson HM, Gossett LK, Piper ME, et al. Effects of smoking and smoking cessation on endothelial function: 1-year outcomes from a randomized clinical trial. J Am Coll Cardiol. 2010;55:1988–1995. doi: 10.1016/j.jacc.2010.03.002. [DOI] [PMC free article] [PubMed] [Google Scholar]