|Year : 2014 | Volume
| Issue : 3 | Page : 70-75
Risk factors for acute myocardial infarction in coastal region of india: A case-control study
Vinay Rao1, Prasannalakshmi Rao2, Nikita Carvalho1
1 Department of Community Medicine, Father Muller Medical College, Mangalore, Karnataka, India
2 Department of Pharmacology, Father Muller Medical College, Mangalore, Karnataka, India
|Date of Web Publication||5-Sep-2014|
Department of Community Medicine, Father Muller Medical College, Mangalore - 575 003, Karnataka
Source of Support: None, Conflict of Interest: None
Background: Various studies have shown that people of Indian origin have an increased risk of ischemic heart disease (IHD) compared with most other ethnic groups. This increased risk has been attributed to multiple risk factors related to lifestyle. Patients and Methods: A total of 100 cases and 100 age and sex-matched controls were taken into this prospective case-control study from Intensive Coronary Care Unit. Prevalence of the following risk factors for myocardial infarction: Age, sex, diet, smoking, alcohol consumption, history of hypertension, history of diabetes mellitus, and lipid profile were studied. Patient data were extracted from the medical records department and by interview. Results: The most important predictor of acute myocardial infarction (AMI) was high low-density lipoprotein (adjusted odds ratio [OR]: 4.124, confidence interval [CI]: 1.44-11.73, P = 0.008) history of hypertension and of overt diabetes mellitus were also independent risk factors (OR: 2, CI: 1.4-3 and OR: 2.29, CI: 1.5-3.5), respectively. Low high-density lipoprotein was found to have no significant association with AMI. Heavy drinkers were found to have a high-risk (OR: 68), while moderate drinkers were found to have protection (OR: 1). Conclusion: Smoking and heavy drinking cessation, treatment of hypertension and reduction in blood glucose, correction of abnormal lipid profile either through use of statins or by dietary modification may be important in preventing IHD in Asian Indians.
Keywords: Acute myocardial infarction, coronary risk factors, smoking
|How to cite this article:|
Rao V, Rao P, Carvalho N. Risk factors for acute myocardial infarction in coastal region of india: A case-control study
. Heart India 2014;2:70-5
|How to cite this URL:|
Rao V, Rao P, Carvalho N. Risk factors for acute myocardial infarction in coastal region of india: A case-control study
. Heart India [serial online] 2014 [cited 2019 Jul 18];2:70-5. Available from: http://www.heartindia.net/text.asp?2014/2/3/70/140229
| Introduction|| |
The incidence of myocardial infarction (MI) in the world varies greatly. According to a Spanish study, the crude coronary heart disease (CHD) incidence rate was 300.6/100,000 person-years for men and 47.9/100,000 person-years for women.  The incidence of MI in India is 64.37/1000 people  in men aged 29-69 years, alcohol intake led to 30% lower CHD incidence.  Smoking is known to cause arterial thrombosis and MI, and is known to cause endothelial dysfunction.  More than 80% of the cases of cardiovascular disease are in developing countries however studies on risk factors are mostly conducted in developed countries.  Hence, it is important to carry out relevant studies in a developing country such as ours, in order to study the risk factors and their influence. The association between substance abuse and CHD has been widely studied. Many such studies have shown that moderate alcohol intake reduces the risk of CHD  and smoking increases it.  As not many studies have been done to show the incidence of substance abuse in patients with MI in this region, this study aims to elicit a history of substance abuse among patients with MI and correlate the two. Consumption of small to moderate amounts of alcohol (2 oz [59.2 ml] or less daily) is associated with lower incidence of coronary death.  This has been attributed to improved plasma lipid profiles, particularly an increase in high-density lipoprotein (HDL) cholesterol, increased adiponectin, reduced plasma fibrinogen, viscosity, platelet activity, C-reactive protein, and improved insulin sensitivity.  A negative association between alcohol consumption and a first MI in 464 patients was found in a study.  There was a larger proportion of people who did not consume alcohol among those who had an MI (P < 0.01) as well as a smaller proportion of moderate (two or less drinks per day) and heavy (three or more drinks per day) drinkers. According to the study, the lower consumption of alcohol by persons who subsequently had an MI was found to be related to ethnic origin, psychological traits or other unknown risk factors for MI. Furthermore, according to the study, alcohol consumption and cigarette smoking were habits that were found together often. The relative risk of MI increased with consumption of tobacco and was higher in inhalers than in non-inhalers.  In another American study, it was proved that cigarette smoking causes marked inhibition of substance P-induced tissue plasminogen activator release in vivo and this could provide the mechanism whereby endothelial dysfunction may increase the risk of atherothrombosis through a reduction in the acute fibrinolytic capacity.  South Asians have an increased risk of ischemic heart disease (IHD) compared with most other ethnic groups, including urban Indians, , which is due to various preexisting reasons leading to IHD. ,,,, Despite these studies, variables associated with IHD may differ among patients from different regions within India. Most studies study Indians who have migrated to other countries or those living in major cities within India. These studies may not reflect the true relation between risk factors of MI and their influence on population from smaller cities. This hospital-based case-control study of patients with a first MI in Mangalore, India, is primarily to assess the relative importance of the risk factors for IHD among dwellers of smaller cities and towns along the coastal belt of Karnataka.
| Patients and methods|| |
A total of 100 patients aged 30-85 years (both inclusive) admitted to the Intensive Coronary Care Unit of the Medical College Hospital with acute myocardial infarction (AMI) were taken as cases. AMI was defined as typical chest pain lasting minimum half an hour and an electrocardiogram (ECG) showing ST elevation of at least 2 mm in two or more contiguous leads with subsequent evolution of the ECG and diagnostic enzyme (creatine kinase-MB) changes. Patients were excluded if they had a history of preexisting cardiac illness.
A total of 100 controls were chosen from the other wards of the hospital, from those admitted for conditions that would not confound the results. Individuals with preexisting heart disease or AMI were excluded. Controls were matched to cases for age (within 5 years range) and sex.
Data were prospectively recorded by patient interview and from patient charts by the same research assistant each time. In all participants, age, sex, religion, details of diet, smoking, alcohol use, and known history of diabetes mellitus and hypertension were recorded. Fasting lipids (total, low-density lipoprotein [LDL] and HDL cholesterol, and triglycerides) were measured in all participants. Total cholesterol and triglycerides were estimated on an automated system with standard kits (Boehringer Manheim GmbH). Enzymic methods for cholesterol and triglycerides were used: Cholesterol oxidase/peroxidase-aminophenazone and glycerol phosphate oxidase/peroxidase-aminophenazone, respectively. HDL cholesterol was estimated with the precipitation method and glucose by the glucose oxidase method. Analyses were done on a Beckman Synchron CX4 random analyzer. LDL cholesterol was calculated as total cholesterol minus (HDL cholesterol + triglyceride/5). All biochemical analyses were done without the knowledge of clinical information.
Comparisons of mean or median values or prevalence of a risk factor were conducted after matching each case with the next control subject recruited of the same sex and age within 5 years. A comparison of discrete variables in cases and controls was done with logistic regression accounting for the matching of cases with controls. Estimates of relative risk and 95% confidence intervals (CIs) were also done. For continuous variables, unpaired t-test was done. Multivariate analyses were conducted with logistic regression methods on transformed values. The Statistical Package for Social Sciences version 16 IBM corporarion were used for analyses. P values were two-tailed. Collected data were analyzed by frequency, percentage, mean, standard deviation, and by odds ratio (OR) and its CI. An OR of 2 or more was taken as significant.
| Results|| |
In order to avoid a confounding bias, cases and controls were matched for age and sex (potential confounders in the study). Cases and controls were then selected based on the matched variables, such that both groups have a similar distribution in accordance with the variables. The demographic characteristics and lipid data of the 100 cases and 100 controls are shown in [Table 1] and [Table 2], respectively. Among all risk factors analyzed, smoking was the most important risk factor on comparison of lifestyle factors. About 61% of cases and 16% of controls had smoked or were current smokers of cigarettes (OR: 3.3, 95% CI: 2-5.1). A dose response effect is evident from [Table 3], where the higher numbers of heavy smokers (taken as more than 10 pack-years) were found among the cases (51%). On the other hand, among the controls only 12% were found to be heavy smokers. The higher number of nonsmokers was among controls (84%), whereas among cases this percentage was only 39%. On binary logistic regression [Table 4] too it was found that smoking was a significant risk factor (adjusted OR: 0.152, P = 0.001, CI: 0.72-0.321). About 52% of controls were drinkers compared to 29% of cases (OR: 2.65, CI: 1.47-4.7). This may suggest a protective effect of alcohol on the controls. On plain Chi-square analysis for alcohol exposure [Table 5], it was found that heavy drinkers had the highest risk, 17% of cases being heavy drinkers as opposed to none of the controls (OR: 68), followed by nondrinkers. It was found that a high number of cases (71%) were nondrinkers as compared with 48% of controls (OR: 6.41). Furthermore, all controls surveyed, were moderate drinkers (taken as <179 ml). This indicates a protective effect up to a moderate level of alcohol consumption and high-risk thereafter. In previous studies, vegetarianism has been shown to have a protective effect.  Among the cases in our study, 93% consumed a nonvegetarian diet as compared with the controls, where 20% of the controls surveyed were vegetarian (OR: 3.3). This indicates the significance of meat consumption as a risk factor in the incidence of MI. Diabetes is another independent risk factor in the study. About 67% of cases had higher fasting blood glucose (FBG) compared to 36% of controls (OR: 1.9, CI: 1.3-2.7). Cases had a mean FBG value of 175 mg/dl, while controls had a mean FBG value of 145 (t = 2.3, P = 0.022) from [Table 1]; however, a higher FBG value among cases may be attributed to a higher number of diabetics among the cases (47%) as compared with controls (17%) (OR: 2.29, CI: 1.5-3.5). Cases were also seen to have a longer duration of diabetes (mean value: 7.5 years) as compared with controls (mean value: 4.7 years) [Table 6]. More cases (52%) were found to be hypertensive that controls (22%). As with diabetes, here too the cases were seen to have a longer duration of hypertension as compared to the controls (mean value of 9.4 years vs. mean value of 6.4 years). On the comparison of lipid profiles among cases and controls, it was found that the HDL value was not a significant risk factor for IHD (OR: 1.29, CI: 0.98-1.7). However, high LDL values were found to be very significant with 68% cases having a high LDL value as opposed to 36% of controls (OR: 2.3, CI: 1.6-3.2). The mean value of LDL among cases was 151 mg/dl and among controls was 110 mg/dl (t-test 3.043, P < 0.003). The higher number of cases had high total cholesterol values (68%) as opposed to controls (35%) (OR: 1.9, CI: 1.4-2.6). Mean values too were higher among cases (222 mg/dl) than in controls (184 mg/dl) (t-test 4.006, P < 0.001). A higher triglyceride value was found among cases (152 mg/dl) than among controls (127 mg/dl) (t-test 2.75, P < 0.006). A binary logistic regression was done [Table 4]. The variables entered were heavy smoking, history of diabetes, history of hypertension, high cholesterol (>200), high LDL (>130), heavy consumption of alcohol (>180 ml). It was found that high LDL was the most significant risk factor (adjusted OR: 4.124, P = 0.008, CI: 1.44-11.73) followed by high consumption of alcohol (adjusted OR: 2.47, P = 0.14, CI: 1.205-5.06) heavy smoking proved to be an independent risk factor on regression analysis (adjusted OR 0.152, CI: 0.072-0.321, P = 0.001). Hypertension was an important risk factor for MI according to the analysis (adjusted OR: 0.274, CI: 0.132-0.572, P = 0.001). Conversely, a high value of cholesterol was found to be unrelated to MI (adjusted OR: 1.245, CI: 0.44-3.527, P = 0.68).
|Table 3: Comparison of cases with controls according to current smoking status|
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| Discussion|| |
Not many case-control studies have been done to identify the relation between risk factors and AMI in people living along the coastal belt of Karnataka, a South Indian state. This study, which is most likely the first to illustrate the relation, shows that tobacco smoking, a history of hypertension, history of diabetes, heavy consumption of alcohol, and a nonvegetarian diet are independent risk factors for AMI. Our study was conducted in a tertiary care hospital in Mangalore. All our cases are confirmed cases of AMI without any previous heart disease, thus ruling out any likelihood of modification of risk factors by treatment of IHD. As the data were extracted from patients belong to Mangalore and surrounding areas only, environmental factors, which are likely to contribute to the variation in arterial disease susceptibility, were assumed to be the same.
Studies conducted in developed countries have shown smoking of tobacco to be major risk factor for IHD.  Furthermore, in our country, the number of smokers is increasing versus a decrease in smokers in the western countries.  Though some studies have deliberated on the prevalence of coronary artery disease in Asian Indians, the importance of smoking as a risk factor has not been considered in them. , According to our analysis, smoking was found to be adversely related the incidence of AMI. Pais et al.  have shown a similar result in their study with respect to smoking as a risk factor. In addition, a study by McKeigue et al.  have reported a similar relation between smoking and IHD among South Asians residing in the UK. Our study signifies that cutting back on smoking could reduce the incidence of IHD in the population. At the very least, heavy smoking must be curtailed as it carries a relatively higher risk compared to moderate smoking.
A nonvegetarian diet was found to be associated with a higher incidence of AMI in our study, with a higher number of cases being meat eaters as compared to controls. This is in accordance with studies that indicate a relationship between consumption of meat and increased risk of MI.  Furthermore, the protective effect for vegetarians may be due to the fact that their diet is low in saturated fat and relatively high in unsaturated fats. 
Atherogenesis and thrombogenesis is also believed to be lower in vegetarians as their platelet phospholipid linoleate and antioxidant concentrations are higher, which is likely to lead to reduced oxidation of LDL.  From our study, it can be considered that following a nonvegetarian diet may lead to an increased risk of IHD and hence encouraging a vegetarian diet among Indians may help bring about a lower incidence of AMI.
Certain large studies such as The Framingham Heart study have revealed the importance of LDL and HDL cholesterol levels in determining risk for coronary artery disease, which in turn is a risk factor for MI. Some other studies too have underscored the importance of HDL cholesterol in predicting the risk of MI and demonstrated the protective effects of both the HDL 3 and HDL 2 subfractions of HDL cholesterol.  Indian populations in other countries have been shown to have lower HDL cholesterol and higher triglyceride concentrations. ,,,,, Our study showed both groups the study population to have a lower mean HDL value. That being said, low HDL was found to be a nonsignificant risk factor for MI in our study. This is concurrent with the results of the case-control study done by Pais et al. with regard to influence of HDL.  On the other hand, where their study shows not much difference between cases and controls in any of the other lipid variables as well, our study shows a high Triglyceride, high LDL and high total cholesterol level to be of significant influence in the development of IHD as seen among cases. This is comparable with other small studies from India, , which showed that total cholesterol and triglycerides were higher in individuals with IHD than in those without IHD. All our blood samples were taken within the first 24 h to rule out alteration in serum lipids due to AMI, which occurs after the first 48 h. , It has been shown that each 1 mmol/l (39 mg/dl) decrease in LDL cholesterol equates to a reduction in relative risk for stroke of 21.1% and that lowering of cholesterol concentrations with statins reduces the risk of stroke in high-risk populations and in patients with non-cardioembolic stroke or transient ischemic attack.  Univariate analysis from other case-control studies have indicated that MI cases had higher cholesterol level and were more likely to have a previous history of diabetes than controls.  Our study is in conformity with above findings from other studies and underlies the importance of stricter lipid control for prevention of IHD either through use of statins or diet control as appropriate.
Data from The Framingham Heart Study indicates a relation between glycosylated hemoglobin and IHD.  An increasing risk with increasing blood glucose concentrations has been observed in a previous study, which suggested that even high blood glucose within the euglycemic range identified individuals at higher risk of IHD.  FBG was higher in cases than in controls, in our study and this finding was significant. The increased risk of cardiovascular disease in type 2 diabetes is well-recognized  and is associated with both diabetes specific risk factors  and increased frequency of conventional risk factors for cardiovascular disease.  It has been suggested that the risk of death from CHD in patients with type 2 diabetes may even be as high as in patients who have had a MI.  In addition, a high prevalence of noninsulin dependent diabetes mellitus has been made known in Asians. ,, A history of diabetes mellitus was found to be a risk factor for AMI in our study. It was also seen that a longer duration of diabetes mellitus prevailed among the cases in comparison with the controls. This indicated a higher risk of IHD among long-standing diabetics. The above findings are in accord with studies suggesting diabetes as a risk factor for IHD. , A study of the relationship between alcohol consumption and nonfatal MI, involving 399 cases and 2486 reference subjects, indicated absence of any major overall association (rate ratio point estimate of 0.9 with 95% confidence limits of 0.6 and 1.2), but there was some evidence of a lower rate in subjects consuming six or more drinks per day (rate ratio point estimate of 0.6 with 95% confidence limits of 0.3 and 1.1).  In our study, the larger number of drinkers were found among the control group. This indicated a protective effect of alcohol against IHD. In spite of this, heavy drinking was seen exclusively in the cases, indicating heavy drinking (taken as more than 180 ml/day) to be a salient risk factor in the incidence of AMI. The inverse association between moderate alcohol intake and CHD is documented in over 40 prospective studies in diverse populations. ,,,, In our study, moderate drinkers were found to be the lowest risk category. This may partly be explained by a study  according to which, a polymorphism in the gene for alcohol dehydrogenase type 3 (ADH3) alters the rate of alcohol metabolism and hence moderate drinkers who are homozygous for the slow-oxidizing ADH3 allele have higher HDL levels and substantially decreased risk of MI. In a quantitative review, strong and consistent evidence was found linking moderate alcohol intake with higher concentrations of HDL cholesterol and apolipoprotein A-I and lower concentrations of fibrinogen.  Our results are in concurrence with studies that report a J-shaped curves, whereby light to moderate drinkers have less risk than abstainers, and heavy drinkers are at the highest risk.  Hypertension is known to induce endothelial dysfunction, exacerbate the atherosclerotic process and contribute to making the atherosclerotic plaque more unstable. Left ventricular hypertrophy, which is the usual complication of hypertension, promotes a decrease of "coronary reserve" and increases myocardial oxygen demand, both mechanisms contributing to myocardial ischemia.  Hypertension is also frequently associated to metabolic disorders, such as insulin resistance with hyperinsulinemia and dyslipidemia, which are additional risk factors of atherosclerosis.  More than half of the cases in our study had a history of hypertension and an average of 3 years longer duration than in controls. Treatment aimed at attaining optimal values of blood pressure may therefore be helpful.
| References|| |
|1.||Arriola L, Martinez-Camblor P, Larrañaga N, Basterretxea M, Amiano P, Moreno-Iribas C, et al. Alcohol intake and the risk of coronary heart disease in the Spanish EPIC cohort study. Heart 2010;96:124-30. |
|2.||Newby DE, Wright RA, Labinjoh C, Ludlam CA, Fox KA, Boon NA, et al. Endothelial dysfunction, impaired endogenous fibrinolysis, and cigarette smoking: A mechanism for arterial thrombosis and myocardial infarction. Circulation 1999;99:1411-5. |
|3.||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. |
|4.||Hennekens CH, Willett W, Rosner B, Cole DS, Mayrent SL. Effects of beer, wine, and liquor in coronary deaths. JAMA 1979;242:1973-4. |
|5.||Kabagambe EK, Baylin A, Ruiz-Narvaez E, Rimm EB, Campos H. Alcohol intake, drinking patterns, and risk of nonfatal acute myocardial infarction in Costa Rica. Am J Clin Nutr 2005;82:1336-45. |
|6.||Klatsky AL, Friedman GD, Siegelaub AB. Alcohol consumption before myocardial infarction. Results from the Kaiser-Permanente epidemiologic study of myocardial infarction. Ann Intern Med 1974;81:294-301. |
|7.||Prescott E, Hippe M, Schnohr P, Hein HO, Vestbo J. Smoking and risk of myocardial infarction in women and men: Longitudinal population study. BMJ 1998;316:1043-7. |
|8.||Sarvotham SG, Berry JN. Prevalence of coronary heart disease in an urban population in Northern India. Circulation 1968;37:939-53. |
|9.||Chadha SL, Radhakrishnan S, Ramachandran K, Kaul U, Gopinath N. Epidemiological study of coronary heart disease in urban population of Delhi. Indian J Med Res 1990;92:424-30. |
|10.||McKeigue PM, Miller GJ, Marmot MG. Coronary heart disease in South Asians overseas: A review. J Clin Epidemiol 1989;42:597-609. |
|11.||Enas EA, Yusuf S, Mehta JL. Prevalence of coronary artery disease in Asian Indians. Am J Cardiol 1992;70:945-9. |
|12.||McKeigue PM, Marmot MG, Adelstein AM, Hunt SP, Shipley MJ, Butler SM, et al. Diet and risk factors for coronary heart disease in Asians in Northwest London. Lancet 1985;2:1086-90. |
|13.||Miller GJ, Kotecha S, Wilkinson WH, Wilkes H, Stirling Y, Sanders TA, et al. Dietary and other characteristics relevant for coronary heart disease in men of Indian, West Indian and European descent in London. Atherosclerosis 1988;70:63-72. |
|14.||Guptha S, Gupta R, Deedwania P, Bhansali A, Maheshwari A, Gupta A, et al. Cholesterol lipoproteins and prevalence of dyslipidemias in urban Asian Indians: A cross sectional study. Indian Heart J 2014;66:280-8. |
|15.||Stason WB, Neff RK, Miettinen OS, Jick H. Alcohol consumption and nonfatal myocardial infarction. Am J Epidemiol 1976;104:603-8. |
|16.||Hines LM, Stampfer MJ, Ma J, Gaziano JM, Ridker PM, Hankinson SE, et al. Genetic variation in alcohol dehydrogenase and the beneficial effect of moderate alcohol consumption on myocardial infarction. N Engl J Med 2001;344:549-55. |
|17.||Amarenco P, Labreuche J. Lipid management in the prevention of stroke: Review and updated meta-analysis of statins for stroke prevention. Lancet Neurol 2009;8:453-63. |
|18.||Stampfer MJ, Sacks FM, Salvini S, Willett WC, Hennekens CH. A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction. N Engl J Med 1991;325:373-81. |
|19.||Fang J, Madhavan S, Cohen H, Alderman MH. Measures of blood pressure and myocardial infarction in treated hypertensive patients. J Hypertens 1995;13:413-9. |
|20.||Lim SS, Vos T, Flaxman AD, Danaei G, Shibuya K, Adair-Rohani H, et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet 2012;380:2224-60. |
|21.||Pais P, Pogue J, Gerstein H, Zachariah E, Savitha D, Jayprakash S, et al. Risk factors for acute myocardial infarction in Indians: a case-control study. Lancet 1996;348:358-63. |
|22.||Farmer JA, Gotto AM. Risk factors for coronary artery disease. In: Braunwald E, editor. Heart Disease. A Textbook of Cardiovascular Medicine. 4 th ed. Philadelphia: WB Saunders; 1992. p. 1125-60. |
|23.||Miller GJ, Beckles GL, Maude GH, Carson DC, Alexis SD, Price SG, et al. Ethnicity and other characteristics predictive of coronary heart disease in a developing community: Principal results of the St James Survey, Trinidad. Int J Epidemiol 1989;18:808-17. |
|24.||Beckles GL, Miller GJ, Kirkwood BR, Alexis SD, Carson DC, Byam NT. High total and cardiovascular disease mortality in adults of Indian descent in Trinidad, unexplained by major coronary risk factors. Lancet 1986;1:1298-301. |
|25.||McKeigue PM, Ferrie JE, Pierpoint T, Marmot MG. Association of early-onset coronary heart disease in South Asian men with glucose intolerance and hyperinsulinemia. Circulation 1993;87:152-61. |
|26.||Thomas I, Gupta S, Sempos C, Cooper R. Serum lipids of Indian physicians living in the U.S. compared to U.S.-born physicians. Atherosclerosis 1986;61:99-106. |
|27.||Chadha SL, Gopinath N, Ramachandran K. Epidemiological study of coronary heart disease in Gujaratis in Delhi (India). Indian J Med Res 1992;96:115-21. |
|28.||Dhawan J, Bray CL, Bennet DH, Miller JP, Fragher B. Lipid abnormalities in British Asian and white patients and in Asian patients in India with coronary artery disease. Br Heart J 1991;66:81. |
|29.||Ryder RE, Hayes TM, Mulligan IP, Kingswood JC, Williams S, Owens DR. How soon after myocardial infarction should plasma lipid values be assessed? Br Med J (Clin Res Ed) 1984;289:1651-3. |
|30.||Gore JM, Goldberg RJ, Matsumoto AS, Castelli WP, McNamara PM, Dalen JE. Validity of serum total cholesterol level obtained within 24 hours of acute myocardial infarction. Am J Cardiol 1984;54:722-5. |
|31.||Stamler J, Vaccaro O, Neaton JD, Wentworth D. Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the multiple risk factor intervention trial. Diabetes Care 1993;16:434-44. |
|32.||Stratton IM, Adler AI, Neil HA, Matthews DR, Manley SE, Cull CA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): Prospective observational study. BMJ 2000;321:405-12. |
|33.||Claudi T, Midthjell K, Holmen J, Fougner K, Krüger O, Wiseth R. Cardiovascular disease and risk factors in persons with type 2 diabetes diagnosed in a large population screening: The Nord-Trøndelag diabetes study, Norway. J Intern Med 2000;248:492-500. |
|34.||Haffner SM, Lehto S, Rönnemaa T, Pyörälä K, Laakso M. Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med 1998;339:229-34. |
|35.||McKeigue PM, Shah B, Marmot MG. Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians. Lancet 1991;337:382-6. |
|36.||Seedat YK, Mayet FG, Khan S, Somers SR, Joubert G. Risk factors for coronary heart disease in the Indians of Durban. S Afr Med J 1990;78:447-54. |
|37.||Ramachandran A, Jali MV, Mohan V, Snehalatha C, Viswanathan M. High prevalence of diabetes in an urban population in South India. BMJ 1988;297:587-90. |
|38.||Singer DE, Nathan DM, Anderson KM, Wilson PW, Evans JC. Association of HbA1c with prevalent cardiovascular disease in the original cohort of the Framingham Heart Study. Diabetes 1992;41:202-8. |
|39.||Escobar E. Hypertension and coronary heart disease. J Hum Hypertens 2002;16 Suppl 1:S61-3. |
|40.||DeFronzo RA, Ferrannini E. Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes Care 1991;14:173-94. |
|41.||O'Keefe JH, Bybee KA, Lavie CJ. Alcohol and cardiovascular health: Alcohol and health: The J-shaped curve. J Am Coll Cardiol 2007;50:1009-14. |
|42.||Moore RD, Pearson TA. Moderate alcohol consumption and coronary artery disease. A review. Medicine (Baltimore) 1986;65:242-67. |
|43.||Marmot M, Brunner E. Alcohol and cardiovascular disease: The status of the U shaped curve. BMJ 1991;303:565-8. |
|44.||Maclure M. Demonstration of deductive meta-analysis: Ethanol intake and risk of myocardial infarction. Epidemiol Rev 1993;15:328-51. |
|45.||Klatsky AL. Epidemiology of coronary heart disease- Influence of alcohol. Alcohol Clin Exp Res 1994;18:88-96. |
|46.||Verschuren PM, Renaud S, Criqui MH, Farchi G, Veenstra J. Alcohol drinking and coronary heart disease. In: Verschuren PM, editor. Health Issues Related to Alcohol Consumption. Washington, DC: ILSI Press; 1993. p. 18-124. |
|47.||Rimm EB, Williams P, Fosher K, Criqui M, Stampfer MJ. Moderate alcohol intake and lower risk of coronary heart disease: Meta-analysis of effects on lipids and haemostatic factors. BMJ 1999;319:1523-8. |
|48.||Thorogood M, Roe L, McPherson K, Mann J. Dietary intake and plasma lipid levels: lessons from a study of the diet of health conscious groups. BMJ 1990;300:1297-301. |
|49.||Tepper SA, Goodman GT, Kritchevsky D. Diet, nutrition intake, and metabolism in populations at high and low risk for colon cancer. Binding of bile salts to dietary residues. Am J Clin Nutr 1984;40 4 Suppl:947-8. |
|50.||Pan A, Sun Q, Bernstein AM, Schulze MB, Manson JE, Stampfer MJ, et al. Red meat consumption and mortality: Results from 2 prospective cohort studies. Arch Intern Med 2012;172:555-63. |
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]