- Email: [email protected]
Relation of family history of premature coronary heart disease and metabolic risk factors to risk of coronary arterial calcium in asymptomatic subjects
Relation of Family History of Premature Coronary Heart Disease and Metabolic Risk Factors to Risk of Coronary Arterial Calcium in Asymptomatic Subjects Erin D. Michos, MD, Khurram Nasir, MD, MPH, John A. Rumberger, MD, PhD, Chandra Vasamreddy, MD, Joel B. Braunstein, MD, MBA, Matthew J. Budoff, MD, and Roger S. Blumenthal, MD We studied 6,141 consecutive, asymptomatic, nondiabetic patients who underwent electron beam tomography and explored the interaction between metabolic risk factors (RFs) and premature family history (FH) of coronary heart disease (CHD) in predicting the presence and severity of coronary arterial calcium (CAC). In the presence of >2 metabolic RFs, patients with a positive FH of premature CHD had a significantly higher prevalence of any CAC, CAC >100, and CAC >75th age-gender percentile than those without a FH of CHD. Our study demonstrated that a familial propensity to subclinical atherosclerosis interacts with the presence of >2 metabolic RFs, magnifying the risks for those exposed to both. 䊚2005 by Excerpta Medica Inc. (Am J Cardiol 2005;95:655– 657)
e hypothesized that subjects with a family history (FH) of premature coronary heart disease W (CHD) may be more susceptible to the adverse effects of an increasing number of metabolic risk factors (RFs) than subjects without a FH. We assessed whether the presence of multiple metabolic RFs posed a higher risk for coronary arterial calcium (CAC) among asymptomatic patients with a FH of premature CHD than for those without any familial predisposition. •••
We performed a cross-sectional study on 13,389 consecutive, physician-referred patients who presented to a single, independent scanning facility in Columbus, Ohio, to undergo an electron beam tomographic study between 1999 and 2003. Patients with incomplete data regarding their metabolic RFs were excluded (n ⫽ 1,875). We excluded patients who reported any personal history of CHD defined by previous myocardial infarction, coronary/peripheral arterial revascularization (n ⫽ 322), or any current symptoms potentially suggestive of angina (n ⫽ From the Ciccarone Preventative Cardiology Center, Johns Hopkins University, School of Medicine, Baltimore, Maryland; Division of Cardiology, The Ohio State University, Columbus, Ohio; and Division of Cardiology, Saint John’s Cardiovascular Research Center, Torrance, California. This work was supported by an unrestricted educational grant by the Maryland Athletic Club Charitable Foundation, Lutherville, Maryland. Dr. Blumenthal’s address is: Ciccarone Preventive Cardiology Center, Blalock 524 C-Division of Cardiology, The Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, Maryland 21287. E-mail: [email protected]. Manuscript received August 24, 2004; revised manuscript received and accepted October 27, 2004. ©2005 by Excerpta Medica Inc. All rights reserved. The American Journal of Cardiology Vol. 95 March 1, 2005
TABLE 1 Baseline Coronary Heart Disease Risk Factors (RF) (n ⫽ 6,141) 55 ⫾ 9 68% 29% 28% 7% 4% 9% 32%
Age (yrs) Men Hypertension Dyslipidemia Low HDL High triglycerides Current smoker Obesity Metabolic RFs None 1 ⱖ2
47% 36% 17%
HDL ⫽ high-density lipoprotein cholesterol.
4,518) defined by self-reports of chest pain, chest pressure, or chest tightness. Subjects with diabetes mellitus were also excluded (n ⫽ 534), because it is considered to be a CHD risk equivalent, leaving a total study population of 6,141 asymptomatic patients free of known CHD at the time of screening. This study was approved by the local institutional review board and received a waiver of patient consent. Metabolic RFs assessed were hypertension, hypertriglyceridemia, low high-density lipoprotein cholesterol, and obesity (body mass index ⱖ30 kg/m2). Patients were considered hypertensive if they reported a previous physician diagnosis of hypertension and were currently taking antihypertensive medications. Triglycerides and high-density lipoprotien cholesterol levels were self-reported and classified as high, normal, and low. Body mass index was calculated from patients who provided a self-report of height and weight. Patients with body mass index ⱖ30 kg/m2 were considered obese. FH of CHD was obtained by asking patients whether any member in their immediate family (parents or siblings) experienced a fatal or nonfatal myocardial infarction and/or coronary revascularization before or after age 55 years by the questionnaire. The event was considered premature if it occurred at ⬍55 years. Each patient underwent electron beam tomographic scanning using an Imatron scanner (Imatron, South San Francisco, California). Coronary arteries were imaged with rapid acquisition of approximately 30 to 40 contiguous images operating with a slice thickness of 3 mm, a spatial resolution of 1.3 mm full-width at half-maximum, a field-of-view of 26 cm, a threshold of 130 HU, and image acquisition of 100 0002-9149/05/$–see front matter doi:10.1016/j.amjcard.2004.10.045
655
The total calcium score was calculated by summing CAC scores from the left main, left anterior descending, left circumflex, and right coronary arteries. RF ⫽ 0 RF ⫽ 1 RF ⱖ2 p Value Age-gender–adjusted median CAC No FH of CHD 14 (12–15) 16 (14–18) 20 (17–23) 0.0001 scores according to FH and increasFH of premature CHD 19 (16–22) 25 (21–28) 39 (33–43) ⬍0.0001 ing numbers of metabolic RFs were compared by median tests. The prevalence of any coronary calcium (positive scores ⬎0), as well as the prevalence of CAC ⱖ100 (moderate calcification)2 and CAC ⱖ75th percentile matched for age and gender,3 was determined in the population across metabolic RFs and FH of premature CHD categories. CAC ⱖ75th percentile for age-gender was considered “advanced CAC.” Logistic regression was used to examine the odds of having CAC associated with increasing metabolic RFs, adjusting for covariates, in the group without any metabolic RFs as the reference. All covariates (age, gender, physical activity, smoking status, and selfreported hypercholesteremia) were forced into the models simultaneously. We tested whether the odds of calcification associated with increasing metabolic RFs were the same in those with and without a FH of premature CHD by including a metabolic RF-by-FH of premature CHD interaction term in the model. All statistical analyses were performed using Stata software, version 8.0 (Austin, Texas). The study population consisted of 6,141 asymptomatic patients (mean age 55 ⫾ 9 years; 68% men) whose baseline characteristics are listed in Table 1. Twenty-six percent of the study population had a FH of premature CHD. Two or more metabolic RFs were presented in 17% of study participants. The age-gender–adjusted median CAC scores across increasing numbers of metabolic RF were higher in patients with a positive FH for premature CHD than in those without a FH, indicating increased coronary atherosclerotic burden (Table 2). The prevalence of any CAC (Figure 1), CAC ⱖ100 (Figure 1), and CAC ⱖ75th age-gender percentile (Figure 1) were all significantly higher with increasing metabolic RF as well with the presence of a FH of premature CHD. The prevalence of any CAC, as well as the extent of CAC, was the lowest among those with no FH of CHD and no metabolic RFs, whereas the highest prevalence was observed among patients with a positive FH of CHD as well ⱖ2 metabolic RFs. The relation persisted after adjusting for covariates among participants with or without a FH of premature CHD (Table 3). The odds ratio for any CAC associated with the presence of ⱖ2 metabolic RFs was significantly higher in those who had a FH of premaFIGURE 1. (A) Prevalence (percent) of any CAC by increasing ture CHD than in those without any FH of CHD. Similar metabolic RFs and categories of FH of premature CHD. (B) Prevainteractions were also observed for CAC ⱖ100 and CAC lence (percent) of CAC >100 by increasing metabolic RFs and ⱖ75th percentile. There was no significant interaction categories of FH of premature CHD. (C) Prevalence (percent) of with gender plus increasing metabolic RFs on CAC; any CAC >75th percentile by increasing metabolic RFs and catealso, effects were similar whether FH of premature CHD gories of FH of premature CHD. was reported in a parent or sibling. ms prospectively triggered at 60% to 80% of the RR ••• (electrocardiographic) interval. CAC was quantified usWe previously described that a FH of premature ing the previously described Agatston scoring method.1 CHD is independently associated with higher burden TABLE 2 Age-gender–adjusted Median (95% CI) Coronary-arterial Calcium Scores according to Metabolic Risk Factors (RFs) and Family History (FH) of Premature Coronary Heart Disease (CHD)
656 THE AMERICAN JOURNAL OF CARDIOLOGY姞
VOL. 95
MARCH 1, 2005
TABLE 3 Odd Ratios (95% confidence intervals) for Presence and Extent of Arterial Coronary Calcium (CAC) With Increasing Metabolic Risk Factors (RFs) Among Subjects With and Without a Family History (FH) of Premature Coronary Heart Disease (CHD) RF ⫽ 1
CAC ⬎0 CAC ⱖ100 CAC ⱖ75th percentile
No FH of CHD
FH of Premature CHD
1.4 (1.0–1.6) 1.3 (1.1–1.7) 1.5 (1.2–1.8)
1.6 (1.3–2.1) 1.3 (1.0–1.8) 1.7 (1.3–2.2)
RF ⱖ2
Interaction
No FH of CHD
FH of Premature CHD
Interaction
1.1 (0.8–1.5) 1.0 (0.7–1.4) 1.1 (0.8–1.5)
2.4 (1.9–2.9) 1.7 (1.4–2.1) 1.9 (1.5–2.4)
3.3 (2.4–4.7) 2.3 (1.6–3.3) 2.8 (2.0–3.7)
1.4 (1.0–2.2) 1.4 (1.0–2.4) 1.5 (1.0–2.2)
Reference category is RF ⫽ 0, adjusted for age, gender, smoking status, hypercholesterolemia, and physical activity.
of CAC.4 Arad et al5 previously described the presence of higher CAC scores with an increasing number of metabolic RFs. Our study extends the findings by demonstrating that patients with a FH of premature CHD were more likely to have a higher burden of coronary atherosclerosis in the presence of multiple (ⱖ2) metabolic RFs than those without any FH of CHD. The presence of just 1 metabolic RF was not associated with a higher risk of CAC among those with a self-reported FH of premature CHD. The results of our study should be interpreted in the context of several limitations. We used self-reported RFs and FH of CHD. Despite the potential for some under-reporting or misclassification of RFs, Hoff et al6 described the validity of self-reported histories of hypercholesterolemia, diabetes, and hypertension in self-referred patients for electron beam tomographic scanning, although the validity of self-reported low high-density lipoprotein cholesterol and high triglycerides is not well studied. Also, because CHD RFs were self-reported, potential “residual confounding” cannot be ruled out. Studies have demonstrated a sensitivity of 68% to 86% and specificities ranging from 86% to 98% for a reported FH of CHD7,8; most likely the bias in recalling a FH of CHD is toward the null.9 In our study, fasting blood glucose was not recorded; as a result, we could not assign a definition of “metabolic syndrome” to the participants. However, it has been recently shown that an increase in the metabolic syndrome score (even if the score is ⬍3) confers an increase in severity of angiographic CHD
and overall cardiac risk.10 In the same study, it was shown that distribution of metabolic RFs follows a Gaussian distribution, and most patients are likely to have a metabolic syndrome score of 2 to 3.10 1. Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte M Jr, Detrano R. Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol 1990;15:827– 832. 2. Rumberger JA, Brundage BH, Rader DJ, Kondos G. Electron beam computed tomographic coronary calcium scanning: a review and guidelines for use in asymptomatic persons. Mayo Clin Proc 1999;74:243–252. 3. Nasir K, Raggi P, Rumberger JA, Braunstein JB, Post WS, Budoff MJ, Blumenthal RS. Coronary artery calcium volume scores on electron beam tomography in 12,936 asymptomatic adults. Am J Cardiol 2004;93:1146 –1149. 4. Nasir K, Michos ED, Rumberger JA, Braunstein JB, Post WS, Budoff MJ, Blumenthal RS. Coronary artery calcification and family history of premature coronary heart disease: sibling history is more strongly associated than parental history. Circulation 2004;110:2150 –2156. 5. Arad Y, Newstein D, Cadet F, Roth M, Guerci A. Association of multiple risk factors and insulin resistance with increased prevalence of asymptomatic coronary artery disease by an electron-beam computed tomographic study. Arterioscler Thromb Vasc Biol 2001;21:2051–2058. 6. Hoff JA, Daviglus ML, Chomka EV, Krainik AJ, Sevrukov A, Kondos GT. Conventional coronary artery disease risk factors and coronary artery calcium detected by electron beam tomography in 30,908 healthy individuals. Ann Epidemiol 2003;13:163–169. 7. Murabito JM, Nam BH, D’Agostino RB Sr, Lloyd-Jones DM, O’Donnell CJ, Wilson PW. Accuracy of offspring reports of parental cardiovascular disease history: the Framingham Offspring Study. Ann Intern Med 2004;140:434 – 440. 8. Watt G, McConnachie A, Upton M, Emslie C, Hunt K. How accurately do adult sons and daughters report and perceive parental deaths from coronary disease? J Epidemiol Community Health 2000;11:859 – 863. 9. Silberberg JS, Wlodarczyk J, Fryer J, Ray CD, Hensley MJ. Correction for biases in a population-based study of family history and coronary heart disease. The Newcastle Family History Study I. Am J Epidemiol 1998;147:1123–1132. 10. Solymoss BC, Bourassa MG, Campeau L, Sniderman A, Marcil M, Lesperance J, Levesque S, Varga S. Effect of increasing metabolic syndrome score on atherosclerotic risk profile and coronary artery disease angiographic severity. Am J Cardiol 2004;93:159 –164.
BRIEF REPORTS
657
e hypothesized that subjects with a family history (FH) of premature coronary heart disease W (CHD) may be more susceptible to the adverse effects of an increasing number of metabolic risk factors (RFs) than subjects without a FH. We assessed whether the presence of multiple metabolic RFs posed a higher risk for coronary arterial calcium (CAC) among asymptomatic patients with a FH of premature CHD than for those without any familial predisposition. •••
We performed a cross-sectional study on 13,389 consecutive, physician-referred patients who presented to a single, independent scanning facility in Columbus, Ohio, to undergo an electron beam tomographic study between 1999 and 2003. Patients with incomplete data regarding their metabolic RFs were excluded (n ⫽ 1,875). We excluded patients who reported any personal history of CHD defined by previous myocardial infarction, coronary/peripheral arterial revascularization (n ⫽ 322), or any current symptoms potentially suggestive of angina (n ⫽ From the Ciccarone Preventative Cardiology Center, Johns Hopkins University, School of Medicine, Baltimore, Maryland; Division of Cardiology, The Ohio State University, Columbus, Ohio; and Division of Cardiology, Saint John’s Cardiovascular Research Center, Torrance, California. This work was supported by an unrestricted educational grant by the Maryland Athletic Club Charitable Foundation, Lutherville, Maryland. Dr. Blumenthal’s address is: Ciccarone Preventive Cardiology Center, Blalock 524 C-Division of Cardiology, The Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, Maryland 21287. E-mail: [email protected]. Manuscript received August 24, 2004; revised manuscript received and accepted October 27, 2004. ©2005 by Excerpta Medica Inc. All rights reserved. The American Journal of Cardiology Vol. 95 March 1, 2005
TABLE 1 Baseline Coronary Heart Disease Risk Factors (RF) (n ⫽ 6,141) 55 ⫾ 9 68% 29% 28% 7% 4% 9% 32%
Age (yrs) Men Hypertension Dyslipidemia Low HDL High triglycerides Current smoker Obesity Metabolic RFs None 1 ⱖ2
47% 36% 17%
HDL ⫽ high-density lipoprotein cholesterol.
4,518) defined by self-reports of chest pain, chest pressure, or chest tightness. Subjects with diabetes mellitus were also excluded (n ⫽ 534), because it is considered to be a CHD risk equivalent, leaving a total study population of 6,141 asymptomatic patients free of known CHD at the time of screening. This study was approved by the local institutional review board and received a waiver of patient consent. Metabolic RFs assessed were hypertension, hypertriglyceridemia, low high-density lipoprotein cholesterol, and obesity (body mass index ⱖ30 kg/m2). Patients were considered hypertensive if they reported a previous physician diagnosis of hypertension and were currently taking antihypertensive medications. Triglycerides and high-density lipoprotien cholesterol levels were self-reported and classified as high, normal, and low. Body mass index was calculated from patients who provided a self-report of height and weight. Patients with body mass index ⱖ30 kg/m2 were considered obese. FH of CHD was obtained by asking patients whether any member in their immediate family (parents or siblings) experienced a fatal or nonfatal myocardial infarction and/or coronary revascularization before or after age 55 years by the questionnaire. The event was considered premature if it occurred at ⬍55 years. Each patient underwent electron beam tomographic scanning using an Imatron scanner (Imatron, South San Francisco, California). Coronary arteries were imaged with rapid acquisition of approximately 30 to 40 contiguous images operating with a slice thickness of 3 mm, a spatial resolution of 1.3 mm full-width at half-maximum, a field-of-view of 26 cm, a threshold of 130 HU, and image acquisition of 100 0002-9149/05/$–see front matter doi:10.1016/j.amjcard.2004.10.045
655
The total calcium score was calculated by summing CAC scores from the left main, left anterior descending, left circumflex, and right coronary arteries. RF ⫽ 0 RF ⫽ 1 RF ⱖ2 p Value Age-gender–adjusted median CAC No FH of CHD 14 (12–15) 16 (14–18) 20 (17–23) 0.0001 scores according to FH and increasFH of premature CHD 19 (16–22) 25 (21–28) 39 (33–43) ⬍0.0001 ing numbers of metabolic RFs were compared by median tests. The prevalence of any coronary calcium (positive scores ⬎0), as well as the prevalence of CAC ⱖ100 (moderate calcification)2 and CAC ⱖ75th percentile matched for age and gender,3 was determined in the population across metabolic RFs and FH of premature CHD categories. CAC ⱖ75th percentile for age-gender was considered “advanced CAC.” Logistic regression was used to examine the odds of having CAC associated with increasing metabolic RFs, adjusting for covariates, in the group without any metabolic RFs as the reference. All covariates (age, gender, physical activity, smoking status, and selfreported hypercholesteremia) were forced into the models simultaneously. We tested whether the odds of calcification associated with increasing metabolic RFs were the same in those with and without a FH of premature CHD by including a metabolic RF-by-FH of premature CHD interaction term in the model. All statistical analyses were performed using Stata software, version 8.0 (Austin, Texas). The study population consisted of 6,141 asymptomatic patients (mean age 55 ⫾ 9 years; 68% men) whose baseline characteristics are listed in Table 1. Twenty-six percent of the study population had a FH of premature CHD. Two or more metabolic RFs were presented in 17% of study participants. The age-gender–adjusted median CAC scores across increasing numbers of metabolic RF were higher in patients with a positive FH for premature CHD than in those without a FH, indicating increased coronary atherosclerotic burden (Table 2). The prevalence of any CAC (Figure 1), CAC ⱖ100 (Figure 1), and CAC ⱖ75th age-gender percentile (Figure 1) were all significantly higher with increasing metabolic RF as well with the presence of a FH of premature CHD. The prevalence of any CAC, as well as the extent of CAC, was the lowest among those with no FH of CHD and no metabolic RFs, whereas the highest prevalence was observed among patients with a positive FH of CHD as well ⱖ2 metabolic RFs. The relation persisted after adjusting for covariates among participants with or without a FH of premature CHD (Table 3). The odds ratio for any CAC associated with the presence of ⱖ2 metabolic RFs was significantly higher in those who had a FH of premaFIGURE 1. (A) Prevalence (percent) of any CAC by increasing ture CHD than in those without any FH of CHD. Similar metabolic RFs and categories of FH of premature CHD. (B) Prevainteractions were also observed for CAC ⱖ100 and CAC lence (percent) of CAC >100 by increasing metabolic RFs and ⱖ75th percentile. There was no significant interaction categories of FH of premature CHD. (C) Prevalence (percent) of with gender plus increasing metabolic RFs on CAC; any CAC >75th percentile by increasing metabolic RFs and catealso, effects were similar whether FH of premature CHD gories of FH of premature CHD. was reported in a parent or sibling. ms prospectively triggered at 60% to 80% of the RR ••• (electrocardiographic) interval. CAC was quantified usWe previously described that a FH of premature ing the previously described Agatston scoring method.1 CHD is independently associated with higher burden TABLE 2 Age-gender–adjusted Median (95% CI) Coronary-arterial Calcium Scores according to Metabolic Risk Factors (RFs) and Family History (FH) of Premature Coronary Heart Disease (CHD)
656 THE AMERICAN JOURNAL OF CARDIOLOGY姞
VOL. 95
MARCH 1, 2005
TABLE 3 Odd Ratios (95% confidence intervals) for Presence and Extent of Arterial Coronary Calcium (CAC) With Increasing Metabolic Risk Factors (RFs) Among Subjects With and Without a Family History (FH) of Premature Coronary Heart Disease (CHD) RF ⫽ 1
CAC ⬎0 CAC ⱖ100 CAC ⱖ75th percentile
No FH of CHD
FH of Premature CHD
1.4 (1.0–1.6) 1.3 (1.1–1.7) 1.5 (1.2–1.8)
1.6 (1.3–2.1) 1.3 (1.0–1.8) 1.7 (1.3–2.2)
RF ⱖ2
Interaction
No FH of CHD
FH of Premature CHD
Interaction
1.1 (0.8–1.5) 1.0 (0.7–1.4) 1.1 (0.8–1.5)
2.4 (1.9–2.9) 1.7 (1.4–2.1) 1.9 (1.5–2.4)
3.3 (2.4–4.7) 2.3 (1.6–3.3) 2.8 (2.0–3.7)
1.4 (1.0–2.2) 1.4 (1.0–2.4) 1.5 (1.0–2.2)
Reference category is RF ⫽ 0, adjusted for age, gender, smoking status, hypercholesterolemia, and physical activity.
of CAC.4 Arad et al5 previously described the presence of higher CAC scores with an increasing number of metabolic RFs. Our study extends the findings by demonstrating that patients with a FH of premature CHD were more likely to have a higher burden of coronary atherosclerosis in the presence of multiple (ⱖ2) metabolic RFs than those without any FH of CHD. The presence of just 1 metabolic RF was not associated with a higher risk of CAC among those with a self-reported FH of premature CHD. The results of our study should be interpreted in the context of several limitations. We used self-reported RFs and FH of CHD. Despite the potential for some under-reporting or misclassification of RFs, Hoff et al6 described the validity of self-reported histories of hypercholesterolemia, diabetes, and hypertension in self-referred patients for electron beam tomographic scanning, although the validity of self-reported low high-density lipoprotein cholesterol and high triglycerides is not well studied. Also, because CHD RFs were self-reported, potential “residual confounding” cannot be ruled out. Studies have demonstrated a sensitivity of 68% to 86% and specificities ranging from 86% to 98% for a reported FH of CHD7,8; most likely the bias in recalling a FH of CHD is toward the null.9 In our study, fasting blood glucose was not recorded; as a result, we could not assign a definition of “metabolic syndrome” to the participants. However, it has been recently shown that an increase in the metabolic syndrome score (even if the score is ⬍3) confers an increase in severity of angiographic CHD
and overall cardiac risk.10 In the same study, it was shown that distribution of metabolic RFs follows a Gaussian distribution, and most patients are likely to have a metabolic syndrome score of 2 to 3.10 1. Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte M Jr, Detrano R. Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol 1990;15:827– 832. 2. Rumberger JA, Brundage BH, Rader DJ, Kondos G. Electron beam computed tomographic coronary calcium scanning: a review and guidelines for use in asymptomatic persons. Mayo Clin Proc 1999;74:243–252. 3. Nasir K, Raggi P, Rumberger JA, Braunstein JB, Post WS, Budoff MJ, Blumenthal RS. Coronary artery calcium volume scores on electron beam tomography in 12,936 asymptomatic adults. Am J Cardiol 2004;93:1146 –1149. 4. Nasir K, Michos ED, Rumberger JA, Braunstein JB, Post WS, Budoff MJ, Blumenthal RS. Coronary artery calcification and family history of premature coronary heart disease: sibling history is more strongly associated than parental history. Circulation 2004;110:2150 –2156. 5. Arad Y, Newstein D, Cadet F, Roth M, Guerci A. Association of multiple risk factors and insulin resistance with increased prevalence of asymptomatic coronary artery disease by an electron-beam computed tomographic study. Arterioscler Thromb Vasc Biol 2001;21:2051–2058. 6. Hoff JA, Daviglus ML, Chomka EV, Krainik AJ, Sevrukov A, Kondos GT. Conventional coronary artery disease risk factors and coronary artery calcium detected by electron beam tomography in 30,908 healthy individuals. Ann Epidemiol 2003;13:163–169. 7. Murabito JM, Nam BH, D’Agostino RB Sr, Lloyd-Jones DM, O’Donnell CJ, Wilson PW. Accuracy of offspring reports of parental cardiovascular disease history: the Framingham Offspring Study. Ann Intern Med 2004;140:434 – 440. 8. Watt G, McConnachie A, Upton M, Emslie C, Hunt K. How accurately do adult sons and daughters report and perceive parental deaths from coronary disease? J Epidemiol Community Health 2000;11:859 – 863. 9. Silberberg JS, Wlodarczyk J, Fryer J, Ray CD, Hensley MJ. Correction for biases in a population-based study of family history and coronary heart disease. The Newcastle Family History Study I. Am J Epidemiol 1998;147:1123–1132. 10. Solymoss BC, Bourassa MG, Campeau L, Sniderman A, Marcil M, Lesperance J, Levesque S, Varga S. Effect of increasing metabolic syndrome score on atherosclerotic risk profile and coronary artery disease angiographic severity. Am J Cardiol 2004;93:159 –164.
BRIEF REPORTS
657