Those with AMI before screening were excluded. The model is adjusted for all other variables. Furthermore, an increased future risk for AMI was associated with age, smoking, large WHR, living in a deprived area and high blood pressure not statistically significant in the main effect model , Table 3. Women generally suffer from AMI at a later age than men, and it has been suggested that other mechanisms, e.
Moreover, it is known that estrogen contributes to an antiatherogenic lipid profile by decreasing LDL and increasing HDL-C [ 12 , 35 ]. However, the results of the present study strengthen the importance to initiate preventive actions focused on blood lipids in middle-aged women. The definition of AMI has changed over time. Nowadays, AMI is divided into ST-elevation myocardial infarction and Non-ST-elevation myocardial infarction, with different patterns regarding course, treatment and prognosis.
According to a Swedish study of the declining rates of coronary heart disease mortality between and , more than half of the decrease was attributable to reductions in major cardiovascular risk factors, mainly a large decrease in TC [ 36 ]. During approximately the same period, dietary fat intake and serum cholesterol levels have been decreasing in many countries [ 36 , 37 , 38 , 39 ]. However, a more recent Swedish study analysed dietary patterns between and and found a recent increase in dietary fat intake [ 41 ].
This could be related to the increased interest in the public to eat a low-carb and high-fat diet although it has not been proven that is a healthier choice than other types of diets. The last decades obesity has dramatically increased globally, as a consequence of poor lifestyle habits.
In Sweden, mean body mass index BMI in women increased from This indicates that the consequences to obesity, e. AMI, may be an increasing problem if we do not manage to identify subgroups for early prevention. In cases these changes are not sufficient, lipid-lowering medication may be relevant in individuals with high or moderate risk for AMI, also as primary prevention [ 43 , 44 ].
However, the use of lipid-lowering drugs as primary prevention is a debated question and is not completely defined in primary prevention for women [ 45 , 46 ].
Current international guidelines emphasize to identify high-risk individuals who would benefit from primary prevention [ 43 ]. The strengths of the present study are the prospective design and the large sample of women drawn from the general population, who were followed for AMI during a long follow-up time.
The data has also been adjusted for several potential confounders. Another strength is the design with a clinical baseline examination including blood tests, anthropometric measurements and blood pressure, completed with a thorough self-reported questionnaire including a range of health problems. The study also has some limitations.
Even if we were able to control for several potential confounding factors, it is possible that residual confounding exists, such as inflammatory markers. AMI is a highly complex disorder and different types of confounders may occur in different individuals and change over time, which we could not control for.
Lipid levels may differ throughout populations and therefore it may not be possible to generalize our results to other populations. Laboratory methodological differences may yield different results for lipid levels; however, these variations will occur in both individuals with and without AMI.
Furthermore, we had no information about lipid lowering medication; however, in the s statin medication was not recommended in Sweden as primary prevention to people without previous cardiovascular disease, so it is likely that only very few individuals had lipid lowering medication.
Because of several missing values on NDI, we had to exclude these individuals. The non-responders may be different from the responders and non-responders may have an increased risk of AMI [ 48 ].
To some extent, we tried to overcome this limitation by analysing non-responders and found no increased risk of AMI in non-responders. Finally, a problem of using baseline questionnaires in follow-up studies is that the data, e.
The results indicate that more commonly clinical use of the ratio may contribute to early identification of individuals at risk of AMI, and support the idea of including the ratio in risk assessment tools for women. The data that support the findings of this study are available from the Swedish National Board of Health and Welfare and the Center for Primary Health Care Research, but restrictions apply to the availability of these data, which were used under license for the current study, and so are not publicly available.
Data are however available from the authors upon reasonable request and with permission of the Swedish National Board of Health and Welfare and the Center for Primary Health Care Research.
Mack M, Gopal A. Epidemiology, traditional and novel risk factors in coronary artery disease. Cardiol Clin. National Board of Health and Welfare. Causes of Death Stockholm; Epidemiology of coronary heart disease and acute coronary syndrome. Ann Transl Med. Lifelong gender gap in risk of incident myocardial infarction: the Tromso study.
Sex differences in age-related cardiovascular mortality. PLoS One. Effectiveness-based guidelines for the prevention of cardiovascular disease in women update: a guideline from the American Heart Association.
J Am Coll Cardiol. Wenger NK. Cardiovascular disease: the female heart is vulnerable: a call to action from the 10Q report. Clin Cardiol. Predicting coronary heart disease events in women: a longitudinal cohort study. J Cardiovasc Nurs. Ischemic heart disease in women: a focus on risk factors. Trends Cardiovasc Med. Health problems and acute myocardial infarction in women - a year follow-up study. Protocol for the HAPPY hearts study: cardiovascular screening for the early detection of future adverse cardiovascular outcomes in middle-aged and older women: a prospective, observational cohort study.
BMJ Open. Acute myocardial infarction in women: a scientific statement from the American Heart Association. Do lipids, blood pressure, diabetes, and smoking confer equal risk of myocardial infarction in women as in men?
The Reykjavik study. J Cardiovasc Risk. Risk of incident myocardial infarction by gender: interactions with serum lipids, blood pressure and smoking. The Tromso study Sex differences in lipid profiles and treatment utilization among young adults with acute myocardial infarction: results from the VIRGO study.
Am Heart J. You may need to have your blood tested more often if you have risk factors for heart disease or stroke. Talk with your healthcare provider. You may need this test as part of your regular medical checkup. You may have this test done more often if:. Your healthcare provider may also order other tests to check for other coronary heart disease risk factors. These may include other blood tests. They may also include tests for diabetes and diseases of your thyroid, liver, or kidneys.
Test results may vary depending on your age, gender, health history, the method used for the test, and other things. Your test results may not mean you have a problem. Ask your healthcare provider what your test results mean for you. Here are the ranges for total cholesterol in adults:. If your total cholesterol is high, you may have a higher risk for heart disease than a person with normal total cholesterol. A low HDL cholesterol level is associated with an increased risk for coronary heart disease.
Your total-cholesterol-to-HDL ratio can be figured out by dividing your total cholesterol number by your HDL cholesterol number.
Together, these numbers provide more information about your coronary heart disease risk than knowing only 1 of the numbers. The test is done with a blood sample.
Fasting apolipoprotein B and insulin levels and low-density lipoprotein LDL peak particle size among triglyceride TG tertiles in men in the Quebec Cardiovascular Study. Arch Intern Med. There is, however, no consensus on which of these 2 indices is superior. Methods A total of middle-aged men in whom measurements of the metabolic profile were performed in the fasting state were recruited from 7 suburbs of the Quebec metropolitan area.
DESPITE considerable advances during the past 40 years, there is increasing awareness among scientists, epidemiologists, and clinicians that current approaches to evaluation of coronary heart disease CHD risk in asymptomatic individuals remain suboptimal.
Regarding the traditional fasting plasma lipid profile triglycerides [TGs], total cholesterol [TC], low-density lipoprotein cholesterol [LDL-C] [which is most often calculated rather than measured directly], and high-density lipoprotein cholesterol [HDL-C] , there is no universal acceptance of how this information should be used and interpreted, although several consensus documents have been produced.
Thus, because TG levels are ignored in the National Cholesterol Education Program algorithm, the clinician is left with LDL-C and HDL-C levels to assess risk while considering the presence or absence of other important risk factors, such as family history of early CHD, age, smoking, hypertension, diabetes mellitus, low physical activity, and obesity.
This dyslipidemic state lipid triad has been described as atherogenic dyslipidemia. The population and evaluation procedures of the Quebec Cardiovascular Study have been described previously. Each participant completed a standardized questionnaire administered by trained nurses.
During this period, men developed a first ischemic event, which included typical effort angina, coronary insufficiency, nonfatal myocardial infarction, and coronary death. After participants had fasted for 12 hours, blood samples were obtained from an antecubital vein while participants were sitting.
Plasma was separated from blood cells by centrifugation and immediately used for measurement of lipoprotein-lipid and APOB levels. Aliquots of fasting plasma were frozen at the time of collection for subsequent assessment of insulin levels.
Plasma APOB concentrations were measured using the rocket immunoelectrophoretic method of Laurell, 29 as previously described. Fasting insulin concentrations were measured using a commercial double-antibody radioimmunoassay human insulin—specific radioimmunoassay method; LINCO Research, St Louis, Mo.
A volume of 7. A plasma pool was used as an internal standard. Lamarche, PhD, A. Tchernof, PhD, S. Moorjani, PhD, et al, unpublished data, Group differences for continuous variables were examined using either the t test or the general linear model, and the Duncan post-hoc test was used in situations in which a significant group effect was observed.
Pearson product moment correlation coefficients were used to quantify associations between variables. Table 1 gives the baseline characteristics of the men who developed IHD compared with those who remained IHD free during 5-year follow-up.
Overall, men with IHD were characterized by an unfavorable metabolic profile compared with asymptomatic men. We believe that there is a metabolic rationale underlying this finding. It is well documented that high TG—low HDL-C dyslipidemia, which is often linked to abdominal obesity and insulin resistance, is associated with marginal or even no change in LDL-C levels. Moreover, the IHD event rate was 2 times higher among these men. This phenomenon is further illustrated in Figure 3 , in which participants in the Quebec Cardiovascular Study were stratified into tertiles of fasting TG levels.
However, the intercept of the relationship between the 2 ratios was different among the 3 TG tertiles. Our results are in accordance with those of Leroux et al, 36 who demonstrated that the relative cholesterol content of the calculated VLDL fraction increased across TG quintiles, whereas there was also relatively less cholesterol associated with the HDL fraction as a function of increasing triglyceridemia.
Moreover, a study conducted by McNamara et al 37 demonstrated that the difference between the estimated LDL-C concentrations and values obtained by measuring cholesterol in the LDL fraction isolated by ultracentrifugation was substantially greater in hypertriglyceridemic individuals than in those with normal TG levels.
Lamarche et al 38 also previously reported that patients with high TG—low HDL-C are characterized by clustering metabolic abnormalities described as the atherogenic metabolic triad of nontraditional risk factors, which included hyperinsulinemia, elevated APOB level, and small, dense LDL particles.
Thus, a higher proportion of men with elevated TG levels were also characterized by the features of the atherogenic metabolic triad. Additional metabolic alterations found in these individuals include, among others, elevated APOB levels, an exaggerated postprandial lipemia, and small, dense LDL particles.
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