Risk Of Coronary Heart Disease Mortality Research Articles

Subclinical Cardiovascular Disease and Death, Dementia, and Coronary Heart Disease in Patients 80+ Years

BackgroundThe successful prevention and treatment of coronary heart disease (CHD) and stroke has resulted in a substantial increase in longevity, with subsequent growth in the population of older people at risk for dementia. ObjectivesThe authors evaluated the relationship of coronary and other peripheral atherosclerosis to risk of death, dementia, and CHD in the very elderly. Because the extent of vascular disease differs substantially between men and women, sex- and race-specific analyses were included, with a specific focus on women with low coronary artery calcium (CAC) Agatston scores. MethodsWe evaluated the relationship between measures of subclinical cardiovascular disease (CAC, carotid intimal medial thickness, stenosis, and ankle brachial index) and risk of dementia, CHD, and total mortality in 532 participants of the Cardiovascular Health Study-Cognition Study from 1998/1999 (mean age, 80 years) to 2012/2013 (mean age, 93 years). ResultsThirty-six percent of participants had CAC scores >400. Women and African-Americans had lower CAC scores. Few men had low CAC scores. CAC score and number of coronary calcifications were directly related to age-adjusted total mortality and CHD. The age-specific incidence of dementia was higher than for CHD. Only about 25% of deaths were caused by CHD and 16% by dementia. Approximately 64% of those who died had a prior diagnosis of dementia. White women with low CAC scores had a significantly decreased incidence of dementia. ConclusionsIn subjects 80+ years of age, there is a greater incidence of dementia than of CHD. CAC, as a marker of atherosclerosis, is a determinant of mortality, and risk of CHD and myocardial infarction. White women with low CAC scores had a significantly decreased risk of dementia. A very important unanswered question, especially in the very elderly, is whether prevention of atherosclerosis and its complications is associated with less Alzheimer disease pathology and dementia. (Cardiovascular Health Study [CHS]; NCT00005133)

Hyperuricemia and the risk for coronary heart disease morbidity and mortality a systematic review and dose-response meta-analysis.

Considerable controversy exists regarding the association between hyperuricemia and coronary heart disease (CHD). Therefore, we performed a systematic review and dose-response meta-analysis of prospective studies to examine the controversy. Prospective cohort studies with relative risks (RRs) and 95% confidence intervals (CIs) for CHD according to serum uric acid levels in adults were eligible. A random-effects model was used to compute the pooled risk estimate. The search yielded 29 prospective cohort studies (n = 958410 participants). Hyperuricemia was associated with increased risk of CHD morbidity (adjusted RR 1.13; 95% CI 1.05 to 1.21) and mortality (adjusted RR 1.27; 95% CI 1.16 to 1.39). For each increase of 1 mg/dl in uric acid level, the pooled multivariate RR of CHD mortality was 1.13 (95% CI 1.06 to 1.20). Dose-response analysis indicated that the combined RR of CHD mortality for an increase of 1 mg uric acid level per dl was 1.02 (95% CI 0.84 to 1.24) without heterogeneity among males (P = 0.879, I2 = 0%) and 2.44 (95% CI 1.69 to 3.54) without heterogeneity among females (P = 0.526, I2 = 0%). The increased risk of CHD associated with hyperuricemia was consistent across most subgroups. Hyperuricemia may increase the risk of CHD events, particularly CHD mortality in females.

Antidepressant Medication Use and Its Association With Cardiovascular Disease and All-Cause Mortality in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) Study.

Mixed evidence suggests that second-generation antidepressants may increase the risk of cardiovascular and cerebrovascular events. To assess whether antidepressant use is associated with acute coronary heart disease (CHD), stroke, cardiovascular disease (CVD) death, and all-cause mortality. Secondary analyses of the Reasons for Geographic and Racial Differences in Stroke (REGARDS) longitudinal cohort study were conducted. Use of selective serotonin reuptake inhibitors, serotonin and norepinephrine reuptake inhibitors, bupropion, nefazodone, and trazodone was measured during the baseline (2003-2007) in-home visit. Outcomes of CHD, stroke, CVD death, and all-cause mortality were assessed every 6 months and adjudicated by medical record review. Cox proportional hazards time-to-event analysis followed patients until their first event on or before December 31, 2011, iteratively adjusting for covariates. Among 29 616 participants, 3458 (11.7%) used an antidepressant of interest. Intermediate models adjusting for everything but physical and mental health found an increased risk of acute CHD (hazard ratio [HR] = 1.21; 95% CI = 1.04-1.41), stroke (HR = 1.28; 95% CI = 1.02-1.60), CVD death (HR = 1.29; 95% CI = 1.09-1.53), and all-cause mortality (HR = 1.27; 95% CI = 1.15-1.41) for antidepressant users. Risk estimates trended in this direction for all outcomes in the fully adjusted model but only remained statistically associated with increased risk of all-cause mortality (HR = 1.12; 95% CI = 1.01-1.24). This risk was attenuated in sensitivity analyses censoring follow-up time at 2 years (HR = 1.37; 95% CI = 1.11-1.68). In fully adjusted models, antidepressant use was associated with a small increase in all-cause mortality.

Serum Magnesium and the Risk of Death From Coronary Heart Disease and Sudden Cardiac Death.

BackgroundLow serum magnesium has been implicated in cardiovascular mortality, but results are conflicting and the pathway is unclear. We studied the association of serum magnesium with coronary heart disease (CHD) mortality and sudden cardiac death (SCD) within the prospective population‐based Rotterdam Study, with adjudicated end points and long‐term follow‐up.Methods and ResultsNine‐thousand eight‐hundred and twenty participants (mean age 65.1 years, 56.8% female) were included with a median follow‐up of 8.7 years. We used multivariable Cox proportional hazard models and found that a 0.1 mmol/L increase in serum magnesium level was associated with a lower risk for CHD mortality (hazard ratio: 0.82, 95% CI 0.70–0.96). Furthermore, we divided serum magnesium in quartiles, with the second and third quartile combined as reference group (0.81–0.88 mmol/L). Low serum magnesium (≤0.80 mmol/L) was associated with an increased risk of CHD mortality (N=431, hazard ratio: 1.36, 95% CI 1.09–1.69) and SCD (N=217, hazard ratio: 1.54, 95% CI 1.12–2.11). Low serum magnesium was associated with accelerated subclinical atherosclerosis (expressed as increased carotid intima‐media thickness: +0.013 mm, 95% CI 0.005–0.020) and increased QT‐interval, mainly through an effect on heart rate (RR‐interval: −7.1 ms, 95% CI −13.5 to −0.8). Additional adjustments for carotid intima‐media thickness and heart rate did not change the associations with CHD mortality and SCD.ConclusionsLow serum magnesium is associated with an increased risk of CHD mortality and SCD. Although low magnesium was associated with both carotid intima‐media thickness and heart rate, this did not explain the relationship between serum magnesium and CHD mortality or SCD. Future studies should focus on why magnesium associates with CHD mortality and SCD and whether intervention reduces these risks.

Magnesium Levels in Drinking Water and Coronary Heart Disease Mortality Risk: A Meta-Analysis.

Epidemiological studies have demonstrated inconsistent associations between drinking water magnesium levels and risk of mortality from coronary heart disease (CHD); thus, a meta-analysis was performed to assess the association between them. Relevant studies were searched by the databases of Cochrane, EMBASE, PubMed and Web of Knowledge. Pooled relative risks (RR) with their 95% CI were calculated to assess this association using a random-effects model. Finally, nine articles with 10 studies involving 77,821 CHD cases were used in this study. Our results revealed an inverse association between drinking water magnesium level and CHD mortality (RR = 0.89, 95% CI = 0.79–0.99, I2 = 70.6). Nine of the 10 studies came from Europe, and the association was significant between drinking water magnesium level and the risk of CHD mortality (RR = 0.83, 95% CI = 0.69–0.98). In conclusion, drinking water magnesium level was significantly inversely associated with CHD mortality.

The Prognostic Value of Family History for the Estimation of Cardiovascular Mortality Risk in Men: Results from a Long-Term Cohort Study in Lithuania.

AimTo evaluate the additional prognostic value of family history for the estimation of cardiovascular (CVD) mortality risk in middle-aged urban Lithuanian men.MethodsThe association between family history of CVD and the risk of CVD mortality was examined in a population-based cohort of 6,098 men enrolled during 1972–1974 and 1976–1980 in Kaunas, Lithuania. After up to 40 years of follow-up, 2,272 deaths from CVD and 1,482 deaths from coronary heart disease (CHD) were identified. Multivariate Cox proportional hazards models were used to estimate hazard ratios (HR) for CVD and CHD mortality.ResultsAfter adjustment for traditional CVD risk factors, the HR for CVD mortality was 1.24 (95% CI 1.09–1.42) and for CHD mortality 1.20 (1.02–1.42) in men with first-degree relatives having a history of myocardial infarction (MI), compared to men without positive family history. A significant effect on the risk of CVD and CHD mortality was also observed for the family history of sudden cardiac death and any CVD. Addition of family history of MI, sudden death, and any CVD to traditional CVD risk factors demonstrated modest improvement in the performance of Cox models for CVD and CHD mortality.ConclusionsFamily history of CVD is associated with a risk of CVD and CHD mortality significantly and independently of other risk factors in a middle-aged male population. Addition of family history to traditional CVD risk factors improves the prediction of CVD mortality and could be used for identification of high-risk individuals.

Abstract 10804: Incidence and Prognostic Significance of Silent Versus Clinically Manifest Myocardial Infarction in the Atherosclerosis Risk in Communities (ARIC) Study

Background: Differences in the incidence and prognostic significance of silent myocardial infarction (SMI) vs. MI with clinical manifestations (CMI) are not well-established in racially diverse populations. Methods: We compared the incidence of SMI and CMI and their associations with coronary heart disease (CHD) death and death from all causes in 9,498 participants (mean age 54 years, 56.9% women, 20.3% African-American) from the Atherosclerosis Risk in Communities (ARIC) study who were free of cardiovascular disease at baseline visit (1987-89). Incident SMI was defined as ECG evidence of MI without documented CMI occurring after the baseline visit until visit 4 (1996-98). CHD and all-cause deaths were ascertained starting from ARIC visit 4 until 2010 (median follow up 12 years). Results: There were 386 (4.1%) incident CMIs and 317 (3.3%) SMIs. Both CMI and SMI were more common in men (6.8% and 4.3%, respectively) than in women (2.0% and 2.6%, respectively) p<0.001. Although SMI rates were comparable in blacks and whites (3.8% vs.3.2%, respectively), CMI was higher in whites (4.4% vs. 2.8%, respectively), p=0.003. In multivariable adjusted Cox Proportional models, both SMI and CMI (compared to no MI) were associated with increased risk of CHD and all-cause deaths, but the risk was higher in the CMI group ( Table ). A significant interaction by sex was observed; SMI and CMI were associated with higher risk of CHD and all-cause deaths in women compared to men (interaction p-value= 0.014). No significant interactions by age or race were detected. Conclusions: SMI is as common as CMI, and both are associated with increased risk of CHD and all-cause mortality. Racial and sex differences in the distribution of SMI and CMI, as well as sex differences in the prognostic significance of SMI and CMI exist. These findings suggest that an ECG finding of MI in persons without a history of MI may warrant consideration in personalized CHD prevention risk management efforts particularly in women.

Abstract 13699: Cardiovascular Health Impact of Air Pollution Control in Beijing and Urban China: Projections From the Cardiovascular Disease Policy Model-China

Background: Air pollution ranks the 4th among risk factors responsible for China’s avoidable disease burden. We projected the potential cardiovascular health benefits achievable with sustained air quality improvement in Beijing and all of urban China. Methods: Coronary heart disease (CHD) and stroke mortality and life years gained were projected in adults aged 35-84 years in Beijing and urban China using the Cardiovascular Disease Policy Model-China. We simulated two air quality improvement scenarios from 2015-2030, each achieved gradually over 10 years: 1) the 2008 Beijing Olympics fine particle matter (PM2.5) level of 55 μg/m3, and 2) the World Health Organization (WHO) recommendation of 10 μg/m3. For comparison, we simulated a 50% reduction in active and secondhand smoking and reduction of systolic hypertension to 140 mmHg, each over 5 years. Relative risks of CHD, stroke and all-cause mortality associated with long term PM2.5 exposure were obtained from a meta-analysis of observational studies. Systolic blood pressure and smoking relative risks were estimated from China Multi-provincial Cohort Study. Results: PM2.5 reduction to 2008 Olympic levels in Beijing would reduce stroke deaths by 2.7%, CHD deaths by 7.2% over 2015-2030 and would gain life-years on the order of about a third of that projected for a 50% smoking reduction, and a fourth of that projected for systolic hypertension control (Table). However, achieving more aggressive WHO PM2.5 goal would yield greater life year gains than either tobacco or systolic blood pressure control. Achieving 2008 Olympics levels in urban China would prevent 304,000 stroke deaths, 619,000 CHD deaths, and gain 4.2 million life years over 2015-2030. Conclusions: Air pollution is a leading cardiovascular risk factor in Beijing and all urban China. We projected that lowering air pollution to Beijing Olympics level could prevent about 900,000 cardiovascular deaths and gain about 4.2 million life years in urban China by 2030.

Hyperuricemia as risk factor for coronary heart disease incidence and mortality in the general population: a systematic review and meta-analysis.

Previous meta-analyses reported no significant or weak association between hyperuricemia (HU) and coronary heart disease (CHD). We updated the literature search, systematically reviewing retrieved papers. The peer-reviewed literature published from 1965 to December 2014 was searched using Medline and Embase. We included prospective cohort studies involving adults (sample size ≥100) with no cardiovascular disease (CVD) and a follow-up of at least 1 year. Studies were excluded if they considered as outcome the CVD incidence/mortality without separately reporting data on CHD, did not adjusted for major confounders and if the 95% confidence interval (CI) for risk ratio (RR) was not available. Relative risk or hazard ratio estimates, with the corresponding CIs, were obtained. For CHD incidence 12 populations were included (457,915 subjects [53.7% males]). For CHD mortality seven populations were included (237,433 subjects [66.3% males]). The overall combined RR were 1.206 (CI 1.066-1.364, p=0.003) for CHD incidence and 1.209 (CI 1.003-1.457, p=0.047) for CHD mortality, respectively. Subgroup analysis showed a marginal (incidence) and not significant (mortality) association between HU and CHD in men, but an increased risk for CHD incidence and mortality in hyperuricemic women (RR 1.446, CI 1.323-1.581, p<0.0001, and RR 1.830, CI 1.066-3.139, p=0.028, respectively). The risk markedly increases for urate concentrations >7.0 mg/dL. HU appears to increase the risk of CHD events in the general population, mainly in adult women. This finding requires, however, further investigation.

Erectile dysfunction and coronary heart disease.

This narrative review discusses the associations of erectile dysfunction with coronary heart disease (CHD) morbidity and mortality, all-cause death and CHD risk factors. Treatment strategies for erectile dysfunction are also mentioned. Erectile dysfunction shares common pathways and risk factors with vascular diseases. Erectile dysfunction has been reported to independently predict CHD events, thus highlighting its role as a marker of early atherosclerosis. Erectile dysfunction prevalence may be followed by the presentation of CHD symptoms in 2-3 years, and a CHD event may occur in 3-5 years. Furthermore, erectile dysfunction has been associated with stroke, peripheral artery disease, diabetes and chronic kidney disease as well as with several CHD risk factors including hypertension, dyslipidaemia, smoking, obesity, metabolic syndrome, hyperuricaemia, arterial stiffness and obstructive sleep apnea syndrome. On the basis of these data, erectile dysfunction may be regarded as a part of polyvascular disease. Patients with erectile dysfunction are at an increased risk for CHD morbidity and/or mortality as well as for all-cause death. Clinicians should monitor patients with erectile dysfunction by assessing their vascular risk and preventing or adequately treating CHD risk factors. In this context, lifestyle interventions should be recommended in addition to drug treatment to attain better outcomes.

Fruit intake and cardiovascular disease mortality in the UK Women's Cohort Study.

In observational studies, fruit intake is associated with a reduced risk of cardiovascular disease (CVD), though fruit type has been less frequently explored. The aim of the current study was to explore the association between total fruit and fruit subgroup intake according to polyphenol content and CVD mortality in the UK Women's Cohort Study. Total fruit intake (g/day) derived from a 217-item food frequency questionnaire was obtained from 30,458 women (aged 35-69 years) at baseline from 1995-1998. Fruit intakes were sub-categorised according to similarities in polyphenol profile from Phenol Explorer, including berries, citrus, drupes, pomes and tropical fruits. Mortality events were derived from the NHS Central Register. During the mean follow-up period of 16.7 years, 286 fatal CVD deaths [138 coronary heart disease (CHD), 148 stroke] were observed. Survival analysis was conducted using participants free from history of CVD at baseline. Total fruit intake was associated with lower risk of CVD and CHD mortality, with a 6-7 % reduction in risk for each 80 g/day portion consumed (99 % CI 0.89, 1.00 and 0.85, 1.01 respectively). Concerning particular fruit types, the direction of the associations tended to be inverse, but point estimates and tests for trend were not generally statistically significant. However, women in the highest intake group of grapes and citrus experienced a significant reduction in risk of CVD and stroke respectively compared with non-consumers [HR 0.56 (99 % CI 0.32, 0.98) and 0.34 (0.14, 0.82) respectively]. These findings support promoted guidelines encouraging fruit consumption for health in women, but do not provide strong evidence to suggest that fruit type is as important.

A wide QRS/T angle in bundle branch blocks is associated with increased risk for coronary heart disease and all-cause mortality in the Atherosclerosis Risk in Communities (ARIC) Study

BackgroundRepolarization abnormality in bundle branch blocks (BBB) is traditionally ignored. This study evaluated the prognostic value of QRS/T angle for mortality in the presence and absence of BBB. Methods and resultsTotal 15,408 participants (mean age 54years, 55.2% women, 26.9% blacks, 2.8% with BBB) were from the Arteriosclerosis Risk in Communities Study. Sex stratified Cox regression models were used to compute hazard ratios (HRs) with 95% confidence intervals (CIs) for coronary heart disease (CHD) and all-cause mortality for wide spatial QRS/T angle with and without BBB including right BBB (RBBB), left BBB (LBBB) and indetermined-type ventricular conduction defect (IVCD) and RBBB combined with left anterior fascicular block. During a median 22-year follow-up, 4767 deaths occurred, 728 of them CHD deaths. Using the No-BBB with QRS/T angle below median value as gender-specific reference groups, the mortality risk increase was significant for both women and men with No-BBB and QRS/T angle above the median value. In the pooled ICVD/LBBB group, the risk for CHD death was increased 15.9-fold in women and 6.04 fold in men, and for all-cause deaths 3.01-fold in women and 1.84-fold in men. However, the mortality risk in isolated RBBB group was only significantly increased in women but not in men. ConclusionA wide spatial QRS/T angle in BBB is associated with increased risk for CHD and all-cause mortality over and above the predictive value for BBB alone. The risk for women is as high as or higher than that in men.

Association between sauna bathing and fatal cardiovascular and all-cause mortality events.

Sauna bathing is a health habit associated with better hemodynamic function; however, the association of sauna bathing with cardiovascular and all-cause mortality is not known. To investigate the association of frequency and duration of sauna bathing with the risk of sudden cardiac death (SCD), fatal coronary heart disease (CHD), fatal cardiovascular disease (CVD), and all-cause mortality. We performed a prospective cohort study (Finnish Kuopio Ischemic Heart Disease Risk Factor Study) of a population-based sample of 2315 middle-aged (age range, 42-60 years) men from Eastern Finland. Baseline examinations were conducted from March 1, 1984, through December 31, 1989. Frequency and duration of sauna bathing assessed at baseline. During a median follow-up of 20.7 years (interquartile range, 18.1-22.6 years), 190 SCDs, 281 fatal CHDs, 407 fatal CVDs, and 929 all-cause mortality events occurred. A total of 601, 1513, and 201 participants reported having a sauna bathing session 1 time per week, 2 to 3 times per week, and 4 to 7 times per week, respectively. The numbers (percentages) of SCDs were 61 (10.1%), 119 (7.8%), and 10 (5.0%) in the 3 groups of the frequency of sauna bathing. The respective numbers were 89 (14.9%), 175 (11.5%), and 17 (8.5%) for fatal CHDs; 134 (22.3%), 249 (16.4%), and 24 (12.0%) for fatal CVDs; and 295 (49.1%), 572 (37.8%), and 62 (30.8%) for all-cause mortality events. After adjustment for CVD risk factors, compared with men with 1 sauna bathing session per week, the hazard ratio of SCD was 0.78 (95% CI, 0.57-1.07) for 2 to 3 sauna bathing sessions per week and 0.37 (95% CI, 0.18-0.75) for 4 to 7 sauna bathing sessions per week (P for trend = .005). Similar associations were found with CHD, CVD, and all-cause mortality (P for trend ≤.005). Compared with men having a sauna bathing session of less than 11 minutes, the adjusted hazard ratio for SCD was 0.93 (95% CI, 0.67-1.28) for sauna bathing sessions of 11 to 19 minutes and 0.48 (95% CI, 0.31-0.75) for sessions lasting more than 19 minutes (P for trend = .002); significant inverse associations were also observed for fatal CHDs and fatal CVDs (P for trend ≤.03) but not for all-cause mortality events. Increased frequency of sauna bathing is associated with a reduced risk of SCD, CHD, CVD, and all-cause mortality. Further studies are warranted to establish the potential mechanism that links sauna bathing and cardiovascular health.

Abstract MP44: Leukocyte Telomere Length and Risks of Incident Coronary Heart Disease and Mortality in a Racially Diverse Population

Background: Telomeres are nucleotide repeat regions at the ends of chromosomes that maintain chromosomal structural integrity and genomic stability. Telomeres from circulating leukocytes can be readily measured; mean leukocyte telomere length (LTL) tends to decrease with age, vary by race/ ethnicity and is a putative marker of cellular aging. In studies of mainly white populations, shorter LTL has been associated with cardio-metabolic risk factors and increased risks of mortality and coronary heart disease (CHD), yet it is not clear whether these findings extend to other race/ethnicity groups. We sought to assess the relationship of LTL with risks of incident CHD and total mortality in a racially diverse population of post-menopausal women. Methods: Using a nested case-cohort design, African American (AA) and white women with incident CHD or mortality during a maximal follow-up of 19.4 years were randomly selected from the Women’s Health Initiative. LTL from baseline blood samples was assayed by Southern blotting. Race-stratified and risk factor-adjusted Cox proportional hazards models, weighted to account for the sampling scheme, were used to estimate the hazard of CHD or mortality. Results: A total of 1,525 women (858 whites and 667 AA) were included in the analyses. In whites, there were 367 incident CHD (292 mortality) events, while AA experienced 269 incident CHD (265 mortality) events. Cross-sectional LTL associations (p&lt;0.05) with age, current smoking, and US recruitment region were observed in AA, whereas in whites, LTL was associated with age, current smoking and HDL cholesterol. Whites with longer LTL at baseline were less likely to have incident CHD, HR=0.58 (95%CI: 0.40-0.84), p=0.004, yet no significant association was observed in AA, HR=1.07 (95%CI: 0.71-1.61), p=0.74. This LTL-CHD association varied significantly by race/ethnicity, p=0.028. Similar trends were observed for total mortality, with longer LTL associated with reduced hazard in whites, HR=0.70 (95%CI: 0.46-1.06), but a slightly increased hazard in AA, HR=1.10 (95%CI: 0.80-1.53), though neither association was significant. In exploratory analyses of cause-specific mortality, increased LTL was associated with an increased, but non-significant hazard of cancer mortality in both AA and whites, p=0.17 and 0.28 respectively. Conclusion: We describe LTL associations with incident mortality, CHD and cardiovascular risk factors in post-menopausal women; these findings appear to vary by race/ethnicity. As a marker of chronic inflammation and cellular stress, LTL is robustly associated with CHD in whites, even after adjustment for cardio-metabolic risk factors including C-reactive protein, yet it does not appear to be associated with CHD in AA. Future studies exploring these race-specific differences may be warranted.

Isolated Systolic Hypertension in Young and Middle-Aged Adults and 31-Year Risk for Cardiovascular Mortality: The Chicago Heart Association Detection Project in Industry Study

BackgroundIsolated systolic hypertension (ISH), defined as systolic blood pressure (SBP) ≥140 mm Hg and diastolic blood pressure (DBP) <90 mm Hg, in younger and middle-aged adults is increasing in prevalence. ObjectiveThe aim of this study was to assess the risk for cardiovascular disease (CVD) with ISH in younger and middle-aged adults. MethodsCVD risks were explored in 15,868 men and 11,213 women 18 to 49 years of age (mean age 34 years) at baseline, 85% non-Hispanic white, free of coronary heart disease (CHD) and antihypertensive therapy, from the Chicago Heart Association Detection Project in Industry study. Participant classifications were as follows: 1) optimal-normal blood pressure (BP) (SBP <130 mm Hg and DBP <85 mm Hg); 2) high-normal BP (130 to 139/85 to 89 mm Hg); 3) ISH; 4) isolated diastolic hypertension (SBP <140 mm Hg and DBP ≥90 mm Hg); and 5) systolic diastolic hypertension (SBP ≥140 mm Hg and DBP ≥90 mm Hg). ResultsDuring a 31-year average follow-up period (842,600 person-years), there were 1,728 deaths from CVD, 1,168 from CHD, and 223 from stroke. Cox proportional hazards models were adjusted for age, race, education, body mass index, current smoking, total cholesterol, and diabetes. In men, with optimal-normal BP as the reference stratum, hazard ratios for CVD and CHD mortality risk for those with ISH were 1.23 (95% confidence interval [CI]: 1.03 to 1.46) and 1.28 (95% CI: 1.04 to 1.58), respectively. ISH risks were similar to those with high-normal BP and less than those associated with isolated diastolic hypertension and systolic diastolic hypertension. In women with ISH, hazard ratios for CVD and CHD mortality risk were 1.55 (95% CI: 1.18 to 2.05) and 2.12 (95% CI: 1.49 to 3.01), respectively. ISH risks were higher than in those with high-normal BP or isolated diastolic hypertension and less than those associated with systolic diastolic hypertension. ConclusionsOver long-term follow-up, younger and middle-aged adults with ISH had higher relative risk for CVD and CHD mortality than those with optimal-normal BP.

Joint Effects Of Serum 25(OH) D And C-Reactive Protein Concentration On Coronary Heart Disease And All-Cause Mortality In Patients With Diabetes Mellitus

The study aimed to examine the joint predicting effect of serum 25(OH) D (a biomarker of vitamin D level in blood) and C-reactive Protein (CRP) concentration on the risk of mortality from Coronary Heart Disease (CHD) and all-causes in patients with type 2 Diabetes Mellitus (T2DM) using data from the third National Health and Nutrition Examination Survey (NHANES III). Of 14965 subjects aged ≥ 30 years who participated in the NHANESIII, 2146 patients with T2DM at baseline (1988-1994) were followed up through December 31 of 2006. The associations of baseline serum 25(OH) D and CRP with outcomes were examined prospectively using Cox’s hazard proportional regression models. The results show that during a median follow-up of 12.3 years, 1257 (58.6%) of the patients with T2DM died, and 370 deaths were from CHD. Multivariate adjusted Cox’s models indicate that decreased 25(OH) D level significantly predicted risk of death. The corresponding hazard ratios for the risk of CHD mortality among those with serum 25(OH) D levels 20-29.9, 10-19.9, and <10 ng/mL were 1.35, 1.38 and 2.19, as compared to those with 25(OH) D ≥ 30 ng/mL, respectively. Similar associations between decreased 25(OH) D and risk of all-cause mortality were observed. Furthermore, a joint effect of decreased 25(OH) D and increased CRP significantly predicted an increased risk of CHD and all-cause mortality. In conclusion, using data from a nationally representative and longitudinal survey, findings from the study suggest that decreased serum vitamin D and increased CRP concentrations significantly predicted the risk of CHD and all-cause mortality in patients withT2DM.

Thyroid function within the normal range and risk of coronary heart disease: an individual participant data analysis of 14 cohorts.

Some experts suggest that serum thyrotropin levels in the upper part of the current reference range should be considered abnormal, an approach that would reclassify many individuals as having mild hypothyroidism. Health hazards associated with such thyrotropin levels are poorly documented, but conflicting evidence suggests that thyrotropin levels in the upper part of the reference range may be associated with an increased risk of coronary heart disease (CHD). To assess the association between differences in thyroid function within the reference range and CHD risk. Individual participant data analysis of 14 cohorts with baseline examinations between July 1972 and April 2002 and with median follow-up ranging from 3.3 to 20.0 years. Participants included 55,412 individuals with serum thyrotropin levels of 0.45 to 4.49 mIU/L and no previously known thyroid or cardiovascular disease at baseline. Thyroid function as expressed by serum thyrotropin levels at baseline. Hazard ratios (HRs) of CHD mortality and CHD events according to thyrotropin levels after adjustment for age, sex, and smoking status. Among 55,412 individuals, 1813 people (3.3%) died of CHD during 643,183 person-years of follow-up. In 10 cohorts with information on both nonfatal and fatal CHD events, 4666 of 48,875 individuals (9.5%) experienced a first-time CHD event during 533,408 person-years of follow-up. For each 1-mIU/L higher thyrotropin level, the HR was 0.97 (95% CI, 0.90-1.04) for CHD mortality and 1.00 (95% CI, 0.97-1.03) for a first-time CHD event. Similarly, in analyses by categories of thyrotropin, the HRs of CHD mortality (0.94 [95% CI, 0.74-1.20]) and CHD events (0.97 [95% CI, 0.83-1.13]) were similar among participants with the highest (3.50-4.49 mIU/L) compared with the lowest (0.45-1.49 mIU/L) thyrotropin levels. Subgroup analyses by sex and age group yielded similar results. Thyrotropin levels within the reference range are not associated with risk of CHD events or CHD mortality. This finding suggests that differences in thyroid function within the population reference range do not influence the risk of CHD. Increased CHD risk does not appear to be a reason for lowering the upper thyrotropin reference limit.

Glycemic load and coronary heart disease in a Mediterranean population: The EPIC Greek cohort study

Background and aimsHigh glycemic load (GL) has been associated with increased coronary heart disease (CHD) risk. We evaluated whether preference of low-GL foods conveys incremental benefits with respect to CHD, especially to people adhering to the traditional Mediterranean diet (MD). Methods and resultsWe analyzed data from the Greek European Prospective Investigation into Cancer and Nutrition, including 20,275 participants free of cardiovascular diseases, cancer, or diabetes at baseline and without incident diabetes. Subjects completed a validated, semi-quantitative food frequency questionnaire at enrollment. We calculated a 10-point MD adherence score and the dietary GL, and estimated hazard ratios (HRs) for CHD incidence and mortality through Cox proportional hazard regression. After a median follow-up of 10.4 years, 417 participants developed CHD, and 162 died from the disease. A significant positive association of GL with CHD incidence emerged (HR for the highest versus the lowest tertile = 1.41, 95% confidence interval, CI: 1.05–1.90). HRs for CHD mortality exceeded unity but were not statistically significant. The association with GL was stronger among subjects with higher body mass index. High adherence to MD with low/moderate GL was associated with lower risk of CHD incidence (HR = 0.61, CI: 0.39–0.95) and mortality (HR = 0.47, 95% CI: 0.23–96). ConclusionHigh dietary GL increases the risk of CHD. Compared to a high GL diet with suboptimal adherence to the traditional Mediterranean pattern, a low/moderate GL diet that also conforms to the traditional MD principles could lead to a 40% reduced risk for CHD, and over 50% reduced risk for death from CHD.

Is inflammatory chronic obstructive pulmonary disease a coronary heart disease risk equivalent? A longitudinal analysis of the third National Health and Nutrition Examination Survey (NHANES III), 1988-1994.

BackgroundEvidence suggests that there is an association between chronic obstructive pulmonary disease (COPD) and coronary heart disease (CHD). An important etiological link between COPD and CHD may be an underlying systemic inflammatory process. Given that COPD patients are at greater risk of cardiovascular mortality, understanding the burden of CHD on COPD patients could permit future risk attenuation.MethodsLongitudinal cohort analyses of the Third National Health and Nutrition Examination Survey from 1988–1994 were performed. 3,681 individuals ≥40 years of age with good quality spirometry data were included. Participants were divided into 5 groups: 1) no COPD, no CHD; 2) COPD without inflammation, no CHD; 3) COPD with inflammation, no CHD; 4) CHD only, and 5) CHD + COPD. A novel “inflammatory” COPD designation included those with COPD and clinical evidence of inflammation (i.e., CRP ≥95.24 nmol/L).ResultsThe risk for CHD mortality was significant only for the CHD group (HR 5.56, 95% CI 3.24-9.55) and the COPD + CHD group (HR 5.02, 95% CI 2.83-8.90). Similarly, the risk for cardiovascular disease (CVD) mortality was significant only for the CHD group (HR 4.25, 95% CI 2.70-6.69) and the CHD + COPD group (HR 4.12, 95% CI 2.60-6.54) after adjusting for nonmodifiable CHD risk factors (age, gender, race/ethnicity, family history of CHD). After adjusting for modifiable CHD risk factors (diabetes, BMI, physical activity, systolic blood pressure, cholesterol, and smoking), hazard ratios of the two groups remained similar but attenuated. For total mortality, the risk was significant for the four groups: the non-inflammatory COPD group; the COPD with inflammation group, the CHD group, and the COPD + CHD group.ConclusionsOur study did not confirm that inflammatory COPD may be a CHD risk equivalent. However, due to the small size of the “inflammatory” COPD group, further prospective replication and validation is needed. Moreover, given that COPD results from inflammation, the systemic inflammation associated with COPD may have worsened comorbid conditions and may have lead to the increased total mortality found in the COPD with inflammation and COPD + CHD groups which requires further investigation.

Abstract 16743: Sauna Bathing, Sudden Cardiac Death and Cause-Specific Cardiovascular Mortality

Introduction: Warm sauna bathing is associated with a better hemodynamic function; however, the association of sauna bathing with fatal cardiovascular outcomes is not known Hypothesis: The frequency and duration of sauna bathing may be related to the risk of sudden cardiac death (SCD), fatal coronary heart disease (CHD) and cardiovascular disease (CVD) events. Methods: This study is based on 2323 (42 to 60 years) participants from the Kuopio Ischemic Heart Disease risk factor study, which is a population-based sample of men from Eastern Finland. During median follow-up of 20.7 years (interquartile range 18.1-22.6 years), a total of 197 SCDs, 282 fatal CHD and 407 CVD events occurred. Results: Frequency, duration, and temperature of sauna bathing were assessed at baseline; 1060 participants reported using sauna once weekly, 1054; 2-3 times per week and 201; 4-7 per week, respectively. After adjustment for conventional CVD risk factors, compared to men reporting 1 sauna per week the hazard ratio (HR) of SCD was 0.87 (95% confidence interval, CI 0.64 to 1.18) for 2-3 sauna/week and 0.46 (95% CI 0.23 to 0.89) for 4-7 sauna/week (p=0.036 for linear trend). Compared to men using sauna 19 minutes per session (highest third) (p=0.002 for linear trend). Similar results were found for the associations between frequency or duration of sauna bathing with fatal CHD or CVD events. Conclusions: The frequency and duration of sauna are associated with a substantial reduced risk of SCD, CHD and CVD mortality. Further studies are warranted to define the potential mechanism behind these associations.