Original Article
Ten-Year Mortality from Cardiovascular Disease in Relation to Cholesterol Level among Men with and without Preexisting Cardiovascular Disease
N Engl J Med 1990; 322:1700-1707June 14, 1990
- Abstract
- Abstract
To determine the associations of total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol with mortality from coronary heart disease and cardiovascular disease, we studied 2541 white men who were 40 to 69 years old at base line and followed them for an average of 10.1 years. Seventeen percent had some manifestation of cardiovascular disease at base line, whereas the others did not.
Among the men who had cardiovascular disease at base line, we found, after multivariate adjustment, that those with "high" blood cholesterol levels (above 6.19 mmol per liter) had a risk of death from cardiovascular disease, including coronary heart disease, that was 3.45 times higher (95 percent confidence interval, 1.63 to 7.33) than that for men with "desirable" blood cholesterol levels (below 5.16 mmol per liter). The corresponding hazard ratios were 5.92 (95 percent confidence interval, 2.59 to 13.51) for LDL cholesterol levels above 4.13 mmol per liter as compared with those below 3.35 mmol per liter, and 6.02 (95 percent confidence interval, 2.73 to 13.28) for HDL cholesterol levels below 0.90 mmol per liter as compared with those above 1.16 mmol per liter. All three lipid levels were also significant predictors of death from coronary heart disease alone (P<0.005).
Total cholesterol and LDL cholesterol levels were also significant predictors of death from cardiovascular and coronary heart disease in men without preexisting cardiovascular disease, although at a lower level of absolute risk of death. Thus, the 10-year risk of death from cardiovascular disease for a man with preexisting cardiovascular disease increased from 3.8 percent to almost 19.6 percent with increasing levels of total cholesterol from "desirable" to "high," whereas the corresponding risk for a man who was free of cardiovascular disease at base line increased from 1.7 percent to 4.9 percent.
Our findings suggest that total, LDL, and HDL cholesterol levels predict subsequent mortality in men 40 to 69 years of age, especially those with preexisting cardiovascular disease. (N Engl J Med 1990; 322:1700–7.)
Media in This Article
Figure 1
Age-Adjusted Rates of Death from Coronary Heart Disease per 1000 Person-Years of Follow-up, According to Lipid Level, for Men with and Men without Evidence of Cardiovascular Disease at Base Line.Figure 2
Age-Adjusted Rates of Death from Cardiovascular Disease per 1000 Person-Years of Follow-up, According to Lipid Level, for Men with and Men without Evidence of Cardiovascular Disease at Base Line.Article Activity
- Article
THE importance of blood lipid levels as risk factors for coronary heart disease is well established.1 , 2 It is uncertain, however, whether their importance applies to men who already have signs and symptoms of cardiovascular disease. In such men, the extent of damage to the myocardium is a powerful prognostic factor,3 , 4 which may have diverted attention from other, modifiable factors, such as blood lipid levels.
Only limited information is available on the association of serum cholesterol levels, especially the lipoprotein cholesterol levels, with mortality from cardiovascular disease among men with preexisting heart disease. However, published reports support the importance of serum lipid levels as predictors of coronary heart disease among such men.5 6 7 8 9 10 11 12 13 14 15 16 There is also good evidence that lowering the serum total cholesterol level has beneficial effects in the secondary prevention of coronary heart disease.17 18 19 20 21 22 In view of the fact that up to half the deaths from coronary heart disease in the United States occur in men with signs of myocardial ischemia,6 7 8 9 10 11 reducing the lipid levels of these men could have a substantial impact on overall mortality from cardiovascular disease.
We evaluated the association of total, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol levels with mortality from coronary heart disease and cardiovascular disease, both for men with preexisting heart disease and for those with no signs of heart disease at base line. The study population consisted of free-living men who participated in the Lipid Research Clinics Prevalence Study and who were followed up for an average of 10.1 years. In our analysis, special attention was given to the cutoff points for lipid levels recommended by the National Cholesterol Education Program.23
Methods
Study Design
All base-line measurements were obtained as part of the Lipid Research Clinics Program Prevalence Study, conducted in 10 North American populations between 1972 and 1976. The methods of the prevalence study have been reported previously in detail.24 25 26 In brief, the study consisted of a preliminary screening (visit 1) of men and women in defined populations who were selected by sampling households, schools, businesses, and one prepaid medical practice. A total of 81,926 persons were eligible for visit 1; 60,502 (74 percent) of those whom we invited participated. Demographic data were obtained and fasting lipid levels were measured at this visit.
Three groups — a 15 percent random sample of the participants in visit 1 (n = 9107), participants who had elevated lipid levels at visit 1 (n = 6882), and participants who were taking lipid-lowering medications at the time of visit 1 (n = 346) — were invited to take part in the second phase of the prevalence study (visit 2), described elsewhere.24 At visit 2, 13,852 men and women (85 percent of those invited) were screened by means of a 24-hour dietary-recall interview, a questionnaire concerning personal habits, requests for information on medications and medical history, a physical examination, resting and exercise electrocardiography, blood-chemistry analyses, and determinations of fasting lipid levels. All the measurements used in the analyses reported here were obtained at visit 2.
Base-Line Measurements
Lipid and lipoprotein levels were measured at the Lipid Research Clinics, according to a standardized protocol.277 An isopropanol extract of plasma was treated with a zeolite mixture to remove phospholipids, glucose, and bilirubin. Plasma triglyceride levels were then estimated fluorometrically with use of an AutoAnalyzer.27 The HDL cholesterol level was estimated from the supernatant fraction of whole plasma after the precipitation of low-density and very-low-density lipoproteins by heparin and manganese chloride. Another aliquot was separated by ultracentrifugation at a density of 1.006 g per milliliter; the bottom fraction (density > 1.006 g per milliliter) contained both HDL and LDL cholesterol. LDL cholesterol was calculated by subtracting the HDL cholesterol value from the total cholesterol value in this bottom fraction.
Smoking histories were obtained for all participants; we asked whether they had ever smoked or currently smoked cigarettes and, for current smokers, the number of cigarettes they usually smoked per day. Blood pressure was measured in the right arm after the participant had been sitting for at least five minutes. For the analyses described here, the first measurement of blood pressure with a standard sphygmomanometer was used. The body-mass index was calculated as the weight in kilograms divided by the square of the height in meters.
Follow-up Procedures
All 8825 men and women who were 30 years of age or older at the time of visit 2 were included in a mortality follow-up study. Beginning in 1977, participants were contacted annually by letter or telephone. No changes in risk-factor levels were measured, and no interventions were attempted. The participants were followed up for a mean of 10.1 years. Vital status is currently known for over 99.6 percent of the participants.
When the annual-contact procedure identified a participant as having died, a death certificate was obtained. Extensive validation information was obtained for deaths that might have been related to cardiovascular disease.3 This information included interviews with the next of kin about the circumstances of death and a review of hospital records or an interview with the subject's personal physician. Two members of a panel of five cardiologists, who were blinded as to the participant's identity and base-line characteristics, coded the cause of death as coronary heart disease, cardiovascular disease (which included coronary heart disease), or "other." Disagreements between the two cardiologists were settled by the entire panel.
Study Population
The present report is restricted to men who were 40 to 69 years of age at visit 2. Of the 2890 eligible men, nonwhites (n = 120), whites in the predominantly nonwhite sample from East Baltimore (n = 3), men with definite diabetes (n = 85), and men who were being treated with lipid-lowering medication (n = 141) were excluded. The final study population therefore consisted of 2541 men.
Categories of Cardiovascular Disease at Base Line
For the purpose of this report, all men examined at visit 2 were assigned to one of the following mutually exclusive categories according to their cardiovascular disease status at visit 2 (categories with lower numbers took precedence over higher-numbered, less specific categories). Category 1 was restricted to men with myocardial infarction, whereas categories 2 and 3 combined the characteristics of coronary heart disease with those of cardiovascular disease not necessarily attributable to coronary heart disease. In our calculations of the numbers presented below, a man who met several criteria to qualify for a given category was counted only once, according to the criterion mentioned first.
Category 1: Definite myocardial infarction (n = 83) — a history of hospitalization for myocardial infarction (n = 68) or major ischemic abnormalities in the resting electrocardiogram (n = 15) (Minnesota codes 1.1, or 1.2 and 5.1 through 5.3)21
Category 2: Abnormal results on the graded exercise test but no definite myocardial infarction (n = 253) — an abnormal S—T-segment change on the exercise test28 (n = 161) or any of the following symptoms suggestive of cardiovascular disease as the cause of termination of the exercise test: cardiac arrhythmia, chest pain, hypotension, or intracardiac block (n = 92)
Category 3: Other manifestations of cardiovascular disease but no definite myocardial infarction or abnormal results on the graded exercise test (n = 135) — category 3 had three subcategories, as follows:
3.1: Abnormalities on the resting electrocardiogram suggestive of chronic ischemia (n = 31) — any of the following, as coded at the field center18: possible acute ischemic injury or suspected unhealed myocardial infarction, second-degree heart block, multifocal or multiple (>10 per minute) premature ventricular complexes, R-on-T—type premature ventricular complexes, ventricular tachycardia, or any of the following Minnesota codes,21 as coded at the central coding center: 1.2,3 and 4.1,2 or 5.1,2; 6.1,2,4; 7.1; or 8.4 3.2: Angina pectoris (n = 64) — a positive Rose Questionnaire29 (n = 49), use of nitrates (n = 9), or dull sternal pain at the termination of a graded exercise test that disappeared in less than six minutes (n = 6)
3.3: Miscellaneous signs and symptoms of cardiovascular disease (n = 40) — use of antiarrhythmia medication (n = 16), heart surgery (n = 1), use of digitalis (n = 4), hospitalization for stroke (n = 8), congestive heart failure (n = 3), evidence of parasystolic focus, atrial flutter, or atrial fibrillation on the resting electrocardiogram (n = 3), termination of the graded exercise test before the subject reached stage 1 (n = 5)
Category 4: No cardiovascular disease at base line (n = 1940) — no signs or symptoms of cardiovascular disease, as defined above, in men who underwent exercise-tolerance testing
A number of men (n = 130) who did not meet the criteria for category 1 or 3 but were excluded from exercise testing, primarily because of preexisting cardiovascular disease, were considered "unclassifiable" (category 5).
Statistical Analysis
Age-specific mortality rates were computed for 10-year age groups on the basis of the age at death or at the last follow-up contact. The rates were adjusted for age by the direct method, with the proportions of person-years of follow-up in each 10-year age group used as weights. Means and proportions (prevalences) of different manifestations of cardiovascular disease at base line were adjusted for age by the direct method, with the proportions of the men in each 10-year age group at visit 2 used as weights. Because men with hyperlipidemia were oversampled at visit 2, the mortality rates, means and their standard errors, and prevalences were weighted to account for the varying sampling proportions within strata defined by age, clinic, and lipid levels.24 Standard errors for the mortality rates were calculated with use of the approximation formula of Chiang.30 The calculated rates were also converted into conditional probabilities of death over a 10-year period.31 These probabilities are conditional on the fact that the person does not die of any other cause during the 10 years.
Age-specific mortality rates and mortality rates calculated on the basis of only the 15 percent random sample of participants were consistent with the age-adjusted, weighted rates presented here. Statistical tests of the effect of each lipid level on mortality from coronary heart disease and cardiovascular disease, adjusted for other risk factors, were performed with use of the discrete proportional-hazards model,32 , 33 appropriately weighted across sampling strata. Lipid levels were included in the statistical models as indicator variables representing the lipid categories shown in the tables. The overall effect of each lipid level was determined with the likelihood-ratio test used for all the indicator variables representing the lipid level in question. Models for LDL cholesterol included triglycerides as a control variable, and models for HDL cholesterol included LDL cholesterol. All models run also included the control variables age and body-mass index as continuous variables and current smoking, hypertension, and level of physical activity as binary variables.
Hypertension was defined as a systolic blood pressure exceeding 140 mm Hg, a diastolic blood pressure exceeding 90 mm Hg, or the use of blood-pressure medication. The physical-activity variable was based on the participant's answer to the question "Do you regularly engage in strenuous exercise or hard physical labor?"
Separate models were fitted for the men with and without cardiovascular disease at base line. Estimated coefficients for the models including men with and without cardiovascular disease at base line were compared by calculating the variance of the difference between two coefficients as the sum of the variances of the individual coefficients. This method assumes zero covariance between the coefficients. In the present case, the covariance is technically not zero, but it is so small that it would have a negligible influence on the test statistics. Hazard ratios and their two-sided 95 percent confidence intervals were calculated according to the following formula: exp (beta ± 1.96 * SE (beta)). All significance tests were two-tailed.
Results
Almost one fifth of the study population had some evidence of cardiovascular disease at the base-line examination (Table 1Table 1
Age-Adjusted, Weighted Prevalence of Manifestations of Cardiovascular Disease (CVD) at the Base-Line Examination and Selected Characteristics of Men in These Categories.*). As expected, the prevalence of all manifestations of cardiovascular disease increased markedly with age (data not shown). The prevalence of any sign of cardiovascular disease at base line was 7.7 percent in the group of men 40 to 49 years old, 20.5 percent in the age group 50 to 59 years old, and 36.5 percent in the group 60 to 69 years old. The cardiovascular disease status at base line of 130 men (category 5) could not be accurately determined because they were excluded from the exercise test, in some instances because of overt or suspected cardiovascular disease. Therefore, the base-line characteristics and mortality rates of these men are shown in Tables 1 and 2Table 2
Age-Adjusted, Weighted Rates of Death from Coronary Heart Disease (CHD), Cardiovascular Disease (CVD), and All Causes per 1000 Person-Years of Follow-up, According to Cardiovascular Disease Category at Base Line.*, but they are excluded from further analyses.As shown in Table 1, men with cardiovascular disease at base line were older, had higher levels of total and LDL cholesterol and triglycerides, and more often had hypertension than men without cardiovascular disease. Within the group that had cardiovascular disease at base line, survivors of a myocardial infarction had a higher mean LDL cholesterol level and more often reported themselves to be physically active than men with a positive graded exercise test and those with other manifestations of cardiovascular disease.
During the average 10.1-year follow-up period, men with previous myocardial infarction had a high risk of death from coronary heart disease (Table 2). Previous myocardial infarction increased the risk of death from coronary heart disease more than 20 times as compared with the risk for men with no signs of cardiovascular disease at base line. Men with positive graded exercise tests had a four times higher risk of death than men without preexisting cardiovascular disease, but their risk was lower than that for men with other manifestations of cardiovascular disease at base line. This difference may reflect the fact that 29 men who were excluded from the graded exercise test because they had signs of severe cardiovascular disease were classified as having "other" cardiovascular disease. These patterns were quite similar for mortality from cardiovascular disease (which included deaths from coronary heart disease) and, to a lesser degree, for mortality from all causes. Men who were categorized as unclassifiable had a higher risk of death than men without cardiovascular disease at base line but a lower risk than men with manifestations of cardiovascular disease.
Age-adjusted rates of death from coronary heart disease and cardiovascular disease were calculated for three levels of total cholesterol, LDL cholesterol, and HDL cholesterol (Fig. 1Figure 1
Age-Adjusted Rates of Death from Coronary Heart Disease per 1000 Person-Years of Follow-up, According to Lipid Level, for Men with and Men without Evidence of Cardiovascular Disease at Base Line. and 2Figure 2Age-Adjusted Rates of Death from Cardiovascular Disease per 1000 Person-Years of Follow-up, According to Lipid Level, for Men with and Men without Evidence of Cardiovascular Disease at Base Line.). With the exception of the upper level for HDL cholesterol, the cutoff points used were those recommended by the National Cholesterol Education Program.23 The risk of death from both coronary heart disease and cardiovascular disease increased with less favorable levels of lipids in both men with cardiovascular disease at base line and those without such disease. For easier interpretation, the rates in Figures 1 and 2 can be converted into conditional probabilities of death in the next 10 years. On the basis of these probabilities, among the men with cardiovascular disease at base line, 19.6 percent of those with total cholesterol levels above 6.19 mmol per liter were projected to die from cardiovascular disease in 10 years, as compared with 3.8 percent of the men with total cholesterol levels below 5.16 mmol per liter. The corresponding probabilities for men without cardiovascular disease at base line were 4.9 percent and 1.7 percent. A high total cholesterol level was associated with an increase of 15.8 percent in the 10-year risk of death from cardiovascular disease among the men who had signs of cardiovascular disease at base line and an increase of 3.2 percent among the men without such signs. Similarly, a high LDL cholesterol level was associated with an increase of 16.8 percent (20.4 percent minus 3.6 percent) in the risk of death from cardiovascular disease among the men who had cardiovascular disease at base line and an increase of 2.4 percent (4.2 percent minus 1.8 percent) among the men without cardiovascular disease. The corresponding percentages for the men with low HDL cholesterol levels were 16.0 percent (20.4 percent minus 4.4 percent) and 3.1 percent (4.7 percent minus 1.6 percent).Men who had cardiovascular disease at base line had considerably higher rates of death from coronary heart disease and cardiovascular disease than those without manifest cardiovascular disease, at each level of values for the lipids we measured. Men without clinically manifest cardiovascular disease at base line who had high blood cholesterol levels (above 6.19 mmol per liter), had a higher risk of death from coronary heart disease and cardiovascular disease than those with evidence of cardiovascular disease who had desirable blood cholesterol levels (below 5.16 mmol per liter). This relation was also true for LDL cholesterol levels, but in the case of HDL cholesterol levels it held only for mortality from cardiovascular disease.
All but one of the observed associations between lipid levels and mortality from coronary heart disease and cardiovascular disease were statistically significant (P<0.05) after adjustment for other risk factors (Table 3Table 3
Weighted, Multivariable-Adjusted Hazard Ratios (HR) for Death from Coronary Heart Disease (CHD) and Cardiovascular Disease (CVD) among Men with and Men without Cardiovascular Disease at Base Line, According to Lipid Level.*). Multivariate adjustment in general changed the results very little. It did, however, decrease to some degree the strength of the association between the total cholesterol level and death from coronary heart disease and cardiovascular disease among men who had cardiovascular disease at base line. When the estimated hazard ratios for men who had cardiovascular disease at base line were compared, one by one, with those for men without cardiovascular disease at base line, no significant differences between the hazard ratios were observed at the 0.05 level.When additional multivariate models were fitted for the men with cardiovascular disease at base line, with adjustment for the severity of the disease as measured by the category of cardiovascular disease at base line, the estimated hazard ratios changed only slightly. The greatest changes occurred in the hazard ratios for mortality from coronary heart disease; for the HDL cholesterol level, the hazard ratio decreased from 6.10 to 5.02, and for the total cholesterol level it increased from 6.43 to 7.47.
Persons with clinical evidence of cardiovascular disease are not a homogeneous group. As indicated in Methods, that was also the case for the men analyzed in this study. Age-adjusted rates of death from cardiovascular disease were therefore calculated separately for men with different manifestations of cardiovascular disease (Table 4Table 4
Age-Adjusted, Weighted Rates of Death from Cardiovascular Disease (CVD) per 1000 Person-Years of Follow-up, According to Lipid Level, among Men with Manifestations of Cardiovascular Disease at Base Line.*). The risk of death from cardiovascular disease generally increased with less favorable levels of all three lipids within each of three categories of cardiovascular disease at base line: myocardial infarction, a positive graded exercise test, and all other manifestations. The major exception was the HDL cholesterol level in men with previous myocardial infarction. Rates were also calculated for mortality from coronary heart disease (data not shown); the associations were similar to those presented in Table 4.Discussion
The objectives of this study were to explore the relations between lipid levels and mortality from coronary heart disease or cardiovascular disease in men who were 40 to 69 years of age and had clinically evident heart disease at base line and to compare these relations with those in men with no such evidence of disease at base line. Less favorable levels of serum total cholesterol, LDL cholesterol, and HDL cholesterol at base line were found to be associated with increased mortality from coronary heart disease and cardiovascular disease in both men with and men without preexisting cardiovascular disease. The risk of mortality increased in a graded fashion according to lipid level and in a consistent manner from the fifth to the seventh decade of age; it was also consistent for different manifestations of cardiovascular disease. It remained strong and statistically significant after multivariate adjustment for risk factors other than lipid levels.
Lipid and lipoprotein levels were measured at base line. Random error in lipid levels (and other measurements) is greater when single rather than multiple measurements are made; thus, the association between lipid levels and the risk of mortality presented here may be an underestimation.34 However, this underestimation should be similar in magnitude for men with and men without preexisting cardiovascular disease.
The results of this study are in agreement with the findings of several types of studies of men with clinically evident coronary heart disease. Population-based studies from the United States,5 , 14 Finland,9 , 15 and England6 , 11 , 16 have demonstrated that an increased risk of coronary heart disease is associated with high total cholesterol levels among persons who have clinically evident coronary heart disease at base line. In these studies, men with electrocardiographic abnormalities and angina pectoris, as well as those who had survived a myocardial infarction, were included in the group with cardiovascular disease at base line. Analysis of the placebo group in the Coronary Drug Project showed a statistically significant association between the base-line total cholesterol level and the risk of death from coronary heart disease among 2789 men with previous myocardial infarction.4 More recently, the Aspirin Myocardial Infarction Study has confirmed this finding in men less than 55 years of age.13
Less information is available on the importance of lipoprotein fractions in men with evidence of cardiovascular disease. In the Coronary Drug Project, a low HDL cholesterol level was associated with increased mortality in a group of 354 men randomly assigned to the placebo group.8 This finding has been supported by a study of 130 Israeli survivors of myocardial infarction,12 but not by the Aspirin Myocardial Infarction Study.13 Among the population-based studies, the British Regional Heart Study11 found a strong association between HDL cholesterol levels and the risk of coronary heart disease in men with preexisting cardiovascular disease.
Meta-analysis of 22 primary-and secondary-prevention trials has convincingly shown that lowering serum total cholesterol levels reduces the incidence of coronary heart disease among survivors of myocardial infarction, both in trials using dietary intervention21 and in those using drugs.22 No prevention trials have been carried out in which the subjects were men with less severe signs of myocardial ischemia, such as angina pectoris or electrocardiographic changes. In the Belgian Heart Disease Prevention Project,35 however, multifactorial intervention was more effective in men with electrocardiographic changes at entry than in men without such changes. Angiographic studies have also shown that favorable changes in total, LDL, and HDL cholesterol levels are associated with slower progression and greater regression of atherosclerotic lesions.17 18 19 20
In our study, the estimated relative risks for the various plasma total cholesterol and lipoprotein lipid levels were not significantly different for men with and men without preexisting cardiovascular disease, and there were no indications that the role of the lipid levels was more important in the men with preexisting cardiovascular disease. However, because of the much higher risk of death among men who had cardiovascular disease at base line, the differences in the absolute risk at different lipid levels were considerably larger in the men with preexisting cardiovascular disease. For example, the 10-year risk of death from cardiovascular disease for a man with preexisting cardiovascular disease increased from 3.8 to almost 20 percent as the level of total cholesterol increased from "desirable" to "high." In contrast, the corresponding increase in risk for a man who was free of cardiovascular disease at base line was from 1.7 to 4.9 percent. Although the design of this study did not allow us to assess the benefits of intervention, since none was attempted, our results suggest that the potential impact of changes in lipid levels on the risk of death from cardiovascular disease may be considerably greater for men with preexisting cardiovascular disease than for healthy men. Depending on the definition of clinically evident heart disease, about half the deaths from coronary heart disease in the general population occur in men with signs of myocardial ischemia.6 , 11 Assuming that the degree of reduction in relative risk resulting from the primary and secondary prevention of coronary heart disease is comparable, as suggested by meta-analyses of the results of published trials,21 , 22 interventions in men with preexisting cardiovascular disease may also have a considerable impact on mortality from cardiovascular disease in the general population.
Considerable evidence indicates that in persons with signs or symptoms of ischemic heart disease, the impairment of cardiac function is an important determinant of subsequent events.3 , 4 This study cannot assess the importance of myocardial damage, as compared with other risk factors such as lipid levels, in determining long-term mortality rates. It is important to note, however, that plasma lipid levels were powerful predictors of mortality from coronary heart disease and cardiovascular disease in this cohort of men, in whom we documented a range of manifestations of cardiovascular disease and a range of degrees of impairment. Lipid levels predicted mortality from coronary heart disease and cardiovascular disease among the men in each cardiovascular disease category (myocardial infarction, a positive graded exercise test, and all other manifestations). These associations persisted after multivariate analyses with adjustment for other risk factors, as well as for the severity of cardiovascular disease at base line.
The guidelines of the National Cholesterol Education Program23 identify the presence of definite signs of myocardial ischemia as an indication for aggressive treatment of high LDL cholesterol levels. The results reported here highlight the prognostic importance of total, LDL, and HDL cholesterol levels in men with clinically evident cardiovascular disease. Because of the high risk faced by these men and because of the social burden of cardiovascular diseases, the potential importance of the secondary prevention of cardiovascular morbidity and mortality is great.36
For a list of participating investigators, see the Appendix.
Supported by contracts (NO1-HV12159, NO1-HV12156, NO1-HV12160, NO1-HV22914, NO1-HV30010, NO1-HV22913, NO1-HV12158, NOl–HV12161, NO1-HV22915, NO1-HV12903, NO1-HV12243, NO1-HV22932, NO1-HV22917, NO1-HV12157, and NO1-HV32961) with the National Heart, Lung, and Blood Institute. These analyses were performed while Dr. Pekkanen was a visiting scholar at the School of Public Health, University of North Carolina, with funding from the Academy of Finland, the National Board of Health, Finland, and the Paavo Nurmi Foundation. Dr. Linn was supported while in Israel by the Brecher Foundation and was a visiting scientist at the Lipid Metabolism—Atherogenesis Branch, Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute.
We are indebted to Lloyd E. Chambless, Ph.D., and Shrikant I. Bangdiwala, Ph.D., for statistical advice, to Allan Rosen and Jeffrey M. Abolafia for programming advice, and to Professor O. Dale Williams and Beth Corder, M.P.H., for their help and support.
Source Information
From the Collaborative Studies Coordinating Center, Department of Biostatistics (J.P., C.M.S.), and the Department of Epidemiology (G.H., H.A.T.), School of Public Health, University of North Carolina, Chapel Hill; the Department of Epidemiology, National Public Health Institute, Helsinki, Finland (J.P.); the Clinical Epidemiology Unit, Rambam Medical Center, Haifa, Israel (S.L.); the Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis (A.L.); and the Lipid Metabolism—Atherogenesis Branch, Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md. (B.M.R.). Address reprint requests to Dr. Rifkind at the Lipid Metabolism—Atherogenesis Branch, Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health, Federal Bldg., Rm. 401, Bethesda, MD 20892.
Appendix
The following investigators participated in this study:
Follow-up Study Executive Committee — H.A. Tyroler, M.D. (chairman); Shrikant I. Bangdiwala, Ph.D.; Elizabeth Barrett-Connor, M.D.; C. Edward Davis, Ph.D.; Manning Feinleib, M.D.; William R. Hazzard, M.D.; David Jacobs, Ph.D.; Leslie Kirkland-Ellis, M.P.H.; Irma Mebane, M.S.; Richard Mowery, M.S.P.H.; Ronald Prineas, M.B.S., Ph.D.; Basil M. Rifkind, M.D.; Carl Rubenstein, M.D.; and William J. Schull, Ph.D.
Follow-up Study Directors — Elizabeth Barrett-Connor, M.D.; Reagan Bradford, M.D., Ph.D.; Bobbe Christensen, D.P.H.; Linda Cowan, Ph.D.; Michael Criqui, M.D., M.P.H.; William Haskell, Ph.D.; Joanne Hoover, M.D., M.P.H.; David Jacobs, Ph.D.; J. Alick Little, MD.; John Morrison, Ph.D.; George Owen, Ph.D.; Pearl Van Natta, M.S.; Patricia Wahl, Ph.D.; and Robert Wallace, M.D.
Mortality Classification Panel — Arthur S. Leon, M.D.; Ronald Prineas, M.D., M.B.S., Ph.D.; Carl Rubenstein, M.D. (chairman); Joseph Ruwitch, M.D.; and John Wilson, M.D.
Lipid Research Clinics Directors Committee — Francis Abboud, M.D.; W. Stewart Agras, M.D.; Edwin Bierman, M.D.; Reagan Bradford, M.D., Ph.D.; Virgil Brown, M.D.; Marilyn Buzzard, Ph.D.; William Connor, M.D.; Gerald Cooper, M.D., Ph.D.; John Farquhar, M.D.; Ivan Frantz, M.D.; Elena Gerasimova, M.D.; Antonio Gotto, M.D., Ph.D.; James Grizzle, Ph.D.; William R. Hazzard, M.D.; Donald Hunninghake, M.D.; Frank Ibbott, Ph.D.; William Insull, M.D.; Anatoli Klimov, M.D.; Robert Knopp, M.D.; Peter Kwiterovich, M.D.; John C. LaRosa, M.D.; J. Alick Little, M.D.; Fred Mattson, Ph.D.; Maurice Mishkel, M.D.; Basil M. Rifkind, M.D.; Gustav Schonfeld, M.D.; Helmut Schrott, M.D.; Yechezkiel Stein, M.D.; Daniel Steinberg, M.D.; George Steiner, M.D.; and O. Dale Williams, Ph.D.
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Komitzer
CrossRef | Web of Science | Medline36
Study Group, European Atherosclerosis Society
Web of Science | Medline
- Citing Articles (179)
Citing Articles
1
J. Roquer, E. Cuadrado-Godia, A. Rodríguez-Campello, J. Jiménez-Conde, J. E. Martínez-Rodríguez, E. Giralt, A. Ois. (2011) Serum cholesterol levels and survival after rtPA treatment in acute stroke. European Journal of Neurologyno-no
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Tamara B. Horwich, Holly R. Middlekauff, W. Robb Maclellan, Gregg C. Fonarow. (2011) Statins Do Not Significantly Affect Muscle Sympathetic Nerve Activity in Humans With Nonischemic Heart Failure: A Double-Blind Placebo-Controlled Trial. Journal of Cardiac Failure 17:11, 879-886
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Karen E. Porter, Neil A. Turner. (2011) Statins and myocardial remodelling: cell and molecular pathways. Expert Reviews in Molecular Medicine 13,
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M.D. Kertai, E. Boersma, C.M. Westerhout, J. Klein, H. van Urk, J.J. Bax, J.R.T.C. Roelandt, D. Poldermans. (2011) Reprinted Article “A Combination of Statins and Beta-blockers is Independently Associated with a Reduction in the Incidence of Perioperative Mortality and Nonfatal Myocardial Infarction in Patients Undergoing Abdominal Aortic Aneurysm Surgery”. European Journal of Vascular and Endovascular Surgery 42, S96-S104
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Myung Ha Lee, Song Vogue Ahn, Nam Wook Hur, Dong Phil Choi, Hyeon Chang Kim, Il Suh. (2011) Gender differences in the association between smoking and dyslipidemia: 2005 Korean National Health and Nutrition Examination Survey. Clinica Chimica Acta 412:17-18, 1600-1605
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Grant T. Generaux, Fiorenza M. Bonomo, Marta Johnson, Kelly M. Mahar Doan. (2011) Impact of SLCO1B1 (OATP1B1) and ABCG2 (BCRP) genetic polymorphisms and inhibition on LDL-C lowering and myopathy of statins. Xenobiotica 41:8, 639-651
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K.J. Joshipura, M.O. Andriankaja, F.B. Hu, C.S. Ritchie. (2011) Relative utility of 1-h Oral Glucose Tolerance Test as a measure of abnormal glucose homeostasis. Diabetes Research and Clinical Practice 93:2, 268-275
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Tomonori Okamura, Yoshihiro Kokubo, Makoto Watanabe, Aya Higashiyama, Yuu Ono, Kunihiro Nishimura, Akira Okayama, Yoshihiro Miyamoto. (2011) A revised definition of the metabolic syndrome predicts coronary artery disease and ischemic stroke after adjusting for low density lipoprotein cholesterol in a 13-year cohort study of Japanese: The Suita Study. Atherosclerosis 217:1, 201-206
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H. Bays, A. Shah, Q. Dong, C. McCrary Sisk, D. Maccubbin. (2011) Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups. International Journal of Clinical Practice 65:4, 436-445
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Marco Metra, Valerio Zacà, Gianfranco Parati, Piergiuseppe Agostoni, Maria Bonadies, Marco Ciccone, Alessandra Dei Cas, Massimo Iacoviello, Rocco Lagioia, Carolina Lombardi, Raffaele Maio, Damiano Magrì, Giuseppe Musca, Margherita Padeletti, Francesco Perticone, Natalia Pezzali, Massimo Piepoli, Angela Sciacqua, Luisa Zanolla, Savina Nodari, Pasquale Perrone Filardi, Livio Dei Cas. (2011) Cardiovascular and noncardiovascular comorbidities in patients with chronic heart failure. Journal of Cardiovascular Medicine 12:2, 76-84
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Michael H. Davidson, Joanne M. Donovan, Soamnauth Misir, Michael R. Jones. (2010) A 50-Week Extension Study on the Safety and Efficacy of Colesevelam in Adults with Primary Hypercholesterolemia. American Journal Cardiovascular Drugs 10:5, 305-314
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Kyung Hoon Cho, Myung Ho Jeong, Youngkeun Ahn, Young Jo Kim, Shung Chull Chae, Taek Jong Hong, In Whan Seong, Jei Keon Chae, Chong Jin Kim, Myeong Chan Cho, Ki Bae Seung, Seung Jung Park. (2010) Low-Density Lipoprotein Cholesterol Level in Patients With Acute Myocardial Infarction Having Percutaneous Coronary Intervention (the Cholesterol Paradox). The American Journal of Cardiology 106:8, 1061-1068
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M. J. L. Peters, A. E. Voskuyl, N. Sattar, B. A. C. Dijkmans, Y. M. Smulders, M. T. Nurmohamed. (2010) The interplay between inflammation, lipids and cardiovascular risk in rheumatoid arthritis: why ratios may be better. International Journal of Clinical Practice 64:10, 1440-1443
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Claus Jünger, Bernhard Rauch, Steffen Schneider, Nadine Liebhart, Geraldine Rauch, Jochen Senges, Kurt Bestehorn. (2010) Effect of early short-term cardiac rehabilitation after acute ST-elevation and non-ST-elevation myocardial infarction on 1-year mortality. Current Medical Research and Opinion 26:4, 803-811
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Tomonori Okamura, Yoshihiro Kokubo, Makoto Watanabe, Aya Higashiyama, Yuu Ono, Yoshihiro Miyamoto, Yasunao Yoshimasa, Akira Okayama. (2010) Triglycerides and non-high-density lipoprotein cholesterol and the incidence of cardiovascular disease in an urban Japanese cohort: The Suita study. Atherosclerosis 209:1, 290-294
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Loic Desquilbet, François Mariotti. (2010) Dose-response analyses using restricted cubic spline functions in public health research. Statistics in Medicinen/a-n/a
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Rasheed A. Balogun, Adesola Ogunniyi, Kimberly Sanford, Chidi Okafor, Peter I. Lobo, Ghodrat Siami, John Barcia, Andre A. Kaplan. (2010) Therapeutic apheresis in special populations. Journal of Clinical Apheresis 25:5, 265-274
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Shepard D. Weiner, LeRoy E. Rabbani. (2010) Secondary prevention strategies for coronary heart disease. Journal of Thrombosis and Thrombolysis 29:1, 8-24
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Weichao Wang, Hui Xie, Lisha Sun, Lailiang Ou, Lianyong Wang, Yaoting Yu, Deling Kong. (2009) Macroporous poly(vinyl alcohol) microspheres bearing phosphate groups as a new adsorbent for low-density lipoprotein apheresis. Biomedical Materials 4:6, 065007
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Francesco Giallauria, Rosa Lucci, Mariantonietta DʼAgostino, Alessandra Vitelli, Luigi Maresca, Maria Mancini, Mario Aurino, Domenico Del Forno, Pantaleo Giannuzzi, Carlo Vigorito. (2009) Two-year multicomprehensive secondary prevention program: favorable effects on cardiovascular functional capacity and coronary risk profile after acute myocardial infarction. Journal of Cardiovascular Medicine 10:10, 772-780
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Hope R. Ferdowsian, Neal D. Barnard. (2009) Effects of Plant-Based Diets on Plasma Lipids. The American Journal of Cardiology 104:7, 947-956
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T. Malati, M. R. U. Mahesh. (2009) Reference intervals for serum total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, Lp (a), apolipoprotein A-I, A-II, B, C-II, C-III, and E in healthy South Indians from Andhra Pradesh. Indian Journal of Clinical Biochemistry 24:4, 343-355
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Tamara Horwich. (2009) Low-density lipoprotein in the setting of congestive heart failure: Is lower really better?. Current Atherosclerosis Reports 11:5, 343-349
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Tracy Y. Wang, L. Kristin Newby, Anita Y. Chen, Jyotsna Mulgund, Matthew T. Roe, Ali F. Sonel, Deepak L. Bhatt, Elizabeth R. DeLong, E. Magnus Ohman, W. Brian Gibler, Eric D. Peterson. (2009) Hypercholesterolemia Paradox in Relation to Mortality in Acute Coronary Syndrome. Clinical Cardiology 32:9, E22-E28
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Diana R. Chirovsky, Veronika Fedirko, Yadong Cui, Vasilisa Sazonov, Philip Barter. (2009) Prospective studies on the relationship between high-density lipoprotein cholesterol and cardiovascular risk: a systematic review. European Journal of Cardiovascular Prevention & Rehabilitation 16:4, 404-423
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G. R. Hajer, Y. van der Graaf, M. L. Bots, A. Algra, F. L. J. Visseren, . (2009) Low plasma HDL-c, a vascular risk factor in high risk patients independent of LDL-c. European Journal of Clinical Investigation 39:8, 680-688
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Peter W. Parodi. (2009) Has the association between saturated fatty acids, serum cholesterol and coronary heart disease been over emphasized?. International Dairy Journal 19:6-7, 345-361
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Tomonori Okamura, Yoshihiro Kokubo, Makoto Watanabe, Aya Higashiyama, Yoshihiro Miyamoto, Yasunao Yoshimasa, Akira Okayama. (2009) Low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol and the incidence of cardiovascular disease in an urban Japanese cohort study: The Suita study. Atherosclerosis 203:2, 587-592
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Umakanta Subudhi, Kajari Das, Biswaranjan Paital, Shravani Bhanja, Gagan B.N. Chainy. (2009) Supplementation of curcumin and vitamin E enhances oxidative stress, but restores hepatic histoarchitecture in hypothyroid rats. Life Sciences 84:11-12, 372-379
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Terri Montague, Barbara Murphy. (2009) Lipid Management in Chronic Kidney Disease, Hemodialysis, and Transplantation. Endocrinology & Metabolism Clinics of North America 38:1, 223-234
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Sanjay Patel, Brian G. Drew, Shirley Nakhla, Stephen J. Duffy, Andrew J. Murphy, Phillip J. Barter, Kerry-Anne Rye, Jaye- Chin-Dusting, Anh Hoang, Dmitri Sviridov, David S. Celermajer, Bronwyn A. Kingwell. (2009) Reconstituted High-Density Lipoprotein Increases Plasma High-Density Lipoprotein Anti-Inflammatory Properties and Cholesterol Efflux Capacity in Patients With Type 2 Diabetes. Journal of the American College of Cardiology 53:11, 962-971
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Tamara B. Horwich, Adrian F. Hernandez, David Dai, Clyde W. Yancy, Gregg C. Fonarow. (2008) Cholesterol levels and in-hospital mortality in patients with acute decompensated heart failure. American Heart Journal 156:6, 1170-1176
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Benjamin A. Steinberg, Deepak L. Bhatt, Shamir Mehta, Philip A. Poole-Wilson, Philip O'Hagan, Gilles Montalescot, Christie M. Ballantyne, Christopher P. Cannon. (2008) Nine-year trends in achievement of risk factor goals in the US and European outpatients with cardiovascular disease. American Heart Journal 156:4, 719-727
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Patrizio Sarto, Laura Merlo, Giampaolo Pasquetto, Pierluigi Zanco, Pietro Pascotto, Donatella Noventa, Bernhard Reimers. (2008) Competitive sport after coronary angioplasty: suggested eligibility criteria for moderate-high intensity sport. Journal of Cardiovascular Medicine 9:6, 631-635
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Alicja Szklarska, Anna Lipowicz, Monika Lopuszanska, Tadeusz Bielicki, Sławomir Koziel. (2008) Biological condition of adult migrants and nonmigrants in Wrocław, Poland. American Journal of Human Biology 20:2, 139-145
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Pantel S. Vokonas, William B. Kannel. 2008. Epidemiology of Coronary Heart Disease in the Elderly. , 215-242.
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Chris Wallace, Stephen J. Newhouse, Peter Braund, Feng Zhang, Martin Tobin, Mario Falchi, Kourosh Ahmadi, Richard J. Dobson, Ana Carolina B. Marçano, Cother Hajat, Paul Burton, Panagiotis Deloukas, Morris Brown, John M. Connell, Anna Dominiczak, G. Mark Lathrop, John Webster, Martin Farrall, Tim Spector, Nilesh J. Samani, Mark J. Caulfield, Patricia B. Munroe. (2008) Genome-wide Association Study Identifies Genes for Biomarkers of Cardiovascular Disease: Serum Urate and Dyslipidemia. The American Journal of Human Genetics 82:1, 139-149
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Csaba P. Kovesdy, John E. Anderson. (2007) CARDIOVASCULAR AND SURVIVAL PARADOXES IN DIALYSIS PATIENTS: Reverse Epidemiology in Patients with Chronic Kidney Disease Who Are Not Yet on Dialysis. Seminars in Dialysis 20:6, 566-569
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James K. Liao. (2007) Does it matter whether or not a lipid-lowering agent inhibits Rho kinase?. Current Atherosclerosis Reports 9:5, 384-388
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Catherine Y. Campbell, Khurram Nasir, Ammar Sarwar, Romeu S. Meneghelo, Jose A.M. Carvalho, Roger S. Blumenthal, Raul D. Santos. (2007) Combined Effect of High Low-Density Lipoprotein Cholesterol and Metabolic Syndrome on Subclinical Coronary Atherosclerosis in White Men Without Clinical Evidence of Myocardial Ischemia. The American Journal of Cardiology 100:5, 840-843
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F. Cohen Aubart, B. Hansel, J.-S. Hulot, P. Lechat, E. Bruckert. (2007) Avancées récentes et perspectives dans le traitement des dyslipidémies athérogènes. La Revue de Médecine Interne 28:8, 537-544
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James E Sharman, Carmel M McEniery, Zahid R Dhakam, Jeff S Coombes, Ian B Wilkinson, John R Cockcroft. (2007) Pulse pressure amplification during exercise is significantly reduced with age and hypercholesterolemia. Journal of Hypertension 25:6, 1249-1254
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D LIU, B HE, S HAN, S WANG, Q LIU, A JUNICHI, T OSA, Q CHEN. (2007) An adsorption behavior of low-density lipoprotein onto cholesterol-modified dextran studied by a quartz crystal microbalance. Materials Science and Engineering: C 27:4, 665-669
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A. V. Antonchick, V. N. Zhabinskii, V. A. Khripach. (2007) Oxysterols: Genesis and basic functions. Russian Journal of Bioorganic Chemistry 33:3, 275-287
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Haofeng Yu, Guoqi Fu, Binglin He. (2007) Preparation and adsorption properties of PAA-grafted cellulose adsorbent for low-density lipoprotein from human plasma. Cellulose 14:2, 99-107
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B. Greg Brown, Xue-Qiao Zhao, Marian C. Cheung. (2007) Should both HDL-C and LDL-C be targets for lipid therapy? A review of current evidence. Journal of Clinical Lipidology 1:1, 88-94
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Eric J. Stanek, Chaitanya Sarawate, Vincent J. Willey, Scott L. Charland, Mark J. Cziraky. (2007) Risk of cardiovascular events in patients at optimal values for combined lipid parameters. Current Medical Research and Opinion 23:3, 553-563
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Yukio Mizuguchi, Yoshifumi Oishi, Hirokazu Miyoshi, Arata Iuchi, Norio Nagase, Takashi Oki. (2007) Impact of Statin Therapy on Left Ventricular Function and Carotid Arterial Stiffness in Patients With Hypercholesterolemia. Circulation Journal 72:4, 538-544
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Michael H Davidson, Jennifer G Robinson. 2006. Management of Elevated Low-Density Lipoprotein Cholesterol. , 255-294.
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John J. CHANG, John CONCATO, Carolyn K. WELLS, Susan T. CROWLEY. (2006) Prognostic implications of clinical practice guidelines among hemodialysis patients. Hemodialysis International 10:4, 399-407
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Deepa Gopalan, Steven M. Thomas. (2006) Pharmacotherapy for patients undergoing carotid stenting. European Journal of Radiology 60:1, 14-19
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José Félix Meco López, Emili Corbella Ingles, Carmen Sanclemente Anso, Marta Miralles Fortuny, Iziar Sarasa Corral, Ramon Pujol Farriols, Xavier Pintó Sala. (2006) Efectividad de un programa de prevención secundaria de la arteriosclerosis en el control de las dislipemias en pacientes con enfermedad arterial coronaria. Clínica e Investigación en Arteriosclerosis 18:4, 128-136
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F. Hadaegh, H. Harati, A. Ghanbarian, F. Azizi. (2006) Association of total cholesterol versus other serum lipid parameters with the short-term prediction of cardiovascular outcomes: Tehran Lipid and Glucose Study. European Journal of Cardiovascular Prevention & Rehabilitation 13:4, 571-577
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Niklas Rudholm. (2006) A comparison of population versus individual based cardiovascular disease prevention programs in Västerbotten, Sweden. Health Policy 78:1, 70-76
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Steven G. Chrysant, Mohammad Ibrahim. (2006) Niacin-ER/Statin Combination for the Treatment of Dyslipidemia: Focus on Low High-Density Lipoprotein Cholesterol. The Journal of Clinical Hypertension 8:7, 493-501
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MG Law, N Friis-Moller, WM El-Sadr, R Weber, P Reiss, A D'Arminio Monforte, R Thiebaut, L Morfeldt, S De Wit, C Pradier, G Calvo, O Kirk, CA Sabin, AN Phillips, JD Lundgren, . (2006) The use of the Framingham equation to predict myocardial infarctions in HIV-infected patients: comparison with observed events in the D:A:D Study. HIV Medicine 7:4, 218-230
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Leiv Ose, Arvind Shah, Michael J. Davies, Jennifer Rotonda, Darbie Maccubbin, Diane Tribble, Enrico Veltri, Yale Mitchel. (2006) Consistency of lipid-altering effects of ezetimibe/simvastatin across gender, race, age, baseline low density lipoprotein cholesterol levels, and coronary heart disease status: results of a pooled retrospective analysis. Current Medical Research and Opinion 22:5, 823-835
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Julia L. Newton, John Allen, Simon Kerr, David E. J. Jones. (2006) Reduced heart rate variability and baroreflex sensitivity in primary biliary cirrhosis. Liver International 26:2, 197-202
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Guoqi Fu, Haiyan Li, Haofeng Yu, Li Liu, Zhi Yuan, Binglin He. (2006) Synthesis and lipoprotein sorption properties of porous chitosan beads grafted with poly(acrylic acid). Reactive and Functional Polymers 66:2, 239-246
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Terry A. Jacobson, Franklin H. Zimmerman. (2006) Fibrates in Combination With Statins in the Management of Dyslipidemia. The Journal of Clinical Hypertension 8:1, 35-41
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É. P. Serebryakov, G. V. Kryshtal’, G. M. Zhdankina, A. G. Nigmatov, V. V. Tertov, L. V. Filatova. (2006) Synthetic analogs of phytanic acid and their effect on human hepatic cholesterol esterase in vitro. Pharmaceutical Chemistry Journal 40:1, 23-28
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Scott Kinlay. (2005) Potential vascular benefits of statins. The American Journal of Medicine 118:12, 62-67
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Ewoud ter Avest, Evertine J. Abbink, Suzanne Holewijn, Jacqueline de Graaf, Cees J. Tack, Anton F. H. Stalenhoef. (2005) Effects of rosuvastatin on endothelial function in patients with familial combined hyperlipidaemia (FCH). Current Medical Research and Opinion 21:9, 1469-1476
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Thomas F. Rehring, Brian G. Sandhoff, Ryan S. Stolcpart, John A. Merenich, H. Whitton Hollis. (2005) Atherosclerotic risk factor control in patients with peripheral arterial disease. Journal of Vascular Surgery 41:5, 816-822
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Shinji Yokoyama, Hisao Ikeda, Nobuya Haramaki, Hideo Yasukawa, Atsushi Katoh, Tsutomu Imaizumi. (2005) HMG-CoA Reductase Inhibitor Protects Against In Vivo Arterial Thrombosis by Augmenting Platelet-Derived Nitric Oxide Release in Rats. Journal of Cardiovascular Pharmacology 45:4, 375-381
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J. K. VIRTANEN, S. VOUTILAINEN, G. ALFTHAN, M. J. KORHONEN, T. H. RISSANEN, J. MURSU, G. A. KAPLAN, J. T. SALONEN. (2005) Homocysteine as a risk factor for CVD mortality in men with other CVD risk factors: the Kuopio Ischaemic Heart Disease Risk Factor (KIHD) Study. Journal of Internal Medicine 257:3, 255-262
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James K. Liao, Ulrich Laufs. (2005) PLEIOTROPIC EFFECTS OF STATINS. Annual Review of Pharmacology and Toxicology 45:1, 89-118
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L. Janoskuti, Z. Forhecz, N. Hosszufalusi, M. Kleiber, S. Walentin, O. Balint, J. Duba, S. Rugonfalvi-Kiss, L. Romics, I. Karadi, G. Fust, Z. Prohaszka. (2005) High levels of C-reactive protein with low total cholesterol concentrations additively predict all-cause mortality in patients with coronary artery disease. European Journal of Clinical Investigation 35:2, 104-111
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Serena Tonstad. (2005) Epidemiology and Genetics, Morbidity and Mortality of Lipid-Associated Cardiovascular Disorders. Heart Drug 5:1, 29-33
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Mehmet Kanbay, Aylin Yildirir, Hüseyin Bozbas, Taner Ulus, Muhammet Bilgi, Haldun Muderrisoglu, Ali Akcay, Fatma Nurhan Ozdemir. (2005) Statin Therapy Helps to Control Blood Pressure Levels in Hypertensive Dyslipidemic Patients. Renal Failure 27:3, 297-303
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Nurzen Sezgin, Alpay T. Sezgin, Hakan Gullu, Aysun Karabulut, Irfan Barutcu, Ergun Topal, Defne Yalcintas, Ismail Temel. (2005) Decreased Serum Lipoprotein Levels as a Guide for Clinical Severity in Patients with Idiopathic Dilated Cardiomyopathy. The Tohoku Journal of Experimental Medicine 206:3, 219-224
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L. D. Woodard, N. R. Kressin, L. A. Petersen. (2004) Is Lipid-Lowering Therapy Underused by African Americans at High Risk of Coronary Heart Disease Within the VA Health Care System?. American Journal of Public Health 94:12, 2112-2117
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M.D. Kertai, E. Boersma, C.M. Westerhout, J. Klein, H. van Urk, J.J. Bax, J.R.T.C. Roelandt, D. Poldermans. (2004) A Combination of Statins and Beta-blockers is Independently Associated with a Reduction in the Incidence of Perioperative Mortality and Nonfatal Myocardial infarction in Patients Undergoing Abdominal Aortic Aneurysm Surgery. European Journal of Vascular and Endovascular Surgery 28:4, 343-352
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Sanjaya Khanal, Omar Obeidat, Mei Lu, Lori Douthat, Michael P. Hudson, Adam B. Greenbaum, Aaron Kugelmass, W. Douglas Weaver. (2004) Dyslipidemia in patients with angiographically confirmed coronary artery disease-an opportunity for improvement. Clinical Cardiology 27:10, 577-580
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J. D. Curb. (2004) High Density Lipoprotein Cholesterol and the Risk of Stroke in Elderly Men: The Honolulu Heart Program. American Journal of Epidemiology 160:2, 150-157
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P.Michael Ho, Frederick A Masoudi, Eric D Peterson, Gary K Grunwald, Anne E Sales, Karl E Hammermeister, John S Rumsfeld. (2004) Cardiology management improves secondary prevention measures among patients with coronary artery disease. Journal of the American College of Cardiology 43:9, 1517-1523
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Jennifer E Zimmer, Charles R Spillert, Sirisha Puppala, Katherine Zamecki, Biren A Bhatt, Rohit R Arora. (2004) Pravastatin potentiates the anticoagulant effects of low molecular weight heparin. Thrombosis Research 113:6, 407-410
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Elke Naumann, Jogchum Plat, Ronald Mensink. 2003. Plant Sterols and Stanols, Lipoprotein Metabolism, and Cardiovascular Disease. .
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Gregg C Fonarow, Tamara B Horwich. (2003) Cholesterol and mortality in heart failure: the bad gone good?. Journal of the American College of Cardiology 42:11, 1941-1943
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Ulrich Laufs, James K. Liao. (2003) Isoprenoid metabolism and the pleiotropic effects of statins. Current Atherosclerosis Reports 5:5, 372-378
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LilyAnn Jeu, Judy W.M. Cheng. (2003) Pharmacology and therapeutics of ezetimibe (SCH 58235), a cholesterol-absorption inhibitor. Clinical Therapeutics 25:9, 2352-2387
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Michael Miller, Min Zhan. (2003) Factors influencing coronary risk in low HDL syndromes. Atherosclerosis 169:2, 347-348
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Paul Durrington. (2003) Dyslipidaemia. The Lancet 362:9385, 717-731
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Shenqi Wang, Yaoting Yu, Tao Cui, Yan Cheng. (2003) A novel amphiphilic adsorbent for the removal of low-density lipoprotein. Biomaterials 24:16, 2799-2802
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Christopher S. Gray. 2003. Cerebrovascular Disease in Diabetes Mellitus. .
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D.R. Lewis, J.F. Bolton, S. Hebard, F.C. Smith, R.N. Baird, P.M. Lamont. (2003) Risk Factor Documentation in Elective and Emergency Vascular Surgical Admissions. European Journal of Vascular and Endovascular Surgery 25:6, 568-572
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Yan Cheng, Shenqi Wang, Yaoting Yu, Yi Yuan. (2003) In vitro, in vivo studies of a new amphiphilic adsorbent for the removal of low-density lipoprotein. Biomaterials 24:13, 2189-2194
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Philip Barter, John Kastelein, Alistair Nunn, Richard Hobbs. (2003) High density lipoproteins (HDLs) and atherosclerosis; the unanswered questions. Atherosclerosis 168:2, 195-211
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Stephen L. Seliger, Catherine O. Stehman-Breen. (2003) Editorials: Are HMG-CoA Reductase Inhibitors Underutilized in Dialysis Patients?. Seminars in Dialysis 16:3, 179-185
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Masazumi AKAHOSHI, Yasuko AMASAKI, Midori SODA, Ayumi HIDA, Misa IMAIZUMI, Eiji NAKASHIMA, Renju MAEDA, Shinji SETO, Katsusuke YANO. (2003) Effects of Radiation on Fatty Liver and Metabolic Coronary Risk Factors among Atomic Bomb Survivors in Nagasaki. Hypertension Research 26:12, 965-970
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R.M. Pigeon, E.P. Cuesta, S.E. Gilliland. (2002) Binding of Free Bile Acids by Cells of Yogurt Starter Culture Bacteria. Journal of Dairy Science 85:11, 2705-2710
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Glenn A. Hirsch, Nidhi Vaid, Roger S. Blumenthal. (2002) The Significance of Measuring Non-HDL-Cholesterol. Preventive Cardiology 5:3, 156-159
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Kunitoshi Iseki, Masanobu Yamazato, Masahiko Tozawa, Shuichi Takishita. (2002) Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney International 61:5, 1887-1893
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Alan Cheng, Joel B. Braunstein, Cheryl Dennison, Caitlin Nass, Roger S. Blumenthal. (2002) Reducing global risk for cardiovascular disease: Using lifestyle changes and pharmacotherapy. Clinical Cardiology 25:5, 205-212
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Albert Ferro. (2002) Statins and vascular protection: a ‘radical’ view. Journal of Hypertension 20:3, 359-361
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C. Parkinson, W. M. Drake, G. Wieringa, A. P. Yates, G. M. Besser, P. J. Trainer. (2002) Serum lipoprotein changes following IGF-I normalization using a growth hormone receptor antagonist in acromegaly. Clinical Endocrinology 56:3, 303-311
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D. Dutta, B. Ogunnaike. (2002) Lipid lowering after myocardial infarction in hospital practice. British Journal of Clinical Governance 7:3, 154-157
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Stephen L. Seliger, Noel S. Weiss, Daniel L. Gillen, Bryan Kestenbaum, Adrianne Ball, Donald J. Sherrard, Catherine O. Stehman-Breen. (2002) HMG-CoA reductase inhibitors are associated with reduced mortality in ESRD patients. Kidney International 61:1, 297-304
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D. P. ALLDRED, C. BOOTH, H. CHRYSTYN. (2001) Development of a pharmacist-led cholesterol screening and lipid-lowering medication review service in coronary artery bypass graft patients. International Journal of Pharmacy Practice 9:4, 275-281
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Leon A. Simons, Judith Simons, Yechiel Friedlander, John McCallum. (2001) Cholesterol and other lipids predict coronary heart disease and ischaemic stroke in the elderly, but only in those below 70 years. Atherosclerosis 159:1, 201-208
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Riikka Malin, Reijo Laaksonen, Juhani Knuuti, Tuula Janatuinen, Risto Vesalainen, Pirjo Nuutila, Terho Lehtimaki. (2001) Pharmacogenetics 11:7, 625-633
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Sidney Rosenblatt, Barry Miskin, N. Bradly Glazer, Melvin J. Prince, Kenneth E. Robertson. (2001) The impact of pioglitazone on glycemic control and atherogenic dyslipidemia in patients with type 2 diabetes mellitus. Coronary Artery Disease 12:5, 413-423
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Matteo Longo, Andrea Crosignani, Mauro Podda. (2001) Hyperlipidemia in chronic cholestatic liver disease. Current Treatment Options in Gastroenterology 4:2, 111-114
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Steven I. Aronin, Vincent J. Quagliarello. (2001) Utility of prognostic stratification in adults with community-acquired bacterial meningitis. Comprehensive Therapy 27:1, 72-77
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Domenico Ferro, Sandro Parrotto, Stefania Basili, Cesare Alessandri, Francesco Violi. (2000) Simvastatin inhibits the monocyte expression of proinflammatory cytokines in patients with hypercholesterolemia. Journal of the American College of Cardiology 36:2, 427-431
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John H. Contois, Alan H.B. Wu, Zemin Li, Amna H. Feroze, Fabienne Grunenberger, Jürg Haller, Lisette deGroot, Carol J. Lammi-Keefe. (2000) Distribution of serum apolipoproteins A-I and B and lipoprotein(a) in European elderly. Clinica Chimica Acta 295:1-2, 1-12
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Maria Fiatarone Singh, Jeanne Wei. 2000. Cardiovascular Disease and Hypertension. , 279-316.
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