Clinical Coronary Heart Disease Research Articles

Cardiovascular Outcomes in Systemic Lupus Erythematosus: Big Studies for Big Questions

Accelerated atherosclerosis is now a well recognized complication of systemic lupus erythematosus (SLE). The overall risk of clinical coronary heart disease (CHD) in women with SLE is estimated to be between 5 and 6-fold greater than in women in the general population1. The prevalence of CHD in lupus cohorts is 6%–10%, and this has remained constant over the last 2 decades1–4. The premature onset of CHD in SLE is also well documented, with the age of first event noted on average to be between 47 and 51 years1,4–6. Several factors contribute to clinical and subclinical CHD in SLE including “classic” Framingham risk factors and SLE-related factors. The Framingham risk factor formula has been shown not to perform as well in SLE compared to a non-SLE cohort for the prediction of coronary events7. A complex interaction involving traditional risk factors, endothelial dysfunction, systemic inflammation, and therapy such as corticosteroids, renal disease and antiphospholipid antibodies is hypothesized to result in accelerated atherosclerosis in SLE. It remains unclear to what extent these risk factors contribute to the risk of CHD and to CHD-related outcomes in SLE. Overall survival in patients with SLE has improved substantially over the last 50 years, with 5-year survival estimates improving from 50% in the 1950s to 93% in 1993 in North American cohorts8,9. The improvement in survival is likely to reflect several factors. Survival rates in the general population have improved, and recognition of SLE and its complications is better and may have resulted in identifying a higher proportion of milder … Address reprint requests to Dr. Bruce. E-mail: ian.bruce{at}manchester.ac.uk

Abnormal T-wave axis is associated with coronary artery calcification in older adults

Objective. To determine whether T-wave axis on the resting electrocardiogram (ECG) is associated with coronary artery calcification (CAC) score, a measurement of coronary atherosclerosis, in older adults. Methods. The sample consisted of 2004 adults aged 66 and over participating in the prospective, population-based Age-Gene/Environment Susceptibility-Reykjavik Study. The cohort was divided into gender-stratified quartiles based upon Agatston CAC score derived from computerized tomography. Frontal T-axis deviation from 45° was assessed using surface ECG. Statistical analysis was performed with Tobit regression models adjusted for demographic and cardiovascular risk factors. Results. In the entire study population, T-axis deviation from 45° was significantly associated with increasing CAC score in men (p<0.001) and women (p=0.03). In men without clinically recognized coronary heart disease (CHD), the association with CAC score remained statistically significant (p=0.02). This association was significant among women without CHD once male CAC cut points were used (p=0.05). Conclusion. An abnormal T-wave axis is associated with an increasing CAC score in this population of Icelandic older adults. This association remains in the subgroup of subjects without clinical CHD.

Progressing From Risk Factors to Omics

Many factors contribute to the development of clinical atherosclerotic disease in adults. Observational studies conducted from the late 1940s onward have helped us to identify cigarette smoking, cholesterol levels, diabetes, blood pressure, and other factors as important determinants of cardiovascular disease (CVD) outcomes.1,2 The effects are multiplicative. For example, smoking, hypertension, and diabetes each double the risk of a heart attack, and having all 3 factors can lead to a risk that was ≈8 times that of an adult of similar age and sex who did not have any of the factors.3 A major focus in the earlier population and clinical studies was identification of persons at increased risk before the clinical atherosclerotic event. Less attention has been directed toward other types of events, such as occurrence of a myocardial infarction in persons presenting with chest pain, recurrent CVD events, and long-term vascular disease complications such as cardiac failure. The determinants of these vascular events are likely to include some of the classical risk factors, but new factors will no doubt be important as well. Improvements in outpatient and inpatient care, diagnosis, and biomarker discovery have reshaped the landscape. It is possible to visualize subclinical CVD with modern atherosclerotic imaging techniques such as carotid intima-media thickness and arterial calcification assessments. Clinical chemists and geneticists identify new biomarkers that promise to help refine assessments of CVD risk, but it is not clear how such tests should be used for research or for clinical care. This article addresses several of the questions posed above and takes the perspective of research and care for clinical atherosclerotic disease, emphasizing the progress we have made from traditional risk factor assessment to the present time that includes newer assessment methods such as genomics, metabolomics, and predictive medicine. ### Traditional Risk Factors for Cardiovascular Disease The traditional risk factors include cholesterol, blood …

Abstract 3262: Impact of the MESA Arterial Age Calculator Incorporating Coronary Calcium on CHD Risk Estimation

Background: The MESA study recently published a web-based calculator for the computation of arterial age incorporating Framingham risk factors and coronary calcium to integrate the incremental predictive value of coronary calcium within the Framingham risk score, a reference-standard clinical coronary heart disease (CHD) risk calculator. We examined the impact of arterial age on the distribution of CHD risk estimation. Methods: We applied CHD risk factor data from the Prospective Army Coronary Calcium Project, a screening cohort of 2000 men and women between the ages of 40 and 50, to the MESA Arterial Age calculator (available at www.mesa-nhlbi.org). Subjects were studied with measured CHD risk factors and electron beam CT for the identification of coronary artery calcium. Framingham risk scores (FRS), using the 10 year CHD risk model with and without arterial age, were calculated using the MESA arterial age calculator. An estimate CHD risk between 6 and 20% was categorized as intermediate risk, and compared for the calculations using chronological age, and arterial age. Results: Demographics of the cohort included mean age 42.9 ± 2.7 yrs, male gender 82%, hypertension 8.0%, systolic blood pressure 123 ± 13 mm Hg, current smoking 7.7%, total cholesterol 203 ± 36 mg/dL, and HDL-C 53 ± 14 mg/dL. Mean FRS was 4.5 ± 3.6%. Coronary calcium was present in 394 subjects (19.7%). Application of the arterial age calculator increased mean age from 42.9 ± 2.7 to 43.6 ± 10.4 years (P &lt; .001), and the mean FRS increased from 4.5 ± 3.6 to 7.3 ± 8.1% (P &lt; .001). Reclassification was seen primarily among male subjects, in whom the mean age (chronological vs. arterial age) increased from 42.9 ± 2.7 to 44.2 ± 11.0 (P &lt; .001) and the prevalence of intermediate CHD risk increased from 26.2% (429 of 1639) to 37.4% (613/1639; P &lt; .001). Among women, mean age (chronological vs. arterial age) was reduced by calcium scoring (42.7 ± 2.6 vs. 40.7 ± 6.3%; P &lt; .001) and a shift to intermediate risk was seen in only 0.6% of subjects (from 10 to 18 out of 349). Conclusions: Among healthy middle-aged individuals, the MESA arterial age calculator modestly shifts predicted CHD risk estimation, and reclassifies 1 in 9 men from low to intermediate risk. Arterial age was lower than chronological age in women.

The risk of marathon runners-live it up, run fast, die young?

Marathon running enjoys an astonishing popularity. Because of the enormous number of applicants, it is quite difficult to get a starting place for one of the marathon races in Berlin, London, or New York. Almost every European city appears to have its own marathon race in the months between April and October. Regularly, out of the tens of thousands of runners, one or two succumb to an acute coronary syndrome or sudden arrhythmias. It is quite evident that the extreme exertion of a marathon race, as mentally rewarding as it may be, offers little benefit in terms of health and longevity. Indeed, in clinically healthy runners, markers of cardiac injury are elevated after a race.1,2 An inverse relationship between myocardial injury and the amount of training for the race has been described, with the greatest amount of injury incurred by runners with the least training mileage.2 However, the clinical relevance of acute post-race elevations in markers of myocardial injury remains open. There is little evidence to suggest permanent cardiac damage in healthy runners, but the issue is complex. With increasingly sophisticated biomarkers and imaging methods to measure cardiac damage—what is a healthy runner? Mohlenkamp and colleagues from the University Clinic Essen, Germany, have collected unique data in 108 male recreational marathon runners aged ≥50 years.3 The runners had completed at least five marathon races during the preceding 3 years and were free of clinical coronary heart disease, diabetes mellitus, and other major cardio-renal disease. An important aspect of this study is that the authors in part are investigators of the Heinz Nixdorf Recall study, a large epidemiological study in the general, unselected population in the Ruhr area in Germany. This ongoing study examines the predictive value of state-of-the-art risk factor analysis compared with … *Corresponding author. Tel: +49 69 9450 28 0, Fax: +49 69 461613, Email: A.Schmermund{at}ccb.de

Alcohol consumption and risk of coronary heart disease among Chinese men

Background Observational studies suggest that moderate alcohol consumption may lower risk of myocardial infarction (MI) and coronary heart disease (CHD); yet, evidence for this comes almost entirely from Western populations. Methods We conducted a prospective cohort study in 64,597 Chinese men aged ≥ 40 years who were free of clinical CHD at baseline examination. Data on frequency and type of alcohol consumed were collected at the baseline examination in 1991 using a standard protocol. Follow-up evaluation was conducted in 1999–2000, with a response rate of 94%. Results Over 494,084 person-years of follow-up, we documented 725 (361 fatal) incident MI and 976 (588 fatal) incident CHD events. After stratification by province to account for multi-stage sampling design and adjustment for age, education, physical activity, cigarette smoking, body mass index, systolic blood pressure, urbanization (urban vs. rural), geographic variation (north vs. south) and history of diabetes, relative risk (95% confidence interval) of MI was 0.93 (0.70–1.24) for participants consuming 1 to 6 drinks/week, 0.66 (0.54–0.82) for those consuming 7 to 34 drinks/week, and 0.58 (0.41–0.81) for those consuming ≥ 35 drinks/week ( p for linear trend < 0.0001) compared to non-drinkers. The corresponding relative risks for CHD events were 0.99 (0.77–1.27), 0.67 (0.56–0.81), and 0.58 (0.44–0.78), respectively ( p for linear trend < 0.0001). Conclusion Alcohol consumption may be related to lower risk of MI and CHD in middle-aged and older Chinese men. However, heavy alcohol consumption may lead to increased mortality from other causes; therefore, the implications of these findings should be interpreted cautiously.

Oxidation, Type 2 Diabetes, and Coronary Heart Disease: A Complex Interaction

OBJECTIVE—The purpose of this study was to analyze the interrelationship among oxidation, myocardial infarction (MI), and type 2 diabetes in a population-based case-control study of MI.RESEARCH DESIGN AND METHODS—Participants were 1,709 individuals from western New York: 257 women and men with incident MI and 1,452 healthy control subjects (aged 35–70 years). Lipid peroxidation was measured by plasma levels of thiobarbituric acid reactive substances (TBARS). History of type 2 diabetes was determined by self-reported history of medical diagnosis.RESULTS—In multivariate analyses, there was no significant difference in TBARS levels between case and control subjects in both sexes. In subgroup analyses by diabetes status, diabetic subjects, regardless of MI status, exhibited significantly higher TBARS values than nondiabetic subjects. For diabetic women, TBARS values were 1.84 and 1.83 nmol/ml for case and control subjects, respectively. Values for nondiabetic women were 1.29 and 1.31 nmol/ml, respectively. In diabetic men, values were 1.65 and 1.97 nmol/ml for case and control subjects, respectively. Values for nondiabetic men were 1.36 and 1.36 nmol/ml, respectively.CONCLUSIONS—Whereas type 2 diabetes may be an important correlate of lipid peroxidation, clinical coronary heart disease may not.

Visceral Adiposity and Subclinical Coronary Artery Disease in Elderly Adults: Rancho Bernardo Study

Despite growing attention to central obesity as a predictor of clinical coronary heart disease (CHD), there are few reports about the association between directly measured visceral obesity and subclinical coronary atherosclerosis in elderly adults. We examined this association in elderly, community-dwelling adults without clinically recognized CHD. Elderly adults (190 men, BMI 27.2 +/- 3.6 kg/m(2); 220 women, BMI 25.8 +/- 4.6) aged 55-88 years (median 69 years) with no history of CHD or coronary revascularization had an electron beam computed tomography (EBCT) to measure coronary artery calcification score (CACS), an estimate of coronary plaque burden. Visceral and subcutaneous adiposity were assessed by a triple-slice EBCT scan at the lumbar 4-5 disc level and height, weight, and waist and hip circumferences were measured. In sex-specific ordinal logistic regression analyses, no measure of obesity or body fat distribution, including BMI, waist-to-hip ratio, waist girth, and visceral and subcutaneous fat by EBCT, was significantly associated with CACS before or after adjusting for multiple covariates of CACS (age, smoking, alcohol intake, exercise, pulse pressure, low-density lipoprotein (LDL)/high-density lipoprotein (HDL)-cholesterol ratio, and fasting plasma glucose). In elderly adults without clinically recognized CHD, body weight and fat distribution do not predict coronary artery plaque burden. These results raise questions about the value of weight reduction diets for preventing heart disease in elderly survivors without clinical heart disease.

Diabetic Retinopathy and Risk of Heart Failure

The purpose of this study was to examine the association of diabetic retinopathy with incident heart failure (HF). Microvascular disease might play a more prominent role in the pathogenesis of diabetic cardiomyopathy, a major cause of HF in diabetes. Whether diabetic retinopathy, a microvascular complication of diabetes, predicts HF is unclear. A population-based study included 1,021 middle-aged type 2 diabetic persons with normal renal function and free of clinical coronary heart disease or HF at baseline. Diabetic retinopathy signs were graded from retinal photographs. Incident HF events were prospectively identified from hospital stay and death records. There were 125 (12.8%) participants with diabetic retinopathy. After 9-year follow-up, 106 (10.1%) participants developed incident HF events. Persons with retinopathy were more likely to develop HF (cumulative incidence of 21.6%) than those without retinopathy (cumulative incidence of 8.5%). After controlling for age, gender, race, smoking, diabetes duration, insulin use, blood pressure, lipid profile, and other risk factors, participants with retinopathy had more than 2.5-fold higher risk of developing HF than those without retinopathy (hazard ratio [HR] 2.71; 95% confidence interval [CI] 1.46 to 5.05). This association remained significant after further adjustments for glycemic control, carotid atherosclerosis, and serum markers of endothelial dysfunction (HR 2.20, 95% CI 1.08 to 4.47). The presence of diabetic retinopathy signifies an excess risk of HF, independent of known risk factors. This further supports a contribution of microvascular disease to the development of HF in people with diabetes.

Relation of Heart Rate Parameters During Exercise Test to Sudden Death and All-Cause Mortality in Asymptomatic Men

Heart rate (HR) profile during exercise predicts all-cause mortality. However, less is known about its relation to sudden (vs nonsudden) death in asymptomatic people. The relation of exercise HR parameters (HR at rest, target HR achievement, HR increase, and HR recovery) with sudden death, coronary heart disease (CHD) death, myocardial infarction, and all-cause mortality was assessed in 12,555 men who participated in MRFIT. Subjects were 35 to 57 years old without clinical CHD, but with higher than average Framingham risk. Trial follow-up was 7 years, and extended follow-up after the trial for all-cause mortality was 25 years. After adjusting for cardiac risk factors, having to stop exercise before achieving 85% of age-specific maximal HR was associated with increased risk of sudden death (hazard ratio 1.8, 95% confidence interval [CI] 1.3 to 2.5, p = 0.001), CHD death (hazard ratio 1.4, 95% CI 1.2 to 1.5, p <0.001), and all-cause mortality (hazard ratio 1.3, 95% CI 1.2 to 1.4, p <0.001). Increased HR at rest (p = 0.001), attenuated HR increase (p = 0.02), delayed HR recovery (p = 0.04), and exercise duration (p <0.0001) were independent predictors of all-cause death in the overall study population and also in the subgroup that achieved target HR. In conclusion, middle-aged men without clinical CHD who stopped exercise before reaching 85% of maximal HR had a higher risk of sudden death. Other exercise HR parameters and exercise duration predicted all-cause mortality.

An apolipoprotein A-I mimetic dose-dependently increases the formation of preβ1 HDL in human plasma

Prebeta1 HDL is the initial plasma acceptor of cell-derived cholesterol in reverse cholesterol transport. Recently, small amphipathic peptides composed of D-amino acids have been shown to mimic apolipoprotein A-I (apoA-I) as a precursor for HDL formation. ApoA-I mimetic peptides have been proposed to stimulate the formation of prebeta1 HDL and increase reverse cholesterol transport in apoE-null mice. The existence of a monoclonal antibody (MAb 55201) and a corresponding ELISA method that is selective for the detection of the prebeta(1) subclass of HDL provides a means of establishing a correlation between apoA-I mimetic dose and prebeta1 HDL formation in human plasma. Using this prebeta1 HDL ELISA, we demonstrate marked apoA-I mimetic dose-dependent prebeta1 HDL formation in human plasma. These results correlated with increases in band density of the plasma prebeta1 HDL, when observed by Western blotting, as a function of increased apoA-I mimetic concentration. Increased prebeta1 HDL formation was observed after as little as 1 min and was maximal within 1 h. Together, these data suggest that a high-throughput prebeta1 HDL ELISA provides a way to quantitatively measure a key component of the reverse cholesterol transport pathway in human plasma, thus providing a possible method for the identification of apoA-I mimetic molecules.

Impaired coronary flow reserve in patients with metabolic syndrome

Background Metabolic syndrome (MetS) is a strong predictor of cardiovascular events. Coronary flow reserve (CFR), as determined by transthoracic echocardiography, is an indicator of microvascular function. In this study, we sought to determine whether CFR is impaired in patients with MetS without clinical coronary heart disease. Methods Thirty-three patients with MetS (mean age, 67 ± 8 years) and 35 age- and sex-matched controls were studied prospectively. Transthoracic two-dimensional and Doppler echocardiography was performed on all patients. Baseline and hyperemic (after dipyridamole infusion) coronary flow rates were measured using pulsed Doppler echocardiography. CFR was calculated as the ratio of hyperemic to baseline diastolic peak velocities. Results There was no difference with regard to baseline systolic and diastolic coronary flow rates in patients with MetS compared with control subjects (19.9 ± 3.1 cm/s vs. 19.7 ± 2.9 cm/s, P > .05; and 27.7 ± 4.2 cm/s vs. 27.1 ± 3.6 cm/s, P > .05, respectively). Hyperemic diastolic flow and CFR were significantly lower in patients with MetS than in controls (61.7 ± 9.4 cm/s vs. 70.2 ± 9.2 cm/s, P < .0001; and 2.2 ± 0.5 vs. 2.6 ± 0.4, P = .001, respectively). In a logistic regression analysis that included age, sex, body mass index, hypertension, and dyslipidemia and MetS, MetS was the only predictor of a CFR < 2.5 ( P = .007, OR = 6.1, 95% CI: 1.6–23.3). Conclusion In conclusion, CFR is impaired in patients with MetS suggesting that coronary microvascular dysfunction, an early finding of atherosclerosis, is present in this patient population. Metabolic syndrome is associated with a CFR < 2.5.

Cardiovascular Risk Factors and Incident Acute Renal Failure in Older Adults

Although the elderly are at increased risk for acute renal failure, few prospective studies have identified risk factors for acute renal failure in the elderly. The associations of cardiovascular disease risk factors, subclinical cardiovascular disease, and clinical coronary heart disease with the risk for development of acute renal failure were examined in older adults in the Cardiovascular Health Study, a prospective cohort study of community-dwelling older adults. Incident hospitalized cases of acute renal failure were identified through hospital discharge International Classification of Diseases, Ninth Revision codes and confirmed through physician diagnoses of acute renal failure in discharge summaries. Acute renal failure developed in 225 (3.9%) of the 5731 patients during a median follow-up period of 10.2 yr. In multivariate analyses, diabetes, current smoking, hypertension, C-reactive protein, and fibrinogen were associated with acute renal failure. Prevalent coronary heart disease was associated with incident acute renal failure, and among patients without prevalent coronary heart disease, subclinical vascular disease measures were also associated with acute renal failure: Low ankle-arm index (< or =0.9), common carotid intima-media thickness, and internal carotid intima-media thickness. In this large, population-based, prospective cohort study, cardiovascular risk factors and both subclinical and clinical vascular disease were associated with incident acute renal failure in the elderly.

Relation of Retinopathy to Coronary Artery Calcification: The Multi-Ethnic Study of Atherosclerosis

Microvascular disease, reflected by retinal vascular changes, has been shown to predict clinical coronary heart disease. Whether retinal vascular changes are associated with subclinical coronary artery disease is unclear and was examined in this study. The authors conducted a multiethnic, population-based study of 6,147 persons aged 45-84 years, sampled from six US communities in 2002-2004, who were free of clinical cardiovascular disease. Coronary artery calcification (CAC), a noninvasive measure of subclinical coronary artery disease, was assessed by cardiac computed tomography scanning and categorized into three groups of increasing severity: none (average CAC score = 0), mild (1-100), and moderate-to-severe (>100). Retinopathy signs and retinal vascular caliber were graded from retinal photographs following standardized protocols. After adjustment for age, gender, race/ethnicity, blood pressure, diabetes, lipid profile, smoking, and other risk factors, retinopathy was associated with having a moderate-to-severe CAC score (odds ratio = 1.43, 95% confidence interval: 1.18, 1.75). This association remained significant in both men and women and in persons with and without diabetes or hypertension. Variations in retinal vascular caliber were not significantly associated with CAC score. This study shows that retinopathy signs are independently associated with CAC, supporting the concept that common pathophysiologic processes may underlie both micro- and macrovascular disease.

Psychological Stress and the Development of Heart Disease

Until recently it was thought that no more than 50% of clinical coronary heart disease was explicable in terms of classical cardiac risk factors such as dyslipidemia, cigarette smoking, high blood pressure and diabetes. Recent large scale epidemiological studies have increased our understanding of the mechanisms generating cardiac risk and have provided evidence indicating that psychosocial factors, including stress at work and at home, financial stress, recent major life events and the presence of depressive illness are involved here, “triggering” clinical cardiovascular events, and possibly also contributing to hypertension and atherosclerosis development. The underlying mechanisms in play are most likely multi factorial in origin, involving the autonomic nervous system, platelet activation, thrombogenesis and endothelial dysfunction. Given that strategies for preventive therapy remain largely unformulated, future research should focus on generating a better understanding of the neurobiology of psychogenic heart disease as a basis for rational and effective therapy.

Association of Back Pain Frequency With Mortality, Coronary Heart Events, Mobility, and Quality of Life in Elderly Women

A 5-year observational cohort design using data from a randomized controlled trial of calcium intervention. To describe the epidemiology of back pain and determine the association of back pain frequency to mortality, coronary heart events, mobility, and quality of life in elderly women. Although back pain is a common physical symptom in the elderly, little is known of its effects and long-term outcomes. The study subjects were 1484 community dwelling Australian women 70 to 85 years of age. At baseline and 5 years, back pain frequency was assessed by self-report, mobility by the Timed Up and Go Test (TUAG) and Quality of Life by the SF-36 questionnaire. The all cause of death data were ascertained from death certificates available for all deaths over 5 years, and incident clinical coronary heart disease (CHD) data were adjudicated from patient diaries verified by primary care physician and medication records. At baseline and 5 years, 21.7% and 26.9% subjects experienced daily back pain (> or = 1/day) and 27.6% and 24.4% subjects experienced frequent back pain (1/mo to 1/day), respectively. Compared with those with infrequent (< 1/mo) back pain, subjects with daily back pain had significantly lower quality of life physical component score and mobility as assessed by TUAG at both baseline and 5 years. Daily back was associated with greater overall mortality risk (hazards ratio = 2.03; 95% confidence interval, 1.14-3.60) and greater risk of CHD mortality and new CHD diagnosis (hazards ratio = 2.13; 95% CI, 1.35-3.34) after adjusted for baseline age. The effects remained significant after further adjustment for cardiovascular risk factors and physical activity level. Daily back pain is associated with reduced quality of life, mobility and longevity and increased risk of coronary heart events. The adverse health effects of chronic back pain deserve greater recognition.

Census-based and personally reported income measures as long-term risk-adjusted mortality predictors

Census-based and personally reported income measures as long-term risk-adjusted mortality predictors

Framingham risk score and prediction of coronary heart disease death in young men

We tested the ability of the Framingham Risk Score (FRS) and the online ATP III risk estimator to estimate risk and to predict 10-year and longer-term coronary heart disease (CHD) death in younger adults (age 18-39 years). Although prediction with individual risk factors has been tested in individuals <30 years, current multivariate risk prediction strategies have not been applied to prediction of clinical CHD in this age range. We included 10,551 male participants of the CHA study who were aged 18 to 39 years and free of baseline CHD and diabetes at enrollment from 1967 to 1973. Risk of CHD was estimated using both FRS and ATP III online risk estimator for each individual. Men were stratified into deciles according to the magnitude of predicted risk calculated from measured baseline risk factors (CHA-predicted risk). Observed CHD mortality rates for 10, 20, and 30 years of follow-up were compared with estimated risks. Death rates of CHD were low across 30 years of follow-up. The FRS remained <10% for all deciles of CHA-predicted risk in the 18- to 29-year-old cohort. Framingham-predicted risk reached 12% only in the 30- to 39-year-old cohort in the highest decile of CHA-predicted risk despite substantial risk factor burden. Neither method classified individuals <30 years as high risk despite substantial risk factor burden. Future clinical guidelines should consider alternative strategies to estimate and communicate risk in populations <30 years.

Fatty Liver and Uric Acid Levels Predict Incident Coronary Heart Disease but Not Stroke among Atomic Bomb Survivors in Nagasaki

Relationships between fatty liver and coronary heart disease (CHD) and stroke risk remain ill defined. We investigated whether fatty liver is a predictor of CHD and stroke risk. Until December 2000 we followed 2,024 atomic bomb survivors (775 men: 62.0 +/- 9.9 years old; 1,249 women: 63.2 +/- 8.4 years old) who had basic examinations between November 1990 and October 1992 for clinical and laboratory CHD risk factors and fatty liver and who were initially free of CHD and stroke. Forty-nine cases of CHD and 84 cases of stroke were observed. At the time of the baseline examinations, significant clinical associations were found between fatty liver and obesity (p<0.001), hypertension (p<0.001), dyslipidemia (p<0.001), and glucose intolerance (p<0.001). A slight but nonsignificant association was found between fatty liver and hyperuricemia (p=0.07) as well. By using multiple Cox regression analyses, age (relative risk [RR] 1.05, 95% confidence interval [CI] 1.01-1.08), smoking (RR 2.20, 95% CI 1.02-4.74), hyperuricemia (RR 2.30, 95% CI 1.08-4.89), and fatty liver (RR 2.53, 95% CI 1.06-6.06) were shown to be significant predictors of CHD, whereas age (RR 1.08, 95% CI 1.06-1.10), smoking (RR 2.06, 95% CI 1.14-3.72), and hypertension (RR 2.14, 95% CI 1.38-3.30) predicted stroke risk. Fatty liver, which clusters clinical and laboratory CHD risk factors, is an independent predictor of CHD, but not of stroke. Fatty liver should be followed as a feature of metabolic syndrome, with the aim of preventing CHD.

Hypothyroidism in coronary heart disease and its relation to selected risk factors

Hypothyroidism (HT) has been found a predictor of cardiovascular diseases. We aimed to ascertain the prevalence of HT in patients with manifest coronary heart disease (CHD), and to establish its association with conventional risk factors. 410 patients, 6-24 months after hospitalization for acute coronary syndrome, and/or revascularization, were included into the cross-sectional study. The prevalence of thyroid dysfunction was found in males and females as follows: overt HT, ie, thyroid stimulating hormone (TSH) > 3.65 mIU/L and free thyroxine (fT4) < 9 pmol/L and/or L-thyroxine substitution, in 2.6% and 8.4%, respectively; subclinical HT (TSH > 3.65, fT4 9-23 and no substitution) in 4.3% and 15.0%, respectively. Higher prevalence of HT was found in females with hypercholesterolemia, and in males and females with concomitant positive thyroid peroxidase antibodies. Hypothyroid subjects had higher total homocysteine in both genders and von Willebrand factor in males only. Hypothyroid females had higher total and LDL cholesterol, and were more often treated for diabetes. HT was found highly prevalent in patient with clinical coronary heart disease, mainly in females, and was associated with several cardiovascular risk factors.